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Neuro Block

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									              Neuroscience Block
               Problems 25 – 28
Problem 25 – Parkinson‟s Disease .......................................................................................................... 2
     Pathophysiology of degenerative CNS disorders ............................................................................... 3
     Pharmacology of Drugs to treat Parkinsons ...................................................................................... 4
     Management and diagnosis of Parkinson‟s ....................................................................................... 5
     More clinical guff – Dyskinesias and Differentiation of P/EP lesions ..................................................... 6
     Neuropsychiatry ............................................................................................................................ 7
     Clinical – Neuro exam .................................................................................................................... 8
Problem 26 – Headache ...................................................................................................................... 14
     Dx of Headache .......................................................................................................................... 15
     Pathophysiology of Headache ....................................................................................................... 16
     Treatment of Headache ............................................................................................................... 17
     Neuro Path I ............................................................................................................................... 18
     Uncertainty and Defensive Medicine (again)................................................................................... 20
     Ethics – Confidentiality & Privacy .................................................................................................. 21
     Complementary Therapies............................................................................................................ 23
Problem 27 – Epilepsy ......................................................................................................................... 24
     Seizures & Epilepsy – Diagnosis .................................................................................................... 25
     Epilepsy - Pathophysiology ........................................................................................................... 27
     Neuro Pathology II ...................................................................................................................... 28
     Epilepsy – Treatment................................................................................................................... 30
     Stigma and Social Consequences of Epilepsy.................................................................................. 32
     Public Health - Driver‟s License ..................................................................................................... 32
Problem 28 – Meningitis ...................................................................................................................... 33
     Pathophysiology of Meningitis....................................................................................................... 34
     Diagnosis of Meningitis ................................................................................................................ 35
     Prevention and Treatment of Meningitis ........................................................................................ 37
     Neuro Pathology III ..................................................................................................................... 37
     Septic Shock ............................................................................................................................... 39
     Immunisation ............................................................................................................................. 39
     Ethics of Immunisation ................................................................................................................ 43
     Public Health – Infectious Diseases (Meningitis as Example) ............................................................ 46
Problem 25 – Parkinson‟s Disease
                                  Week 25 Learning Objectives

Wk Dom            LO Title                                            LO Detail
 25 BCS Pathophysiology of           1. To be familiar with a range of degenerative diseases of the CNS
        degenerative disorders of    (Parkinson‟s, Huntington‟s, Alzheimer‟s, Multiple Sclerosis), their
        the CNS                      underlying pathophysiology, and their clinical manifestations.
 25 BCS Diagnosis and management     1. To be able to recognise the symptoms and signs of Parkinson's
        of Parkinson's disease       disease and outline what is known about the changes that occur
                                     within the central nervous sytem to elicit these changes.
                                     2. To be aware of intellectual changes that occur in the later stages
                                     of Parkinson's disease and other neuropsychiatric illnesses.
                                     3. To outline the mechanism of action of drugs used to treat
                                     Parkinson‟s disease.
                                     4. To be able to evaluate the response to drug treatment of a patient
                                     with Parkinson‟s disease.
                                     5. To be aware of the effects of long term treatment with levodopa-
                                     containing preparations.
 25 ICCP Clinical examination        1. Perform a focussed central nervous system examination for:
                                     (a) Cranial nerves (including ophthalmoscopy)
                                     (b) Upper or lower limb (power and sensation)
                                     (c) Cerebellar function
                                     (d) Locomotion.
 25 PPH Retirement (Social Sciences) 1. List key issues that are likely to impact upon an individual‟s
                                     adjustment to early retirement.
 25 PPH Parkinson‟s disease and      1. Discuss the psychosocial consequences of Parkinson‟s disease to
         coordinated care (Social    patients, their families and carers, and the community.
         Sciences)                   2. (a) Describe the role of multidisciplinary teams in the management
                                     of patients with complex medical conditions.
                                     2. (b) Suggest potential barriers to, and possible strategies to
                                     enhance, successful multidisciplinary management.
                                     3. List benefits of the general practitioner‟s coordinating role in the
                                     management of a patient with a complex medical condition.
                                     4. Be able to develop a care plan for a patient with a complex medical
                                     condition such as Parkinson‟s disease.
Pathophysiology of degenerative CNS disorders

Huntington Disease
 An inherited autosomal dominant disease characterised clinically by progressive movement disorders and
  dementia, and histologically by neuronal degeneration of striatal neurons
 Chorea – jerky, hyperkinetic, sometimes dystonic, affecting all parts of the body
      o Pts may later develop parkinsonism with bradykinesia and rigidity
 Functional loss of striatal neurons is to dysregulate the basal ganglia circuitry that modulates motor
      o Degeneration of GABA-containing neurons -> loss of striatal inhibitory output to external portion
           of the globus pallidus
      o ->  inhibitory input to subthalamic nuclei -> prevents subthalamic nuclei from exerting
           regulatory effects
 Morphology:
      o Brain is small and shows atrophy of the caudate nucleus and putamen
      o Globus pallidus may be atrophied secondarily
      o Microscopically, severe loss of striatal neurons, especially in the caudate nucleus
 Clinical:
      o Age of onset is usually 40-50
      o Usually presents with choreiform movements
      o Higher cortical symptoms include forgetfulness and thought and affective disorders -> eventually
           leads to dementia

Alzheimer disease
 Degenerative cortical disease
 Most common cause of dementia in elderly – becomes clinically apparent as insidious impairment of
   higher intellectual function with alterations in mood and behaviour
 Morphology:
       o Macroscopic:
                 Cortical atrophy with widening of the cerebral sulci, most pronounced in the frontal,
                    temporal and parietal lobes
                 Compensatory ventricular enlargement secondary to loss of parenchyma
       o Microscopic:
                 Neurofibrillary tangles – bundles of filaments in the cytoplasm of the neurons that displace
                    or entangle the nucleus. They are characteristic of Alzheimer, but not specific
                 Senile (neuritic) plaques – focal, spherical collections of dilated, tortuous, silver-staining
                    neuritic processes surrounding a central amyloid core
                 Amyloid angiopathy

Multiple Sclerosis
 A demyelinating disorder characterised by distinct episodes of neurologic deficits, separated in time,
   attributable to white matter lesions that are separated in space
 Unknown pathogenesis, but suggestions of environmental, genetic and immune factors
 Morphology:
        o Lesions may appear on the surface of the brain stem or along the spinal cord, where myelinated
           fiber tracts course superficially
                 There may appear to be multiple, well-circumscribed, somewhat depressed, glassy, gray-
                    tan irregularly shaped plaques
                 In fresh state, these have firmer consistency than the surrounding white matter (sclerosis)
        o Microscopically, in an active plaque, there is evidence of ongoing myelin breakdown with
           abundant macrophages
 Clinically:
        o Because it can occur anywhere in the CNS, as a consequence, it may induce a wide range of
           clinical manifestations
        o Unilateral visual impairment during the course of a few days due to involvement of the optic
           nerve (optic neuritis, retrobulbar neuritis) is a frequent initial manifestation of MS
        o Invovlement of the brains tem produces CN signs, ataxia, nystagmus and internuclear
       o   Spinal cord lesions give rise to moto and sensory impairment of the trunk and limbs, spasticity,
           and difficulties with the voluntary control of bladder function

Pharmacology of Drugs to treat Parkinsons

Dopamine (DA) is active in the nigrostriatal pathway – which is involved with motor control. In Parkinson‟s
disease, there is a deficiency of DA in this pathway. Drugs to treat this fall into the following categories:
 Drugs that replace DA (eg. levodopa)
 Drugs that mimic the action of DA at the D2 or D3 receptors (eg. bromocriptine)
 MAO-B inhibitors (eg. selegiline)
 Drugs that release dopamine (eg. amantadine)
 Muscarinic acetylcholine receptor antagonists (eg. benzatropine)

 First line treatment, L-dopa acts as a dopamine precursor in the presynaptic nigrostriatal neurone
 Usually always combined with a peripheral dopa decarboxylase inhibitor (eg. carbidopa or benserazide)
       o Reduces the dose needed by about 10 fold
 An inhibitor of catechol-0-methyl transferase (COMT) may also be used to inhibit DA inactivation (eg.
       o Levodopa undergoes 0-methylation by catechol-0-methyl transferase, entacapone inhibits this
 Short plasma half life (2 hours)
 The decarboxylase inhibitor prevents the conversion to dopamine in the periphery
       o Since the decarboxylase inhibitors do not cross the blood brain barrier, decarboxylation occurs
           rapidly within the brain.
 Mechanism of dopamine action not really known. Theories include:
       o Flooding of the striatum with exogenous dopamine
       o  release of dopamine from the few surviving dopaminergic neurons
       o Probably due to both of the above
 Therapeutic effectiveness:
       o About 80% of pts show initial improvement (of rigidity and hypokinesia), and about 20% of those
           are restored to virtually normal motor function
       o As time progresses, the effectiveness of L-dopa gradually declines
 Unwanted effects:
       o Dyskinesia/chorea
                 Involuntary writhing movements
                 Movements usually affect face and limbs
                 These disappear when dosage is reduced, but rigidity reappears – therefore dose needs to
                   be titred
       o „On-off‟ effect
                 Rapid fluctuations can occur where hypokinesia and rigidity may suddenly worsen from
                   anything between a few hours to minutes, and then suddenly improve
                 Mechanism is not understood – it is suggested that the fluctuating plasma levels of
                   levodopa have a role to play in this
 Preventing unwanted effects:
       o Shortening the interval between each levodopa dose and  each dose
       o Segegiline may smooth the response to levodopa
       o Add DA agonists
       o Add a COMT
       o Drug holiday

 MAO inhibitor that is selective for MAO-B (predominates in DA containing regions of the CNS)
 Inhibition of MAO-B protects DA from intraneuronal degradation
 Often used in combo with L-dopa

Dopamine receptor agonists
 Bromocriptine is a D1, D2 agonist also on D3-5
 Has a longer plasma half life (6-8hrs) to L-dopa, so it does not need to be administered so frequently
 Antiviral that was discovered by accident to be beneficial in PD
 Enhances dopamine release
 Less effective than L-dopa or bromocriptine, and it‟s action decreases with time
 Side effects are less severe

Acetylcholine antagonists
 Used before L-dopa became the new kid on the block – atropine and its brothers and sisters
 Muscardinic ACh receptors exert an excitatory effect (opposite to that of DA) on striatal neurons. They
   also exert a presynaptic inhibitory effect on DA nerve terminals
       o Thus, suppression of these effects makes up, in part, for a lack of dopamine
 These diminish tremor more than rigidity and hypokinesia
 Many side effects of course
 Mainly used in PD pts also receiving antipsychotic drugs (ie. because anti-ψ drugs are DA antagonists –
   and thus nullify the effect of L-dopa)

Management and diagnosis of Parkinson‟s


                        Tremor                                    Bradykinesia

Tremor:                                                  Bradykinesia means difficulty initiating movement.
 Usually 4-7Hz                                          It can manifest itself via:
 „Pill rolling‟                                          Difficulty rising from chair
 Usually  by action, and  by emotion                   Micrographia
                                                          Mask-like face
                                                          Monotonous voice
                                                          Festinant gait
                                                          Stoop
                                                          No arm swing with gait
                                                          Difficulty turning corners

Rigidity:                                                Evaluating a Parkinsonism gait:
 Stiffness throughout the range of limb movement          step size – festinant
 Lead pipe rigidity                                      Difficulty getting started
 When stiffness is combined with tremor, smooth           distance between legs
   lead pipe rigidity gets broken up into jerky           No arm swing
   resistance to passive movement -> cogwheel             Narrow walking base
   rigidity                                               When pushed backwards, pt responds by doing
                                                             the gait in reverse

To test for bradykinesia, get the pt to unbutton shit.

Pathology of idiopathic PD
 Progressive degeneration of the pars compacta of the substantia nigra
 Neuronal eosinophilic inclusion bodies (Lewy bodies) are seen – these contain protein filaments of
   ubiquitin and alpha-synuclein
   Degeneration also occurs in other basal ganglia nuclei
   Biochemically, there is loss of DA (and melanin) in the striatum that correlates well with the areas of cell
    loss and also with the degree of akinesia

Natural history
 Worsens over some years
 Pts have joint and limb discomfort. No sensory loss
 Reflexes are brisk, plantar response flexed, cognitive function preserved
 Dementia may develop in later stages. Anxiety and depression are common

 Dx is entirely clinical
 Certain diffuse or multifocal brain disease cause some features of parkinsonism
      o Alzhiemer‟s
      o Multi-infarct dementia
      o Sequalae of repeated head injury (eg. in boxers)
      o Late effects of severe hypoxia or CO poisoning
      o Hypothyroidism
      o Depression

Drug treatment above. Also available is:
 Stereotactic neurosurgery
        o Small stereotactic lesions, usually unilateral placed in the ventrolateral nucleus of the thalamus or
           globus pallidus
        o Provides effective, temporary improvement in severe tremor, and dyskinesia with minor relief of
        o Thalamic stimulation is also used
 Tissue transplantation
        o Of foetal or autologous DA containing adrenal medulla and glial cell-line neurotrophic releasing
           factor into cerebral ventricles or basal ganglia
        o Has not really produced any major clinical improvement in the majority of pts with PD

Need to have a team based effort:
 GP
 Neurologist
 Physiotherapy
       o Can improve gait
 Occupational therapy
       o Clothing – avoid zips, buttons, lace up shoes
       o Cutlery, chairs, rails, shoes, flooring
 Psychiatrist

More clinical guff – Dyskinesias and Differentiation of P/EP lesions

 Resting – characteristic of PD, usually pill rolling
 Movement tremor – may be a parietal/cerebellar lesion
 Action tremor – benign essential tremor
      o Common and inherited, usually seen when pt puts hands out
      o May also be due to thyrotoxicosis, nervousness and -agonist use
 Red nucleus tremors – multiple sclerosis

 Jerky, quasi-purposive and sometimes explosive fidgety movements around the body
 Causes:
      o Huntington‟s disease
      o Sydenham‟s chorea
      o Benign hereditary
       o   Drugs – phenytoin, levodopa, alcohol
       o   Thyrotoxicosis, pregnancy and OCP
       o   SLE
       o   Encephalitis lethargica
       o   Stroke in the basal ganglia
       o   Rarities: tumour, trauma, subdural haematoma, CO poisoning, Wilson‟s etc

Descending pathways:
 Ventromedial
      o Includes the vestibule-, reticulo- and tectospinal pathways
      o Often referred to as the extra-pyramidal tract
      o Innervates distal muscles
 Lateral
      o Includes the corticospinal and rubrospinal tracts
      o Often referred to as the pyramidal tract
      o Innervates axial muscles

Differentiating an extra-pyramidal lesion

                                     Corticospinal                          Extrapyramidal
Alteration of tone                   Clasp knife                            Plastic throughout, cogwheeling
                                     (this is best felt in the knee, must   and lead pipe. This is best felt in
                                     move the limb quickly though)          the wrist flex/ext
Distribution of tone                 Flexors of the arms                    Generalised
                                     Extensors of the legs
Involuntary movements                Absent                                 Tremor
Tendon reflexes                                                            Normal
Extensor plantar response            Maybe present                          Absent
Paralysis of voluntary               Present                                Absent

                                                                         Causes of dementia:
                                                                            Alzheimers
 Multiple cognitive deficits, one of which must be memory impairment       Vascular
      o Deficits are stable, do not occur during the course of a            PD (Lewy body)
          delirium, cause functional impairment or severe distress          Pick‟s
 Example cognitive impairments                                             Head trauma
      o Aphasia                                                             Huntingtons
                                                                            Creuztfedlt-Jakob
      o Agnosia
                                                                            General medical conditions
      o Apraxia                                                             Multiple aetiologies
      o Disturbance in executive functioning
 Assoc features: psychotic symptoms, mood disorders, behaviour disturbance, sleep disturbance,
  personality change                                                   Common causes of delirium:
 Sometimes differentiate between cortical and sub-cortical dementia      Intoxication
      o Cortical – Alzheimers                                             Withdrawl states
      o Sub-cortical – Parkinsons                                         Nutritional def
                                                                               Metabolic disorders
                                                                               Infections
Delirium                                                                       Endocrine
 An acute mental disorder characterized by confusion and altered              Structural CNS disease
   (possibly fluctuating) level of consciousness. Delusions, illusions         Hypoxia
   and/or hallucinations may be present. It is a reversible condition          Post-op states
   except when followed by dementia or death
                                                                            Good way to remember (3):
                                                                              CNS disturbance
                                                                              Systemic disease
                                                                              Substance intox/withdrawl
       o     10-15% surgical patients and 15-25% of medical patients experience delirium during admission.
       o     This rises to 30-50% for special populations - ICU, post #NOF, CCU, Severe burns, AIDS
       o     Predisposing Factors include: age (elderly and very young) , substance dependence, preexisting
             CNS disorder, Diabetes, Cancer, malnutrition and sensory deficits
   Clinical features:
        o Fluctuating disorientation.
        o Impaired attention.
        o Psychomotor agitation or psychomotor retardation.
        o Illusions or hallucinations.
        o Delusions (poorly organized).
        o Memory deficits.
        o Difficulties with speech (dysarthria) or language (disorganized speech or word finding difficulties)
        o Disturbances of mood

Clinical – Neuro exam

 Headache
 Pins and needles (parasthesia)
 Weakness
 Numbness
 Fits, faints or funny turns
 Dizziness or vertigo
 Disturbances of vision, hearing or smell
 Disturbances of gait
 Involuntary movements
 Speech and swallowing disturbances

Risk factors for cerbrovascular disease:
 HT
 Smoking
 DM
 Hyperlipiadaemia
 AF, IE, MI (emboli)
 Haematological disease
 FHx stroke

General Signs
 Neck stiffness
       o Hand under occiput, passively flex pts neck and move head towards chest
       o Kernig‟s sign – for meningitis – flex hips, and attempt to straighten knee while hip is flexed. This
          is limited by spasm of the hamstring when there is meningism due to inflammatory exudates
          around lumbar spinal roots
 Handedness – 94% of R‟s and 50% of L have a dominant L hemisphere. Dominant hemisphere controls
   language and mathematical function
 Orientation – person, place and time
 Speech
       o Dysarthria – difficulty with articulation
       o Dysphonia – altered quality of the voice with reduction in vol
       o Dysphasia‟s
                Receptive (posterior) dysphasia – pt cannot understand the spoken (auditory) or written
                   (alexia) word. Speech is fluent but disorganised. Usually due to a lesion in Wernicke‟s
                Expressive (anterior) dysphasia – when pt understands, but cannot answer properly.
                   Usually due to a lesion in Broca‟s area. Pt may still use emotive language, sing songs, but
                   be unable to speak the words
                Nominal dysphasia – objects cannot be named. Pt may use circumlocution
                   Conductive dysphasia – pts repeat statements and name objects poorly, but can follow
                 Test for the dysphasia‟s by getting pt to talk freely. Then ask pt to: name objects, repeat
                    statement, comprehend commands, read and write
   Parietal lobe function
        o PL is concerned with reception and analysis of sensory info
        o Dominant lobe signs – lesions of the dominant PL in the angular gyrus causes a distinct clinical
            syndrome called Gerstmann‟s syndrome. Test by the following:
                 Arthimetic calculations (inability is acalculia)
                 Ask pt to write – inability is agraphia
                 Left sided disorientation (ask pt to show L hand, then R, then to touch R ear with L hand)
                    -> L-R disorientation
                 Ask pt to name their fingers – finger agnosia
        o Non-dominant and non-localising parietal lobe signs
                 Sensory and visual inattention – when one arm/leg is tested at a time, sensation is normal,
                    when both are tested simultaneously, sensation is only appreciated on the normal side
                 Visual field testing
                 Astereognosis (tactile agnosia) – inability, with eyes closed, to recognise an object placed
                    in the hand when ordinary sensory modalities are present
                 Agraphaesthesia – inability to appreciated a number drawn on the hand on the opposite
                    side of the parietal lesion
                 Spatial neglect – pt fills in the numbers on an empty clock face. Pts with R parietal lesion
                    may only fill numbers on the left side of the face
   Temporal lobe function
        o Short term and long term memory
        o Test short term memory and long term memory by asking for example, what year WWII ended
        o Some pts may try to confabulate – make up stories to fill gaps in their memory
                 Common presentation of Korsakoff‟s psychosis
   Frontal lobe function
        o Deals with emotion, memory, judgement, carelessness about personal habits and disinhibition
        o Test with primitive reflexes (grasp reflex, ipsilateral contraction of orbicularis oris muscle when
            the thenar eminence is stroked, pout/snout reflex on tapping above the upper lip)
        o Interpretation of a proverb – frontal lobe disease will give a literal interpretation
        o Shuffling gait

Cranial Nerves
I – Olfactory
 Test each nostril separately with a variety of familiar smells

II – Optic
 Assess visual acuity
       o Pt wears their glasses
       o Use a snellen chart
       o Test each eye separately while covering the other
 Visual fields
       o Remove pts glasses
       o Get pt to cover one eye, and stare into yours
       o Move a coloured pen or wiggle fingers outside of the
           visual field bringing it in on a diagonal in 4 directions
 Fundi

III - Occulomotor, IV - Trochlear, VI – Abducens
 Pupils
       o Light reflex
              Direct
              Consensual
              Afferent pupillary
       o Accomodation
               Pt focuses in distance, then focuses on a finger 30cm in front of their nose
               Argyll-Robertson syphilis pupil – accommodates, but not light reflex
   Eye movements
       o Ask pt to voluntarily move eyes
       o Move your finger in an H
   Nystagmus
       o Direction of nystagmus is that of the fast correcting movement
       o Ask pt to follow your finger out to 30 degrees from the central gaze position
       o Nystagmus may be jerky or pendular
               Acute vestibular lesions -> nystagmus away from the side of the lesion
               Chronic vestibular lesions -> nystagmus to the side of the lesion
               Unilateral cerebellar lesion -> nystagmus to side of lesion

V – Trigeminal
 Corneal reflex
       o Lightly touch cornea with a wisp of cotton wool -> pt will blink both eyes
 Facial sensation in the three divisions of the nerve – compare one side with the other
       o Sharp and dull with a pin
       o Cotton wool for light touch
 Test motor division
       o Get pt to clench teeth and palpate for contraction of the masseter muscles above the mandible
       o Get pt to open mouth and stop you closing it
 Jaw jerk reflex

VII – Facial
 Inspection for facial asymmetry
 Muscles:
       o Get pt to look up and wrinkle forehead – test corrugation
       o Get pt to shut the eyes tightly – try to open them
       o Get pt to grin
       o Get pt to blow cheeks out and then examiner pushes them in
 Very seldom do you test for taste on the anterior 2/3rds of the tongue

VIII – Vestibulocochlear
 Examine for a hearing aid, examine the pina, and external auditory meatus
 Test hearing
       o Cover opposite ear and whisper 68 for high freq and 100 for low freq
 If partial deafness is suspected, perform Rinne‟s and Weber‟s tests
       o Rinnes – 512Hz tuning fork on mastoid process, when sound is no longer heard, then bring it in
           line with the external meatus. Sound should still be heard at external
                 If AC > BC -> Rinne positive, the middle and outer ears are functioning normally
                 If BC > AC -> Rinne negative, defective function of the outer or middle ear
                 Rinne‟s test tells you nothing about cochlear function, it is a test of middle ear
       o Weber‟s - Base of tuning fork is held on the vertex of the head, and the patient is asked whether
           the sound is heard centrally or is referred to one or other ear
                 Normal -> sound heard in centre
                 In conductive deafness -> sound is heard in deafer ear
                 In sensorineural deafness -> sound is heard in better-hearing ear
                 This is useful to determine the type of deafness a patient may have, and to determine
                   which ear has the better-functioning cochlea
 If pt complains of vertigo, the Hallpike manoeuvre should be performed
       o Pt sits and is warned about what is to happen
       o Examiner grabs pt head and gets him to lie back quickly so head is at 30 degrees below the
       o The head is also rotated 30 degrees towards the examiner at the same time
       o Pt keeps eyes open – a positive test, after a short latent period, reveals vertigo and nystagmus
           towards the affected (lowermost) ear for sever seconds
IX – Glossopharyngeal and X – Vagus
 Inspect palate with a torch, check the uvula
 Get pt to say „Ah‟ – iff the uvula is drawn to one side, this indicates a unilateral X nerve palsy
 Test for the gag reflex (IX is sensory, X is motor)
 Maybe get pt to swallow some water

XI – Accessory
 Get pt to shrug the shoulders, then attempt to push them down
 Turn head against resistance (left and right, up and down)
       o Remember the R sternoimastoid turns the head to the left

XII – Hypoglossal
 Inspect the tongue at rest
       o Look for wasting
       o And Fasciculations (fine irregular non-rhythmical muscle fibre contractions)
 Get pt to poke out tongue and wiggle it from side to side
       o If XII nerve lesion, tongue will deviate towards affected side if there is a LMNL (weaker extensors)

Upper Limbs                                                                  General examination of periphery:
 Shake hands for a start                                                       General inspection
 Inspection:                                                                         o Posture
       o Expose shoulders and arms, look for:                                         o Muscle bulk
                 Abnormal posture                                                    o Abnormal movements
                                                                                Fasciculations
                 Muscle bulk/wasting
                                                                                Tone
                 Abnormal movements (eg. tremor)                               Power
                 Skin                                                          Reflexes
                 Fasciculation (irregular contractions of small groups of      Coordination
                   muscles with no rhythm – if present with weakness and        Sensory:
                   wasting -> LMNL)                                                   o Pain
                                                                                      o Temperature
 Ask pt to hold out both arms, palms upward with eyes closed – watch
                                                                                      o Vibration
   for drift. Causes of drift:                                                        o Proprioception
       o UMN weakness (downward drift)                                                o Light touch
       o Cerebellar disease (upward drift)
       o Loss of proprioception
 Tone
       o Test tone at wrists and elbows
                 Support pt‟s elbow
                 Wrists are rotated (pronated and supinated)
       o UMN ->  tone
       o PD -> cogwheel rigidity
 Power
       o 0 (paralysis) ->3 (against gravity) -> 5 (normal power)
       o Shoulder
                 Abduction – deltoid and supraspinous (C5, C6)
                 Adduction – pec major and latissimus dorsi (C6, C7, C8)
       o Elbow
                 Flexion – biceps and brachialis (C5, C6)
                 Extension – tricepts brachii (C7, C8)
       o Wrist
                 Flexion – flexor carpi ulnaris and radialis (C6, C7)
                 Extension – extensor carpi group (C7, C8)
       o Fingers
                 Extension – extensor digitorum communis, extensor indicis and extensor digiti minimi (C7,
                 Flexion – flexor digitorum profundus and sublimes (C7, C8) (finger squeeze)
                 Abduction – dorsal interossei (C8, T1)
                 Adduction – volar interossei (C8, T1)
                 Abduction of thumb (side of palm, straight up – median nerve)
 Reflexes
       o Biceps jerk (C5, C6)
       o Triceps jerk (C7, C8)
       o Brachioradialis (supinator) jerk (C5, C6)
       o Finger jerks (C8)
   Coordination
       o Finger-nose
       o Rapidly alternating movements
       o Rebound (get pt to lift arms rapidly from sides and then stop)
               Hypotonia from cerebellar disease causes a delay in stopping the arms
   Sensory
       o Spinothalamic
               Pinprick (pain) over all the dermatomes
               Temperature
       o Posterior columns
               Vibration (128Hz)
               Proprioception
   Light touch testing (with cotton wool)

Lower Limbs
 Begin by testing gait
      o Normal walking
      o Heel toe
      o Romberg – pt stands with feet together, eyes closed for 10 seconds
 Inspect the legs
      o All of the above
      o Fasciculations
 Tone
      o When pt is lying back, roll the thigh from side to side
      o Tone at knees and ankles
               Plase one hand under a chosen knee, and then abruptly pull the knee upwards causing
               Flex and extend the knee at varying rates
               Same with the ankle
      o Clonus (sustained rhythmical contraction of the muscles when put under sudden stretch) of the
          ankle and knee. It is due to hypertonia from an UMNL – it represents an increase in reflex
          excitability (from   motor neurone activity)
               Sharply dorsiflex the foot with the knee bent and the thigh externally rotated
               When ankle clonus is present, recurrent ankle plantar flexion movement occurs
               Test for patellar clonus by resting the hand on the lower part of the quadriceps with the
                  knee extended and moving the patella down sharply
               There is sustained rhythmical contraction of the quads as long as the downward stretch is
 Power
      o Hip
               Flexion – psoas and iliacus (L2, L3)
               Extension – gluteus maximus (L5, S1, S2)
               Abduction – gluteus medius and minimus, sartorius and TFL (L4, L5, S1)
               Adduction – adductors longus, brevis and magnus (L2, L3, L4)
      o Knee
               Flexion – hamstrings (L5, S1)
               Extension – quadriceps femoris (L3, L4)
      o Ankle
               Plantarflexion – gastrocnemius, plantaris, soleus (S1, S2)
               Dorsiflexion – tibialis anterior, extensor digitorum longus and extensor hallicus longus (L4,
      o Tarsal joint
               Eversion – peroneus longus and brevis and extensor digitorum longus (L5, S1)
               Inversion – tibialis posterior, gastrocnemius and hallucis longus (L5, S1)
 Reflexes
       o Knee jerk (L3, L4)
       o Ankle jerk (S1, S2)
       o Plantar reflex (L5, S1, S2) -> flexion is normal, Babinski is extensor -> UMNL
   Coordination
       o Heel-shin test
       o Foot tapping test
   Sensation
       o Pain in each dermatome
       o Vibration
       o Proprioception
       o Light touch

    Four signs of UMN lesion:                    Five signs of LMN lesion:
     Hyperreflexia                               Hypotonia
     Weakness                                    Hyporeflexia
     Hypertonic                                  Atrophy
     Positive Babinski‟s sign                    Fasciculation
                                                  Weakness
Problem 26 – Headache
Wk Dom            LO Title                                           LO Detail
 26 BCS Diagnosis of headache         1. To be able to obtain a relevant history and examination from a
                                      patient with a headache and subsequently construct a differential
                                      diagnosis of the headache in that patient.
                                      2. To be able to discuss the investigation of headache due to
                                      cerebral aneurysms or tumours.
 26 BCS Pathophysiology of headache 1. To list and discuss the underlying mechanisms of the common
                                      types of headache, namely tension-contraction or tension headache
                                      and migraine.
                                      2. To list and discuss the pain sensitive structures in the head.
 26 BCS Treatment of headache         1. To describe the mechanism of action of drugs used in the
                                      treatment of migraine headaches, both acutely and prophylactically.
                                      2. To investigate the psychosocial issues associated with pain and
                                      how these influence pain management.
 26 EPPD Patient values and choice    1. Assist patients to make decisions about diagnostic and therapeutic
                                      interventions by:
                                      (a) communicating complex medical concepts so that patients
                                      understand them;
                                      (b) providing alternative expressions of benefits and risks of
                                      (c) exploring and appraising patients' beliefs, values and use of
                                      information in forming preferences about interventions.
 26 EPPD Uncertainty, resources and   1.Review the principles governing breaches of the medical duty of
         the duty of care             care and actions in negligence in the context of investigation under
                                      conditions of diagnostic uncertainty and finite resources.
                                      2. Describe the medico-legal controversies surrounding who defines
                                      the standard of care.
 26 ICCP Clinical examination         1. Perform a focussed central nervous system examination for:
                                      (a) Cranial nerves (including ophthalmoscopy)
                                      (b) Upper or lower limb (power and sensation)
                                      (c) Cerebellar function
                                      (d) Locomotion.
 26 PPH Complementary therapies       1. Describe the extent of use of complementary medicine in
         (Social Science; EBM; Public Australia.
         Health)                      2. Discuss the main reasons for patient use of complementary
                                      3. Describe medical concerns regarding patient use of
                                      complementary medicine.
                                      4. Be able to discuss with patients, the issues surrounding the use of
                                      complementary medicine.
Dx of Headache

In taking a history of a headache, you pretty much let the pt talk all about it. Ask the usual NILDOCARF
questions to help them along. Each category below has additional questions to narrow it down.

Examination involves:
 Vitals
 Complete CNS exam
 Psychological state assessment
 Head exam - ears, eyes, teeth, scalp arteries
 Temperature

Here is a differential of types of headaches they might describe:

Acute Single Episode
 We are interested in:
      o Suddenness of the onset
      o Neck stiffness
      o Fever
      o Vomiting
 Meningitis         - also with fever, photophobia, stiff neck, rash, coma
 Encephalitis       - also with fever, odd behaviour, fits or  consciousness
 Tropical illness   - also with „flu-like‟ symptoms
 Haemorrhage        - SAH - sudden „explosive‟ onset, +/- stiff neck
 Sinusitis          - also with tender face, coryza, post-nasal drip
 Head injury        - cuts/bruises,  consciousness, lucid intervals, amnesia

Acute Recurrent Attacks
 Migraine          - maybe prodromal aura, visual spots or vomiting, precipitant (eg. foods etc)
 Cluster headache - unilateral, excruciating, male, time course (clusters), often arising from sleep
 Glaucoma          - with red eyes, seeing haloes, fixed oval pupils,  visual acuity

Subacute onset
 Giant cell arteritis - tender scalp, >50yo,  visual acuity (late), ESR

Chronic headache
 Tension headache - dull, band-like, generalised, worsening throughout day, days-weeks duration
 Chronic ICP     - worse on wakening, focal neuro signs, vomiting, worse on eg. coughing, lying down
      o Malignant hypertension
      o SOL – tumours, slow bleeds, abscess
      o Hydrocephalus
 Analgesic h‟ache - rebound headache on stopping analgesic use
 Withdrawl h‟ache
 Paget‟s disease

Facial pain
 Trigeminal neuralgia         - unilateral lancing facial pain on trigeminal nerve distribution
 Post-herpetic neuralgia      - hx of shingles

Investigation of headache
 Bloods (Venous)
       o FBC – bacterial endocarditis, multiple myeloma, leukaemia, anaemia and polycythaemia
       o ESR – temporal artertitis
 Pictures
       o CXR – exclude lung ca
       o CT
       o Bilateral cerebral angiogram
       o MRI
   Fancy
       o Electroencephalogram
       o Lumbar puncture – encephalitis, meningitis, SAH or benign intracranial HT
              Presence of papilloedema is an absolute contraindication until a CT scan excludes a SOL

Pathophysiology of Headache

Pain sensitive structures in the head:
 Scalp
 Orbital contents
 Middle meningeal artery (or any branch of the carotid)
 Dural/venous sinuses
 Falx cerebri
 Proximal segments of the large pial artery
 Teeth
 Gums

   Pain can be referred from:
        o Eyes
        o Nasal sinuses
        o Upper neck -> C1,2,3

A headache may result from direct noxious stimulation of pain receptors, or inappropriate activation of CNS
pain pathways.

Headaches according to site of origin

Cranium                                                  Unknown origin
 Lesions inside bones, stretching periosteum             Migraine
 Inflammation of cranium or scalp                        Cluster headache
                                                          Acute cerebral vascular insufficiency
Extracranial Arteries:
 Temporal arteritis                                     Tension headache:
                                                          Primary muscle overcontraction
Cranial Nerves:                                           Secondary to other factors (eye strain,
 Excessive stimulation of trigeminal or                    temporomandibular joint disfunction, cervical
   glossopharyngeal (eg. eating ice cream, diving into      spondylitis)
   cold water)                                            Idiopathic chronic tension headaches
 Distortion or inflammation                              Tension-vascular headaches
 Tumour, aneurysm
 Gradenigo‟s syndrome (lesions in apex of tempoiral     Psychogenic headache:
   bone – involves V1 and VI)                             Secondary to a delusional, conversion or
 Postherpetic neuralgia                                    hypochondriacal state
 V and IX neuralgia

Referred pain:
 Ears, eyes, nose, throat, teeth and neck

 Vasodilation from
       o Concussion
       o Epileptic fit (postictal)
       o Pressor reactions:
               Phaeochromocytoma
               Tyramine ingestion (MAOI)
               Post-coital (orgasmic)
               Malignant HT
       o Toxic:
                Systemic infections
                Hangover
                Foreign protein
                Withdrawl
                Meds (indomethacin)
        o Metabolic
                Hypoxia
                Hypoglycaemia
                Hypercapnia
        o Vasodilator agents
   Meningeal irritation
        o SAH
        o Meningitis, encephalitis
   Displacement of intracranial vessels
        o SOL – tu, haematoma, abscess
        o  ICP – obstructive hydrocephalus, cerebral
            oedema, benign intracranial HT
        o  ICP – post LP
   Exertion and cough headache

Treatment of Headache

 Common episodic headache. Affects ~10% of males and ~20% females
 Preceded in about 20% of cases by an aura of neurological symptoms (eg. blurred vision, flashes of light,
   zig zags, or less commonly, parasthesiae and dysphasia)
       o Classical migraine – migraine with aura (scintillating scotoma)
       o Common migraine – migraine without aura
 Characteristically, episodic, separated by intervals of freedom.
       o Unilateral in 2/3rds of pts
       o Commonly affects frontotemporal region, radiating to the occiput
       o Usually accompanied with nausea (90%)
       o Vomitting (60%)
       o Diarrhoea (20%)
       o Photophobia (80%)
 Variations on migraine
       o Vertebrobasilar migraine
       o Retinal migraine
       o Opthalmoplegic migraine
       o Facial migraine
       o Hemiplegic migraine
       o Migrainous infarction
 Pathophysiology
       o Commonly associated with a diminution of cortical blood flow of about 20%, which starts in the
           occiput and moves forward accompanied by a spreading depression of cortical function
       o Blood platelets discharge 5-HT at the onset of the migraine headache
       o There is an initial vasoconstriction associated with an aura, and then a rebound vasodilation
 General management
       o Psychological counselling and relaxation therapy
 Treatment of acute attacks
       o Ergotamine tartrate - prevention of dilation. Should be given as early as possivle
       o Sumatriptan – constricts cranial vessels through the 5-HT1D receptor. It is ineffective in the aura
           phase, but is effective during the headache phase
       o NSAIDs – aspirin, ibuprofen
       o Watch out for people with CAD!
 Preventive therapy
       o  blockers – propanolol/metoprolol
       o Anticonvulsives (valproate)
       o   Pizotifen – antiserotonin, antihistamine
       o   Methysergide – antiserotonin – partial 5-HT1 agonist as well as a 5-HT2 antagonist
       o   Amitriptyline – prevents reuptake of serotonin
       o   NSAIDs
       o   Calcium channel blockers

Cluster headaches
 3% as common as migraine
 Unilateral headache, usually affects one eye and radiates upwards over the fronto-temporal region or
   downwards over the face
 „Cluster‟ means that it happens over a length of time, and then the pt is free for months to years
 An attack usually has severe pain, lasting 15mins – 2 hours
 Treatment:
       o During an attack - 100% oxygen or a subcut injection of sumatriptan
       o Ergotamine
       o Methysergide
       o Prednisone

Neuro Path I


Skull Fractures
 Kinetic energy that cause a fracture is dissipated at a fused suture
 Basal skull fractures typically follow a blow to the occiput or sides
 Symptoms include:
       o Referral to lower cranial nerves
       o Presence of orbital (raccoon eyes) or mastoid haematomas (battle sign) – distant from the point
           of impact
       o CSF discharge from nose or ear, and infection may follow

Parenchymal Injury
 Contusion and laceration
      o Contusion – bruise with extravasation of blood, but with pia-arachnoid intact
      o Laceration – pia-arachnoid is torn
      o Coup injury – a cerebral contusion under the point of contact
      o Countercoup – surface diametrically opposite
      o Usually cause haemorrhage and extravasation of blood
      o Early lesions show oedema and haemorrhage.
      o Old lesions appear as retracted yellow brown patches on the crests of gyri (called plaque jaune)
         and can be the origin of epileptic discharge.
 Concussion
      o This is a clinical syndrome of altered LOC secondary to head injury, typically brought about by a
         change in momentum of the head (movement of head arrested by rigid surface)
      o The biochemical sequence of events is not well known
 White matter injury/Diffuse axonal injury
      o May be axonal swellings or focal haemorrhagic lesions
      o Coma shortly after trauma, even without contusions, may indicate white matter damage
      o Two main features:
              Small haemorrhagic lesions in the corpus callosum and dorso-lateral quadrant of the
                 brainstem (macroscopic)
              Widespread tearing of axons (microscopic)
      o Axonal retraction balls and focal haemorrhages are seen. It is believed mechanical forces damage
         the integrity of the axons at nodes of Ranvier.

Traumatic haemorrhages
 Epidural haematoma
       o    Trauma to the skull over the temporal bone can sometimes cause laceration to the middle
            meningeal artery
        o Under arterial pressure, there is an accumulation of blood, and the dura peels off the skull
        o Underlying brain is compressed
   Subdural haematoma
        o Underneath the dura, above the arachnoid
        o Usually due to a tear of one of the bridging veins (from the cortex) that penetrate the dura
        o Clotted blood
   Subarachnoid haematoma
        o Associated with vessel rupture and bleeding into the CSF of the arachnoid space
        o Three main causes:
                Rupture of an aneurysm (in the circle of Willis or Basilar artery)
                Rupture of an AVM
                No underlying vascular abnormality
        o Can also result from hypertension, embolisms or infarction
   Intracerebral haemorrhage
        o Direct rupture of the intrinsic cerebral vessels at the time of injury

Congenital/Perinatal brain injury

Causes of neural tube defects:
 Genetics
 Maternal infections
 Toxicity
 Metabolic factors
 Irradiation in utero

Neural tube defects
 Anencephaly – absence of cranial vault, and failure in development of cerebral hemispheres
 Encephalocoele – ossification defects in bones of skull result in hernition of brain and Meninges

Neural tube defects with spinal involvement
 Spina bifida occulta – abnormal development of the vertebral arches, but the cord and Meninges are
   normal – usually asymptomatic
 Spina bifida custica – presents as either meningomyelocoele (90%) or meningocoele (10%). Abnormal
   development of vertebral arches results in cystic outpouching

Posterior fossa abnormalities
 Arnold-chiari malformation – prolongation of the cerebellum downwards through the foramen magnum
   often resulting in obstructive hydrocephalus
 Dandy-walker malformation – obstruction of foramina of Luschka and Magendie (exit of the fourth
   ventricle) results in the formation of a cyst like structure between the cerebral hemispheres

Syringomyelia and hydromyelia
 Syringomyelia – a cyst (syrinx) develops within the spinal cord, usually posterior to the central canal
      o Cavity is lined by gliosis (astrocytes), it is most common in the cervical spinal cord, but it may
           extend into the medulla (syringobulbia)
 Hydromyelia – dilated central canal contain CSF and lined by ependyma
 Causes of these conditions:
      o Acquired – secondary to trauma or ischaemia, or occurring in association with tumours of the
           spinal cord
      o Congenital – may be associated with maldevelopment of the cord or other developmental
           abnormalities of the craniocervical junction, especially in Arnold-Chiari syndrome
 Clinical presentation
      o Muscle weakness and atrophy in upper limbs due to compression of anterior horn cells
      o Loss of sensations of pain and temperature – due to damage to nerve fibres crossing the cord in
           the lateral spinothalamic tracts
      o Preservation of position and vibration
Perinatal Injury

Cerebral palsy
 Brain malformation or damage affecting motor areas of the brain
 2 per 1000 live births
 Damage may occur in foetal life, may be birth related, or occur postnatally
 Causes:
      o Cerebral malformation
      o CVA
      o Hypoglycaemia
      o Hypoxia
      o Infection
      o Kernicterus (bilirubin-induced brain damage)
      o Poisoning
      o Toxins
      o Trauma (peri- and postnatal)
 Types of cerebral palsy
      o Spastic (70%) – hypertonia, ankle clonus, extensor plantar response
      o Dystonic (athetoid) 10% - irregular, involuntary muscle movements
      o Ataxic (10%) – hypertonia, weakness, uncoordinated movements and intention tremor
      o Mixed (10%)

Ischaemia and hypoxia
 Major cause of perinatal brain damage
 Perinatal hypoxia usually due to asphyxiation associated with trauma of birth
 Perinatal ischaemia commonly caused by intracranial haemorrhages
      o Premature infants are highly susceptible to developing haemorrhages because of disturbances in
          the cerebral circulation possibly caused by in-utero hypoxia/ischaemia

  in vol of CSF within the brain, resulting in the expansion of the cerebral ventricles. Can occur via:
      o Obstruction to flow of CSF (most common)
      o Impaired absorption of CSF at the arachnoid villi (rare)
      o Overproduction of CSF by choroids plexus neoplasms (very rare)
 Obstructive hydrocephalus is either congenital or acquired
      o Communicating – extraventricular obstruction within the SA space
      o Non-communicating – obstruction within the ventricular system leading to blockage of CSF flow
          from ventricles to the SA space
 Congenital hydrocephalus
      o Occurs in 1 in 1000 live births
      o Principle causes are congenital malformation:
                Arnold-Chiari malformation
                Congenital stenosis of the cerebral aqueduct
                Atresia of the foramina of Magendie and Luschka (Dandy-Walker)
                Some genetic causes associated with X-linked inheritance
 Acquired
      o Lesions that obstruct the CSF pathway
                Tumours – esp in posterior fossa (obstructs the 4th ventricle)
                Scarring – post inflammatory fibrosis of the Meninges at exit foramina following meningitis
                  or SAH
                Haemorrhage – intraventricular or in the posterior fossa

Uncertainty and Defensive Medicine (again)

Diagnostic strategy:
 Probability diagnosis
 Serious disorders not to be missed
 Pitfalls (often missed)
 The seven masquerades
        o     Depression
        o     Diabetes
        o     Drugs
        o     Anaemia
        o     Thyroid disease
        o     Spinal dysfunction
        o     UTI
   Is the   pt trying to tell me something?

Ethics – Confidentiality & Privacy

Factors  fragility of confidence:
 Written/electronic medical records
 Multidisciplinary health team/referral lawyers
 Claims for access to medical info eg. insurance
 IT/DBs/Smart cards
 Research/public health requirements
 Genetics/genome/criminal blueprinting/research

Ethical aspects of confidentiality
 Four types of philosophical arguments have been used to support the concept of confidentiality:
       o Principle-based argument derived from respect for autonomy
                Maintaining confidence is a crucial part of respecting pt autonomy – for if people are to be
                   self-determining, they must be able to maintain their sense of personal integrity and
                   control what personal information others have about them
       o Virtue-based argument – maintains that trust and fidelity to an implicit or explicit promise to
           maintain confidentiality, is a fundamental part of the health worker-pt relationship
       o Moral right to protection of secrets and the corresponding duty to maintain confidentiality is
           fundamental to all human relationships
       o Consequentialist – the assurance of pt confidentiality is necessary for achieving the medical goals
           of effective diagnosis and treatment
 Pt benefit is the most important aspect served by confidentiality (in the interest of health)
       o Individual interest -> knowing that your confidentiality will be protected (usefulness of trust)
       o Public interest -> general community trust of physicians
 A breach in confidence will disrupt both individual pt and public trust
 The utilitarian aspect of breaching confidentiality (benefit outweighing harm)
       o E.g. divulging a pt‟s drug problem to a friend that will be able to help them through it
 But a right to confidentiality is tied with the identity of the pt
       o If a competent pt makes decisions in their best interest, they should be allowed to keep such info
           confidential, even if breaching confidentiality is in their best interests
       o Deontological – duty to respect rights
 Nonetheless, breaching confidence is associated with a moral harm

1996 AMA Code of Ethics -> allows a breach of confidentiality when: the law requires it, or when the health
of others is at risk.
     No guidance as to the criteria to use to know when to breach confidentiality
     Confidentiality needs to be absolute, otherwise it loses its point

2004 AMA Code of Ethics -> allows a breach of confidentiality when: serious risk to pt or another person;
required by law; approved research; or overwhelming societal interest
     Reflects that there is increasing acceptance that there are occasions where confidentiality may be
        justifiably breached
     But also the fact that justifications must be serious

The codes look at a breach of confidentiality as a „moral violation of a professional ethic‟, where the law sees
a BOC in terms of two kinds of public interest: public interest in keeping medical consults private vs keeping
the public free from harm.
Everyday failures of respecting confidentiality
 Completing consultation moving from consult room to waiting room
 Giving results within earshot of others
 Indicating to the partner of the current pt, your concerns about their problem
 Allowing charts, results or computer screens to be viewed by other people
 Corridor discussions of pts with colleagues
 Discussion of known pts with one‟s own family or friends
 Providing details on medical certificates that are not authorised by pts

Legal duties of confidentiality

Confidence between health care provider and pt may be protected (and thus enforced) in four ways:
 Contract
       o Implicit contract between dr and pt
       o Breach of confidence = breach in contract
 Equity
       o An equitable obligation of confidence will arise where:
                Info has „the necessary quality of confidence about it‟;
                It „must have been imparted in circumstances importing an obligation of confidence‟
                „There must be an unauthorised use of that info to the detriment of the party
                  communicating it‟
       o An injunction can be sought against an anticipated breach of confidence
 Tort
       o Standard of care includes protection of confidences
       o Breach of confidence = breach of standard of care
       o Provided some damage resulted, then an action in negligence will be likely
 Specific statutory provisions

 Commonwealth Privacy Act 1998
 Health Services Act 1991 (QLD) – all employees of QH must maintain pt confidentiality

Professional misconduct
 Health Practitioner‟s (Professional Standards) Act 1999
      o BOC would not result in deregistration, but a reprimand

Common Law
 Usually handled under a breach of contract heading, which involves the duty of care, which comes under
  the torts of negligence
 Contracts -> implied sense that confidentiality will be maintained
      o Pt must prove that the breach of contract (ie. BOC) caused damage in some way
      o This is hard to quantify

 Provides for natural justice in certain matters and complements the common law
 Breaching the confidentiality of the doctor-patient relationship is deemed by equity to be taking unfair
   advantage of the person who has divulged the information, in a situation where the information is
   mutually understood to have been given in confidence.

Exceptions to breaching confidence

Mandatory disclosure under law
 Notifiable conditions
 Court orders
 Disciplinary matters
 Substitute decision makers

Pt consent and implied consent
 Medical certificates
   Referrals
   Prescriptions
   Insurance reports

Medical research and quality assurance
 De-identified
 NHMRC checks it all

The „public interest‟ exception
 Differs from what the statutes demand –ie. statues offer indemnity to drs who have to BOC due to legal
 No statute to cover a „public health‟ interest exception
 In the relevant common law cases, justification has usually depended on the existence of an immediate
   and clearly foreseen danger to be avoided by urgent disclosure to another party. The conditions most
   likely to support disclosure in the public interest are therefore likely to be
        o A serious and immediate risk of harm occurring;
        o The risk is likely to be reduced by the disclosure;
        o Disclosure is kept to the minimum required to avert the risk;
        o Resulting damage to public interest in maintaining confidentiality is outweighed by the public
            interest served by averting the risk.

Complementary Therapies

In Australia, as in many Western countries, there is increasing consumer demand for complementary and
alternative medicines (CAM). Already, 60% of Australians use CAM, with 1 in 2 using some non-prescribed
complementary medicine and 1 in 5 visiting a CAM practitioner at least once per year. Australians spend
roughly $A 2 billion per year on CAM, with 2/3 of this being on medicines and 1/3 on practitioners.

The reasons for the extent of CAM use are many. Some arise from the failure of biomedicine to alleviate
symptoms, particularly in chronic illness and pain. The “small planet syndrome” is a reason put forward which
suggests that globalisation is leading to those who live in Western countries having an increased appreciation
of non-western cultures, including their traditional eco-friendly health systems. Economic globalisation is
leading to an increase in the availability for sale of these traditional medicines in Australia.

There are several reasons for the medical professions to be concerned with the increasing use of CAM. The
ready availability of the medicines makes it accessible to the larger population, while the lack of regulation of
CAM industries has limited the control over what is in them etc. In addition, there are several side effects to
CAM, which the consumer should be aware of. In response to the increasing use by the Australian population
of CAM, the Australian government has introduced legislation to help regulate it. There is now an office of
Complimentary medicine within the TGA. Victoria has introduced legislation to support the use of CAM,
allowing the inclusion, alongside scientific evidence, of evidence based on tradition.

In practice, CAM is becoming increasingly accepted by the community at large, and by orthodox medical
practitioners. In recent studies it has been found that: 1 in 5 GPs provide CAM; 75% of GPs refer patients to
CAM practitioners and 1 in 7 GPs perform acupuncture (although this figure must be looked at under the light
of acupuncture being medicare funded when performed by an orthodox medical physician – though not when
performed by a traditional medicine practitioner). Private health insurers now pay benefits for CAM.

The role of complementary medicine in Australia is complex. It is used by people from all backgrounds,
though middle aged, educated women are the highest use group. There is increasingly evidence available to
support the use of some CAM, though further studies would provide a much needed insight. The CAM
approach to medicine from a more holistic viewpoint is something that biomedicine seems to be aiming
towards as well, and community understanding of lifestyle/ behaviour ideas to support better health
outcomes will improve overall community wellbeing. Individuals seeking CAM should exercise caution and
possibly be critical in ascertaining whether the intervention is safe, effective and suitable for their individual
Problem 27 – Epilepsy

Wk Dom          LO Title                                          LO Detail
 27 BCS Diagnosis of epilepsy 1. To be able to elicit an appropriate history from and perform an
                               examination on a patient with a recent seizure.
                               2. To be able to outline an appropriate management plan for a patient
                               presenting to hospital with a seizure.
                               3. To be aware of the common investigations used to evaluate patients with
                               epilepsy, such as the electroencephalogram, and imaging procedures such
                               as computerised axial tomography or magnetic resonance imaging of the
                               4. Detailed understanding of these procedures IS NOT REQUIRED.
 27 BCS Mechanisms of          1. To describe the common syndromes of epilepsy.
         epilepsy and seizures 2. To outline the biochemical mechanisms of seizures.
 27 BCS Treatment of epilepsy 1. To outline the mechanism of action of the common anticonvulsants used
                               to treat epilepsy.
                               2. To be aware of the surgical options for the management of epilepsy
                               (detailed knowledge NOT required).
 27 ICCP Clinical examination 1. Perform a focussed central nervous system examination for:
                               (a) Cranial nerves (including ophthalmoscopy)
                               (b) Upper or lower limb (power and sensation)
                               (c) Cerebellar function
                               (d) Locomotion.
 27 PPH Psychosocial           1. Describe the possible psychosocial consequences of a diagnosis of
         consequences (Social epilepsy.
 27 PPH Stigmatization (Social 1. Describe stigmatisation.
         Sciences)             2. Differentiate between „felt‟ and „enacted‟ stigma, using a clinical example.
 27 PPH Health policy and      1. What key information should you provide a newly diagnosed patient with
         guidelines (Public    epilepsy regarding the general principles relating to their driving eligibility
         Health)               and responsibilities?
Seizures & Epilepsy – Diagnosis

Seizure – temporary alteration of brain function caused by paroxysmal, abnormal, neuronal discharge; it
may manifest as alterations in motor, sensory or psychological function.

Types of seizures

Generalised (bilateral brain and motor manifestation, with LOC)
 Tonic-clonic (Grand mal)
      o Some have prodromal aura (suggests a focal origin) of elation, depression, irritation, headache
      o Tonic phase
               Facial, jaw, limb and trunk muscles contract
               Falls can be common, also biting of the tongue
               Incontinence of urine or faeces
      o Clonic phase
               Limb jerking
      o After
               Pt in stupor/confusion
               Headache and painful muscles
      o Status epilepticus
               Succession of tonic-clonic seizures without pt regaining consciousness
 Typical absence (petit mal)
      o Brief lapse of consciousness for 10 seconds or more
      o Usually occurs in childhood, very rare to continue to adulthood
      o Child usually appears to not be paying attention, may be fluttering of the eyelids, rolling upwards
          of eyes, automatisms, myoclonus, or akinetic attacks (falling down)
 Myoclonic/atonic
      o Myoclonic – isolated muscle jerking
      o Tonic – intense stiffening of the body not followed by convulsive jerking
      o Atonic – sudden loss of tone, with falling and loss of consciousness

Focal/Localised/Partial Seizures (Simple – normal LOC; Complex – altered conscious level)
 Partial focal seizures (simple/complex)
      o An area of brain has generated abnormal electrical activity that may spread
      o An aura is suggestive of a focal seizures
 Jacksonian (focal motor seizure)
      o Originates in motor cortex
      o Starts at the side of the mouth and spreads down limbs on the opposite side of the focus
                „March‟ of the seizure
      o There may be a post-ictal loss of motor function for a few days (Todd‟s paralysis)
 Temporal lobe (simple/complex)
      o Often relates to a structural abnormality (eg. scarring from prolonged childhood febrile
      o Presents with an aura
                Over-under familiarity with surroundings (deja/jamais vu)
                Unpleasant taste/smell
                Epigastric discomfort
      o Seizure may involve:
                Facial grimacing
                Complex motor actions (eg. undressing)
                Bizzare behaviour
 Occipital seizures (simple/complex)
      o Produce flashing lights or complex distortion of vision
Differential diagnoses:

Grand mal seizure:                                      Simple, partial
 Intracranial infection (abscess, encephalitis)         Brain abscess
 Idiopathic epilepsy                                    Tumour
 Metabolic (CRF, hepatic encephalopathy,                Head trauma
   hypoglycaemia, hyponatraemia,                         Stroke
 Brain neoplasm
 Eclampsia
 Head trauma
 Hypoxic encephalopathy
 Neurofibromatosis
 Stroke
 Drugs (theophylline, lignocaine, penicillins,
   cimetidine, meperidine)
 Arsenic poisoning
 Barbituate withdrawl
 Radiological contrast

Complex partial:                                        Absence:
 Brain abscess                                          Idiopathic epilepsy
 Head trayma (to frontal lobe)
 Herpes simplex encephalitis
 Temporal lobe tumour

 Epilepsy is the continuing tendency to have seizures, even if a long interval separates attacks
 2% of the population have two or more seizures in their life
 Types of epilepsy can be any of the above types of seizures
 Epilepsy is a syndrome, need a pathological diagnosis

Aetiology and precipitants
 Genetic predisposition and developmental abnormalities
       o 30% of pts have a FHx of epilepsy in first degree relatives
       o Absence seizures and primary generalised epilepsy are commonly inherited
 Trauma, hypoxia and surgery
       o Perinatal trauma (cerebral contusion and haemorrhage) and foetal anoxia are common causes of
          childhood seizures
       o As is hypoxic damage to the hippocampi
       o To cause epilepsy, brain injury must (usually) be sufficient to cause coma
 Pyrexia (febrile convulsions) in the young
 Brain tumours and abscesses
       o Mass lesions in the cortex
 Vascular
       o Seizures sometimes follow cerebral infarction
       o A brain AVM may present with seizures
 Alcohol, drugs and drug withdraw;
       o Phenothiazines, MAO inhibitors, TCAs, amphetamines, lignocaine, propofol and nalidixic acid
       o Withdrawl of anticonvulsant drugs (esp phenobarbital) and BZD withdrawl may provoke seizures
 Encephalitis and inflammatory conditions
 Metabolic abnormalities
       o Hypocalcaemia, hypoglycaemia, hyponatraemia, acute hypoxia, porphyria, uraemia, hepatocellular
          failure, mitochondrial disease
 Degenerative brain disorders
       o Alzheimer‟s, MS
 Provoked (eg. photosensitivity)
       o Flashing lights or a flickerng TV screen
 Sleep deprivation
Diagnosis and Investigations of Epilepsy
 History from a witness is critical
      o Onset, setting and stages of the attacks are important
 Neurological exam

 Bloods
       o FBC
       o U&Es, LFTs, Glucose
       o ESR
 Photos:
       o CT and/or MRI
 Fancy
       o EEG – should be performed after a first fit
              During seizure – always abnormal
              EEG evidence of seizure activity is shown by focal cortical spikes or by a generalised
                spike-and-wave activity
              3 Hz spike-and-wave is specific to petit mal
              A normal EEG between attacks does not exclude epilepsy

Emergency treatment of epilepsy
 It is best simply to ensure the pt comes to as little harm as possible
 Maintain airway (ABC‟s)
 Most seizures last only minutes and end spontaneously

Epilepsy - Pathophysiology

   A seizure is an abnormal paroxysmal discharge of cerebral neurons due to cortical hyperexcitability.
   Partial seizures result from a seizure discharge within a particular brain region or focus, and they manifest
    focal symptoms. Generalized seizures probably begin in the thalamus and other subcortical structures, but
    on scalp EEG recordings they may appear to start simultaneously in both cerebral hemispheres; therefore,
    they manifest symptoms bilaterally in the body and are always associated with loss of consciousness

Generalized epilepsy is thought to be initiated by 3 different mechanisms:
 Abnormal response of hyperexcitable cortex to initially normal thalamic input
 Primary subcortical trigger, and
 Abnormal cortical innervation from subcortical structures

   Physiologically, a seizure results from a paroxysmal high-voltage electrical discharge of susceptible
    neurons within an epileptogenic focus.
        o These neurons are known to be hyperexcitable and, for unknown reasons, remain in a state of
            partial depolarization.
                 This may come about due to damage of the neuronal cells via trauma, SOL etc
                 Changes in neurotransmitter release
        o The neurons surrounding the epileptogenic focus are GABA-ergic and hyperpolarized, and they
            inhibit the epileptogenic neurons.
        o At times, when the epileptogenic neurons overcome the surrounding inhibitory influence, the
            seizure discharge spreads to neighbouring cortical structures and then to subcortical and
            brainstem structures.
   Various animal models of generalized epilepsy implicate brainstem structures in the pathogenesis of
    generalized seizures.
   These brainstem structures include
        o A lateral geniculate body, which produces a generalized tonic-clonic seizure (GTCS) when kindled
            in the cat
        o Ascending pathways through the mamillary bodies and anterior thalamus; and
        o The substantia nigra, including a nigrotectal GABA-ergic projection and locus ceruleus.
   The spread of excitability to subcortical, thalamic, brainstem, and spinal cord structures corresponds with
    the tonic phase of the seizure.
       o   Following this, an inhibitory impulse starts from the thalamus and interrupts the tonic phase into
           discontinuous bursts of electrical activity, known as the clonic phase.

Neuro Pathology II

   About half of tumours are metastatic, the rest primary
   Tumours of the CNS account for 20% of all Ca of childhood
        o 70% of tumours arise in the posterior fossa,
   In adults, 70% tumours arise within the cerebral hemispheres above the tentorium
   Tumours of the NS are unique because:
        o Distinction between benign and malignant is less evident in the CNS
        o Ability to surgically resect infiltrating glial neoplasms without compromising neurologic function is
        o Anatomic site of the neoplasm can have lethal consequences irrespective of histologic
        o Pattern of spread is different – highly malignant gliomas rarely metastasize outside of the CNS
   Complications of brain tumours:
        o General
                   ICP
                  Herniation from compression
                  Hydrocephalus
                  Oedema
        o Local
                  Loss of function
                  Epilepsy
                  Haemorrhage
   Four major classes of brain tumours:
        o Gliomas
        o Neuronal tumours
        o Poorly differentiated neoplasms
        o Meningiomas

 50% of all brain tumours

 Types:
      o Fibrillary astrocytoma
             80% of adult primary brain tumours, usually found in cerebral hemispheres
             Most common CNS tumour of children, usually found in cerebellum
             Most common presenting sx: headache, seizures, focal neurological defects
      o Gliblastoma multiforme
      o Pilocytic astrocytoma
      o Pleomorphic xanthoastrocytoma

 5% of all gliomas
 Ill-defined, slow growing tumours arising from the oligodendrocytes of the white matter, especially in the
    temporal lobe
 Rare in children
 Usually associated with a good prognosis

 Arise from ependymal cells lining ventricle and central cord of the spinal cord
 Most common tumour of the spinal cord, accounting for 5% of all primary CNS neoplasms
 Common in children and young adults
 Cause hydrocephalus, usually associated with poor prognosis

Poorly Differentiated Neoplasms
 Of primitive neuroepithelial cells arises in the cerebellum in children, in whom it is the most common CNS
 Malignant, with a rapid growth rate.
 Usually obstructs the fourth ventricle and results in hydrocephalus

Neuronal tumours
 These occur mainly in children and rarely in young adults.
 Neuroblastomas usually arise in the adrenals or in association with the autonomic nervous system.
       o Rare in the central nervous system.
 Gangliocytomas include mature ganglion cells and occur in the third ventricle, hypothalmus and temporal
 Medulloblastomas occur in the cerebellar region in young children.
       o Obstruct the flow of the CSF and seed within the subarachnoid space.

Parenchymal tumours

Primary brain lymphoma
 Associated with immunosuppression, especially AIDS
 Most primary brain lymphomas are high grade, non-Hodkin‟s lymphomas of B cell type with a poor

Germ cell tumours
 Rare tumours, often seen in children, m>f
 Most arise near pineal gland and they behave as malignant teratomas

Other tumours

 Account for approximately 15% of adult intracranial tumours (f>m)
 Arise from the arachnoid matter, usually bening, but may invade adjacent bone, resulting in erosion and
 Produce symptoms by compression of brain tissue rather than invasion

Metastatic tumours
 CNS is a common site for mets and tumours are usually multiple
 May arise from haematogenous or direct spread
 Cerebellum is preferred site, but they can affect any part of the brain as well as other intracranial
   structures (Meninges etc)
 Mets often occur at the boundary between grey and white cancer
 Most common neoplasms to mets to brain:
       o Breast
       o Bronchus
       o Kidney
       o Colon
       o Malignant melanoma

Peripheral Nerve Sheath Tumours

Schwannoma (Neurilemmoma)
 Arise from schwann cells and are associated with neurofibromatosis type 2
 Sx come from local compression of involved nerve
 Most common site is vestibular branch of CN VIII

 Can occur in the skin (cutaneous neurofibroma) or peripheral nerve (solitary neurofibroma)
      o Airse sporadically in neurofibromatosis type I
       o  Skin lesions are evident as nodules, sometimes with overlying hyperpigmentation and become
   Tumour of the neural crest cells derived from the epineurium and endoneurium

Epilepsy – Treatment

Anticonvulsant drugs                                                      Side effects of anticonvulsants:
 Use carries the stigma of epilepsy                                          Intoxication with all anticonvulsants
 Acceptance by pts is essential, as is their understanding of possible
                                                                                    o Ataxia
   side effects                                                                     o Nystagmus
 Only used when there is a firm clinical diagnosis of recurrent                    o Dysarthria
   seizures, or a substantial risk of recurrence                              Idiosyncratic side effects (non-dose
 For both partial and generalised seizures, prescribe monotherapy             related):
   with an established anticonvulsant of proven efficacy                  Phenytoin            Rashes
                                                                                               Blood dyscrasias
 Four main drugs are used – carbamazepine, lamotrigine, phenytoin
   and sodium valproate                                                                        SLE
                                                                                               Toxic epidermal necolysis
Three mechanisms of ACD‟s:                                                Carbamazepine        Rashes
 Enhance GABA action                                                                          Blood dyscrasias
       o Act on GABAA receptors to facilitate opening of Cl- channels                          Leucopenia
          -> hyperpolarise neuron                                                              Toxic epidermal necrolysis
                                                                          Sodium               Anorexia
       o Examples: phenobarbitol, benzodiazepines, gabapentin             valproate            Hair loss
 Inhibit Na+ channel function                                                                 Liver damage
       o Affect voltage gated Na+ channels -> prevent spreading of        Lamotrigine          Toxic epidermal necrolysis
          AP                                                              Vigabatrin           Retinal damage
       o Voltage gates: inactive -> resting -> active -> inactive                              Psychological change
       o Use-dependent -> affect the cells that are continually firing
          (ie. the ones that get back to inactive)
                 freq of firing -> greater block potential
       o eg. phenytoin, carbamazepine, valproate, lamotrigine
 Inhibit Ca2+ channel function
       o Blockage of T-type Ca2+ channel -> plays a role in absence seizures
       o Eg. ethosuximide

Phenytoin (Dilantin)
 A bit different to other ACDs, this does several things:
      o Tonically inhibits voltage sensitive sodium channels in the neuronal cell membrane
      o Gates release of excitatory agent glutamine
 Impairs the rapid train of impulses, but does not interfere with isolated impulses or slow trains of
   neuronal discharge
 Highly effective for grand mal and focal epilepsies, NOT absence
 SE:
      o Vertigo, ataxia, headache, nystagmus, gum hyperplasia, hirsuitism, megaloblastic anaemia,
           hypersensitivity rashes, foetal malformations (cleft palate)

Carbamazepine (Tegretol)
 Structurally related to the TCAs
 Works on the Na+ channels
 Leukopenia is common, but rarely severe enough to warrant cessation of treatment
 Good for grand mal and focal epilepsies, often used with neuropathic pain
 SE:
      o Drowsiness, dizziness, ataxia, mental/motor disturbance, water retention, bone marrow
 Powerful inductor of hepatic microsomal enzymes – affects several drugs, especially concentrations of the

Sodium valproate (Epilim, Valpro)
 Unrelated to any ACD, MOA is relatively unknown, suggested:
      o  synthesis of GABA and slows its breakdown
   SE:
          oRelatively few:
          oThinning and curling of hair, hepatotoxicity, teratogenic (spina bifida and other neural tube
       o Usually makes pts brighter rather than drowsier, and may sometimes cause tremor and insomnia
   Used for primarily generalised epilepsies such as childhood petit mal or juvenile myoclonic epilepsy

Lamotrigine (Lamictal)
 Same MOA as phenytoin
 „Add on‟ drug

Barbiturates (phenobarbitone)
 Modulate the GABA-A receptor complex
 Causes sedation and irritability in some pts

 Benzodiazepine – has a more effective and sustained anticonvulsant action than diazepam
 Modulates the GABA-A receptor complex, same as barbiturates
      o Mediates fast inhibitory synaptic transmission in the CNS
      o BZDs enhance response to GABA by facilitating opening of Cl channels
 Benzodiazepines are best treatment for status epilepticus

Vigabatrin (Sabril)
 Inhibits GABA transaminase
 Usually only as a last-line treatment
 May cause drowsiness, weight gain, depression and psychosis

GABApentin (Neurontin)
 Another GABA analogue, MOA not known
 Side effects include somnolence, fatigue and ataxia

Ethosuximide (Zarontin)
 Used only for control of petit mal absences

 Fertility
      o Small  of fertility in epileptic population – this is multifactorial
                 1/3rd of women with epilepsy have ovarian pathology – menorrhagia, anovulatory cycles
                     and PCOS
                 Probably more common in pts taking sodium valproate
 Birth defects
      o Overall risk of birth defects in babies of mothers who take one anticonvulsant is ~7-9%, 3x higher
            than the 3% in the general population
      o Carbamazepine is safest to use
      o Counselling before conception is essential
      o Malformations of phenytoin – craniofacial abnormalities such as cleft palate, also congenital heart
      o Sodium valproate is associated with spina bifida
      o Regular folic acid administration should be given to women taking anticonvulsant medications
            who intend to become pregnant so as to reduce risk of neural tube defects
 Contraception
      o Anticonvulsants that induce enzymes (eg. carbamazepine, phenytoin, and Phenobarbital) reduce
            the efficacy of oral contraceptives
                  metabolism of the OCP
      o Valproate does not
      o A COCP containing at least 50mg of oestrogen should be used, or an IUCD or barriers
 Breast feeding
      o Unknown effects in the breastmilk
 Cosmetic side effects
       o   Phenytoin causes facial hirsutes, coarsening of the features, acne, and gum hypertrophy
       o   Sodium valproate causes weight gain and thinning of the hair
       o   Carbamazepine and lamotrigine are relatively free of cosmetic side effects

Drug withdrawl
 Successful withdrawl is only achieved in < 50%
 Recurrence of seizures can cause considerable difficulty when a driving license has been regained

Stigma and Social Consequences of Epilepsy

 An discrediting attribute such that the individual with this attribute is disqualified from full social
 Stigmatising conditions set their possessors apart from „normal‟ people & imply their inferiority e.g.
    physical deformity, prison record, mental disorders, homosexuality
 It is not the disability, the life episode or the attribute itself – but the sociocultural meaning which is
    attached to the condition -> meaning is not fixed or inherent but culturally relative
 Diagnosis as labelling
 Diagnosis can be a welcome label -> ends uncertainty & provides explanation of symptoms
 When a patient is diagnosed with a condition which is stigmatised they are given a label with a negative
    image; possible associations with guilt & shame and detrimental implications of social acceptance

Felt v Enacted Stigma
Enacted Stigma – discrimination due to the perceived unacceptability or inferiority of those with the condition
Felt Stigma – fear of enacted stigma and the accompanying shame

   Felt stigma makes patients adopt a policy of non-disclosure in order to avoid enacted stigma -> most feel
    more unhappiness, anxiety & self-doubt through felt stigma than they do either directly or indirectly
    through enacted stigma
   Predisposes patients to secrecy & concealment to pass as “normal” e.g. a study showed 28% informed
    employer they had epilepsy & 55% made no disclosures of any kind
   This can result in withdrawal -> the isolation can be more detrimental than the intermittent physical
    symptoms of the condition -> isolation ameliorated by contact with support group

       Example of the distinction (as requested by the Faculty LO)
       Enacted Stigma – not letting people with epilepsy into a particular restaurant
       Felt Stigma – a person with epilepsy avoiding all restaurants for fear they will be refused
       entry or make a scene

   When giving a diagnostic label which has an associated stigma doctors MUST be aware of its likely impact
    & allow additional time to talk about the psychosocial consequences of the diagnosis to help the patient
    begin to cope with their emotional reaction
   Terms in which diagnosis is described make a considerable differences & aid patient‟s cognitive
    restructuring in learning to live with a stigmatised condition
   Provide information, support & counselling

Public Health - Driver‟s License

In Qld
 If single episode of seizure -> no driving for 3-6 months
 If chronic epilepsy -> must be seizure free for >= 2 years
 No driving of commercial vehicles
 Must be reported when applying for licence
Problem 28 – Meningitis

Wk Dom       LO Title                                            LO Detail
 28 BCS Diagnosis of          1. To be able to develop a differential diagnosis for the febrile child.
        meningitis            2. To be able to recognize the clinical syndrome of bacterial meningitis.
                              3. To be aware of the various CSF profiles in different types of meningitis.
                              4. To describe the types of investigations and their role in evaluating
 28 BCS Pathophysiology of 1. To discuss the pathophysiology of meningitis and the changes that occur in
         meningitis           the blood brain barrier in meningitis.
                              2. To be familiar with the common organisms (viral, bacterial, fungal and
                              parasitic) causing meningitis in various age groups (eg neonatal vs young
 28 BCS Prevention and        1. To be aware of the role of vaccines in preventing or reducing the incidence
         treatment of         of meningitis.
         meningitis           2. To identify which causative agents have vaccines available for their
                              3. To be aware of the current treatment guidelines for meningitis in children
                              and the pharmacology of those drugs.
                              4. To understand how the blood brain barrier affects the delivery of drugs to
                              the CNS.
 28 EPPD Immunisation issues 1. Describe the related ethical issues in maintaining adequate infant
                              immunisation rates.
 28 ICCP Clinical reasoning   1. To be aware of decision making implications regarding further
                              investigations, eg lumbar puncture, CT scan when physical examination
                              findings for meningitis are equivocal.
 28 ICCP Clinical examination 1. Perform an examination that would focus on the relevant clinical features
                              when acute meningitis was suspected.
 28 PPH Infectious disease 1. Document the public health implications of a disease outbreak such as
         outbreak; Child care bacterial meningitis.
         centres (Public      2. What general public health measures are recommended for child care
         Health)              centres to minimise the occurrence of infectious disease outbreaks?
                              3. Be able to discuss with a parent, the possible reasons why his/her toddler
                              has developed several infectious illnesses since enrolling in a childcare centre
                              6 months previously.
 28 PPH Immunisation          1. Describe the related public health and policy issues in maintaining adequate
         (Public Health)      infant immunisation rates.
Pathophysiology of Meningitis

Meningitis – inflammation of leptomeninges (pia + arachnoid) due to infection from pathogens which
invade the CSF.


Bacterial meningitis (septic/purulent                  Viral meningitis (aseptic meningitis)
meningitis)                                             Enteroviruses
 Neisseria meningitides *                                    o Echo
 Streptococcus pneumoniae *                                  o Coxsackie
 Staphylococcus aureus                                 Mumps
 Strep group B                                         HSV
 Listeria monocytogenes                                HIV
 G- bacilli                                            EBV
 Mycobacterium tuberculosis
 Treponema pallidum

Fungi                                                  Pathogens associated with bacterial meningitis in:
 Cryptococcus neoforms                                 Neonates
 Candida                                                     o Group B streptococcus
                                                              o E. coli
                                                        Children
                                                              o S. pneumoniae
                                                              o H. influenzae B
                                                        Adults
                                                              o S. pneumoniae
                                                              o N. meningitidis
                                                        Elderly
                                                              o L. monocytogenese
                                                              o S. pneumoniae
                                                        Immunocompromised
                                                              o Klebsiella
                                                              o Other anaerobic organisms

Organisms reach meninges via:
 Direct extension (eg. penetrating traum, inections of aears, nasopharynx)
 Haematogenous spread (eg. septic emboli, IE, etc)
 Iatrogenic infection (eg. lumbar puncture)
 Congenital abnormalities (eg. meningomyelocoeles)

 Disease begins as an infection by normal body flora of:
      o URT (S. pnemoniae, N. meningitides, H. influenzae, Grp B Strep)
      o Skin and subcutaneous tissue (Staph aureus)
      o Intestine (E. coli)
 Localised infection -> bacteraemia ->
 Infection of the meninges ->
 Subarachnoid inflammation ->
      o Increased BBB permeability
               Vasogenic cerebral oedema
      o Blockage of normal CSF pathways
               Interstitial cerebral oedema
      o Toxic factors from macrophages and or bacteria
               Cytotoxic cerebral oedema
      o Cerebral vasculitis
               Cerebral infarction
 These lead to decreased cerebral blood flow either directly or due to increased intracranial pressure. ->
   Cerebral hypoxia -> CSF acidosis -> Encephalopathy -> Death

Ways through the BBB/BCB:
 Invasion engineered by pathogen
      o Pathogen signals the cell to take it from the blood and discharge it in the CSF
      o eg. L. monocytogenes, H. influenzae B.
 Paracellular transmigration
      o eg. H. influenzae B (has a capsule)
 Enhanced vesicular transport
      o eg. Meningococcus
 Receptor mediated uptake
      o eg. pneumococcus + PAF-receptor, malaria +ICAM-1

Predisposing factors for meningitis
 Infection
      o Systemic (particularly respiratory)
      o Direct extension (ears, nasopharynx)
      o Parameningeal/congenital meningeal defect
 Head trauma
 Neurosurgical procedures
 Cancer
 Alcoholism
 Immunodefficiency
 Absence of spleen

Pathology of Bacterial Meningitis
 Pia-arachnoid (leptomeninges) and the CSF is congested with neutrophils and a layer of pus is formed
   that may organise to form adhesions causing:
       o Cranial nerve palsies
       o Hydrocephalus
 Causative organisms above

Complications of acute bacterial meningitis:
 Ventriculitis
 Intracerebral abscess
 Cerebral infarction
 Epilepsy
 Adrenal haemorrhage (Addisonian crisis)
      o Bleeding into brain and andrenals (Waterhouse-Fridrichsen)

Diagnosis of Meningitis

Differential diagnosis of febrile child
 Infection, with Associated Fever
       o Viral:
                Respiratory tract infection, check for RTI signs such as sniffles, cough, crackles, CXR
       o Bacterial
                Acute otitis media: unilateral ear ache, confirmed by otoscope.
                Tonsillitis: presents with a sudden severe sore throat with pain radiating to the ears.
                Urinary Tract Infection: presents with dysuria, frequency and apparent on urine
                Pneumonia: as covered previously, presents with cough, painful shallow breathing and
                  lower respiratory signs.
                Meningitis: rash, nausea, headache, photophobia, bulging fontanelle. As covered above.
 Other
       o Metabolic insults such as congenital enzyme deficiencies.
        o   Toxin ingestion: always keep this in the back of your mind. Mercury poisoning used to be a big
        o   Physiological: the bub‟s overdressed or something, and therefore can‟t thermoregulate.

„Classic‟ triad of:                                       Other symptoms:
 Headache                                                 Photophobia
 Neck stiffness                                           Irritability
 Fever                                                    Vomiting
                                                           Malaise, rigors, fever
                                                           Petichial rash (meningococcal)

Acute bacterial meningitis:
 Onset is sudden with rigors and a high fever
 Meningococcal meningitis -> petechial rash
 Acute septicaemic shock may develop

Viral:                                                                                  Layers Traversed in a LP
 Almost alwas benign and self limiting condtion of 4-10 days
 Headache may follow, but no serious sequelae                                              skin & underlying fat
Kernig‟s sign – pt supine, examiner flexes pt‟s hip, but cannot extend the                 supraspinous ligament
knee without causing neck pain and flexion (Kernig‟s = Knee)                                          
                                                                                           interspinous ligament
Brudzinski‟s sign – Flexion of the neck causes flexion of the legs at the                             
knees, hips and ankles                                                                       ligamentum flavum
Investigations                                                                                  epidural space
 Bloods                                                                                              
       o FBC                                                                                      dura mater
       o U&E‟s, LFTs, Glu                                                                             
 Bacto                                                                                         subdural space
       o Systemic                                                                                     
       o CSF (if possible)                                                                     arachnoid mater
 Pictures                                                                                            
       o Skull XR, CXR                                                                 subarachnoid space containing
       o CT/MRI                                                                                      CSF
 Fancy
       o PCR tests
       o LP

Risks of LP include: infection, bleeding and brain herniation of cerebellar tonsils.

CSF findings in meningitis
Type               Pleocytosis                   Glucose                 Protein                 Appearance
Bacterial           (neutrophils)                                                        Turbid/purulent
Viral               (Lymphocytes)               Normal                                         Clear/turbid
Fungal              (Lymphocytes)                                     
TB                  (Lymphotyctes)                                                         Turbid/viscous

 H influenzae type B
      o G- coccobacilli
      o URT inhabitant
 N. meningitidis
      o G- diplococci
      o Types A, B, C, Y, W135
      o Carried by 20% of population
      o No vaccine for group B which causes 50% of disease
        o   Exclusively human pathogen, nasopharynx reservoir, spreads via aerosols
        o   Endotoxin is highly toxic
   S. pneumoniae
        o   G+, -haemolytic cocci
        o   More than 90 serotypes, capsule is major virulence factor

Virulence factor             N. meningitidis             H. influenzae            S. pneumoniae
Capsule                                √                            √                      √
IgA protease                           √                            √                      √
Autolysins                             √                            √                      √
Pili                                   √                            √                      X
Endotoxin                              √                            √                      X
Outer Membrane Proteins                √                            √                      X

Prevention and Treatment of Meningitis

Treatment should be commenced without delay:
 Organism
      o Unknown – ceftriaxone
      o Meningococcus – benzylpenicillin
      o Pneumococcus – cefriaxone
      o Haemophilus – ceftriaxone
 Steroids are sometimes used in children (controversial apparently)
      o Has been shown to reduce frequency of complications (especially deafness)

Mortality of bacterial meningitis:
 25% with pneumococcus
 10% with meningococcus
 5% with H. influenzae

Prevention of meningitis
N. meningitidis Rifampicin prophylaxis for close contacts
                Polysaccharide vaccine (poor protection against
                group B)
H. influenzae   Polysaccharide vaccine against type B (Hib)
S. pneumoniae Prompt treatment of otitis media and RTI‟s
                Polyvalent, polysaccharide vaccine
E. coli         No vaccines available
M. tb           BCG vaccination, isoniazid prophylaxis
Cryptococcus    No vaccines

Neuro Pathology III

Four principal routes of entry for infections of the nervous system:
 Haematogenous spread
 Direct implantation (traumatic, iatrogenic, congenital)
 Local extension (sinuses, teeth, neurosurgical site)
 Peripheral nervous system (herpes, rabies)

 Meningitis may result from:
      o Acute pyogenic (bacterial)
      o Acute aseptic (viral)
      o Chronic (bacterial, fungal or tuberculosis)
 Plenty of info in week 28 notes
 Morphology (bacterial):
       o CSF is cloudy and frankly purulent
       o Exudate is evident within leptomeninges over the surface of the brain
       o Meningeal vessels are engorged and stand out prominently
   Morphology (viral):
       o No distinctive macroscopic characteristics except for brain swelling in some instances
       o Lymphocytic pleocytosis microscopically

 May arise
      o Direct implantation of organisms
      o Local extensions from adjacent foci (mastoiditis, paranasal sinusisits)
      o Haematogenous spread (heart, lungs, distal bones, tooth extraction)
 Predisposing conditions:
      o Acute bacterial endocarditis
      o Cyanotic congenital heart disease
      o Chronic pulmonary sepsis (bronchiectasis)
 Streptococci and staphylococci are most common identified
 Pts invariably present clinically with progressive focal deficits in addition to general  ICP
 CSF is under pressure, white cell count and protein levels are raised, but glucose is normal
 Complications:
      o  ICP -> herniation
      o Rupture -> ventriculitis, meningitis and sinus thrombosis
 Morphology:
      o Macroscopic – abscesses are discrete lesions with central liquefactive necrosis, a surrounding
          fibrous collagenised response, and oedema
      o Commonly affected: frontal lobe, parietal lobe, cerebellum
      o Microscopically – exuberant neovascularisation around necrosis that is responsible for marked
          vasogenic oedema and formation of granulation tissue
      o Collagen of capsule is produced by fibroblasts derived from the walls of blood vessels
      o Outside capsule is a zone of reactive gliosis with numerous astrocytes

 Primary infection of the brain is not common, but may result from:
      o Viral (mostly)
      o Bacterial (eg. syphilis, TB and mycobacterioses)
      o Fungal (eg. Cryptococcus)
      o Parasitic (eg. toxoplasmosis in AIDS pts)
 Viral meinigoencephalitis
      o Viral encephalitis is almost always invariably associated with meningeal inflmamtion and
          sometimes the spinal cord
      o Most characteristic histologic features of viral encephalitides are:
                Perivascular and parenchymal mononuclear cell infiltrates (lymphocytes, B cells and
                Glial cell reactions
                Neuonophagia
      o Examples:
                Herpes zoster (varicella-zoster) -> shingles
                HSV-1 & 2 (temporal lobes!)
                Rabies
                Rubella (foetal malformations)
                CMV (foetuses and immunoscompromised
                Poliomyelitis
      o May be arthropod-borne (arbo) viral encephalitis as well. Eg. Japanese B, Murray Valley
 Spongiform encephalopathies (prion disease)
      o Creutzfeld-Jakob and kuru
      o They are all associated with abnormal forms of a specific protein, termed prion protein, and are
          both infectious and transmissible
      o Predominantly characterised by „spongiform change‟ – caused by intracellular vacuoles in neural
Clinically pts develop progressive dementia

Septic Shock

   Occurs from G- endotoxin release in 70% of cases
   May also be from G+ (eg. toxic shock syndrome toxin-1 from staph) and fungi
   Results from the spread and expansion of an initially localised infection (eg. abscess, peritonitis,
    pneumonia) into bloodstream

Stages of Shock
 An initial nonprogressive phase during which reflex compensatory mechanisms are activated and
   perfusion of vital organs is maintained
 A progressive stage characterized by tissue hypoperfusion and onset of worsening circulatory and
   metabolic imbalances, including acidosis
 An irreversible stage that sets in after the body has incurred cellular and tissue injury so severe that
   even if the hemodynamic defects are corrected, survival is not possible.


Vaccine is a form of active acquired immunity. A person is deliberately exposed to an avirulent version of the
pathogen, and this will stimulate the person‟s immune system to produce protective antibodies and memory
The requirements of a good vaccine
 A vaccine should be effective, safe, stable and of low cost.
 Must give effective response: for example an antibody response is unlikely of benefit against tuberculosis.
 The response must give long-lasting immunity: in general living vaccines give stronger and more lasting
 Must be Safe: because vaccines are the only compounds routinely given to healthy people.
 Must be Stable: because they tend to remain on the shelf for long periods and must endure extreme
 Cost must be relative to risks, but not high for use in developing countries
 Must be targeted to prevent a disease of sufficient severity
 Must be targeted to prevent a common disease
 Must have a stable antigenic profile
 Must have a high compliance rate and sufficient public education programs.

Types of vaccines:
 Attenuated vaccines
       o Live vaccines of weakened pathogens, avirulent pathogens derived from weakening pathogenic
       o Examples: viral vaccines (adenovirus, varicella, rubeola, mumps, rubella, polio, rotavirus, smallpox,
           yellow fever); bacterial (BCG, cholera, tularaemia, typhoid fever)
 Inactivated vaccines
       o Pathogens killed by heat or chemicals. Less effective than live vaccines because antigens on dead
           cells are less effective
       o Examples: viral vaccines (hepatitis A, influenza, Japanese encephalitis, other encephalitis vaccines,
           polio, rabies); bacterial (anthrax, typhoid fever, Q fever)
 Subunit vaccines
       o Uses antigenic (antibody stimulating) portions of a pathogen (rather than the whole thing)
       o Examples: hepatitis B (surface protein), Lyme disease, whooping cough
 Conjugate vaccines
       o Conjugating bacterial capsular antigens (not very antigenic) to molecules that stimulate immune
           system to produce antibodies against less antigenic capsular antigens
       o Examples: HIB, Neisseria meningitidis, pnemococcal
 Toxoid vaccines
       o Toxoid – inactivated exotoxin. Can be injected to stimulate production of antibodies that
           neutralise exotoxins of pathogens
       o Examples: diphtheria, tetanus
 DNA vaccines
       o Gene from a pathogen is inserted into plasmids, plasmids are injected. Inside host cells, genes
           direct the synthesis of antigens. The body then starts producing antibodies directed against the
 Autogenous vaccines
       o One that has been prepared from bacteria isolated from a localised infection. Pathogens are then
           killed and injected into the same person to induce production of more antibodies
Meningicoccal specific vaccines:
 Polysaccharide vaccine
       o Mencevax and Menomune
       o Protects against serogroups A, C, W-135, Y
       o Efficacy against serogroup C67-90%
       o Limited duration of efficacy
       o Ineffective in young children
       o No role in management of sporadic disease
       o Does not cover serogroup B (predominant sporadic serogroup)
       o Limited response < 2yo who are at greatest risk
       o >2 weeks to induce optimal immune response
       o Does not induce long-term immunity
       o Recommended for:
                Travel to countries where group A epidemics are not infrequent
                Control of outbreaks of group A, W135 or Y
                Lab staff handling meningococcus (+ conj)
                >2yoa with inherited defects of properdin or complement or functional/anatomical
                   asplenia (+ conjugate)
                Pilgrims attending annual Hajj (Saudi Arabian authorities require valid vaccination
 Conjugate vaccine
       o Meningitec, Menjugate, NeisVac-C
       o For all children at 12 months + catch up program in process to 19yoa
       o Protection against serogroup C – “long lasting”
       o In infants
                Immunogenic in 98-100% after 3 doses
                Primes immunological memory
       o In children > 12 months
                Immunogenic in 81-97% after 1 dose
       o Conjugated with a protein
       o No thiomersal, human albumin or human fetal material
       o One milk-derived component (from countries where no BSE has ever been reported)

Ethics of Immunisation

Causes of Under-immunisation
 Office and clinical barriers.
 Parental misconceptions or fears.
 Failure to track and recall children.
 Missed opportunities.
 Invalid contraindications
 Lack of simultaneous administration.

The Anti-vaccination Lobby
There is a certain group of people in the society that are against immunisation. These are usually intelligent
people, from a variety of backgrounds, with a variety of motives, that often lack a strong scientific
background. They tend to selectively use information. Anti-immunisation advocates tend to get a fair bit of
media attention, probably because it rates well to come out and say something that contradicts everything

Argument #1: “Infectious Diseases are not serious and are a Normal Part of growing up”
This is one of the major anti-immunisation arguments. It‟s fairly easily disproved. Between 1989 and 1998
there were 581 recorded deaths from diseases preventable by vaccines on the current childhood
immunisation schedule, with 440 from Hep B, 88 from Hib, 1 from diphtheria, 19 from measles, 14 from
pertussis, 3 from mumps and 16 from tetanus.

Argument #2: “Immunisation is not responsible for the decline in communicable diseases as
improved living standards and sanitation have reduced the incidence of infectious diseases.”
Although a slightly more rational argument, this too is clearly wrong. Although the decline in communicable
diseases has been multifactorial, and living standards do play a major role, vaccination has also had a clear
and significant impact. For example, measles and pertussis are spread by the respiratory route and attack
rates aren‟t affected by living standards or standards of sanitation. The attack rate is about 100% irrespective
of social and sanitary conditions, and they affect virtually everyone in unvaccinated countries. Vaccination
reduced transmission of these diseases, sanitation won‟t.

The other argument related to this is that the prevalence of the vaccine-preventable diseases was reducing
before the vaccine introduced. This is actually true, for all diseases except measles and pertussis. However,
look at the table included above, and tell me that immunisation didn‟t make a significant difference to the
incidence and mortality of these diseases.

Argument #3: “The vaccines do not protect against disease, as many cases of disease occur in
immunised children”
This is the paradox – when immunisation coverage increases, there are increasing proportions of cases of
vaccine-preventable diseases in immunised children. Basically, if 95% of the population‟s inoculated, and the
vaccine isn‟t perfect (as none as them are), then a lot of the cases are going to occur in vaccinated people.
Proportionally, however, there will be more cases in unvaccinated people.

An argument of statistics.

Argument #4: “Vaccines are Unsafe”
This is one of the major arguments against immunisation, and is hard to counter, because no biological
product can be considered 100% safe. However all vaccines in Australia pass stringent testing standards set
by the TGA. There are some specific arguments, covered below.

“The side-effects of DTP include brain damage”
The DTP has components to induce immunity to tetanus, diphtheria and pertussis. The pertussis vaccine used
to be manufactured from whole-cell pertussis organisms, and commonly caused severe local adverse events
such as redness, swelling and pain, and mild systemic events such as drowsiness, fretfulness and loss of
appetite. More severe effects occurred in about 1 in 1750 doses, including convulsions, with or without fever,
and hypotonic, hyporesponsive episodes. There was concern in the 1970s that pertussis vaccine caused
encephalopathy and brain damage. There is no conclusive evidence to prove this.

The acellular pertussis vaccine used now has much smaller incidence of mild side-effects, and very few
documented major side-effects. Therefore the argument‟s old, anyway, and probably wasn‟t right in the first

“Vaccines cause the diseases they are supposed to prevent”
Oral polio vaccine (OPV) is often said by critics to be the major cause of paralytic polio in developed countries
like Australia and the US. Indeed, live oral polio vaccine may cause paralysis in 1 per 2.5 million distributed
doses. In the US, this meant about 8 cases per year following the introduction of OPV. Because the virus is
shed for about 6 weeks after administration, there were also occasionally cases of paralysis in contacts. In
Australia, there have been 2 cases of vaccine-associated paralytic poliomyelitis in the last 13 years. This is
because Australia uses a non-first generation vaccine, that doesn‟t have as high an incidence as the newer

A quick look at the graph reveals, that over the last 13 year, we would probably expect around 26,000 deaths
due to poliomyelitis if the vaccine hadn‟t have been developed. 26,000 vs 2.

“Vaccines suppress the immune system”
The only situation where this may occur appears to be immune suppression following the use of high-titre
measles vaccines, which were proposed at one time for some developing countries. These have never been
used in developed countries, such as Australia.

“Additives in vaccines are toxic”
Additives in many vaccines are said to be „toxic‟, for example formaldehyde, aluminium and thiomersal.
However, it is an exaggeration and misleading to say that vaccines contain many toxic ingredients.
Formaldehyde, for example, is used to detoxify the tetanus toxin protein produced during manufacture of the
vaccine, and is later removed in the purification process. The maximum amount of formaldehyde registered
by the TGA has been 0.004% weight per volume of formaldehyde, well below the standard 0.02% limit.
Thiomersal contains 49.6% mercury and has been used in small amounts in vaccines since the 1930s, as it
prevents bacterial and fungal contamination. There is no evidence that it causes any adverse health effects in
children due to its role in vaccines, however, in low birth weight children with repeated vaccinations, may
theoretically lead to levels of mercury above the recommended guidelines. However, in Australia, there‟s only
one vaccine that contains theomersal, and there is a current directive to remove this.

Green tea is also toxic in high doses. These doses are not high.

“Vaccines cause Sudden infant death syndrome (SIDS)”
This belief came about because a moderate proportion of children who die of SIDS have been recently
vaccinated. This argument, confuses association with causality. Consider that many people who crash their
cars have eaten bread in the last 24 hours before a car crash. Eating bread therefore causes car accidents....
SIDS death occur within the age range where many vaccinations are given, and therefore precede it purely
by chance. Several studies have revealed that there‟s no increased risk.

“Vaccines contain foreign proteins”
Egg protein and gelatin, for example, in vaccines may cause allergic reactions. Opponents of immunisation
say that this is particularly dangerous for young infants who are said to be vulnerable because of their
immaturity. The claim is that vaccines cause encephalitis, convulsions, brain damage, multiple sclerosis and
other neurological syndromes.

Yes, there are proteins in vaccines, such as egg proteins in the MMR. However studies have revealed that any
immune reaction is limited to a mild skin reaction, even in children with confirmed egg allergy.

“Some vaccines may cause mad cow disease”
Bacteria for use in some vaccines are grown on a medium with bovine heart and brain components, therefore
there is a danger of transmitting BSE. This risk is negligible, and there have been no reported cases,

“Vaccine viruses persist after immunisation”
Apparently, the viruses from vaccines hang around for years, leading to chronic disease. A variant on the
view is that immunisation drives viruses directly into the bloodstream and thus deep into the body, where the
attack „vital organs‟. Viruses in vaccines are eliminated by the very immune response they cause, except for
varicella, which may cause herpes zoster many years after vaccination, but at a much lower rate than natural
varicella infection.

“MMR vaccine causes inflammatory bowel disease and autism”
In 1993, a group of researchers in London suggested an association between both the natural and vaccine
types of measles virus and inflammatory bowel disease. A few years later they found a similar link with
autism. The data for IBD was based on a group of 25 children with Crohn‟s disease. Both studies have widely
been considered to be very flawed. The onset of autism and MMR coincidentally appear about the same time.

“Vaccines are contaminated with other viruses”
It has been said that vaccines are cultured on animal tissue and therefore contain many vaccines and viruses
other than the ones they were supposed to immunised against. For starters, only viral vaccines are cultured
in material derived from animal tissues. They are propagated in chicken eggs, primary cell cultures, and
continuous cell lines. These are all thoroughly screened for other viruses or bacteria. Although between 1955
and 1963 there was one cases of contamination of polio vaccine with a simian virus that „might‟ cause cancer,
this was later proven to have no connection. There is no evidence linking AIDS to polio vaccines.

“The rubella and chicken pox vaccines are cultured on cell lines of aborted fetuses”
This is based on old information, about one strain of the rubella virus, which was raised originally in a cell
culture originally derived from human foetal lung tissue obtained from a foetus aborted at about 3 months
gestation from a Caucasian female, in about 1966. The cell line used was obviously not identical, and, after
30 years culturing, of course barely resembled the original.
This was one cell line. The catholic church has no problems with any vaccinations, and they tend to be picky
about these things.

“Vaccines can cause diabetes”
Again, an isolated result from bad research. Not confirmed by any larger, better studies.

Argument #5: “The germ theory of disease is false”
The theory is that infectious agents aren‟t the cause of infection but merely one of its manifestations.

Argument #6: “Immunisation is unnatural‟
Immunisation is said to be an artificial stimulus to the immune system which is somehow harmful.

Everything that improves human suffering is unnatural. So if you don‟t want immunisation, also get rid of
your big soccer-mum 4WD, riverside house, clothes, eye-glasses, and run back to nature, cavorting playfully
with the animals.

Argument #7: “Specific immunity is not important for protection against disease”
These people believe that diet, health life-style and avoidance of stress are said to be the most important
factors in preventing disease. Gradual strengthening of the immune system through things such as vitamin C
is said to be the best way of preventing infection.

Public Health – Infectious Diseases (Meningitis as Example)

Risk Factors for Meningitis Outbreaks
 Socioeconomic (poor, crowding)
 Household contact (up to 600x)
 Damage to resp mucosa (adverse environmental conditions, antecedent viral infection especially influenza,
   smoking –active or passive)
 Immunological (IgG/IgM deficiency, complement deficiencies, high IgA, ABO non-secretor status)

 Respiratory droplets
 Infections acquired from carriers (human host)
 Carriage may last months
 Western society: asymptomatic (usually adult) carrier
 African setting: child to child
 Dies quickly outside human host

Highest incidence 0-4 years and 15-24 years.

 It‟s a rare but potentially fatal disease
 Early presentation, prompt diagnosis
 Presumptive parenteral antibiotics (throat swab and blood cultures)
 Contact definition
 Chemoprophylaxis
 Vaccination

Public Health Response:
 Information about the disease
 Chemoprophylaxis to selected contacts (still possibility of disease)
 No particular quarantine or behaviour requirements of contacts
 Maintenance of surveillance for further cases
 No value of immunisation for sporadic cases

Rationale for chemoprophylaxis:
 Antibiotics are given to close contacts NOT to abort incubating disease but to prevent them giving it to
   others in their network of close contacts
   We are looking for the carrier that gave the infection to the case through their close degree of contact (or
    could have acquired it through their close contact with the case since onset of the disease)– “who is the
    case‟s family”

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