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          THE CENTRAL NERVOUS                        PRIMARILY AFFECTING                  AND MOVEMENT               DISEASES OF THE NERVOUS
          SYSTEM                                     CENTRAL NERVOUS SYSTEM               DISORDERS                  SYSTEM
           Meningitis                                Huntington’s                        Parkinson’s               Alzheimer’s Disease
           Encephalitis                              Inherited Cerebral Ataxia            Disease

          NERVOUS SYSTEM                                                                                             DEMYELINATING DISEASES OF
           Hydrocephalus                                                                                            THE CENTRAL NERVOUS
                                                                                                                      Multiple Sclerosis
          CEREBRAL PALSY AND OTHER                                                                                    Neuromyelitis Optica
           Cerebral Palsy
           Plegias                                               WHO INTERNATIONAL
                                                                  CLASSIFICATION OF
                                                                                                                     EPISODIC AND PAROXYSMAL
                                                                   DISEASE (ICD-10):                                 DISORDERS
                                                                   NERVOUS SYSTEM                                     Epilepsy
          JUNCTION AND MUSCLE                                                                                         Migraine
           Myasthenia Gravis                                                                                         Headache Syndromes
           Muscular Dystrophies                                                                                      Sleep Disorders
           Congenital Myopathy

          THE PERIPHERAL NERVOUS SYSTEM                                       Trigeminal Neuralgia
           Inherited: Charcot-Marie-Tooth; Déjerine-Sottas                   Facial Nerve Disorders: Bell’s Palsy
           Inflammatory: Guillain-Barré syndrome                             Other Cranial Nerve Disorders (exc II + VIII)
           More: See Polyneuropathies                                        Nerve Root Compressions
                                                                              Mononeuropathies- Upper limb: Carpel Tunnel Syndrome
                                                                              Mononeuropathies- Lower limb: (exc sciatica)

 PRESYNCOPE & SYNCOPE                                                                               compromising heart filling time and bradycardias by causing a
 Def      Transient LOC associated with  cerebral blood flow.                                     low cardiac output (cardiac output=heart rate x stroke volume).
 PP       30% lifetime risk.                                                                               Bradycardia: Ischaemia / Fibrosis of conduction. Heart
 Cause    Cardiac / Non Cardiac. Cardiac assoc with > mortality. May                                       block (Sycope due to HB is named a Stokes-Adams
            sudden death                                                                                     attack). Drugs: Digitalis, β blockers, Ca channel
 Non      VASOVAGAL SYNCOPE (aka Neurocardiogenic)                                                          blockers. Tx: Pacemaker.
 Crdiac   Most common form in Young people. Normal physiology…                                             Tachycardia (11% all syncope): Divided: VT or SVT.
 Cause                                                                                                     Other causes: Recreational Drugs: Cocaine,
                    / BP is sensed by Aortic Arch Baroreceptors                                            Amphetamines.
                                                                                                           ECG useful but definitive Dx only if temporal
                  Respective: / Sympathetic drive via vagus nerve                                          relationship b/w symptoms and arrhythmia.
                                                                                                STRUCTURAL HEART DISEASE (MECHANICAL)
                   Respective: Vasoconstriction / dilation + / HR                                         Exertion  Light-headedness / Syncope…
                                                                                                           Causes: Severe aortic / mitral stenosis (> common
                                Respective: / BP                                                           causes), Hypertrophic Cardiomyopathy, Critical
                                                                                                             coronary artery disease, Obstructed vessels (PE)
               In Vasovagal syndrome,  BP is not compensated by this                S&S        Light headedness  Vision darkens, Ringing in ears.
                reflex (Bezold-Jarisch reflex), probably due to vagal                            Cardiac              Vasovagal            Neurogenic
                overactivation after initial adrenergic response. Triggered by       S&S        Light-headed,        Light-headed,        Confusion, Headache,
                Venous return:                                                                   Palpitations,        Nausea,              Hyperexcitability, Olfactory
                       Emotionally charged event                                                Pale, Chest          Sweating             hallucinations, Aura.
                       Prolonged standing                                                       Pain, SOB
                        Heat                                                       LOC        Extreme death        Pallor. Gradual      Prolonged (>1min) LOC,
                       Large meal                                                               like pallor          and brief.           Motor seizure activity,
                       Urinating (micturition syncope)                                                                                    Tongue biting, Urinary
                       Defecating (defecation syncope)                                                                                    Incontinence.
                       Swallowing (deglutition syncope)                              Recovery   Rapid (<1 min),      Slow, Nausea,        Prolonged, Confusion
                       Coughing (cough syncope)                                                 Flushing             Light-               (>5mins), Headache,
                       Post-exercise/Post-prandial syncope                                                           headedness.          Focal neurological signs.
             Dx: Tilt Table test (70o angle for 45 mins)                             DDx        See Causes
             Tx: Often unnecessary but BBlockers in severe cases.                    Inv /    ECG     Arrhythmia
             HYPERSENSITIVE CAROTID SINUS SYNDROME                                   Dx       U&E     Assessing hydration status and rule electrolyte disorders
                       Hypersensitivity of cardotid sinus baroreceptors may          Mx         Supine position, legs slightly elevated, loosen clothing
                           recurrent episodes of  consciousness by                             If necessary: Rehydration and correct ions e.g. Na, K
                          promoting inappropriate bradycardia + vasodilation.                    Pacemaker for bradyarrhythmias, Catheter mediated ablation
                                                                                                    for tachyarrhythmias
                       Causes: Mechanical deformation of CS in turn caused
                          by: Looking up, Turning Head, Wearing Tight Collar.
                       Dx: ECG and Sinus massage.                                    HEADACHE & FACIAL PAIN
             POSTURAL (aka Orthostatic) HYPERTENSION                                 Path    AREAS SENSITIVE TO PAIN: dura (inc dural sinsuses, falx
                                                                                                  cerebri), proximal parts of large pial blood vessels.
                       Caused by failure of N compensatory mechanisms.
                                                                                                         Mainly innervated by following: Trigeminal and Upper
                       Dx:  at least 20 mm Hg in systolic blood pressure
                                                                                                            Cervical nerves…accounts for pain referral when
                          when moving from a supine to a standing position.
                                                                                                            sensitive parts are stretched, distended, irritated.
                       Triggered by:
                                                                                              AREAS INSENSITIVE TO PAIN: Brain parenchyma, pial
                                  Relative hypovolaemia…Most common
                                                                                                  arteries over convexities, cerebral ventricles, choroid plexus.
                                    cause (Excessive diuretics)
                                  Sympathetic degeneration (Dm, PD, Age)             S&S     ACUTE...Suddenly:
                                  Other drugs (vasodilators, antidepressants)                           SAH: See CCC: SAH.
 Crdiac   CARDIAC SYNCOPE: Caused by sudden decline in Cardiac output                                    Migraine variant.
 Cause      Cerebral perfusion. May be provoked by exertion with aortic                                Meningitis: Less dramatic in onset.
          stenosis or out of blue with heart block.                                           ACUTE…Hours: Less likely to be assoc with structural disease.
             ARRHYTHMIA: (Most common cause of Syncope / Dizziness)                              More likely to be due to…
             Rates < 180 or > 135 do not compromise cerebral blood flow.                                Migraine (unless other S&S).
             HR outside this range   CBF. Tachycardias do this by                                     Meningitis: Normally assoc with meningism S&S.
                                                                                              CHRONIC…weeks or more:
WILL WESTON                                                                                                                                          Page 1 of 18
                                                                                                           occur so don’t be put off if -ve).
       TENSION HEADACHE                                                                                    Methotrexate if relapse (30%)
       Features        Constant, Generalised, Often radiating from                         Comp           Immediate risk is blindness, but long term steroids
                        occiput.                                                                            is main cause of mortality / morbidity
                       Dull / Tight / Band.                                                POST LUMBAR PUNCTURE ( PRESSURE HEADACHE)
                       Progressively worse throughout day.                                 Features      
                       Normal activities may be carried out, less                          Timing        
                        noticeable when occupied.                                           Assoc         
                       Unresponsive to simple analgesia.                                   Precipitating 
       Timing          May continue for months without interruption.                       MENINGITIS: See elsewhere
                        Contrast to migraine.
       Assoc           Emotional strain, Anxiety                               VISUAL FIELD LOSS (See: Systems: Nervous- Cranial Nerves)
       Precipitating   Excessive analgesics may worsen.                           On way to primary visual area in occipital cortex
                       Contraction of neck / scalp muscle. Stress. Eye                    Lower fibres pass through temporal lobe  UQopia*
                        strain. Sleeping in funny uncomfortable position.                  Upper fibres pass through parietal lobe  LQopia*
       PP              Most common.                                               Low = UQ and High = LQ due to flipping of image.
       Treatment        Anxiety. Excessive analgesia may worsen S&S.             Transient Visual loss: Vascular cause likely if loss lasts 1-20 mins.
                       Muscle relaxation +/- Amitriptyline.                              Carotid Circulation: Uniocular
       MIGRAINES                                                                           Vertebrobasilar Circulation: Homonymous Hemianopia
       Features        Triad of Paroxysmal headache, Nausea +/-                   Transient Visual loss: Migraine likely if loss lasts 20-30 mins.
                        vomiting, Aura (20 mins) of focal neurological.         Site      Cause              PC                  Loss           Assoc
                        (Classical = all three, Common = Without Aura.)         Retina /      Vascular             Partial /           Altituninal      Acuity
                       Often persisting for several days.                      Optic          disease              Complete             field defect    Visual distortion
       Timing          Likely if intermittent                                  Disc          Glaucoma             visual loss         Arcuate         Abnormal retinal
       Assoc           Prodrome: Malaise, Irritability                                       Inflammation         depending on         scotoma          appearance
                       Assoc: Vomiting, Photophobia, Transient Aphasia
                                                                                Optic           Optic neuritis     Partial /           Central          Acuity
                        (if dominant lobe affected).                            Nerve           Sarcoidosis        Complete loss        Scotoma          Colour vision
                       Aura: Visual- Ziz zag lines, vision loss                                Tumour             of vision in one    Paracentral     Rel Afferent
                       Aura: Sensory- Numbness moving from one part to                         Leber’s            eye. Often           scotoma          pupilliary defect
                        other                                                                    hereditary optic   painful. Central    Uniocular       Optic atrophy
       Precipitating   CHOCOLATE, CHeese, Oral Contraceptive,                                   neuropathy         vision affected      blindness        (late)
                        Caffeine, AlcohOL, Anxiety, Travel, Exercise.
                                                                                Optic         Pituitary tumour     May be none.       Bitemporal        Pituitary function
                        Cerebral Blood Flow  Aura                            Chiasm        Craniopharyngi       Rarely diplopia    hemianopia         abnormalities
                        Cerebral Blood Flow  Migraine                                       oma
       PP              Lifetime prevalence: 20% ♀:6% ♂                                       Sarcoidosis
                       Over 90% have first attack by 40.                       Optic         Tumour               Disturbed          Incongrous        NA
       Cause           FHx, Hormonal (Menstrual related, ♀>♂, assoc            Tract         Inflammatory         vision to one      contralateral
                                                                                               disease              side of midline    homonymous
                        with pill),                                                                                                    hemianopia
       Treatment       Avoid precipitants.                                     Temporal      Stroke               Disturbed          Contralateral     Memory / Lang
                       Acute: Simple analgesia (aspirin, Paracetamol,          Lobe          Tumour               vision to one      homonymous         disorders
                        Antiemetics e.g. Metclopramide). Avoid long term                      Inflammatory         side of midline    upper
                        use of codeine.                                                        disease                                 quadrantopia
                       Severe: Triptans (serotonin agonists)                   Parietal      Stroke               Disturbed          Contralateral     Contralateral
                                                                                Lobe          Tumour               vision to one      homonymous         sensory
       CLUSTER HEADACHE (MIGRAINOUS NEURALGIA)                                                Inflammatory         side of midline.   upper              disturbance.
       Features        Periodic, severe, unilateral periorbital pain.                         disease              Bumping into       quadrantopia       Asymmetry of
       Timing          Brief (30-90 mins), often at same time of day esp                                           things.                               optokinetic
                        early morning. May occur repeatedly (clusters) for                                                                                nystagmus.
                        weeks and then disappear for months.                    Occipital     Stroke               Disturbed          Homonymou         Damage to other
                                                                                Lobe          Tumour               vision to one      s hemianopia       structures
       Assoc           Conjunctival injection, unilateral lacrimation, nasal                 Inflammatory         side of midline    (may be mac        supplied by
                        congestion / rhinorrhoea, Horner’s syndrome.                           disease                                 sparing)           posterior cerebral
       Precipitating   NA                                                                                                                                circulation.
       PP              10-50 x < common than Migraines. M>F (5:1)              DIFFERENTIAL DIAGNOSES
       Cause           Unknown. Though pts often smokers + OH.              Sudden       Vitreous Haemorrhage; Central Retinal Artery Occlusion;
       Treatment       Acute: SC Sumatriptan / Inh 100% O2. Often not          Visual          Central Retinal Artery Vein Occlusion; Retinal Detachment;
                        responsive to analgesia.                                Loss            Retrobulbar Neuritis; Anterior Ischaemic Optic Neuropathy
                       Preventative: Often ineffective though short                            (Atheroma or Arteritis), Migraine.
                        courses of Verapamil, Methysergide, Steroids may        Visual       Central Scotoma: Optic Nerve Disease
                        help. Lithium for very severe.                          Field        Peripheral Constriction: Retinal Disease
       COITAL AND EXERCISE INDUCED CEPHALGIA                                    Defect:      Altitudinal Defects: Retinal Vascular Lesions; Optic Nerve
       Features        Sudden often severe headache.                           Uniocular       head ischaemia
       Timing          Climax of sexual intercourse /  exercise. Severe       Visual       Central Field Loss: Retinal Diseases; Bilateral Optic Nerve
                        ache: 10-15 mins, < severe may persist for hours.       Field           Disease; Tobacco & OH Amblyopia; Leber’s Optic Atrophy
       Assoc           NA                                                      Defect:      Peripheral: Retinal Disease (e.g. Retinitis Pigmentosa); 
       Precipitating   NA                                                      Bilateral       ICP
       PP              Almost exclusively middle aged men.                                  Bitemporal Hemianopia: Supracellar Meningioma; Pituitary
       Cause           Unknown                                                                 Tumour; Craniopharyngiomas; Hypothalmic tumour; Carotid
       Treatment       Needs distinguishing by CT +/- CSF from SAH.                            Aneurysm.
                                                                                             Homoymous Hemianopia (Lesion behind chiasma):
                                                                                                Tumour; Vascular lesion; Migraine.
       Features        Dull ache, often mild (Severe in hypdrocephalus:
                        May be no other S&S, except for gait ataxia +/-
                        papilloedema).                                          CATARACTS (& BLINDNESS)
                       Responsive to simple analgesia.                         Def      Clouding of the lens of the eye or its surrounding transparent
       Timing          Present on waking, improving as upright (due to                    membrane that obstructs the passage of light
                        in ICP) or simple analgesia.                                  CLASSIFICATION: by N lens appearance (also by maturity)
       Assoc           Morning vomiting
       Precipitating   Worse bending forward                                               NUCLEAR (Central) CATARACTS
       GIANT CELL ARTERITIS (Cranial / Temporal Arteritis)                                    Common in old age
                                                                                              Lens   improvement in your reading vision  ‘2nd sight’
       Features        Pain localised to one or more temples or occipital
                                                                                                disappears as the lens gradually  yellow or greenish  cloud
                        region. Scalp tenderness.
                                                                                                vision ( brown).
       Timing          May be abrupt or insidious over weeks / months.
                                                                                              Seeing in dim light and driving at night may be especially
       Assoc           Jaw pain (ischaemia of masseters)
                       Visual disturbance ( acuity e.g. sudden blindness
                                                                                            POSTERIOR SUBCAPSULAR
                        in one eye,  visual fields)
                                                                                              From steroid use
                       Polymyalgia in 25%                                                    Starts as a small, opaque area just under the capsule shell.
       Precipitating   NA                                                                      (usually forms at the back of lens, in visual axis
       PP              Over 60 year olds. Rare in < 55s. F>M (4:1)                           May occur in both eyes but tends to be > advanced in 1 eye
       Cause          ?                                                                        than other.
       Inv              ESR, CRP, Platelets, ALP                                            Often interferes with
       Treatment       Immediate prednisolone                                                         Reading vision,  vision in bright light, Causes glare
                       Temporal artery Bx in next few days (skip lesions                                 or halos around lights at night.
WILL WESTON                                                                                                                                             Page 2 of 18
         PERIPHERAL                                                                                 haemorrhage
            Common in old age
            Cortical Cataracts, Radial Spoke like pattern                          PUPILS: CONSTRICTED aka MIOSIS
            Begins as whitish, wedge-shaped streaks on the outer edge of           Phys    Diameter Controlled: Sphincter Pupillae & Dilator Pupillae
              the lens cortex  slowly progresses, streaks extend to the            CONSTRICTION REFLEX (PARASYMPATHETIC):
              centre and interfere with light passing through the nucleus.                                 Light                             Pupil Constriction
            Both distance and near vision can be impaired.                                                                                           
         DOT OPACITIES                                                                                    Retina                             Sphincter Pupillae
            Common in normal lenses                                                                                                                  
            Also in fast developing cataracts in Dm / dystophia myotonica                             Optic Nerve                             Ciliary Ganglion
         IMMATURE CATARACTS                                                                                                                           
            Are defined as cataracts through which a red reflex can still be                Pretectal Nucleus in Midbrain              Occulomotor Nucleus (III)
              seen.                                                                 DILATION REFLEX (SYMPATHETIC): A Three Neuron Arc
         MATURE CATARACT                                                                            st
                                                                                                  1 Neuron Midbrain                              Pupil Dilation
            Have obscured red reflex and often are associated with                                                                                   
              weakness of the suspensory ligament of the lens.                                           Medulla                                Dilator Pupillae
         HYPERMATURE CATARACTS                                                                                                               (Muller’s Muscle)
            Have leaked protein as a result of the action of                                            T1 Cord                                       
              endopeptidases, resulting in a wrinkled lens. This sort of lens                                                              Short Ciliary Nerve
              ought to be removed before  lens-induced uveitis / glaucoma.                              T1 Root                                       
 PP         75% of over 65s, 20% of 45-65 year, ♀>♂                                                                                        Long Ciliary Nerve
 Risk    ‘DADS GUTS’                                                                                   Synapse with                                    
            Dm- often bilateral and cortical                                                     2 Order Neuron at                             Carotid Plexus
            Age                                                                                   Thoracic Ganglion                      (via Cavernus Sinus 
            Disease- Occular e.g. uveitis AND rubella                                                                                          Uveal Tract)
            Steroid Use- po, top, inh                                                              Axons Pass over                                    
            Genetic to unknown extent                                                                  Lung Apex                                Synapse with
            UV exposure                                                                                                                   3 Order Neuron at
            Trauma                                                                            Sympathetic chain In Neck                Superior Cervical Ganglion
            Surgery - Occular                                                              Postganglionic fibers also innervate:
                     High myopia                                                              Muller’s Muscle within eyelid, (responsible for initiation of eyelid
            In children                                                                           retraction during opening).
                     Genetic                                                                  Sweat glands of face (follow path of external carotid artery).
 Path                                                                               Cause   NARCOTICS
                                                                                              Cause constriction of pupil and  Drainage of aqueous (acts
                                                                                              through ciliary muscle). Used in Tx of glaucoma. E.g. Pilocarpine
                                                                                            HORNER’S SYNDROME
                                                                                              Triad of features resulting from interruption of sympathetic pathway
                                                                                              from hypothalamus to orbit, as follows:
                                                                                                          PTOSIS: Slight, Ipsilateral
                                                                                                          MIOSIS: Ipsilateral. Paralysis of Muller's muscle.
                                                                                                          ANHYDROSIS: Ipsilateral. Over the forehead
                                                                                                Light Reflex + Accommodation still intact.  Dilation to dark.
                                                                                              CAUSE: (Central Lesions)
                                                                                               Vascular: Post Inf cerebellar A occlusion / lateral medullary
                                                                                                   syndrome. Basilar artery occlusion
                                                                                               Demyelinating disease. (E.g. MS), Syringomyelia or
                                                                                                   syringobulbia, Tumours, Cervical cord tumours
 S&S           Aymptomatic- incidental finding…very common                                   CAUSE: (Peripheral Lesions)
               Blurred vision                                                                 Apical pulmonary disease - Pancoast's syndrome
               Glare: Daylight, Low sunlight, Head lights                                     Cervical rib, Mediastinal tumour, Carotid aneurysm
               Unilateral cataracts are often unnoticed                                       Thyroid enlargement - goitre, tumour
               Bilateral cataracts may cause gradual visual loss +/- frequent                 Neck trauma - carotid arteriography, cervical sympathectomy
                glasses changes                                                                Cervical lymphadenopathy, Cervical sympathectomy
            Monocular diplopia                                                                Brachial plexus lesions, e.g. Klumpke's palsy
            Children: Squint, Loss of binocular function, White pupil,                     UVEITIS
                Nystagmus (infants), Amblyopia                                                Uveal tract comprises iris, ciliary body, and choroid.
 DDx     Blindness (gradual onset bilateral loss)                                           POINTINE LESIONS
            1st in Dev World: Macular degeneration (> common in NIDDM)                       Pontine haemorrhage / tumour may  Bilateral miosis possibly by
            2nd in Dev World: Diabetic retinopathy                                           affection of both sympathetic pathways.
            Worldwide, chlamydial infection causing trachoma                               ARGYLL ROBERTSON PUPIL (Prostitute Pupil: Accom, Not React!)
            Diabetic maculopathy, HT retinopathy, Cataracts, Chronic                          Pupil usually bilateral and characterised by:
                glaucoma, Chiasmal or bilateral optic nerve compression,                                  Small, Irregular Pupils
                Bilateral optic nerve damage, e.g. Tobacco amblyopia                                      Size Of Pupils May Be Unequal
 Inv /   Visual acuity test                                                                              Absence Of Light Reflex
 Dx      Slit-lamp exam             Allows your eye doctor to see the                                    Prompt Accommodation Reflex
                                        structures at the front of your eye under                         Pupils Slowly Dilate With Mydriatics
                                        magnification                                          COMMON CAUSE: SYPHILIS. Pupils generally unequal &
                                    Called a slit lamp because it uses an                         irregular. Also atrophy & depigmentation. Ciliospinal reflex lost.
                                        intense line of light                                  OTHER CAUSES: Dm, Chronic OH, Encephalitis, MS,
         Retinal exam                                                                             Peroneal muscular atrophy, Midbrain tumours
 Tx      TEMPORARY HELP: sunshades / sunglasses
          SURGERY only Tx: PHACO EMULSIFICATION                                    PUPILS: DILATED
            Lens implantation: 3mm incision, US breaks up original,                Phys    See Pupils: Constrict
                Aspiration of original, Insertion of new                            Cause   MYDRIATICS
            Indications: Symptoms restrict lifestyle/ Pts cannot see well
                                                                                               Parasympathetic Paralysis, e.g. Atropine (Acts via CN III)
                enough to drive
                                                                                               Sympathetic Stimulation, e.g. Cocaine, Adrenaline
 Comp    CATARACT                                                                              Others: TCAs
            Longstanding cataract with time  White and Swollen =
                                                                                            Associated with Near / Light Dissociation
                ‘Mature’  Uveitis /  ICP
                                                                                               THIRD NERVE LESION: See Phys
                                                                                               HOLMES-ADIE PUPIL:
            Thickening of posterior capsule (5-30%)  Blurred vision: Tx
                                                                                               PARINAUD SYNDROME: Midbrain lesion.
                with laser
            Astigmatism induced from wound incision                                        LESION OF OPTIC NERVE:
            Post operative uveitis: Tx with top steroids                                      Pupil reacts sluggishly to direct light i.e. light not received!
            Cytoid macular oedema (Retinal Fluid accumulates  acuity)                       Normal reaction to consensual light and accommodation.
            Eye not entirely N afterwards: Glare /  near vision                           DEEP COMA
            Rare: Intraocular infection, Retinal detachment, Corneal                          See Elsewhere
                Decompensation (Corneal endothelial cells  in no), Choroidal               OTHER LESIONS OF THE EYE:

WILL WESTON                                                                                                                                         Page 3 of 18
            Trauma / Ischaemia to Iris                                                 Redness          Gen conjunctiva    Circumcornea              Circumcornea
            Cataract                                                                                                       Redness                   duskiness
            Vitreous haemorrhage                                                       Cornea           Normal             Deposits on Inf           Haze over Ant
          CONGENITALLY DILATED PUPIL                                                                                        surface                   surface
            ----------                                                                 Pupil            Normal             Fixed (small at first)    Fixed (dilated
                                                                                        (Key to                             Irregular                 oval)
 RED EYE                                                                                Red Eye)                            (adhesions)
 PP             Eye-Related complaints = 57 / 1000 consultations in GP.                IO Prssre        Normal             Normal                    Increased
                ~ 10-15% Of which will involve conjunctivitis.                         Vision           Blurred- Temp      Blurred- ocular media     Visual Field 
 Gen            COMMON CAUSES: Conjunctivitis, Dry Eyes, Foreign Bodies                                 due to discharge   obscured by
                EMERGENCY: Anything not seen regularly: Iritis, Acute                                                      inflammatory exudate.
                 Glaucoma & Ophthalmic Herpes.
             Avoid Steroids unless sure eye not infected e.g. recurring iritis         GLAUCOMA
             Suspicious of unilateral red eye - infective conjunctivitis usually       Def               Group of eye diseases characterized by pathological change in
                 bilateral by time it presents                                                             intraocular pressure.
             Itching nearly always allergy - Cromoglycate (aqueous) is safe                              Almost invariably an  in pressure  damage optic nerve head
                 and works well but Nedocromil needs to be used less often                                  changes in visual field.
             To instil eyedrops, pull down lower lid especially in children: lid                         Mean value for intraocular pressure is 15-16 mm Hg with SD of
                 is much less sensitive than eyeball                                                       +/- 2.5. Upper limit of normal is considered to be 21 mm Hg.
             Chloramphenicol  Aplastic Anaemia so rarely that antibiotic              Path              Intra-ocular pressure maintained by aqueous within anterior
                 still first choice. May  Allergic Blepharitis in chronic use                             and posterior chambers.
 Cause                                       Side       Where            Pupils                           2 Anatomical areas separated by iris. Communicate via pupil.
          Bact Conjunctivitis                Both       Periph                                                    Cornea marks anterior border of these regions;
          Acute Iritis                       One        Cornea           Irreg, Small                             Anterior lens surface, the posterior border.
          Glaucoma                           One        Cornea           Oval, Fixed                      Aqueous produced in ciliary body region, adjacent to posterior
          Scleritis                          Either     Focal / Difus                                      chamber. It enters this area by ultrafiltration and active
          Episcleritis                       One        Segment                                            secretion by epithelium on surface of ciliary body. It then
          Corneal Ulcer                      One        Cornea                                             passes into anterior chamber and leaves by one of two routes.
          Conjunctival Haemorrhage           Local haemorrhage                                                    The major flow - 75% - is via trabecular meshwork in
 Path     CONJUNCTIVITIS:                                                                                            angle formed by the iris and cornea.
 & Tx        Bacterial: Acute- S pneumoniae, Chronic- S aureus                                                   The remainder leaves through uveoscleral route close
                           Tx: Chloramphenicol                                                                      to trabecular region.
             Viral: Adenovirus                                                                           Intra-ocular pressure depends upon balance between
                           Tx: - Chloramphenicol- To prevent 2o Bacterial.                                production and drainage of aqueous.
             Atopic / Allergic: Hayfever
                           Tx: - Antihistamine (Top).
             S&S Not above: Severe, deep pain and tissue destruction even
                 leading to loss of the eye. Episclera almost always involved.
                 Vision often affected. F>M. 4-5th Decades
             Assoc: 21% RA & Other collagen disease; 12% Ank Spond;
                 15% Herpes zoster, TB, Syphilis, Gout and Reiter's disease.
             Mx: Early referral; Generally resistant to treatment. NSAIDS.
             Assoc: 30%-Collagen Disease, Herpes Zoster, Gout, Syphilis.
             Tx: NSAIDS +/- Topical Steroids (Dexamethasone).
             Comp: 15% develop a mild iritis
             S&S: Pain, Lacrimation, Photophobia, Blepharospasm ( blink)
             Tx: Exclude foreign body. ABx Ointment, Padding, Analgesia.
             Comp: If infection may  Corneal Ulceration.
             S&S Not above: Pain, Vision blurring, Photophobia, Keratits (ID
                 as white/grey patch on cornea. Represent WBC collection)
             Mx: Refer!
          IRITIS:                          (Arthopathy, IBD, Psoriasis, Sarcoidosis)
             Idiopathic or…Ankylosing Spondylitis, Chronic Stage Of Reiter's
                 Disease, Sarcoidosis, Behcet's Disease, Juvenile Rheumatoid
                 Arthritis, UC, Crohn's, Psoriasis
             See elsewhere
             Age > 40; FHx: 10x, Afro-Caribbeans, Dm, Thyroid eye
                 disease, Myopia.                                                       Types       Two main types of glaucoma are angle closure and open angle.
          SUB CONJUNCTIVAL HAEMORRHAGE:                                                               In ANGLE-CLOSURE GLAUCOMA, normal drainage canals
             Hx: Squash ball, Champagne Cork! Sneezing / Coughing.                                      within eye physically blocked. Can be acute / chronic.
             Tx: None needed. Blood is gradually absorbed  yellow in 14/7                                      Acute angle-closure glaucoma: Sudden  in IOP
 Inv /    History                  Onset? Precipitant? Dust? Trauma? Sore /                                       occurs because of build up of aqueous humor.
 Dx                                   Itchy? Discharge?                                                            Emergency because optic nerve damage and vision
          Examination                                                                                             loss can occur within hours of onset of problem.
          Others                   Site of injection: If cornea: Corneal Ulcer; If                              Chronic angle-closure glaucoma may cause vision
                                      peripheral: Conjunctivitis.                                                  damage without symptoms.
                                   Visual Acuity, Pupil Reactions, Red Reflex                        In OPEN-ANGLE GLAUCOMA, drainage system remains open.
                                      Fundoscopy, Eyelid Eversion (foreign body /                        Open-angle glaucoma also may cause vision damage without
                                      pus)                                                               symptoms.
 Mx       REFER FOR OPTHALMOLOGY:                                                       Other         CHILDHOOD GLAUCOMA is rare and starts in infancy,
              Acuity, Abnormal pupillary reactions, Corneal ulceration                                 childhood, or adolescence. Similar to open-angle glaucoma.
             Conjunctival injection most marked around pupil (suggestive of                          SECONDARY GLAUCOMA refers to  IOP that is a result of a
                 keratitis, corneal ulcer or intraocular pathology)                                      structural problem within eye. May be result of injury to eye or
             History of possible penetrating injury, Fundus is cloudy                                   other medical conditions. different because treatment aimed at
                                                                                                         treating underlying cause as well as lowering  pressure.
                  ACUTE                ACUTE IRITIS                  ACUTE              Inv /         GOLDMANN APPLANATION TONOMETER - Requires Top
             CONJUCTIVITIS              (aka Uveitis)              GLAUCOMA             Dx               anaesthesia and fluorescein but accurate.
 Hx          Eyelid sticking on     See Assoc                                                         "AIR-PUFF" TONOMETER - cornea flattened using small puff
             waking                                                                                      of air. Does not require anaesthesia but is not very accurate.
 Where       Often Bilateral        Unilateral                  Unilateral                            SCHIOTZ TONOMETER - weight required to indent cornea
 Pain        Roughness on           Ache within eye             Severe eye pain                          measured and converted to pressure value. requires topical
             lid movement                                                                                anaesthesia but portable.
 Photop      Slight                 Severe (Even from           Moderate                Mx            Medical and Surgical options are available depending on the
                                    contralateral eye!)                                                  case and type of glaucoma.
 Discharge   Clear / Purulent       Watering                    Watering                Comp          Blindness

WILL WESTON                                                                                                                                             Page 4 of 18
                                                                                                TX: Optical (Prescription Glasses), Orthoptic Exercise,
 OPTIC DISC SWELLING                                                                             Occlusion (force squinting amblyopic eye to fixate), Sx.
 Def       Several causes. Papilloedema reserved for swelling due to                       PARALYTIC SQUINT
              ICP (Generally bilateral).                                                       PATH: Caused by damage to extraocular muscles or their
 Path      ICP of any cause  swollen nerve fibres  capillary and                              innervation. (3 / 4 / 6 Nerve Palsies. Brainstem Syndromes)
              venous congestion  optic disc swelling.                                         FEATURES: Usually acquired, Diplopia Present
 Cause     RAISED ICP                                                                         Diplopia maximal when attempting to look in direction requiring
                     Cerebral mass lesion: Tumour, Abscess.                                     action of weak muscle. Image from paralysed eye always
                     Hydrocephalus, Haemorrhage, Haematoma.                                     peripheral to image from N eye. Angle between longitudinal
                     Idiopathic intracranial hypertension                                       axies of eyes varies during testing of eye movements.
           OBSTRUCTION OF OCULAR VENOUS DRAINAGE                                              CAUSE: See Path: Head Trauma CVA, Demyelinating Disease,
                     Central retinal vein occlusion                                             Space Occupying Lesions (Tumour, Haemorrhage, Abscess,
                     Cavernous sinus thrombosis                                                 Cerebral Aneurysm,  ICP, Dm)
           SYSTEMIC DISORDERS AFFECTING RETINAL VESSELS.                                      TX: Dx & Tx Cause. Double vision may be managed by:
                                                                                                 Spectacle prisms (minimise amount of 2 muscle contracture),
                     Hypertension, Vasculitis, Hypercapnia
                                                                                                 Supervised patching, Muscle Sx if paralytic squint shows no
                                                                                                 sign of spontaneous improvement after 6/12.
                     Demyelination (optic neuritis / papillitis)
                                                                                    Inv /      Facial appearance, Corneal reflections - symmetrical on pupil
                     Leber’s hereditary optic neuropathy
                                                                                    Dx         Head Tilt, Test Ocular movements
                     Ischamia                                                                 COVER-UNCOVER TEST: Involves patient fixating on object,
                     Toxins e.g. methanol                                                       one eye is then covered and refixation movement is looked for
                     Infiltration of optic disc                                                 in other (uncovered) eye. Other eye then tested in same way.
                     Sarcoidosis                                                                If, during either manoeuvre, there is movement of unoccluded
                     Glioma                                                                     eye, then that eye must have been squinting before fellow eye
                     Lymphoma                                                                   was uncovered, ie manifest squint is present.
 S&S       Papilloedema: Cessation of normal venous pulsation seen at                         ALTERNATE COVER TEST: Eyes rapidly and alternately
              disc. Disc margins then become red (hyperaemic)  Margins                          occluded - from one eye to other and then back again.
              become distinct and whole disc is raised up, often with                            Procedure  breakdown of binocular fusion mechanism and
              haemorrhages in the retina.                                                        reveals refixation movements of each eye at moment of
                                                                                                 uncovering. In absence of manifest squint, such a squint in
 DIPLOPIA                                                                                        fixation implies latent squint.
 Def     Occurrence of multiple images from one object in visual field. It can
         only occur if binocular vision has developed.                              NYSTAGMUS
 Cause   MONOCULAR DIPLOPIA: Double vision in one eye which persists                Def   Rhythmic oscillation of eyes. Sign: Disease of Ear or Posterior Fossa.
         after other eye is covered. Image separation is slight, often described    Class Jerk / Pendular (Jerk >> common). For true nystagmus…must be
         as 'ghosting.' Common causes: abnormalities of cornea, iris, lens, or            binocular and sustained.
         vitreous or aqueous humour                                                 Jerk  Has fast and slow component. Direction dictated by fast movement
            Refractive Error – (commonest problem) - if looking through                  (reflex to correct slower, primary movement). Seen in:
                pinhole abolishes diplopia then spectacles should be worn                         PERIPHERAL LESIONS: (CONTRALATERAL)
            Developing Cataract - areas of differing refractive index                                      Vestibular end organ (middle ear)
                splitting of light beam & diplopia. Usually  as opacification .                 CENTRAL LESIONS: (IPSILATERAL)
            Corneal Scarring                                                                                8th Nerve
         BINOCULAR DIPLOPIA: Double vision caused by paralytic squint.                                       Brainstem
         Separation of two images is maximal when gaze is in direction of the                                Cerebellar
         defective movement.                                                                                 Cortical (rare).
            NEUROGENIC - paralytic squint
            MUSCULAR:                                                                       PERIPHERAL LESIONS:
                        Myasthenia gravis - diplopia usually with a ptosis
                        Exophthalmic ophthalmoplegia                                             Fatigable. Seen on Positional Testing
            MECHANICAL:                                                                          Acute and transient, lasting mins / hours.
                        Blow out fracture                                                        Associated with severe vertigo +/- N&V.
                        Displacement of globe by an orbital tumour                               CAUSES:
 Inv /   BINOCULAR DIPLOPIA                                                                              Cochlear Path: Labyrinthitis, Meniere’s, Head Injury
 Dx         Examine eye movements in six cardinal positions of gaze as in                               VIII Nerve Disease: Acoustic Neuroma
                each position, one eye acts predominantly                                                Viral Neuronitis
            Note direction in which diplopia is maximal
            Cover each eye in turn - the fainter and more peripheral                        CENTRAL LESIONS: Most common form in clinical practice.
                image disappears when affected eye is covered
                                                                                                  Non Fatigable. Present at rest.
 SQUINT                                                                                           Long-lasting (weeks / months)
 Def    Condition in which visual axes of each eye not directed                                   Vertigo tends to wane after days, with nystagmus outlasting.
        simultaneously at same object.                                                            CAUSES: Vestibular Nuclei Damage: Vascular, Neoplastic,
 PP        Affects 3% of children. < 1% recognised by parents.                                    Demyelination, Drugs (Phenytoin, Carbamazepine)
           Childhood Squints Risk: FHx, Prematurity, Neonatatal jaundice,
               Encephalitis, Meningitis, Cerebral P, Mental retardation.                     VERTICAL JERK: Only caused by central lesions
 Terms  Binocular            Ability to use both eyes to create common                       DOWN BEAT JERK: Rare: Caused by lesions around foramen
        Single Vision        perception                                                      magnum (e.g. meningioma, cerebellar ectopia).
        Orthophoria          Perfect ocular balance in the binocular state          Pend     Pendular Nystagmus = Movements are similar in velocity and
        Porphoria            Eyes move out of aligned state when they are                    amplitiude. Almost always binocular, horizontal and present in all
                             dissociated - LATENT SQUINT                                     directions of gaze. Causes mainly ocular, when poor visual fixation
        Exophoria            Eyes diverge                                                    (severe and longstanding visual impairment) or as congenital lesion
        Esophoria            Eyes converge                                                   assoc with head nodding. May rarely occur in brainstem disease (MS,
        Hyperphoria          Visual axis of one eye moves vertically with                    Brainstem glioma).
                             respect to other one
        MANIFEST             If, in binocular state, eyes have different visual     DEAFNESS
        SQUINT               directions                                             Def    HEARING LOSS may be classified as:
        Non-Paralytic        Angle of the squint remains unaltered regardless                 Conductive - due to defect in the sound-conducting apparatus
        Squint               of the direction of gaze                                         Sensorineural - due to lesion of the receptive organ - the hair
        Paralytic Squint     Angle of non-alignment varies with  in direction                   cells/ auditory nerve / central neural pathways
                             of gaze. Squint is incompetent and cause usually                 Distinguished using Rinne's and Weber's tests.
                             infranuclear muscle palsy. Situation can also occur    PP        3 million hearing impaired in UK
                             in mechanical restriction of eye movement                        Benefits: Free hearing aids, Disability Allowance (<65),
 Class  NON-PARALYTIC (CONCOMITANT) SQUINT                                                       Attendance Allowance (>65)….
           PATH: Excess tone in one muscle compared with its antagonist            Cause  Glue Ear and Otitis Media are most common causes.
               resulting in deviation of eye.                                       Child  Genes               Rare. E.g. Alport’s Syndrome
           FEATURES: Usually congenital, diplopia absent, extraocular                     Pregnancy           Rubella, Eclampsia, Severe haemorrhage.
               muscles and nerves are grossly normal, angle between                        Delivery            Any cause of anoxia may  inner ear damage
               longitudinal axes of eyes remains constant on testing eye                   Life so Far         Viral infections (mumps, measles) may 
               movements, both eyes have full movement if tested separately                                        unilateral deafness
           CAUSE: Idiopathic (most common; ½ have FHx), Severe                                                Meningitis, Ototoxic drugs, head injuries 
               Hypermetropia, Severe Myopia, Blindness, Brain damage.                                              bilateral deafness.

WILL WESTON                                                                                                                                      Page 5 of 18
 Cause    CONDUCTIVE                                                               S&S         EARACHE: throbbing, severe (Frequently rubbing ear)
 Gen        EXTERNAL CANAL OBSTRUCTION (wax, discharge from                                   PYREXIA
              otitis externa, foreign body, dev abnormalities).                                OTORRHOEA: profuse, mucoid  thick yellow (bloodstained)
            DRUM PERFORATION (Trauma, Barotrauma, Infection).                                 Irritability, Anorexia, Vomiting
            OSSICULAR CHAIN DEFECT (Otosclerosis, Infection,                      DDx       Wax or foreign body, Eustachian tube obstruction, for example glue
              Trauma).                                                                       ear, Otitis media or otitis externa, Otosclerosis, Paget's disease,
            INADEQUATE EUSTACHIAN TUBE VENTILATION of middle                                Barotrauma
              ear with effusion present (eg 2 to nasopharyngeal carcinoma)         Inv /     Otoscopy          Fluid bubbles behind tympanic membrane. Red
          SENSORINEURAL                                                            Dx                              bulging membrane.
            OTOTOXIC DRUGS (damage 8 CN or inner ear)                                       H Tests           Hearing 
                       AMINOGLYCOSIDES: Esp gentamycin. Since cleared             Tx          Discussion & Reassurance RE natural progression
                         by kidney, risk  with Renal F Regular Blood Tests.                  Analgesia
                         Selective vestibulotoxicity of Genatmycin may be used                 Oral fluids.
                         as Tx in Meniere’s Disease.                                           Antibiotics- Consider
                       FRUSEMIDE: Rare, usually reversible.
                       QUININE: May be reversible.                                          According to Disease progression:
                       ASPIRIN: Usually only in OD. Usually reversible.                        1. Early: Paracetamol + Amoxicillin (no point of eardrops if
                       CYTOTOXICS: Esp Cisplatinum.                                               tympanic membrane intact)
                       BETA-BLOCKERS: E.g. Propranalol.                                        2. Bulging: Myringotomy (gen anaesthetic, incision: tympanic
            POST INFECTIVE (Meningitis, Measles, Mumps, Flu, Herpes,                              membrane) & Grommets
              Syphilis)                                                                         3. Discharging: Nature’s own myringotomy. Swab  culture,
            OTHERS (Cochlear vascular Disease, Meniere’s disease,                                 Antibiotics
              Trauma)                                                              Mx           Younger: Antibiotics: Ampicillin / Amoxicillin (Haemophilus)
            RARE (Vit B12 def, MS, 2 Carcinoma of brain)                                       Older: Antibiotics: Penicillin (Streptococcus)
 S&S        Speed of onset. Unilateral / Bilateral.                                            Use of Abx is controversial.
            Tinnitus / Vertigo. Pain / Discharge. Noise Exposure.                 Comp      IMMEDIATE AND LOCAL COMP:
            Otoscope: Tympanic membranes (to ID middle ear disease)                         1)   Resolution: Most cases
            Tuning Fork: Weber / Rinne                                                      2)   Necrosis: Tissue death (conductive deafness)  Perforation 
 Inv      PTA     Pure Tone Audiogram: Quantify Hearing loss and ID type &                        Cholesteatoma formation.
                  pattern.                                                                   3)   Fibrosis: Collagen replaces effusion  Adhesions of ossicles 
          MRI     If asymmetrical Sensorineural hearing loss (i.e. one ear >                      Conductive deafness
                  than other) to ID Acoustic Neuroma or other central cause.                 4)   Chronic Otitis Media
                                                                                             SECONDARY COMPLICATIONS: Infection Spreads…
 COCHLEAR IMPLANT                                                                               To bone : Mastoiditis +/- Subperiosteal absess
                                                                                                To facial Nerve  Inflammatory oedema: Facial Paralysis
   Used with profound hearing loss to stimulate residual nervous tissue.
                                                                                                To Inner Ear Acute Suppurative Labyrinthitis
   Indications:
                                                                                                To middle or posterior cranial fossa  Venous sinus
           Bilateral profound sensorineural hearing loss.
                                                                                                   thrombosis, Meningitis, Bran / Extra dural / Sub dural abscess
           No benefit from other hearing aids.
           No surgical C/I to cochlear implantation.
                                                                                   OTITIS EXTERNA
           Patient needs to be well motivated.
                                                                                   Def        Inflammation of skin of external ear canal
   First developed 30 years ago.
                                                                                              Acute: As a result of a boil. Always in outer 1/3 as only this part
   Has internal and external components:
                                                                                                 has hair follicles.
           Internal component - body containing decoder and magnet, and
                                                                                   Cause     INFECTION: Bacterial: S aurus, Pseudomonas aeruginosa; Fungal:
              a band of electrodes that are inserted into the cochlea; each
                                                                                             Candida; Viral: Herpes Zoster
              electrode delivers sounds of varying pitch and loudness.
           External component
                                                                                   Risk      Trauma (fingers, cotton buds, foreign bodies); Swimming in dirty
                                                                                             water; Hot / Humid atmosphere.
                 Microphone worn behind the ear  (Sound)
                                                                                  S&S        PAIN: May be severe. Worse on moving pinna, eating.
            Speech processor  (Selects and Codes useful sounds)                              DISCHARGE: Purulent, not mucoid
                                                                                             OEDEMA OF EAR CANAL  Blockage & Deafness.
                           Transmitter  (Code)                                               LYMPHADENOPATHY: Postauricular; May be confused with
                                                                                                mastoiditis.
             Receiver  (Conversion of code to electrical signals)                 Tx         Microbiological swab for C&S.
                                                                                             Removal of debris from ear canal.
                       Stimulate Hearing Nerve fibres                                         Topical ABx: Drops- Aminoglycoside + Hydrocortisone
                                                                                              Avoid water entering ear.
 EARACHE                                                                                    Consider in Elderly Diabetics: Possibility of ‘Malignant’ Otitis
                                                                                           Externa (potentially fatal infection of ear canal extending to skull base)
 Local         Any disease of external ear or middle ear, including:
 Cause                 acute otitis media
                                                                                   ACOUSTIC NEUROMA (& TINNITUS)
                       acute otitis externa
                       furunculosis ( þ acute mastoiditis - rarer )               Def       Benign, slow growing tumour of 8th CN.
             Malignant disease of the ear                                         PP        Occurs bilaterally in Neurofibromatosis Type 2.
 Cause    Pain may be referred to ear from nerves listed below; for each,          S&S       Progressive sensorineural hearing loss and tinnitus.
 Rferd    disorder causing stimulus is detailed.                                             Less common: Sudden hearing loss, Vertigo, Trigeminal
            AURICULO-TEMPORAL BRANCH OF TRIGEMINAL NERVE (V):                                    Numbness.
             Dental abscess, dental caries, impacted molar teeth, temporo-                  Large Tumours: May  Cerebellar signs and  ICP. May be
                mandibular joint lesions - e.g. Costen's syndrome                                fatal if untreated.
            TYMPANIC BRANCH OF GLOSSOPHARYNGEAL NERVE (IX):                        DDx    Tinnitus (perception of sound in absence of appropriate external
             Post-tonsillectomy, tonsillitis or quinsy, carcinoma at the base            auditory stimulus): Commonest by far: Presbyacusis / noise exposure.
                of the tongue or tonsil, neuralgia of the glossopharyngeal nerve          Others: Meniere’s, Trauma, Intracranial vascular lesions e.g. glomus
            SENSORY BRANCH OF THE FACIAL NERVE (VII):                                     tumours, Toxic causes e.g. alcohol, aspirin, streptomycin.
             Geniculate herpes / Ramsay Hunt syndrome                             Inv /  PTA            Pure Tone Audiogram to document hearing loss.
            AURICULAR BRANCH OF THE VAGUS NERVE (X):                               Dx     MRI            To Demonstrate the tumour.
             Carcinoma of the piriform fossa, carcinoma of the larynx, post-      Mx     Sx: Excision performed by ENT and Neurosurgery together.
                cricoid carcinoma
            GREAT AURICULAR NERVE (C2 / C3)                                        VERTIGO
            LESSER OCCIPITAL NERVE (C3):                                           Def       Abnormal perception of movement
             Cervical Spondylosis                                                 PP       
                                                                                   All    Mismatch between information about position in environment reaching
 OTITIS MEDIA                                                                             brain from eyes, limb propriocepive apparatus and vestibular system.
 Def        Inflammation of Middle Ear                                                      LABYRINTHINE CAUSES:
 PP         Peak incidence at 6 months – 3 yrs. Rare in adults.                                       Path: Inappropriate input from Labyrinthine apparatus
             incidence in Down S, ♂>♀                                                                  (same as when spun round on chair).
 Cause                       COMMON                                   RARE                             Duration: Normally short lived.
            Common cold                                         Sinusitis                            Tx: Vestibular sedatives: Cinnarazine,
            Acute tonsillitis                                   Tonsillectomy                          Prochlorperzine, Betahistine. Refer to ENT.
            Flu (pneumococcus, haemophillus)                    Barotrauma                 CENTRAL CAUSES: Duration:
 Path    Acute inflammatory oedema of mucosa blocks Eustachian tube                                   Often persistent. Positionally induced vertigo lasts as
         viral effusion into middle ear (perfect conditions for culturing).                              long as position is maintained, unlike common
                                                                                                         peripheral vertigo that fatigues if position maintained.
WILL WESTON                                                                                                                                        Page 6 of 18
                       Same is true of accompanying nystagmus.                                  sinuses. Treatment may need Sx involvement.
                       Brain stem dysfunction  dysarthria, diplopia              NASAL VESTIBULITIS                                                 (Inflammation)
                        If deafness and not suggestive of Meniere’s, 8 CN          PP         Dm & Immunocompromised patients prone to recurrent
                        lesion e.g. acoustic neuroma should be suspected.                        infections of hair follicles in nasal vestiblules (furunculosis).
                      S&S: Often accomp by S&S of brainstem dysfunction.          Cause      Infected anterior nasal discharge
 Cause      VESTIBULAR ENDO ORGANS & VESTIBULAR NERVES                                        Infection of hair follicles (usually Staph a).
                                                                                              Children: Foreign Body, Unilateral Choanal Atresia.
             VESTIBULAR NEURONITIS (AKA LABYRINTHITIS, AKA                         Inv /   Pus             Send for C&S
             EPIDEMIC VERTIGO)                                                     Dx                     
                                                                                   Mx         Antibiotics according to C&S
                 Most common cause                                                ATROPHIC RHINITIS                                                  (Inflammation)
                 Cause unknown                                                    PP         Rare
                        rd  th
                  PP: 3 / 4 decade                                                 Cause      Assoc with poor hygiene and malnutrition
                 S&S: Most severe at onset, settling down over a few days.        S&S        Nasal crusting. Foetor.
                  During attack, nystagmus may be present but not for long.        Mx         Removal of crusts and application of nasal douches / drops.
                  Vomiting, Ataxia often on wakening. No tinnitus. Occasional                 Sx: May be needed to  size of nasal cavities.
                  deafness.                                                        ALLERGIC RHINITIS                                                  (Inflammation)
                 Tx:: Antiemetics / Vestibular Sed (Prochlorperazine)             PP         1:5 of Populaiton.
                                                                                   Cause      Seasonal: Spring / Summer: Tree / Grass pollen
             BENIGN POSITIONAL VERTIGO                                                        Seasonal: Autumn: Mould
                                                                                              Perennial: Animal dander, House dust mite, Feathers.
                 Path: Presence of degenerative material affective free flow of              Ingested: Eggs, Milk, Nuts.
                  endolympth (cupulolithiasis).                                               Vasomotor: Stress / Tiredness, Hormonal, Temp / Humidity.
                 S&S: Each attack lasts seconds. Pt reluctant to move head        Path       Type 1 Hypersensitivity Reaction (See Septicaemia)
                  which may  muscle type tension headache. Assoc                  S&S        Nasal obstruction, Clear discharge, Sneeaing Bouts.
                  hyperventilation. Positional vertigo may also occur after        Mx         Steroid nasal spray +/- Top Antihistamine e.g. Sodium
                  concussive head injuries. Assoc nystagmus.                                     Cromoglycate.
                 Tx:: Antiemetics / Vestibular Sed (Prochlorperazine)                        Sx: Turbinate Reduction.
                 Tx: Epley's manoeuvre removes debris from semicircular           Comp       Prolonged use of nasal decongestants may  Rhinitis
                  canals & deposit in utricle where hair cells not stimulated.                   medicamentosa.
                                                                                   EPISTAXIS                                                                (Septum)
             MENIERE’S DISEASE                      …Sensor the Green Tin Men!     Cause      Assoc: HT, Arterial Disease, Coagulation Disoresers,
                 Often Dx too early. Attacks may occur in clusters with long      Path       Usually bleed from anterior portion of septum (Little’s Area)
                  periods of remission.                                                          since it is a site of rich vascular anastomosis.
                 Path: Dilation of endolymph system of unknown cause                         More serious bleeds are from posterior vessels: Occur in
                 S&S:                                                                           elderly, hypertensive patients with arterial disease.
                        Tinnitus and distorted hearing.                           Mx         ANTERIOR: Sit up. Pinch anterior portion of nose.
                        Vertigo (mins - hrs) with prior sense of ear fullness.               ANTERIOR: Cautery: Under Local A using Silver Nitrate /
                        Sensorineural hearing loss on affected side.                            Electrocautery.
                        Often nystagmus. Often vomiting during attacks.                      POSTERIOR: Assesss for shock, Cauterise under endoscopic
                 Tx:                                                                            control. If area not identified  Post nasal packing under GA.
                        Acute: Antiemetics / Vestibular Sed (Prochlorperazine)                  Emergency packing may be used with Foley catheter. Packing
                        Prophylaxis: Betahistine                                                requires ABx.
                                                                                              Sx: If Conservative measures are inadequate, Arterial Ligation
                        Dietary Salt restriction.
                                                                                                 may be necessary.
                        Sx: Grommet insertion- Mechanism unknown.
                                                                                   CHOANAL ATRESIA                                                       (Obstruction)
                        Sx: Shunt tube insertion into endolymphatic sac
                                                                                   Path       Failure of breakdown of bucco-nasal membrane.
                        Sx: Ablation of Vestibular function w Gentamycin inj.
                                                                                   S&S        BILATERAL: Acute respiratory onstructino in neonate
                        Sx: Destruction of Labyrinth
                                                                                                 (Neonates are obligate nasal breathers)
                        Sx: Vestibular nerve Division- Int Auditory Meatus.)
                                                                                              UNILATERAL: Present later in infancy / childhood with
                                                                                                 unilateral purulent nasal discharge / obstruction
             OTHERS                                                                Inv /   Catheter         Failure to pass soft catheter through nostril.
                                                                                   Dx      CT               Helps to differentiate bony from membranous atresia.
                Drugs (e.g. genatmycin), Noise (e.g. acoustic trauma), Middle     Mx         BILATERAL: Establish oral airway as emergency  Sx
                 ear infection, Mumps, Advancing age, Intrauterine rubella,                   UNILATERAL: Sx May be delayed.
                 Congenital syphilis.                                              POLYPS                                                               (Obstruction)
              Motion Sickness, Trauma; Ototoxicity (e.g. OH), Herpes Zoster       Cause      Assoc: Non allergic Asthma, Aspirin intolerance. Do not occur
                 Oticus.                                                                         in children except in CF.
            BRAINSTEM & CEREBELLUM                                                            NEONATES: May be congenital: Meningoencepahlocoele
              MS; Infarct / TIA; Haemorrhage; Migraine (rare)                                ADULTS: May be Neoplastic.
            CEREBELLO-PONTINE ANGLE                                                Path       Redundant oedematous mucosa. Usually arise from ethmoid
              Vestibular schwannoma (acoustic neuroma), Meningioma,                             sinuses.
                 Secondary neoplasm, carcinomatous megningitis, inflammatory                  Most commonly bilateral and present in middle meatus 
                 lesions.                                                                        obstruction.
            CEREBRAL CORTEX                                                                   Occasionally arise from maxillary sinus ( antrochoanal
              Vertiginous Epilepsy                                                              polyps)
 COMMON NASAL CONDITIONS…Inflammation, Septum, Obstruction                         DDx        Inferior Turbinates
                                                                                   Inv /   Endoscopy           Appearance: Skinned green grapes.
 RHINITIS                                                      (Inflammation)      Dx                          Insensitive to probing, unlike inferior turbinates.
 PP          
             Most common in young children who have not yet developed              Mx         Large Polyps  Sx Removal…Small Polyps: Steroid spray.
             immunity to viral agents.
 Cause     Most common is common cold caused by viral infection.                  ENT NEOPLASIA (+SWELLINGS) …INC TONSILS / ADENOIDS / PAROTIDS
 S&S       Nasal obstruction, discharge and sneezing.                             Cause  UNPAIRED STRUCTURES (Lie in Midline) Risk: Smoking, OH
           Usually self limiting.                                                          NOSE: BENIGN
           S&S > severe & prolonged in smokers ( muco-ciliary function)                            Osteoma: Fronto-Ethmoid complex with S&S of
 Comp      Sinusitis                                                                                 obstruction of Fronto-nasal duct. May require removal.
 ACUTE SINUSITIS                                                (Inflammation)                       Papilloma: Common in nasal vestibule. Tx with
 Path      Comp of Common cold as paranasal sinuses may be impaired                                  Cautery / Excisino. ~ 10% assoc with SCC.
             by swollen mucosa and thick secretions.                                        NOSE: MALIGNANT…Tx Rad RadTx  Sx. Prog: 66% 5yMR
 Mx        Steam inhalations, Local / Systemic Decongestants.                                       SCC most common but many other histological types.
           Analgesics.                                                                              Wegner’s Granulomatosis: Systemic disease assoc
           Broad Spectrum Abx for 2o Bacterial infection.                                            with necrotising granulation of nose. Death usually by
           Sx: Occasionally required to drain maxilliary / frontal sinuses if                        assoc Renal Disease.
             pain severe or complications. See below                                                 S&S: Maxilliary sinus most common. Diplopia (Orbital
 Comp      Maxilliary sinusitis: Assoc with infection of apices of premolar /                        involvement), Ill fitting teeth (Oral cavity extension),
             molar teeth.                                                                             Nasal Obstruction (Breech into medial wall of antrum).
           Orbital Cellulitis, Threatened intracranial spread of infection.                ORAL CAVITY: MALIGNANT
           Chronic Sinusitis:  Damage to mucosal lining of involved                                Prognosis worse the more posterior the tumour is
WILL WESTON                                                                                                                                         Page 7 of 18
                    situated due to easier cervical lymph spread and out                    Carotid body tumour: Arises in chemoreceptor tissue at caroid
                    of view . As well as normal Risk Factors (Smoking,                       bifurcation, level with hyoid bone. Occurs slightly lower down
                    OH), Also sharp teeth, poor dental hygiene.                              than branchial cyst. It is deep to anterior edge of
                  Management: RadTx / Sx. Poorer Prog the larger the                        sternocleidomastoid and may be pusitile. May be moved from
                    tumour.                                                                  side to side but not up and down. Tx: Sx Removal.
         ORAL CAVITY: OTHERS                                                             Actinomycosis
                  Sublingual dermoid cyst                                                Muscle tumours
         OROPHARYNX                                                                      Clavicular tumours
                  Rich lymphatic supply commonly present with                           Spinal abscesses
                    cervical nodes. Tumours have large space in which to               SUPERFICIAL:
                    grow   S&S (e.g. Otalgia) … Poor Prognosis.                         Sebaceous cysts
                  Tx: RadTx / Layyngopharyngectomy +/-                                   Lipomata (commonest benign tumours)
                    Oesophagectomy                                                        Carbuncles (infection of multiple hair follicles; commonly occur
                  Most common site for extranodal lymphoma i.e. NHL                         on neck / back in Dm)
         NASOPHARYNX                                                                     Neurofibromata
                  BENIGN: Angiofibroma (Rare, Typically in Adolescent         S&S        History. Examination: Neck, Full ENT assessment (Mirror and
                    Males presenting with Nasal obstruction + Epistaxis):                    fibreoptic exam of larynx & pharynx)
                    Histologically begign, but locally aggressive. Tx: Sx                 Scalp & General systemic exam
                  MALGIGNANT: Highest incidence in SE Asia (Esp               Inv /   Bloods                FBC, ESR
                    HK). EPV associated. S&S: Cervical Nodes, Otitis           Dx      Imaging               CXR, US
                    media, Facial Pain / Paraesthaeia, Horner’s S.                     Bx                    Fine Needle Aspiration Cytology
                    Prognosis poor (33% 5 Year Survival).
                  Pharyngeal pouch                                            DYSPHASIA
                  Subhyoid bursa                                              Def          Dysphasia: Acquired deficit in comprehension / production of
         LARYNX BENIGN:                                                                     language whether spoken or written. Main types…
                  Tx with Carbon Dioxide Laser                                                    Receptive (Wernicke’s)
         LARYNX MALIGNANT: Hoarseness +/- Stridor / Dysphagia.                                    Motor (Broca’s)
                  SCC of Larynx: Glottis (Most common)                                           Conduction
                    Hoarseness. Good prognosis if affecting glottis caught                  DYSARTHRIA: Disorder of language / speech disorders limited
                    early as true vocal cords have no lymphatic drainage.                    to motor apparatus of speech.
                  SCC of Larynx: Supraglottis / Subglottis  Present                       ALEXIA: Disorder of reading
                    later. Spread is to Cervical Lymph nodes.                               AGRAPHIA: Disorder of writing
                  Tx with Radical RadTx. Total Layyngectomy reserved                       APRAXIA: Disorder of skilled movements.
                    for those who fail to respond.                             Phys
         LARYNX OTHERS:                                                                                                Auditory input
                  Glottis Thyroglossal cyst
                  Laryngocoele
         Carcinoma, trachea and oesophagus
         Plunging ranula                                                                                       Lateral Geniculate Nucleus
         Lymph node enlargement
                 BENIGN:                                                                                           Primary Visual Cortex
                  Secondary to infection- Acute: Tonsillitis, Glandular
                    Fever; Chronic: TB
                  Sarcoidosis
                                                                                                           Higher Order Visual Cortical Areas
                  Nonspecific reactive lymphadenopathy
                  Primary: Lymphoma (classic rubbery texture)
                  Secondary: Metastases from …                                                                   Post Temporal Cortex:
                             Squamous Cell Carcinoma of upper air / food                                          WERNICKE’S AREA
                              tracts. (Larynx / Pharynx)                                                    (Auditory Word Comprehension)
                             Bronchus, Breast, Thyroid, Kidney, Malignant                                   ----------------------------------------
                              Melanoma.                                                                            Wernicke’s Aphasia
         Thyroid swellings (See elsewhere)                                                                  ----------------------------------------
                  Ask patient to sip some water and carefully watch
                    neck swelling. Only goitre / thyroglossal cyst will rise
                    on swallowing because of attachment to larynx.
                  DIFFERENT TYPES OF CANCER (In order of freq):                             Arcuate Fascicularus                      Parietal-Temporal-Occipital
                             Papillary: May be situated anterolaterally.                                                               ASSOCIATION CORTEX
                             Follicluar: Bone pain (Met via blood).                         ------------------------------              ------------------------------
                             Medullary: Feels stony hard due to amyloid                     Conduction Aphasia                          Transcortical Aphasia
                              infiltration.                                                  ------------------------------              ------------------------------
                             Anaplastic: Middle age / Elderly. Not a
                              discrete lump as infiltrates surrounding area.
                             Malignant Lymphoma: Assoc with
                              Hashimoto’s Thyroiditis.                                                          Ventral Pre-frontal Cortex:
         Salivary gland tumours (Refer if unexplained for 3-6/52)                                                     BROCA’S AREA
                  Parotid, Submandibular, Sublingual, Minor glands.                                          (Motor Word Comprehension)
                  5% head and neck tumours. Affect major salivary                                            ----------------------------------------
                    glands 5x > often than minor, but > malignant in                                                  Broca’s Aphasia
                    smaller glands. Parotid account for 70% of total.                                         ----------------------------------------
                  BENIGN: Pleomorphic Adenoma (Inf Post to earlobe),
                    Monomorphic Adenoma, Warthin’s Tumour (Bilateral
                    and in older men).
                                                                                                                   Speech Motor Output
                  MALIGNANT: Adenoid Cystic Carcinoma, Squamous
                    Cell Carcinoma, Pleomorphic Carcinoma
                  Malignant S&S: Hard, Fixed, Painful. Infiltrating           Anat
                    surrounding structures e.g. facial nerve (with parotid)
                    and local lymph nodes. Cause of overlying skin
                  Tx: Often Paratidectomy +/- Facial Nerve Excision.
         Branchial cysts: Arise from remants of second pharyngeal
            pouch. Typically a painless soft swelling, appearing deep to
            sternomastoid muscle and bulging forward at anterior border.
         Sternomastoid tumour
         Cervical rib
         Cystic hygroma: A type of lymphangioma. Present at birth and
            may be huge. Occur below angle of mandible on site of neck.
         Carotid artery aneurysms
         Arteriovenous fistula

WILL WESTON                                                                                                                                              Page 8 of 18
                                                                                    Def      Difficulty in articulation - no disorder of content of speech.
                                                                                             May be manifested if patient attempts to say a phrase such as,
                                                                                               'Peter Piper picked a peck of pickled pepper'.
                                                                                    PP       Most common cause of dysarthria is alcohol intoxication.
                                                                                    Cause   
                                                                                    Type   LOCAL
                                                                                             SITE:          Mouth ulceration, loose dentures
                                                                                           MYOPATHIC                                             BULBAR PALSY
                                                                                             SITE:          Muscles of Speech
                                                                                             S&S:           Indistinct, poor articulation
                                                                                             ASSOC:         Weakness of Tongue, face, neck
                                                                                           MYASTHENIC            BULBAR PALSY PICTURE (though not strictly)
                                                                                             SITE:          Motor End Plate
                                                                                             S&S:           Indistinct with fatigue & dystonia. Fluctuating sever
                                                                                             ASSOC:         Ptosis, Diplopia, Facial and neck weakness.
                                                                                           BULBAR                                                BULBAR PALSY
                                                                                             SITE:          Brain Stem
                                                                                             S&S:           Indistinct, slurred, nasal.
                                                                                             ASSOC:         Dysphagia, Diplopia, Ataxia
                                                                                           SCANNING                                   PSEUDO-BULBAR PALSY
 Types   SENSORY DYSPHASIA                                                                   SITE:          Cerebellum
            Caused by lesion of dominant temporoparietal cortex                             S&S:           Slurring, Impaired timing and cadence. Sing song
                (Wernicke's area) in posterior part of first temporal gyru.                                  quality...Say: University, Hippopotamus.
            Characterised by:                                                               ASSOC:         Ataxia of limbs and gait. Tremor of head / limbs.
                       Trouble Understanding what has been said, e.g.                     SPASTIC:                                    PSEUDO-BULBAR PALSY
                         unable to execute commands "When I clap my hands,                   SITE:          Pyramidal Tracts i.e. UMN Lesion (ischaemia,
                         and not before, touch your left ear with your right                                 MND, MS)
                         hand".  Command must be delivered with no non-                     S&S:           Indistinct, breathy, mumbling.
                         verbal communication.                                               ASSOC:         Poor rapid tongue movement.  Reflexes & JJerk.
                       Speech: Fluent but disorganised.                                   PARKSINSONIAN
          If lesion posterior to Wernicke's area, it may cause dyslexia.                    SITE:          Basal Ganglia
         MOTOR DYSPHASIA                                                                     S&S:           Indistinct, Rapid, Stammering, Quiet.
            Caused by lesion of inferior frontal gyrus of dominant frontal                  ASSOC:         Tremor, Rigidity, Slow shuffling gait.
                lobe (Broca's area).                                                       DYSTONIC
            Characterised by:
                                                                                             SITE:          Basal Ganglia
                       Understands but cannot answer appropriately
                                                                                             S&S:           Strained, Slow
                       Difficulty finding words
                                                                                             ASSOC:         Dystonia, Athetosis.
                       Reduced rate of word production - non-fluent
          In testing for this form of dysphasia, ask to talk about something
         (choice of subject will vary). Patient might use elaborate descriptions    Def    DYSPHAGIA: Difficulty in swallowing.
         to get around inability to find particular word (circumlocution), and               Painful (ODYNOPHAGIA): Feature of inflammatory conditions-
         may substitute words whose meaning is not quite correct.                                Pharyngitis, Tonsillitis, Acute Supraglottitis
                                                                                             Painless: Suggests mech obstruction / neurological condition.
            Caused by lesion arcuate fasciculus that links Wernicke's and          Cause   LOCAL
                Broca's areas together                                                       IN THE LUMEN
            Characterised by:                                                                           Foreign body, including bolus of food.
                       Inability to repeat statements                                       IN THE WALL
                       Inability to name objects                                                        Congenital Atresia
                       Ability to perform commands                                                      Stricture: Congenital, 2o to Reflux Oesophagitis,
                                                                                                           Ingestion of Caustic Liquids.
            Lesion amidst Association Cortex adjacent to Wernicke's                                     Patterson Brown Kelly Syndrome with post cricoid
                and/or Broca's areas. There are three forms (In all 3, repetition                          structure. (aka Plummer Vinson syndrome. Formation
                of speech is conspicuously normal):                                                        of oesophageal web. Assoc w iron deficiency in
            TRANSCORTICAL SENSORY DYSPHASIA [Lesion: usually in                                           women. Premalignant and assoc w development of a
                the posterior parietal-occipital cortex]                                                   carcinoma in cricopharyngeal region.)
                       Impaired comprehension of written & spoken                                       Pharyngeal pouch
                         language                                                                        Tumour
                       Fluent speech and anomia (automatically repeating                                Achalasia
                         interviewer) & paraphasias (slightly incorrect words)               OUTSIDE THE WALL
                       Normal repetition of speech which may degenerate                                 Enlarged lymph nodes: Lymphoma, Mets, TB
                         into echolalia                                                                  Retrosternal Goitre
            TRANSCORTICAL MOTOR DYSPHASIA                                          Cause   GENERAL
                       Non-Fluent speech and writing                                        Myasthenia gravis, Bulbar palsy, Bulbar poliomyelitis, Myotonic
                       Comprehension is normal                                                  dystrophy, Pseudobulbar palsy, MND, PD, Diphtheria neuritis,
                       Repetition of speech is normal                                           Scleroderma
                       The lesion is usually in one of two locations:              S&S     Specific points in the history are diagnostically helpful:
                                                                                             REGARDING SWALLOWING OF FLUID:
                       Broca's area: the lesion is small or recovering
                                                                                             If can swallow fluid as quickly as usual but has difficulty with
                       frontal lobes: seen in cases of abulia or akinetic
                                                                                                 food apparently getting stuck, suspect stricture. It may be
                                                                                                 benign or malignant.
                                                                                             If cannot swallow fluid as quickly as usual, there is either
                       Impaired comprehension                                                   motility disorder e.g. achalasia (neuromuscular failure of
                       Non-fluent speech                                                        relaxation at lower end of oesophagus), neurological
                       Normal repetition of speech                                              disorder, or severely narrowed oesophageal lumen
         SUMMARY                                                                             If neck bulges / gurgles on drinking, or if patient has to swallow
                                           Fluent     Repetition    Understanding                twice, suspect pharyngeal pouch
         Transcortical Motor                 NO          YES             YES                 REGARDING MOVEMENT OF SWALLOWING:
         Motor                               NO           NO             YES                 If constant and painful suspect a malignant stricture.
         Transcortical Mixed                 NO          YES              NO        Inv    Depends on cause, but Barium Swallow usually most helpful.
         Global                              NO           NO              NO        Mx     Depends on cause.
         No Dysphasia                       YES          YES             YES        BULBAR AND PSEUDOBULBAR PALSY CAUSES
         Conductive                         YES           NO             YES                Bulbar Palsy (i.e. LMN Lesion):          Pseudobulbar Palsy (UMN
         Transcortical Sensory              YES          YES              NO                CNs 9-12 are frequently affected         Lesion i.e. degen of cortico-
         Conductive                         YES           NO              NO                bilaterally  Dysphagia,                 bulbar pathways to V, VII, X,
         + Transcortical Sensory                                                            Dysarthria.                              XI and XII CN nuclei):
         Sensory                            YES       But incomprehensible                     Tongue wasted &                         Tongue small &
 DDx        Dementia, Delirium, Dysarthria                                                        fasciculating.                            contracted, moves
                                                                                               Palate moves very little.                    slowly. (Donald Duck

WILL WESTON                                                                                                                                       Page 9 of 18
                   Nasal Speech                           Speech)                    Mx             Depends on cause but…Eye Care: Inability to blink may 
                  Jaw Jerk & Gag absent.                Jaw jerk brisk.                            corneal drying  blindness.
 Genetic          Kennedy’s Disease (X                                                            Symptomatic: Lubricants, Taping of eye at night.
                   linked bulbospinal                                                               Surgical: Tarsorrhaphy (suturing the eyelid closed).
                   neuronopathy)                                                                    Bell’s Palsy: Steroids- High dose Prednisolone
 Vasc             Medullary infarction                  Bilateral hemisphere
                                                          (lacunar) infarction       SLIPPED DISC (Prolapsed intervertebral disc)
 Degen            Motor Neuron Disease                  Motor Neuron Disease       Def     Gelatinous nucleus pulposus squeezes through annulus fibrosus and
                  Syringobulbia                                                             bulges in posterior or posterolateral direction, beneath posterior
 Inflam,          Myasthenia (Bulbar picture,           Multiple sclerosis                 longitudinal ligament  Pressure S&S on root below level of
 Infective         though strictly not)                  Cerebral vasculitis                herniation - most commonly S1 > L5 > L4. Other defects are rarer,
                  Guillain Barre                                                            and higher defects ought to be investigated for other causes.
                  Poliomyelitis                                                             Disc prolapse can be divided into several regional sub-types:
                  Lyme disease                                                                            CERVICAL
                  Vasculitis                                                                              THORACIC (0.2%)
 Neo-             Brain stem glioma                     High brainstem tumour                            LUMBAR
 plastic          Malignant meningitis                                              PP         Most common: Fit 20-30 years after lifting / strain. < Likely in
                                                                                                    elderly since thickness of intervertebral disc lessened by
 LEFT VOCAL CORD PALSY (HOARSENESS)                                                                 desiccation of the nucleus pulposus.
 Anat     Muscles which move left vocal cord are innervated by the left                        Degeneration of vertebrae in middle aged  hypertrophy of
             recurrent laryngeal nerve (Branch of Vagus).                                           facet joints – b/w superior & inferior articular facets - and
 Cause    DAMAGE to LRL Nerve at any point along its course                                        predisposes to compression of nerve root as it exits spinal
                    Trauma                                                                         canal through intervertebral canal.
                               Operations (esp thyroid, but also                    Cause      Healing usually proceeds by shrinkage and fibrosis of extended
                                   oesophagus, lung.)                                               material rather than by its reposition within disc. Secondary
                               External penetrating trauma.                                        effects of lesion are acceleration of degeneration and
                    Malignancy                                                                     predisposition to the development of spondylosis.
                               Esp thyroid, bronchus, oesophagus.                              Lumbar disc prolapse results from herniation of soft disc
                    Miscellaneous                                                                  material from nucleus pulposus through a tear in the annular
                                                                                                   ligament. It most often occurs laterally but may be central,
          MALIGNANT INFILTRATION by Laryngeal or Pharyngeal                                        compressing cauda equina.
             carcinoma physically fixing cord.                                                  Lateral disc herniations usually compress nerve root exiting
          RA of the cricoarytenoid joint  Fixation.                                               through foramen below affected level.
 S&S      Hoarseness, Poor (bovine i.e. non explosive) Cough                        Path    PAIN
          Other S&S depending on cause.                                                        SUDDEN onset while lifting or stooping
 DDx                                                                                            BACK with limited movement
 Inv /  None Necessary…         If Cause obvious e.g. Thyroid Sx, Bronchial C                   LEG / BUTTOCK (sciatica) - may be 1 or 2 days later.
 Dx     CXR & CT                Otherwise: From Skull base to aortic arch.                      ON TOUCH to middline of lower back.
                                                                                                AGGRAVATED:
 Mx       Treat underlying cause
                                                                                                           Coughing / Straining.
          Speech Tx: To encourage vocal cord to compensate by
             crossing midline to come into contact with paralysed cord.                                    Foot dorsiflexion and bowstringing of popliteal nerve
          Sx: To move paralysed cord to midline (Inj of Teflon into cord.                                 May be ‘crossed sciatic tension - sciatic pain in
             Insertion of Silastic implant into space lateral to cord.)                                       affected leg on raising unaffected leg
 Prog                                                                                        OTHERS:
                                                                                                INABILITY to straighten up: lumbar lordosis may be lost and
                                                                                                    may be a protective sciatic scoliosis
                                                                                                PARAESTHESIA: Leg / Foot.
 Def       Acute tonsillitis is acute inflammation of the tonsils
                                                                                                URINARY RETENTION: If cauda equina compression
 S&S       Sore throat, Otalgia, Headache and Malaise                               DDx        INFLAMMATORY PROCESSES:
           Pyrexial, Fetor, Cervical lymph nodes enlarged & tender.
                                                                                                           Ankylosing Spondylitis } raised
           Tonsils: Enlarged +/- Pus frm tonsillar crypts -follicular tonsillitis
                                                                                                           Tuberculosis of the Spine } ESR
           Pharyngeal mucosa is inflamed
                                                                                                TUMOURS, e.g. of nerves giving continuous pain
 DDx       Infectious mononucleosis may severe membranous tonsillitis.
                                                                                                           Exclude by means of imaging
               Dx confirmed by Bunnell test.
                                                                                     Inv /   XR                          May show disc space narrowing &
           Scarlet fever (rare) - Streptococcal tonsillitis + S&S caused by a
                                                                                     Dx      Myelography scan            osteophytes in cases of chronic recurrence;
               specific toxin. Characterised by punctate erythematous rash,
               whiteness around mouth, and 'strawberry and cream' tongue.                    CT scan                     can show herniation of nucleus pulposus
           Diphtheria; Agranulocytosis                                                      NMR scan                    into the vertebral bodies - Schmorl's nodes
 Mx       Rest. Aspirin held in mouth then swallowed for symptomatic relief.         Tx      Rest +  Anti-Inflammatory
          Oral Fluids. ABs: Penicillin V +/- Sx: Tonsillectomy…See below:                    Reduction:  Continuous reduction is effective in 90%, may be
           Indications:  5 attacks of acute tonsillitis / year or 2 quinsies.              helped with epidural corticosteroid and local anaesthesia
           Comp: Haemorrhage; Injury (lips, gums, teeth, TM joints); Pain                   Removal,  …Indications are: - cauda equina syndrome; Persistent
               (throat / ear referred); Acute Otitis Media.                                  pain & severely limited leg raise after 2/52 conservative Tx -
 Comp      LOCAL: Severe swelling (Resp Obstruction); Abscess                               Neurological Deterioration; Frequent Recurrence
               (Peritonsillar [Quincy], Parapharyngeal, Retropharyngeal)                     Rehabilitation , eg, with isometric exercises & methods of lifting
           GENERAL: Septicaemia, RhF, Glomerulonephritis.
                                                                                     CAUDA EQUINA SYNDROME
 FACIAL PALSY                                                                        Def       Compression of cauda equina (CE) below level of L2  S&S
 Def     Paralysis of facial nerve. Facial nerve is motor supply to scalp, facial    PP        Atraumatic CES occurs primarily in adults.
         muscles and stapedius. Also supplies taste in anterior 2/3 of tongue        Path   The CE is formed by nerve roots caudal to level of spinal cord
         via chorda tympani branch.                                                         termination (L2). CES may result from any lesion that compresses CE
 Cause   UPPER MOTOR NEURONE: Sparing forehead which receives                               nerve roots. These nerve roots are particularly susceptible to injury,
         bilateral enervation                                                               since they have a poorly developed epineurium.
            CVA, MS, Tumours                                                        Cause     Trauma, Lumbar disc disease e.g. L4/5, Abscess, Spinal
 Cause   LOWER MOTOR NEURONE: Includes forehead.                                                   anaesthesia, Tumour / metastatic / CNS elements, Ankylosing
            Idiopathic: Bell’s Palsy (Unknown aetiology [maybe Herpes];                           spondylitis, Idiopathic
                Commonest cause but other pathology must be excluded…)                         Prolapse of disc in lower lumbar region is usually to one side or
            Cholesteatoma (keratinising squamous epithelium growing in                            other due to strong posterior longditudinal ligament of vertebrae
                middle ear  damage dura, lateral sinus, facial nerve, canals)                     which prevents central protrusion. Occasionally this ligament
            Trauma: External penetrating, Sx-Middle ear / Parotid, Skull #                        may be degenerate, and disc in lower lumbar region will
            Ramsey Hunt Syndrome: Herpes Zoster infection of 7th CN with                          prolapse backwards and cause pressure on cauda equina.
                vestibules around the external auditory meatus.                                Syndrome differentiated from demyelination of conus med-
            Tumour: Acoustic Neuroma, Malignant parotid tumour.                                   ullaris by absence of dissociated sensory loss & N plantars.
 S&S        FACIAL ASYMMETRY + sagging of mouth in unilateral lesion                S&S       Pain
            TASTE / DRIBBLING Impaired.                                                                   Low back pain. Acute / Chronic radiating pain.
            WEAKENED ability to wrinkle forehead - ability maintained in                                  May be tender to palpation.
                unilateral UMN palsy due to bilateral cortical representation                  Urinary and faecal incontinence
            EYES: Inability to close forcefully. Lacrimation .                                           Urinary incontinence may be preceded by difficulty in
            BELL'S PHENOMENON (shut eye on affected side which                                             starting / stopping stream)
                upward movement of eyeball and incomplete closure of eyelid.)                  Sensory numbness / paraesthesia
            HYPERACUSIS: Acute sense of hearing.                                                          Buttocks and the backs of thighs (saddle area).

WILL WESTON                                                                                                                                        Page 10 of 18
                          Does loo paper feel different?                                                      Micrographia
              Lower motor neurone weakness                                                        Abdomen : 1 stomach
                          Features depend on level at which CE compressed.                                    Peristalsis  Constipation.
                          Commonly, foot becomes flail with loss of dorsiflexion                  Feet : 2 feet
                            of the foot (L4) and toes (L4,5), and of eversion and                              Festinant gait: Flexed / unstable posture with Short
                            plantarflexion (S1).                                                                 shuffling steps as if one step behind ones centre of
                          Ankle jerks are usually absent on both sides.                                         gravity. Loss of arm swing (Early sign).
 DDx       Back Pain: Mechanical, GB Syndrome, Lumbar (Inter-vertebral) Disk                                      Feet as if frozen to ground: Mx with Stand
           Disorders, Neoplasms, Spinal Cord, Spinal Cord Infections / Injuries                                  still…gather rhythm, counting 1, 2, 3…and step.
   Inv /   Lmbar MR           The definitive investigation if facility available                  Other:
    Dx     XR                 Limited benefit in inv of lumbar disc disease                                  Sweating, Aches / Cramps (Early signs), Obsessional
 (same                        May reveal loss of disc space / spondylolisthesis                                 traits, Depression, Dementia, Lethargy, Fatigue.
  as for                      It is more important in excluding other causes,         DDx      Drug induced Parkinsonism (esp dopamine receptor antagonists:
 inv for                          e.g. metastatic bony changes                                  antiemetics, antipsychotics, reserpine), Essential tremor, Normal
  lumbr    Radicul-           May show filling defect in theca on AP / lateral                 pressure hydrocephalus, Mass lesions (tumour, subdural hematoma),
   disc    ography:               view                                                          Infarct, Wilson’s disease, Poisoning (CO, methanol, manganese)
   slip)                      May Show Obliteration Or Displacement Of                         Diffuse Lewy body disease (Hallucinations + PD S&S).
                                  Nerve Root Sleeve                                             Multi System Atrophy (Swallowing & Breathing problems +/- Stridor,
           Spinal CT          May detect small, laterally-placed protrusions                   Postural Hypotension, PD S&S. Life Expectancy 2-5 Yrs).
                                  which may be missed on radiculography                         Progressive Supranuclear Palsy(Rigidity+/-Trem+/-Eye movemnts).
                              Shows hypertrophied facet joints and diameter           Inv /    Clinical              See above
                                  of spinal cord                                       Dx       Drugs                 Response to Dopamine Agonist therapy
           Electro-           Denervation in muscles supplied by affected                      CT                    Rule out other pathology
           myography              roots may be shown                                            DAT Scan              May show loss of dopamine cells.
                              A low specificity test                                           Autopsy               Only definite way! Indicates Lewy bodies
 Tx            Neurological emergency. Any delay in root decompression                                                  (eosinophilic structures located within the
                  will reduce chance of full motor and sphincter recovery.                                                cytoplasm of neurons: sign of degeneration)
               Full laminectomy necessary for adequate exposure.                     Tx       Aims to  Dopamine levels in CNS
 Comp         Sphincter recovery is often incomplete                                              Redressing Loss of
                                                                                                                                  L Dopa (1 line)
              Sexual difficulties may persist.                                                        DA:                        Dopamine R Agonists (2nd Line):
                                                                                                                                  Ropinerole, Bromocriptine
 PARKINSON’S DISEASE                                                                               Inhibit breakdown of          Selegiline (3rd Line)
 Def           Age-related, chronic, progressive, neurodegenerative disorder                          DA in CNS neurons:
               Progressive degenerative disease resulting from loss of                             Unbalanced action           Benzatropine
                   dopaminergic neurons in substantia nigra & other CNS areas.                         of Ach in striatum:
 PP            1-2/1000,  to 5/1000 > 65,  20/1000 > 80.                                        NB: Do not affect progression of disease
               ♂=♀, Race: ○ > ● (2:1);  Incidence within families.                               NB:  Drug Tolerance = Honeymoon period of  symptoms 
               2nd > common cause of chronic neurological disability in UK                            wearing off of the medication effect before next dose is due 
 Path      Mostly Unknown cause (Idiopathic):                                                         on / off symptoms (‘off’ periods bear no relation to dosing times-
 Basal Ganglia composed of:                       (Numbers =   , Letters = L  R)                   may move from being symptomatically well controlled to being
 1. Caudate Nucleus                                                                                    ‘switched off’ in mins)
 2. a) Putamen [neostriatum: NS], b) Globus Pallidus ext &intc :GPe/GPi                             Thalamotomy ( tremor on contralateral side).
 3. Substantia Nigra (reticulate & compacta: SNr & SNc)                                             +/- Deep brain stimulation (conduction blocks GPi)
 4. Subthalmic Nucleus: STN                                                                         Pallidotomy ( GPi)
         Degeneration of dopaminergic nigrostriatal tract ( from SN  NS)                          ( Implantation of Dopamine rich fetal nigral tissue)
                            Also formation of Lewy bodies                              Mx          High fibre diet +/- prune juice / senna
                                                                                                  Mechanical aids, Velcro > buttons
                   inhibitory effect of Dopamine from NS on GPe                       Prog        No definitive cure  Lifelong Tx
                                                                                                  Meds have prominent S/Es e.g. dyskinesis
                          activity in STN   activity in GPi                                     Idiopathic PD has better prognosis than other causes of
                                                                                                      Parkinsonism
                   inhibitory output to VA-VL nucleus of thalamus                     Comp        See S&S
                 activation of SMA and other adjacent cortical areas                  ALZHEIMER’S DISEASE
                                                                                      Def       Progressive dementia with insidious onset, characterised by
                             Inability to initiate movement                                          atrophy of cerebral cortex.
                    (explanation for tremor / rigidity is less clear)                            Dementia: State of global cognitive decline that impairs normal
 Ach is also in NS. In PD, levels are N but lack of dopamine  imbalance b/w                         social & occupational functioning; normal consciousness is
 the two  further upset muscle coordination. (In attempt to restore this balance,                   preserved.
 drugs are used to block transmitter actions of Ach &  dopamine levels.               PP        Primarily affects older individuals (but also familial form
                                                                                                     affecting younger pts.)
 Also deficits in neurotransmitters outside SN & NS (1+2)  Neurotransmitter                     70% dementia cases = Alzheimer’s
 deficits  So-called 2o symptoms (depression, senility, sleep disorders, speech                 Prevalence <1% < 65. 30-40% > 85;               ♀>♂ (slight)
 problems)                                                                             Cause     Genetic mutations: 1, 14, 19, 21
 1. Dopamine producing neurons in other parts of brain can be affected                           E4 polymorphism of apolipoprotein gene on chromosome 19
 2. Neurotransmitters: norepinephrine, serotonin & GABA may also .                    Path       Associated with development of neurofibrillary tangles (NFTs) &
 S&S         ≥75% of nigro-striatal neurons need to be lost to  S&S                          senile neuritic plaques (SNPs) in parahippocampal & parietotemporal
            Triad of Cardinal Signs: (TRAP: Tremor Rigidity, Akinesia, Posture)                                               cortical areas.
              Tremor- Resting                                                                                                        
                          ‘Pillrolling’, pro/supination, coarser > cerebellar                                           Cell death within cortex
                          Better: movement / sleeping
                                                                                               2o Loss in cholinergic innervation of cortex with associated atrophy of
                          Often more on one side.
                                                                                                                cholinergic neurons in basal forebrain
                          Worse: rest / excitement / upset… not controlled by                                                       
                             medication during these emotions.                                                Progressive memory / language difficulties
              Rigidity +  tone                                                        S&S       Memory impairment
                          Lead Pipe: limbs resist passive ext through movement                  Loss of reasoning ability
                             (rather > spasticity clasp knife)                                   Difficulty with activities on a daily basis
                          Cogwheel (Rigidity + Tremor): Juddering on passive:                   Decline in language function
                             extension of flexed forearm / pronation / supination                Decline in cognition
              Akinesia:Bradykinesis:Slow movement-Test:Finger-Thumb touching                     Viseo-spatial disturbances
              + Loss of Postural Stability                                                       Agitation, Behaviour , Psychosis- may subside.
            Other S&S … From Top to Bottom:                                                      Parkinsonism, Seizures, Incontinence, Wasting, Mutism– all
               Head:: (1 face, 2 eyes, 1 mouth)                                                    may occur
                           Expressionless face (hypomomia)                           DDx    Pick’s disease, Parkinson’s disease, Multi infarct dementia, Infectious
                           Monotonous speech +/-  dysarthria +/- soft voice               (CJD), Metabolic (Wilson’s disease, hypercalcaemia, hyper/o-
                           Blink rate                                                       thyroidism, vit B12 def), Chronic OH abuse, Tertiary syphilis, Subdural
                              Dribbling + Excess salivation: Mx: Chewing gum                hematoma, Drugs (sedatives, neuroleptics, anticholinergics),
               Hands : 2 hands                                                              Depression (pseudo-dementia)
                           Figeting                                                  Inv /  Hx & O/E        Probable Dx from pts with progressive  cognitive
                                                                                       Dx                     ability without neurologic / medical problems (possible
WILL WESTON                                                                                                                                            Page 11 of 18
                            with neurologic / medical problems)
            Ca              Exclude other causes of dementia
            Vit B12
            CT / MRI      ID atrophy of cerebral cortex & vascular infarcts
            Neuropsychological testing
            Urinalysis    Exclude urosepsis
            Autopsy       Provides definitive Dx
 Mx         No Cure                         (Tx is palliative)
            Exclude treatable disease       (B12, Folate, Syphilis, T4, HIV)
            Tx Concurrent illness
            Avoid … Cognition             (Neuroleptics/Sedatives/Tricyclics)
                                                                                                  PP             Worldwide Prevalence: 0.5-1%
            Gastrostomy Tube                (Not as common now…hand feed)
                                                                                                                 Idiopathic Epilepsy in 75% cases
            Nice Guidelines:                                                                                     Absence Seizures: begin in childhood & rarely  >20
               Alzheimer’s should be Dx and Tx by specialists                                                   Incidence at extremes of age spectrum (IU)
               Assess 2-4/52 after maintenance dose established
                                                                                                  Path           If provoked sufficiently any brain can elicit a seizure
               Re asses every 6/12 in specialist unit.
                                                                                                                 Pt may experience a single seizure as a sign of transient
             Donepezil: Reversible inhibitor of acetylcholinesterase 
                                                                                                                  cerebral overload- Only if recurrent & not provoked by systemic
            cogitative function (improves 40% mild-mod pts)
                                                                                                                  disease, is pt Dx with epilepsy.
            SE: Bradycardia,  gastric secretion of H+  ulcers
                                                                                                             Although different causes / manifestations, epileptic seizures
 Prog       Mean of 7 yrs b/w onset and death                                                                     always reflect imbalance between excitation and inhibition in
                                                                                                                  the brain  abnormal hypersynchronous electrical activity of
 EPILEPSY                                                                                                         neurons
 Def               Clinical: Cond where seizures recur, usually, spontaneously.                             Gamma-aminobutyric acid (GABA) is major inhibitory
                   Pathological: Tendency to spontaneous, intermittent, abnormal                                 neurotransmitter of the CNS
                    electrical activity in part of the brain manifesting as seizures.                        Under N conditions, the excitatory post-synaptic potentials are
                   Seizure: Clinical: An intermittent stereotyped disturbance of                                 followed immediately by GABAergic inhibition. Neuronal
                    consciousness, behaviour, emotion or sensory function that on                                 hypersynchronization occurs if excitatory mechanisms
                    clinical grounds is believed to result from cortical neuronal                                 dominate (initiated by  excitation or  inhibition). As
                    discharge.                                                                                    abnormal neuronal hypersynchronous activity continues, more
                                                                                                                  and more neurons will be activated  epileptic seizure.
         LOC                                                                                                Abnormal hypersynhcronization  characteristic abnormalities
        Motor: Jerking, muscle rigidity, spasms, head-turning e.g. Jacksonian E                                   on electroencephalogram.
        (Due to lesion in 1o motor area  Jerking + Tonic spasms of contralateral face & limbs.   Cause      60-70% Idiopathic
        Movement begins at angle of face / thumb & index finger  arm & trunk,  leg & foot.)                Physical: Trauma, space occupying lesions, stroke, V High BP,
        Sensory: Unusual sensations affecting vision, hearing, smell, taste or touch                              tuberous sclerosis, SLE, PAN, sarcoid / vascular
        Autonomic: Stomach sensation                                                                              malformations.
        Psychological: Memory or emotional disturbances eg. Déjà vu, fear                                    Metabolic: OH withdrawal,  Ca2+,  Mg,  Glucose, /
                                                                                                                  Na, Hypoxia, liver disease, Drugs: Abs, Antimalarials, Anti
          Simple             Partial         Complex           LOC                                               arrhymics, Pychotrophic agents- Lithium, TCAs, phenothiazines
        Partial: 12%                        Partial: 20%      Automatisms such as lip                        Infection: Meningitis, Encephalitis, HIV
                                                              smacking, chewing,
                                                                                                  S&S     Before Seizure:
                                                              fidgeting, walking (+ other
                                                                                                             Prodrome- Mood /  behaviour (hrs/days)
                                                              repetitive movement)
                                                                                                          Part of Seizure
                                                                                                             Preceding sensory / psychic AURA: Light-headedness, strange
                                                                                                                  smells / gut feeling, déjà vu, flashing lights
                                                                                                             Seizure
           1o                                  2o             Difficult to distinguish from               After Seizure
        Generalised        Generalised      Generalised       1o:                                            Temporary weakness of affected limbs (Todd’s Palsy)
                                                              Look for Aura & focal                          Headache, myalgia, confusion, sore tongue
                                                              neurological deficit- Todd's        DDx     Seizure: Trauma, Infection (meningitis, encephalitis, HIV), Stroke,
      ALL  LOC                                               paralysis (persistent                       Mass lesion, Hypoglycaemia, Uraemia, Hyperthermia, Electrolyte
      May be FHx                                              weakness [≥ hours] at                       abnormality, Drug overdose / withdrawal, Cerebral ischaemia,
                                                              affected site                               Eclampsia, Porphria, Syncope
                                                                                                          PAEDS: Arrhythmias, Migraine, Narcolepsy, Night Tremors, Faints
            Tonic Clonic      Aka Grand Mal: 60%                                                          (reflex anoxic seizures), Tics, Munchausen’s.
                                                                                                  Inv /   1.     Distinguish seizures from other episodic events
           TONIC (10-30 secs): Consciousness lost  fall  Legs extend, Arms                      Dx      2.     Distinguish acute symptomatic seizure from those of Epilepsy
           abduct, Elbows & wrists flex.                                                                  3.     ID the aetiology & define the Epilepsy syndrome
           +/-CLONIC (1-5 mins): Jerking of the muscles. Incontinence of urine,                           Witness Hx         Faints -ve to following whilst Seizures +ve:
           dribbling from the mouth and tongue-biting. Movements rapid  slow                             U&Es               Aura, Cyanosis, Tongue biting, Post ictal confusion /
           +/-COMA (Up to hours): Deeply unconscious, with complete muscular                              LFTs               amnesia / headache.
           flaccidity. Absence of corneal or tendon reflexes / extensor plantar                           Glucose
           responses. In awakening may be headache and dazed look.                                        Ca2+ / PO43-           Evaluate potential systemic cause of seizure
              Absence         Aka: Petit Mal- Often Children. LOC Brief: 5-10sec.                         INR / PTT
                              No  postural tone.
                                                                                                          MRI                    Detect underlying cerebral pathology
                                                                                                          CT                     <sensitive than MRI but faster, cheaper
             Myoclonic        Often teenagers. Sporadic (isolated) jerking movements,                                            Haemorrhage best evaluated on CT
                              usually in the arms, within 1 hr of waking                                  Toxicology             If drug OD / withdrawal suspected
                                                                                                          LP                     If Meningitis / Encephalitis suspected
                Clonic        Repetitive, rhythmic jerking movements                                      EEG                    Dx of epilectiform activity  classify specific
                                                                                                                                     type of seizure (N ≠ exclusion)
                                                                                                  EEGs    Electroencephalogram: Useful tool esp children and neonates for …
                Tonic         Muscle stiffness, rigidity                                                   Distinguishing ABSENCES from COMPLEX PARTIAL SEIZURES
                                                                                                           Distinguishing PRIMARY and SECONDARY generalised seizures
                                                                                                           Distinguishing ABSENCE EPISODES from DAYDREAMING
                Atonic        Loss of muscle tone                                                          Characterising electromechanical syndromes
                                                                                                           WAVES TO BE AWARE OF:
                                                                                                           Delta (.05-3 hertz)
               Infantile      Eg: 5/12. Jerks forward: arms flexed, hands extended
                                                                                                            Produced in deep, dreamless sleep
                Spasm         (Salaam attack). Rptd every 2-3 secs up to 50x

                                                                                                           Theta (4-7 hertz)
                                                                                                            Drowsiness, inattention, deep meditation. A person with epilepsy
WILL WESTON                                                                                                                                                     Page 12 of 18
        will often produce bursts of theta.                                                                                           
                                                                                                                        Continues 10 Min
                                                                                                                                      
                                                                                                        Lorazepam (IV / IO)        Skip  Next Step: If Still No IV
                                                                                                                        Continues 10 Min
        Alpha (8-12 hertz)                                                                                                         
         General relaxation and meditation                                                                              Paraldehyde (PR)
                                                                                                                        Continues 10 Min
        SMR (sensorimotor rhythm) (12-15 hertz)                                                                               
         Relaxed concentration. Often used for seizure control.                                Call Senior Help: Phenytoin (Phenobarbitone if already taken)
                                                                                                                        Continues 10 Min
        Beta (15-18 hertz)                                                                        Call Anaesthetist and  ITU: Anaesthesia…Thiopental
         Focused attention                                                        Mx        Drinking  / Contraceptive [Some Tx is enzyme inducing] / Driving
                                                                                             advice: Document! (Pt with epileptic attack must not drive for 1 yr.)
                                                                                            One Drug at time. Start Tx after 2 fits. Discuss with pt.
        Gamma (24 hertz and above)                                                         Slowly  dose over 2-3 / 12 until seizure controlled
         Intense concentration or anxiety                                                   When   begin new at starting dose and withdraw old  over
                                                                                             6/52 (quicker if toxicity)
                                                                                           Generalised        1. Sodium Valproate (or Lamotrigene)
                                                                                                              2. Carbemazepine
        EEGs of people with epilepsy look something like this:                            Partial            1. Carbemazepine (or Lamotrigene)
        Spike-and-slow-wave                                                                                  2. Sodium Valproate
                                                                                            Carbemazepine               100mg / 12hr PO
                                                                                            Sodium Valproate            200mg / 12hr PO +INR +LFT testing
                                                                                            Lamotrigene                 50 mg/day: Beware of use in age <12.
                                                                                            Phenytoin                   No longer 1 line:S/E &dose monitor
        3-second spike-and-wave (Absence or Petit Mal)                           Prog     Absence: 50%  Generalised Tonic Clonic
                                                                                           OUTCOME AFTER 20 YEARS: (Davidson’s)
                                                                                           50%: Seizure free, for last 5 years, without medication.
                                                                                           20%: Seizure free, for last 5 years, with medication.
                                                                                           30%: Seizures continue despite treatment.
        During Tonic Clonic seizure
                                                                                  HUNTINGTON’S CHOREA                                                      
                                                                                  Def    Progressive disorder, consisting of a triad of
                                                                                         1) Choreoathetosis, 2) Dementia 3) Autosomal dominant inheritance
                                                                                         with complete penetrance.
                                                                                         CHOREOATHETOSIS : Nervous disturbance marked by involuntary
        An EEG of a person without epilepsy would look something like this:             purposeless & uncontrollable movements characteristic of…
                                                                                         CHOREA: Incoordinated spasmodic moving of limbs & facial muscles
                                                                                         ATHETOSIS: Continual slow movements especially of extremities)
       NORMAL PATTERNS (in adults):                                               PP     Typically: 35-40 yrs (onset may be predicted by no of CAG repeats)
        Alpha - 8-12 Hz in occipital and parietal regions                        Path   Autosomal dominant mutation of chromosome 4   CAG repeats 
        Beta - more than 12 Hz in frontal regions                                       loss of GABA neurons in caudate & putamen
        Wave patterns that are slower during sleep                               S&S      CHOREIC Involuntary movements: hands / face:
       ABNORMAL PATTERNS:                                                                             Worse with voluntary movement
        Theta 8-12 Hz in parietal and occipital regions
                                                                                                       By emotional stimuli
        Delta < 4 Hz - Any slow wave pattern suggests acute problems.
                                                                                                      Disappears with sleep
        Brain death is indicated by absence of activity in normothermic
                                                                                            DEMENTIA: Memory loss, Apathy
         patients not exposed to sedative drugs.
        Specific Patterns…See below:                                                       PERSONALITY :
       PETIT MAL EPILEPSY: Classically a 3 cycle/sec spike-wave EEG                                   Agitation, Psychosis, Irritability, Antisocial behaviour
       which arises from all four quadrants of brain. May be induced by                     Brisk reflexes
       getting subject to hyperventilate, or by flickering lights.                          Unable to maintain tongue protrusion
       1o GENERALISED EPILEPSY: Paroxysmal activity usually                       DDx    Neuroacanthocytosis, Sydenham’s chorea, Various causes of
       generalised & synchronous, often consisting of spike & slow wave                  dementia eg AD, Pick’s disease, Tardive dyskinesia from neuroleptics
       complexes in single bursts or runs with a frequency usually 2 - 4 / sec.   Inv /  Hx             Especially FHx + Exam
       PARTIAL OR 2o GENERALISED TONIC-CLONIC SEIZURES: Often                     Dx     CSF            Normal
       assoc w local spikes, sharp waves, or spike & slow-wave complexes.                CT/MRI         Cerebral Atrophy (Characteristic bilateral marked
       INFANTILE SPASMS: EEG named Hyps arrhythmia: Mix of irregular                                        wasting of putamen & head of caudate nucleus)
       slow activity with high amplitude, and discharges. Spasm itself may               EEG            Diffuse changes
       be associated with sharp waves.                                            Mx     No Tx for disease. Control Choreic movements with:
 Tx    STATUS EPILEPTICUS:                                                                Neuroleptics, Haloperidol, Reserpine
       DEF                  Seizure lasting > 30mins / repeating with no         Prog   Progressive course;  voluntary movements  institute
                                regain of consciousness                                  Death occurs ~ 15 yrs after onset of symptoms
       PP                   Usually occurs in known epileptics
       1st INV              Clinical (usually tonic clonic), EEG                 MYASTHENIA GRAVIS (MG)
       2nd INV              Glucose, ABGs, U&Es, Ca2+, FBC, ECG                  Def   Disease characterised by progressive weakness & exhaustibility of
                            AED levels, tox screen, LP, blood culture                  voluntary muscles without atrophy or sensory disturbance.
                            Pulse Ox, Cardiac Monitoring                         PP    May occur at any age. Often young. ♀>♂ (2:1)
       Treatment Plan – after 1st INV: (Ref: Oxford Handbook)                     Cause Assoc: Thymic tumour, Hyperthyroidism, RA, SLE
                         O2 (100%)  IV access + blood tests                      Path  Autoimmune attack: Development of Abs [detectable in 90% pts] vs
                                                                                       ACh receptors at post synaptic NMJs  interference of
                     Thiamine if OH / malnourishment suspected                          neuromuscular transmission  weakness / disability
                                                                                 S&S     Muscle groups commonly affected: Extraocular (85%) > bulbar >
                             Correct Hypotension with fluids                            face > neck > limb girdle > distal limbs > trunk
                                                                                         Weakness:
                      Phase 1: Slow IV Bolus: Lorazepam: 4mg                               Prominent after persistent activity…Fatigability
                                                                                          Fluctuations > Constant
       Phase 2: IV Infusion: Phenytoin 15mg/kg. (different line from Phase 1-              Resp Muscles: Hypoventilation & Resp compromise in 10%
                           they don’t mix!) Monitor ECG / BP                               Ptosis, Diplopia
                                                                                          Difficulty in chewing, swallowing
              Phase 3: General Anaesthesia: Get Help esp if > 20 mins                      ‘Myasthenic snarl’ on smiling
                                                                                           Voice weakening- on counting to 50
       Prolonged Seizure in Children: (Ref: Barrow Paediatrics Dept)                       Reflexes Normal (may be brisk)
       ABC,  Flow O2, Blood Gluc, Confirm Epileptic Seizure…                              Exacerbated by: Pregnancy / K+ / infection / over treatment /
                 Vascular Access             No Vascular Access                               climate  / emotion / exercise / gentamicin / opiates /
                                                                                            tetracycline / quinine / procainamide / B-Blockers.
                  Lorazepam (IV / IO)       Midazolam (Buccal)
                                                                                  DDx   Amyotrophic lateral sclerosis, Guillain-Barre syndrome, Lambert-
WILL WESTON                                                                                                                                       Page 13 of 18
           Eaton (aka Myasthenic Syndrome), Hyper-thyroidism, Botulism,                             Chronic polymyositis - differentiate by electromyography and
           Poliomyelitis, Organophosphate poisoning, Mitochondrial myopathy,                         muscle biopsy
           Compressive lesions, D penicillamine (temp reaction)                                  Myasthenia gravis - bulbar signs but rarely muscular wasting;
 Inv /     Hx                & Physical signs                                                       responds rapidly to anticholinesterase
 Dx        Anti Ch           Anti Cholinergic Challenge: (Tensilon Test) Admin      Inv /    EMG       MND shows typical pattern of severe chronic denervation:
                                 of edrophonium (short acting anticholinesterase)    Dx                    Spontaneous fibrillation potentials
                                   Muscle function in ~ 1 min in MG                                       Number of spikes on activity due to  motor
                             Only if atropine + resuss to hand.                                               neurones and thus, motor units present
           Normal            Blood, CSF, Urine                                                             Duration & amplitude of AP of surviving units
           Antibody           Antiacetylcholine receptory antibody                 Tx       There is no cure for MND. Professional counselling and support are
           EMG               Repetitive nerve stimulation   muscle                         important. Symptomatic treatment includes:
                                 responsiveness                                                  DYSARTHRIA / DYSPHONIA - speech assessment and
           CT                Rule out thyoma / thymic hyperplasia                                   therapist +/- communication aids
           TSH               Rule out hyperthyroidism                                           DYSPHAGIA - feeding gastrostomy; cricopharyngeal myotomy;
 Mx         Symptomatic Tx: Anticholinesterases: Pyridostigmine                                     pay caution to food consistency - that of porridge is usually
            Underlying Auto I: Prednisolone                                                         swallowed better than solids or liquids
            Thymectomy: Thyoma…may be curative but effects only seen after                      DROOLING - anticholinergics, e.g. benztropine
           months- performed in Ab +ve pts with S&S involving eyes plus others.                  MUSCLE WEAKNESS - physiotherapy, walking aids, splints
                                                                                                 SPASTICITY - baclofen (20-60mg/d) or low dose diazepam -
 Prog      Relapsing / Slow progression. If thyoma: 5 yr survival is 30%.
           If limited to ocular muscles for > 2yrs, rarely extends to more.                          occupational therapists help the patient to remain at home
                                                                                                 RESPIRATORY FAILURE - tracheostomy and artificial
                                                                                                     ventilation may prolong life but should be avoided
                                                                                                 MOOD - The MND Association gives valuable help.
 Def       Most commonly UMN & LMN S&S, but may be more of one.                               Important to consider the patient's QOL in all decision making.
           Affects limb muscles or those supplied by cranial nerves.                          Tx Vs disease process (NICE): Riluzole in Tx of ALS MND.
           Characteristics of lower motor neurone disease include:                           Expensive and not particularly effective.
              weakness and wasting, hypotonicity,  reflexes, fasciculation.
                                                                                     Prog     Based on the type. Generally, PMA and ALS progress to bulbar palsy,
           Characteristics of upper motor neurone disease include:
                                                                                              which is eventually fatal. Prognosis  based on how long conditions
              weakness, spasticity,  tendon reflexes with clonus, extensor
                                                                                              take to progress to bulbar palsy, as follows:
              plantar response.
                                                                                                 Progressive muscular atrophy: 5 - 8 year survival
         Both UMN and LMN S&S can be found in the same limb.
                                                                                                 Amyotrophic lateral sclerosis: 2 - 5 year survival
 PP        Incidence: ~2 / 100 000 / year except in endemic areas e.g.
                                                                                                 Progressive bulbar palsy: less than 2 year survival
              Island of Guam
           Prevalence: 5-6 / 100 000 of population. M > F (2:1)
                                                                                     MULTIPLE SCLEROSIS                        UMN Lesion Condition (NOT LMN!)
           Onset: Mean = 55; Range = 16-77 y, but usually in 60s-80s.
                                                                                     Def     Neurodegenerative disease of unknown cause characterised by
 Class  3 Types but distinction is artificial since most patients eventually
                                                                                             gradual accumulation of focal plaques of demyelination in Spinal Cord
        develop features of all three:
                                                                                             and Brain (Esp in periventricular areas, optic nerves & chiasma,
           Progressive muscular atrophy
                                                                                             subpial region).  Peripheral nerves not affected.
           Amyotrophic lateral sclerosis (most common)
           Bulbar involvement - either:                                                        RELAPSING/REMITTING MS – S&S come and go. Periods of
                                                                                                    good health or remission followed by sudden S&S or relapses
                     Spastic: Pseudobulbar palsy
                                                                                                    (80% people at onset).
                     Flaccid: Bulbar palsy
                                                                                                SECONDARY PROGRESSIVE MS – follows on from relapsing/
                     Mixed: Progressive bulbar palsy
                                                                                                    remitting MS. Gradually more or worsening symptoms with
 Cause  Unknown aetiology. 5-10% of cases show a family link. The others                            fewer remissions (~50% of those with relapsing/ remitting MS
        occur sporadically. Syndromes resembling MND may occur:                                      secondary progressive MS during first 10 years of illness).
           After trauma to a limb                                                              PRIMARY PROGRESSIVE MS – From beginning, gradually
           After chronic poisoning: Mercury, lead, manganese, selenium.                            S&S develop & worsen over time (10-15% people at onset).
           Assoc disorders of metabolism: Hypoglycaemia, Uraemia,
                                                                                     PP         > Common in temperate areas. Lifetime risk: 1:1000
              macroglobulinaemia, and following gastric surgery
                                                                                                Prevalence: 100 – 120 / 100 000.
           Assoc other progressive degenerative nervous system
                                                                                                Incidence: 3-7 / 100 000 / Year
              diseases of unknown cause: Pick's disease, parkinsonism, CJD
                                                                                                Rarer in Africa / Asia
 Path   Results in pathological changes in anterior horn cells, motor nuclei of                 ♀>♂ (1.5:1). 10 x  risk in 1st Relatives.
        the medulla, and corticospinal tracts.                                                  Mean age of onset: 40 yrs (Rare before puberty / after 60).
           Macroscopic:
                                                                                     Cause     
                     Thinning of the anterior roots of the spinal cord
                                                                                     Path    Cell mediated autoimmune attack of myelin sheath producing
           Microscopic:
                                                                                             oligodendrocytes  Demyelination & inflammation of CNS white
                     Loss of neurons in ant horns, CN nuclei, & motor                       matter (Reversible especially with steroids)  Inflamed areas scarred
                        cortex.                                                              in multiple areas (MS)  Axonal loss (Persistent)
                     Among cranial nuclei, the hypoglossal nucleus,                         Most commonly affected areas:
                        nucleus ambiguus and trigeminal motor nucleus are                       Optic Nerve  Optic neuritis / Retrobulbar neuritis (can’t see
                        particularly affected with 3rd & 4th nerve nuclei                           any change on fundoscopy…Pt can’t see + Doctor can’t see!)
                        invariably spared.                                                      Cerebellar  Cerebellar S&S
                     Reduction of corticospinal & corticobulbar tract fibres -                 Spinal Cord  Cervical region: Lateral (Motor  Spastic
                        corticospinal degeneration is asymmetrical.                                 paralysis, Urinary Incontinence, Constipation).
 S&S    Presentation of MND depends on particular pathways involved:                            Spinal Cord  Cervical region: Dorsal (Sensory  VPL loss).
           Combined UMN and LMN S&S are present in 65% of cases                                Periventricular: Useful for Dx on MRI.
           Bulbar features are present in 25%                                       S&S        1st Presentation usually monosymptomatic:
           Muscle weakness and atrophy are present in 10%                                      Progression: Relapses (Days – Weeks)  remissions of full
        S&S develop gradually. Initial complaint is often non-specific, e.g. a                      functional recovery (Weeks - Months)  incomplete remissions
        weakening hand grip. Characteristic complaints:                                              accumulative progressive disability (not always the case)
           HAND - wasting, weakness, fasciculation                                             Lhermitte’s Sign: Limb tingling on flexing of neck
           BULBAR Involvement - dysarthria and dysphagia                                       Babinski’s reflex (Extensor Plantar Reflex): Stroke lateral sole
           LOWER LIMB - weakness with spasticity                                                   from heel to big toe. Norm to flex toes. <2 / UMN lesion (MS) 
           BREATHING difficulty                                                                    Extension of big toe + abduction of other toes.
        Characteristic negative features:                                                       Subacute painless spinal cord lesion
           NO SENSORY loss or cognitive loss               c.f. MS                             Subacute  function of upper limb
           SPHINCTERS are never affected                   c.f. myasthenia gravis              Cranial Nerve Palsy, Recurrent facial palsy
           OCULAR MUSCLES are never affected c.f. myasthenia gravis                 FATIGUE                                          Look for depression.Review 
 DDx    Other diseases which  muscular wasting, especially of upper limbs:          COGNITION          Memory, Dementia             Assessment
           Syringomyelia - fasciculations are rare; dissociated sensory
              loss from an early age
                                                                                     DEPRESSION:       Common, severe, Txable         Antidepressants
           Intramedullary tumour - sensory loss usually prominent
                                                                                                       (Euphoria rare)
           Cervical spondylosis - sensory loss is usually present but the
                                                                                     MOTOR             Weakness (UMN)                 Exercise
              upper limb weakness and lower limb spasticity may be
              remarkably similar to MND. MND has a more rapid myelopathy                               Spasticity                     Baclofen
              and cervical disc protrusion will be absent on X-ray.                  CEREBELLUM        Ataxia, Nystagmus              Specialist Rehab Team.
              Occasionally, MND may co-exist with cervical spondylosis.                                Intention Tremor,              (Dysarthria: Speech Tx.
           Cervical rib - fasciculation absent, pain prominent, sensory loss                          Speech: Dysarthria             Nystagmus: Gabapentin)
              usually present, characteristic radiology                              SWALLOW           Dysphagia in 43%               NG tube - PEG insertion.
           Peripheral nerve lesions - localised wasting, usually                    EYES              Visual defects on              Uthoff’s Syndrome: Air Con,
              accompanied by sensory loss.                                                             Exercise / Temp  e.g.         Cooling Suit,  4-
           Peroneal muscular atrophy - sensory loss                                                   bath [Uthoff’s Syndrome].      Aminopyridine

WILL WESTON                                                                                                                                       Page 14 of 18
                    Optic neuritis (Central                                                         Tuberculous
                    visual loss & pain on                                                Polyneuropathy In Neoplastic Disease
                    movement), Diplopia                                                  Diabetic Polyneuropathy
 SENSATION         Numbness, Pins/Needles       Specialist Rehab Team                   Endocrine And Metabolic Diseases
                     Propr / L Touch / Vib      See Nervous System Notes:               Nutritional Deficiency
                    N: Pain / Temp / C Touch     Dorsal Column Affected.                 Systemic Connective Tissue Disorders
 PAIN               Dysaesthesia                 Musculoskeletal- Analgesia              Musculoskeletal Disorders
                    Trigeminal Neuralgia         Neuropathic- Carbemazepine              Diseases Classified Elsewhere
                                                                                         Uraemic Neuropathy
 BLADDER            General                      US + Inv for UTI.
                    Incontinence                 Pelvic floor exercise.
                                                                                    Causes of Peripheral Neuropathy:
                    Urgency                      Urgency- Oxybutynin
                                                                                    Alcohol, B12, CRF and Ca, Diabetes, Drugs, Every Vasculitis
                    Frequency                    Frequency, Nocturia-
                                                 Desmopressin                       HEREDITARY MOTOR AND SENSORY NEUROPATHIES (HMSNs)
 BOWEL              Constipation                 Laxatives, Suppositories,          Def    Inherited neuropathies affecting motor & sensory peripheral nerves.
                                                 Enemas.                            PP        1:2500
 SEXUAL           ♂ Impotence                    Sildenafil                         Class  HMSN I
 PRESSURE         ( sensation / cognition /     Education, Inspection,                       AKA: Hypertrophic Charcot Marie Tooth disease
 ULCERS           movement)                      Padding.                                     Describes histological appearance of nerves
 RARE                                                                                         Demyelinating neuropathy with slow conduction velocities
                  Aphasia, Epilepsy
                                                                                           HMSN I
 DDx    Other dymyelinating disease (central pontine myelinosis), structural
                                                                                              AKA: Neuronal Charcot Marie Tooth syndrome
        lesions, brain tumour, head trauma, encephalomyelitis, vasculitis,
                                                                                              Ie. With relatively preserved nerve conduction velocity, but
        vascular diseases, chronic infections, Vit B12 def  subacute
                                                                                                  small motor & sensory APs.
        combined degeneration, neurosarcoidosis, neurosyphilis, HIV
                                                                                              Presentation is similar to HMSN I but more wasting
                                                                                              Axonal neuropathy with near N conduction velocities
 Inv /  Clinical     Dx. See above + Slowed evoked responses to visual,
                                                                                           HMSN I
 Dx                  somatosensory, other stimuli.
                                                                                              AKA: Dejerine-Sottas disease.
        CSF          Protein N/ Slight . Oligoclonal bands.  IgG
                                                                                              More severe, presenting in infancy
        MRI          Lesions (sensitive but not specific). Dx in concordance
                                                                                    S&S       Distal wasting / weakness (inverted champagne bottle legs)
                     now with Mcdonald criteria (scarring around white matter).
                                                                                              Areflexia (absence of reflexes)
                     [Dx used to require demonstration of lesion in >1
                                                                                              Pes cavus
                     anatomical place at > 1 time with no other explanation]
                                                                                              Claw toes
        Others       Exclude other conditions: CXR, Serum ACE, Serum B12,
                                                                                              Distal sensory loss
                     Antinuclear antibodies.
                                                                                    Other  Hereditary Sensory Neuropathy: Rare autosomal recessive /
 Mx     MULTIDISCIPLINARY TEAM!!!                                                   s      dominant condition. Usually presents in childhood. Loss of pain
 (Gen)    Polyunsaturated fat ( linoleic acid   anti inflam)                          predominantly in hands / feet +/- charcot joint deformities and
         Methylprednisolone [ IV /  PO] ( relapse rate: no  in prog)
                                                                                           neuropathic ulcers of feet.
         B Interferon (Used mainly for Relapsing / Remitting):
                                                                                           Hereditary Sensory and Autonomic Neuropathy: HSAN I-V
           Can  relapse rate by 1/3 BUT £. Interferon B1A i.e. that
                                                                                    Mx     None. Tx Disability
               used for IM inj has 5% risk of ABs being formed against it, while
               those SC have > 20% chance.)                                         CHARCOT-MARIE-TOOTH DISEASE (Peroneal muscular atrophy)
         Glatiramer acetate (Alternative to B Interferon)                          Def    Autosomal dominant condition characterised by slowly progressive
           Not used as much. Acts as decoy for myelin sheath).                            sensorimotor neuropathy.
         Flu vaccine (Infections may worsen disability due to  in temp)           PP     Most commonly inherited peripheral neuropathy in the UK.
        Benefits Eligibility: Many aids available                                   Path   Autosomal dominant Inheritance. CMT-1A caused by duplication of
 Prog      At 5yrs 70% still employed. (20yrs: 35%)                                       peripheral myelin protein gene on chromosome 17.
           Poor Prognostic factors: ♂, Old age onset, motor signs at               S&S    TYPE I:
               onset, short interval b/w 1st / 2nd attack, many relapses in early             Demyelinating sensorimotor neuropathy
               yrs, early disability, many lesions on MRI                                     Early onset, typically in the first decade
           Death is rare (5% in 5 yrs): may  pneumonia / decubitus ulcer                    Presentation with walking difficulties and pes cavus
                                                                                              Associated deformities include eqinovarus foot and
 MYOPATHY VS NEUROPATHY                                                                           kyphoscoliosis
              MYOPATHY                         NEUROPATHY                                     Wasting occurs:
 Atrophy                 Yes                                  Yes                                       Distally before proximally: legs before the arms
                                                                                                        Distal wasting may produce the classical inverted
 Tone             Normal / Reduced                    Normal / Reduced
                                                                                                          champagne bottle deformity
 Reflexes         Normal / Reduced                    Normal / Reduced
                                                                                              Generalised areflexia
 Weakness           Proximal and                   Distal, or Nerve or Root
                                                                                              May be cerebellar ataxia of the arms
                    Symmetrical                          distribution
                                                                                              Respiratory muscles may be weak
 Sensory Loss            No                                   Yes                             Nerve conduction is slowed to less than 38 m/sec
 Categories    Muscular dystrophies            Mononeuropathies                             Peripheral nerves may be palpably thickened
               Metabolic myopathies            Polyneuropathy asymmetrical):             TYPE II:
               Dermatomyositis and              Mononeuritis multiplex.                      An axonal sensorimotor neuropathy
                polymyositis                    Polyneuropathy (Symmetrical)                 Later onset, in the second decade or later
               Polymyalgia rheumatica          Autonomic Nerve Neuropathy                   Weakness and wasting are less marked
               Drug-induced myopathy                                                         Usually there is areflexia in the legs only
                                                                                              Structural deformities are less common
 CLASSIFICATION OF NEUROPATHIES                                                               Nerve conduction is slow but always > than 38 m/sec
 AUTONOMIC NERVE NEUROPATHY                                                                   There is no palpable thickening of peripheral nerves
    To Do Later                                                                    Prog      Lifespan is normal. Disability is usually mild.
    Diseased                                                                       GUILLAIN-BARRE SYNDROME                                  May be mild / severe.
    Compression- Cranial Nerve, Median Nerve (Carpal Tunnel)                       Def     Acquired inflammatory disorder of peripheral nerves, characterised by
 POLYNEUROPATHY ASYMMETRICAL): MONONEURITIS MULTIPLEX.                                      onset of progressive weakness & sensation in > 1 limb.
    Rare disorder where there is involvement of > 1 Peripheral +/or CN.            PP      1-2/100 000 /year ♂=♀. Onset at any age. Age =  risk
    ACUTE CAUSES: PAN, Dm                                                          Cause   Frequently follows (Mean time is 3/52) viral illness (esp CMV),
    CHRONIC CAUSES: Carcinoma, SLE, RA, Sarcoid, Acromegaly,                               Campylobacter infection, surgery, immunisations.
      Hypothyroidism, Leprosy, Idiopathic                                           Path    Viral infection eg. CMV, EBV  production of antibodies (even though
 POLYNEUROPATHY (SYMMETRICAL)                                                               a virus)  Infection subsides  Antibodies remain  Antibodies
 HEREDITARY AND IDIOPATHIC NEUROPATHY                                                       attack peripheral nerves.
    Charcot-Marie-Tooth                                                            S&S        Ataxia: may be only complaint
    Déjerine-Sottas                                                                           Weakness: Progressive of extremities
 INFLAMMATORY POLYNEUROPATHY                                                                               Subacute onset
    Guillain-Barré syndrome                                                                               Symmetrical
 OTHER POLYNEUROPATHIES                                                                                    Ascending (Distal  Proximal  Respiratory, trunk,
    Drug-induced                                                                                            cranial muscles)
    Alcoholic                                                                                 Hypoventilation: Respiratory Muscles
 POLYNEUROPATHY IN DISEASES CLASSIFIED ELSEWHERE                                               Ocular symptoms,  Swallowing: Cranial Muscles
    Infections                                                                                Reflexes: Absence of deep tendon. Plantars remain normal.
            Diphtheria, Infectious Mononucleosis, Leprosy, Lyme Disease,                      Pain: Severe visceral
               Mumps, Postherpetic, Syphilis- Late, Congenital Syphilis- Late,                  CN Involvement: Facial is most commonly affected. I and
WILL WESTON                                                                                                                                       Page 15 of 18
                  VIII are not affected. Often unilateral DDx Bell’s Palsy.                        Infection – Other? Toxoplasmosis, Q Fever, Brucellosis,
 DDx       Chronic idiopathic demyelinating polyneuropathy, Hexocarbon use /                         Salmonellosis and Lyme Disease
           abuse, Acute intermittent porphyria, Structural lesion, Myasthenia        Path
           gravis, MS, ALS, Poliolyelitis, Botulism, Diptheria, Lyme disease, HIV,   S&S            FATIGUE:
           Heavy metal poisoning.                                                                           Relapsing / persistent
 Inv /     Hx              Required: Progressive weakness in > 1 limb +                                    Unexplained fatigue
 Dx                         areflexia (absent /  tendon reflex)                                            More than 6/12
                           Suggestive: Symmetrical weakness, CN involvement                                Unrelieved by rest
           CSF             Early: N; 1 week:  protein,  cells                                 PHYSICAL SYMPTOMS
           Nrv Cond        Diffuse demyelination,  nerve conduction velocity                              Myalgia, Arthralgia Without S&S of Inflammation, Sore
           Studies                                                                                            Throat, Headache, Rotational Or Postural Dizziness,
           Resp F          Respiratory function: tidal vol, -ve inspiratory force                            Paraesthesiae
           Rule Out        Lyme disease, HIV                                                    COGNITIVE SYMPTOMS
 Mx             Primarily supportive Tx in ITU                                                           Poor Short-Term Memory & Concentration, Word-
              Mon Resp Function 4 hrly: if < than 3  call PRHO from bed!                                    Finding Difficulty, Inability To Cope w Multiple Stimuli
                  (Intubation if resp muscles )                                     DDx       Depression, Anxiety, Lyme Disease
              Physical Therapy                                                      Inv /     Dx of Exclusion: Oxford Criteria
           Most severe symptoms in 1 /52 but may progress for 3/52                   Dx          Fatigue as main symptom: Severe, Disabling & Affects physical
           Complete recovery may take up to 6/12                                                     and Mental Function. Persists for 6/12 and present 50% of
           35% untreated pts have residual weakness.                                                 time. Definite onset and not lifelong.
           Mortality 10%. 10% unable to walk at 1 yr. 2% Recur Rate.                             Other S&S, especially myalgia, sleep and mood disturbance
           5%  Chronic disease (CIDP)                                                         Exclude        FBC, CRP (or ESR), U+Es, LFTs, TFTs, CK
 CIPD      Chronic Inflammatory Demyelinating Polyradiculoneuropathy                           with:          Urine. RhF & ANAs where indicated.
           Demyelinating disorder of peripheral nerves similar to Guillan-Barre      Mx        Graded Exercise; CBT; Alternative Tx; Antidepressants
           syndrome but  chronic weakness which is either progressive /             Prog      Extremely variable; Often lasts ~ 2 years.
           relapsing & remitting. S&S:
              Weakness which continues to evolve over more than 4 weeks             CARPAL TUNNEL SYNDROME
              Weakness which follows a relapsing and remitting course               Def        Results from compression of median nerve in carpal tunnel.
           Tx Includes: Immunosuppression with corticosteroids, Plasma               PP         Anatomical predisposition with females (3:1 F:M Ratio). Sixty
           exchange, IV Immunoglobulin.                                                             percent of patients are aged between 40 and 60 years.
                                                                                     Anat       Carpal tunnel lies deep to flexor retinaculum on anterior aspect
 NEUROFIBROMATOSIS- Peripheral (NF1, Von Recklinghausen's Disease)                                  of wrist, overlying carpal bones.
 Def    Inherited disorder, characterised by spots on the skin, neurofibromas                   The single soft-tissue structure in carpal tunnel is median nerve
        of peripheral nerves, & deformities of subcut tissues & bone.                                susceptible to damage by any lesion compressing contents.
        Neurofibroma: Benign tumor consisting mainly of connective tissue &                     Other structures in are long flexor tendons of fingers.
        produced by proliferation of Schwann cells                                              Sensory supply of the median nerve:
 PP         Prev: 1:2500 [1:35000 in NF2]; ♀=♂;  race;                                                   supplies sensation to palmar surface of hand,
 Cause      Autosomal dominant trait: Gene 17 [22 in NF2]                                                 (thumb, index, middle and radial half of ring fingers).
 Assoc  Renal artery stenosis, Pulmonary fibrosis, Cardiomyopathy, Optic                                   palmar branch of median nerve actually runs
        nerve glioma, Phaeochromocytoma, Glioblastomas, Ependymomas,                                           superficial to flexor retinaculum, unlike main part of
        Astrocytomas, Meningiomas, Medullary thyroid carcinoma                                                 nerve, so sensation preserved
 S&S:       ≥ 6,       CAFÉ AU LAIT SPOTS: flat, coffee coloured, patches of                    Motor supply of the median nerve:
 NF1     (>5mm /       skin seen in 1st yr of life (clearest in UV),  in size and                         provides motor supply to muscles of thenar eminence,
         15 mm *)      no with age. (*pre / post pubertal)                                                     recalled with acronym "LOAF":
                       FRECKLING: Occurs in axillae, groin, neck base,                                                 L = lateral two lumbricals
                       submammary area (♀). Usually present by age 10.                                                 O = opponens pollicis
                       DERMAL NEUROFIBROMAS: Small, violaceous                                                         A = abductor pollicis brevis
                       nodules, gelatinous in texture, appearing at puberty. Not                                       F = flexor pollicis brevis
        ≥ 2 of any                                                                                         Opposition of thumb particularly affected in carpal
                       painful but may itch. Numbers  over time.
          time / 1                                                                                             tunnel syndrome as other movements assisted by
                       NODULAR NEUROFIBROMAS: Arise from nerve trunk.
                       Firm and clearly demarcated. May  Parasthesiae if                                      muscles not innervated by median nerve.
                       pressed.                                                      Cause      ENDOCRINE: acromegaly, myxoedema, hyperparathyroidism.
             ≥2        LISCH NODULES : Haematomas at iris. Only seen                           INFILTRATIVE: amyloidosis, sarcoidosis, leukaemia
                       with slit lamp. Develop in early childhood & harmless.                   OTHERS:
        Others to note: Kyphosis, Tibial bowing, Exopthalmos, Seizures, S&S                                Idiopathic thickening of the flexor ligaments (FHx)
        of Assoc Conditions, Hypertension.                                                                 Pregnancy, Menopause
 DDx    Mcune-Albright’s syndrome, Posterior fossa tumours, Metastatic brain                               Repetitive use of hands
        , Multiple Lentigenes (Leopard Syndrome), Urticaria Pigmentosa                                    RA, Inflammatory tenosynovitis, Scleroderma
 Inv /  Criteria       Any 2 of: Criteria above + distinctive osseous lesion +                             Trauma, Osteoarthritis of wrist joint
 Dx                    1st degree relative with NF1.                                            Pregnancy and RA are most likely causes of in young patients.
 Mx         Multidisciplinary Team: GP, Geneticist, Neurologist, Surgeon            S&S        NUMBNESS & PARAESTHESIA in hand, usually, but not
            Yearly Mx of BP and cutaneous survey                                                   always, of thumb, index, middle, and radial half of ring finger
            Lesions may be excised (removal of all is unrealistic)                             SYMPTOMS WORST AT NIGHT - May be relieved by hanging
            Genetic counselling.                                                                   the arm over side of the bed, or by shaking arm
 Comp   Occur in 1/3 pts: Mild learning disabilities are common                                 PAIN MAY EXTEND PROXIMALLY, to shoulder region
        Malignancy (5% Pts with NF1): optic glioma, sarcomatous  in                            SENSORY CHANGES may be reproduced by keeping wrist
        neurofibroma. Epilepsy risk slightly .                                                     palmar flexed for 1 min, or compressing arm with a
        Local effects of neurofibromas:                                                             sphygmomanometer cuff.
            Nerve Root  Compression                                                           THENAR WASTING And WEAKENED ABDUCTION Of Thumb
            Gut  Bleeding, obstruction                                                    POSITIVE TINEL'S TEST: Tapping over carpal tunnel  tingling in
            Bone  Cystic lesions, pseudoarthritis, scoliosis                              thumb and radial two and a half fingers. (Also: Sign of nerve recovery.
            Blood  Hypertension 6% (RA stenosis / phaeochromocytoma)                      If site of nerve injury is tapped there is tingling along course of nerve.)
 Prog   No Cure                                                                             POSITIVE PHALEN'S TEST: Forcible palmar flexion of wrist causes
 NF2        Aka Bilateral acoustic neurofibromatosis / Central NF                          venous engorgement of canal and an exacerbation of symptoms.
            SYMPTOMS: of Acoustic Neuromas, Meningiomas                                    WRIST FLEXION TEST: Patient flexes both wrists for 30 seconds.
            Hearing, Vertigo, Tinnitus, Gait ataxia, Facial pain, Headache                Paraesthesiae will often be precipitated in affected hand.
            DIAGNOSIS: Bilateral Cranial nerve VIII tumour                          DDx    Other Nerve Entrapment Syndromes (Ulnar nerve compression and
            1st degree relative with NF2 and unilateral vestibular                         C6/7 radiculopathy), Tendon disorders, Demyelinating disease, Dm or
               schwannoma OR: Glioma, meningioma, schwannoma,                               other neuropathy (Dm is commonest cause of mononeuropathy)
               neurofibroma, juvenile cataract                                       Inv /      Electrical Studies ( Nerve conduction across wrist).
            MANAGEMENT: Screening hearing tests if abnormalities on                 Dx         Screening (Esp if bilateral): TFTs, GF, Ca, RF, Preg Test,
               MRI. Clear scan at 30: gene has not been inherited. Tx of facial                     Serum protein electrophoresis and Bence-Jones protein
               schwannoma is neurosurgical.                                          Mx        Non-surgical treatment includes:
            PROGNOSIS: Mean survival after Dx is 15 yrs.                                       Avoidance cause: Important with elements of RSI
                                                                                                Night-Time Splints in neutral position: Helpful in 80%
 MYALGIC ENCEPHALITIS / CHRONIC FATIGUE SYNDROME                                                Local Steroids: After more conservative Tx tried.
 Def                                                                                          Sx: Complete division of flexor retinaculum and decompression of
 PP                                                                                           tunnel. Successful in ~ 80% of patients.
 Cause     Unknown?
           Infection- Viral? EBV, Herpes, enterovirus, hepatitis                    BRAIN TUMOUR

WILL WESTON                                                                                                                                          Page 16 of 18
 Def          Primary brain tumours arise from CNS tissue. Account for                         give a Hx of intermittent headache of duration > 1 year.
               almost ½ all cases of intracranial neoplasms. Rest: metastatic.                TRAUMA: Haematoma, Contusion
           In adults, 2/3 primary brain tumours arise from structures above                  INFECTION: Abscess, Tuberculoma, Sarcoidosis, Encephalitis
               tentorium (supratentorial)                                                      …BUT Abscesses usually have a short hx from onset of S&S, may
           In children, 2/3 brain tumours arise from structures below                                o
                                                                                                be 2 to an obvious penetrating focus.
               tentorium (infratentorial).                                                    CYSTS…BUT arachnoid cysts not usually progressive; parasitic cysts
           Primary Tumours: Gliomas (43%), Meningiomas (10%),                                usually have Hx of geographical exposure to infective agent.
               Pituitary adenomas (10%), and acoustic neuromas.                      Inv /    CXR, LFTs         Metastases?
          Classification by tumour cell type irrelevant to brain emergency          Dx       Scull Xray         Signs of  ICP: Suture separation.
          physician because emergency treatment is same regardless of type.                                      Calcification e.g. hyperostosis of adjacent bone in
 PP        MORTALITY: Leading oncologic cause of death < 35 years.                                               meningioma
               For ♀, mortality rate from CNS neoplastic disease = Ovarian C.                                    Post clinoids erosion, e.g. cranio-pharyngioma;
           RACE: African Americans, esp women, have slightly >                                                  Osteolytic lesions, e.g. dermoid, meningiomas
               incidence of meningiomas and pituitary adenomas.                               CT                Investigation of choice; Note site, e.g. frontal/occipital,
           SEX: Meningiomas and pituitary adenomas are slightly F>M.                                           extrinsic/intrinsic; Mass effects, e.g. midline shift;
           AGE: Incidence of metastatic lesions to CNS  with age.                                             multiplicity of lesions; effect of contrast enhancement
        Posterior Fossa e.g. Medulloblastoma           4-11 Yrs                               MRI               IDs tumours around skull base and in posterior fossa
        Supratentorial tumours                          Adolescence  Adult                  Angiog            Differentiates certain tumours, e.g. meningiomas,
        Low-grade gliomas, e.g. astrocytomas           Young > Old                                              secondary tumours and gliomas; Also used to exclude
        High-grade gliomas, e.g. anaplastic            Old > Young                                              arteriovenous malformations / aneurysms
        astrocytoma & glioblastoma multiforme                                                 Bx                Burr hole, stereotactic, open with decompression
 Path   Brain Tumours  Variety of Neurological S&S.                                          CSF               LP often C/I due to  ICP. Though may obtained from
           Strategically located tumours Damage neurological paths                                            other sources (ventricular drainage on shunt insertion).
           Brain restricted within skull  Tumour growth + accompanying                      Markers           AFP, HCG
               edema  compresses normal tissue.                                     Mx        Each lesion requires due consideration of:
           Tumours proximal to 3rd & 4th ventricles may obstruct flow of                       GRADE - Benign / Malignant
               cerebrospinal fluid  Hydrocephalus.                                             SITE - How approachable
           Tumours generate new blood vessels (ie, angiogenesis),                             TYPE - Known with certainty? Conservative Tx.
               Disrupting normal BBB and promoting edema.                                      Benign Tx by excision except inaccessible / attached to structures.
           Cumulative effects of tumour invasion, peritumour edema, and                       Mx of malignant tumours / non-excisable benign lesions is complex.
               hydrocephalus may  ICP …                                                       Any existing oedema  with steroids (dexamethasone), diuretics
                       Impaired cerebral perfusion.                                           (mannitol) to  ICP.
                       Shifting / herniation of tissue under falx cerebri,                   Difficulty is then deciding when and how to operate.
                         through tentorium cerebelli, or foramen magnum.                       Monitoring with CT appropriate for small, asymptomatic tumours;
        Slow-growing tumours (Esp those in silent areas of brain e.g. frontal                   initial CT provides baseline against which to assess progress.
        love) have > insidious course  larger at detection.                                   Bx may identify histology. Depending upon nature and site of
        Most 1o tumours do not metastasize. Of those that do, intra-                            tumour, this may then be followed by partial or complete removal.
        parenchymal mets generally precede hematogenous dissemination.                         RadioTx: Either alone / following Sx. Many (not all) radiosensitive.
 Risk      Irradiation to head for reasons other than Tx of present tumour.                   ChemoTx: Disappointing. Most Tx will not cross BBB.
           Inherited Conditions: Neurofibromatosis, Tuberous sclerosis,
               multiple endocrine neoplasia (type I), and retinoblastoma.            DIFFERENTIAL DIAGNOSES
           HIV: Primary CNS lymphoma (Relatively frequent)                          DIZZINESS
           Metastatic tumours ( brain via hematogenous dissemination               Vertigo            
               via arterial system. See Metastases above.                            Loss of Balance    
 S&S       Manifestations depend on cause of S&S, but generally:  ICP,             Light Headedness   
               direct compression of essential grey / white matter, shifting of      DEMENTIA
               intracranial contents, or 2o cerebral ischemia.                       Intracranial      Alzheimer’s; Multiple Cerebral Infarcts; Chronic
           NON-SPECIFIC: Headache (often a late Pc),  mental status,                                    Subdural Haematoma; Tumours; Normal Pressure
               ataxia, N&V, weakness, gait disturbance, sensory disturbance.                              Hydocephalus; Neurosyphilis; HIV; Prion Disease
           FOCAL: Seizures, fixed visual changes, speech deficits, or                                    (CJD).
               focused sensory abnormalities (i.e. may mimic stroke)                 Extracranial      Vitamin Deficiency (B12, Folate, Thiamine); Drugs
                      Seizures may be earliest expression of tumour.                                     (OH, Solvents, Organic Poisons)
                      Jacksonian pattern, ie, focal seizure begins in one           Endocrine         Myxoedema; Ca Metabolism Disorders;  Na;
                         extremity and then  generalized, is distinctive.                                Dialysis Dementia; Hepatic Encephalopathy.
                      Depending on rate of growth, seizures may be present          Psychiatric       Depression
                         for months - years before tumour is diagnosed.              FACIAL PAIN
                      Middle-aged presenting with first seizure should be                            
                         presumed to have a tumour until proven otherwise.           HEADACHE
           TIME: Onset of S&S usually insidious, but acute episode may:             All               Tension headache; Migraine; Cluster headache;
                      Bleeding  Tumour occurs                                                           Temporal Arteritis; Raised ICP; Post Lumbar Puncture
                      Intraventricular tumour suddenly occludes third                                    ( Pressure Headache); Meningitis.
                         ventricle by means of a ball valve mechanism.               IMPOTENCE
           LOCATION:                                                                Autonomic         Dm; Crush Fracture of L1; Drugs: Some
                      HEADACHE: Location reliably indicates side of head            Nerve Lesions        Antihypertensives; Chronic Polyneuropathy;
                         affected, but not precise site. > Common with                                    Multisystem Atrophy; Parkinson’s Disease.
                         posterior fossa tumours (and intracranial tumour in         Others            Spinal Cord Lesions; Cauda Equina Lesions;
                         pediatric patients).                                                             Psychological
                      MENTAL STATUS  (esp mem  &  alertness),                    NYSTAGMUS
                         may be subtle clue to frontal lobe tumour.                  Congenital        Usually pendular, noted in infancy; May be associated
                      DEPERSONALISATION / Emotional / Behavioural                                       with poor vision.
                         may be a result of Temporal lobe neoplasm.                  Acquired          Secondary to Visual loss: Usually pendular, in 1o
                      8th NERVE: Hearing  / Disequilibrium / Tinnitus                                   position
                         …Intermittent  Continuous: Acoustic neuroma.                                 Vestibular: Horizontal / Rotary: Caused by disorder of
                                                                                                          vestibular end organ / nerve / nucleus.
              POSTERIOR FOSSA TUMOURS (Paediatric): Ataxia,                                          Gaze Evoked: Commonest form in clinical practice;
               Irritability, , Headache, Vomiting, Progressive Obtundation.                               Common with sedatives and anticonvulsants,
           SUPRATENTORIAL TUMOURS in children > commonly assoc                                           cerebellar and brainstem disease.
               with seizures, hemiparesis, visual field cuts, speech difficulties,                     Special forms: Wide range, eg. Downbeat, seesaw.
               intellectual disturbance.                                                                  Complex.
           PITUITARY ADENOMAS divided into two:                                     PAPILLOEDEMA
                       Nonfunctional pituitary adenomas asymptomatic until                           
                           large enough to encroach optic chiasm and disturb         RAISED ICP
                                                                                     S Occupying       Tumour; Abscess; Haematoma
                       Hypersecretory pituitary adenomas secrete prolactin,         Lesion
                            amenorrhea-galactorrhoea syndrome in women
                                                                                     Hydrocephalus     Obstructive; Communicating (Post Meningitis,
                           and headache, visual problems, impotence in men.
                                                                                                          Subarachnoid,  CSF Protein)
 DDx    VASCULAR: Haematoma, Giant Aneurysm, AV Malformation,
                                                                                     Diffuse Brain     Head Injury; Hypoxic-Ischaemic Injury; Meningitis /
        Infarction + Oedema, Thrombosis, (Migraine - Vascular Aetiology)
                                                                                     Swelling             Encephalitis; Metabolic ( PaCO2,  Na,  Ca);
         …BUT Infarction / haemorrhage: Rapid onset with substantial
                                                                                                          Venous Sinus Obstruction / Thrombosis; Eclampsia /
          deficit, improvement with time.
                                                                                                          Malignant HT.
         …BUT migraine rarely presents for first time in adult life and may
WILL WESTON                                                                                                                                             Page 17 of 18
 Benign IC Hypertension
 All                  Vitreous Haemorrhage; Central Retinal Artery
                        Occlusion; Central Retinal Artery Vein Occlusion;
                        Retinal Detachment; Retrobulbar Neuritis; Anterior
                        Ischaemic Optic Neuropathy (Atheroma or Arteritis),
 Postural             Essential; Anxiety; OH; Thyrotoxicosis
 Rest                 Parkinsonism
 Intention            MS; Stoke; Cerebellar Disease; Hereditary Ataxia
 Uniocular            Central Scotoma: Optic Nerve Disease
                      Peripheral Constriction: Retinal Disease
                      Altitudinal Defects: Retinal Vascular Lesions; Optic
                        Nerve head ischaemia
 Bilateral            Central Field Loss: Retinal Diseases; Bilateral Optic
                        Nerve Disease; Tobacco & OH Amblyopia; Leber’s
                        Optic Atrophy
                      Peripheral: Retinal Disease (e.g. Retinitis
                        Pigmentosa);  ICP
                      Bitemporal Hemianopia: Supracellar Meningioma;
                        Pituitary Tumour; Craniopharyngiomas; Hypothalmic
                        tumour; Carotid Aneurysm.
                      Homoymous Hemianopia (Lesion behind chiasma):
                        Tumour; Vascular lesion; Migraine.
 Vestibular           Meniere’s Disease; Vestibular Neuronitis; Benign
 Endo Organs &          Positional Vertigo; Motion Sickness; Trauma;
 Vestibular             Ototoxtoxicity; Herpes Zoster Oticus.
 Brainstem &          MS; Infarct / TIA; Haemorrhage; Migraine (rare)
 Cerebello-           Vestibular schwannoma (acoustic neuroma)
 Pontine Angle
 Cerebral Cortx       Vertiginous Epilepsy
 OH Intoxication     
 Eyes                 Opthalmoplegia with Diplopia
 Cervical Vertgo     
 All                  Dm; Stroke; Prolapsed Disc; MS; Common Peroneal
 All                  Myaesthenia Gravis;
                      Brainstem lesions affecting 3rd, 4th, 6th,

WILL WESTON                                                                                              Page 18 of 18

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