NEURO-_summary.doc - STJ PA 2012

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					                                                           Neurology

Pain Management (Podd)
Neuropathic Pain
    o   Radiculopathy- compression of nerve root of spinal cord

    o    Etiology: DM (MCC), and alcoholism(MCC systemic neuropathy), leprosy(MC infx cause)
    o    Sx: Pain pronounced esp. at night, numbness, paresthesias, tingling, impotence, balance defecits, sensory
         defecits, paralysis, etc.
    o    PE: orthostatic hypotension, cranial and peripheral nerve defecits, muscular atrophy, hyporeflexia(peripheral
         neuropathy), ulcers, gangrene, café au lait spots on skin, Charcot’s joints
    o    Tx: treat underlying dz, Gabapentin, tricyclic antidepressants(amitriptyline), plasmapharesis



Peripheral Neuropathy(Politi)
Mononeuritis multiplex- two or more nerves are affected on separate areas of body


In most common polyneuropathies nerve fibers most distal to brain and spinal cord are affected first
Important to differentiate if neuropathy is axonal, demyelinating, or both*(Nerve conduction studies and electromyography
is used to differentiate)*



Bell’s Palsy and Erb’s Palsy(Politi)


Bell’s Palsy
      o    a complete interruption of facial nerve at the stylomastoid foramen paralyzes all muscles of facial expression
      o    Etiology: the common cold sore virus, herpes simplex, and other herpes viruses
      o    S/S: usually *unilateral*, drooping of the face, crease and skin folds, eyelids won’t close, drooling, heaviness or
           numbness in face, hypersensitivity of sound in affected ear, and impairment of taste
      o    Tx: steroids, w/ acyclovir if herpes is the cause



Erb’s Palsy
     o    Brachial plexus injury- including the arms, shoulder or hand, and all may be paralyzed
     o    MC occur at birth
     o    Tx: exercise, therapy, or surgery


Acute Confusional States and Coma (Leshinski)

Causes: TIPPS: trauma, infx, psych, poisons, shock; AEIOU: alcohol, epilepsy, insulin, opiates, urea

Herniation: Dx: EEG, CT Tx: ABCs(GCS<8 intubate), IV Naloxone and dextrose w/ AMS


Uncal Transtentorial Herniation
    o    Etiology: supratentorial mass leads temporal lobe moving into tentorial notch
    o    Herniation of uncus(innermost part of temporal lobe) into tentorial opening
    o    Compression of CN 3(oculomotor): ipsilateral pupil enlargement, sluggish pupil response
    o    *Central neurogenic hyperventilation*; contralateral hemiparesis due to compression
    o    Brainstem compression leading to coma
    o    Cushing’s reflex: HTN, bradycardia, widened pulse pressure (incr. SBP, decr. DBP)




Central Transtentorial Herniation
    o     Downward displacement of thalamic region through tentorial opening
    o     Etiology: supratentorial lesions
    o     Midpoint, *non-reactive pupils*, decorticate then decerebrate posturing, lead to coma
    o     + Babinski, Cushing’s Triad: HTN, bradycardia, irregular respiration(Cheyne-Stokes)


Tonsillar Herniation
    o     Compresses medulla through foramen magnum, compresses the cardiovascular and resp. centers
    o     Will present w/ cardiac arrest and *apneustic breathing*(held for 2-3 sec let go then can’t breath)
Infratentorial Lesions/Herniations
     o    Involves brain centers that control cardiopulmonary fx and RAS
     o    Upward herniation- hydrocephalus/coma; Downward herniation: cardiac arrest and death
     o    Unilateral or bilateral limb weakness or sensory loss prior to non reactive pupils, abn. Resp.




Metabolic Encephalopathy
    o    Etiology: hypoglycemia, hyponatremia, hypercalcemia, hypoxia, narcotics, alcohol
    o    Confusion, and stupor, AMS, *pupil response intact*, asterixis, myoclonus, tremors (all bilateral)



Head Trauma (Kruger)

Traumatic Brain Injury
    o    MCC MVA, falls in elderly
    o    Secondary brain injury- after initial insult i.e. ICP, *systemic hypotension*, hypoxia

    o    Pathophys: As ICP inc. *(>40)*, brain swells decreasing volume of other intracranial components such as blood


    o    Deceleration injury: skull stops moving, brain impacts skull (MVA)

    o    Acceleration injury: skull moves and impacts stationary brain (baseball bat to head)

    o    Coup injury: injury at site of direct impact

    o    Contrecoup injury: injury at site opposite to point of impact


    o    States of consciousness:

              o    A. persistent vegetative state- unconscious, unaware, have sleep-wake cycles, open eyes, move, groan,
                   have *reflex responses*


              o    B. locked in syndrome- patient is aware and awake, but completely paralyzed; eye mvmts


    o    Clinical Manifes:
               o   A. Mild TBI: remain conscious or LOC for few min., feel dazed for days/weeks, HA, tinnitus, confusion,
                   behavioral or mood changes, N/V


              o    B. Moderate/Severe TBI: persistent HA and/or vomiting, *seizures*, *unable to wake from sleep*,
                   pupil changes(bilateral fixed and dilated), ataxia, *inability to form and store new memory(MC)*


    o    Dx: GCS(glascow) score- speech, motor, and eye opening
              Skull X-ray: used for penetrating injuries to see how deep and any fragments
              *CT scan(non contrast): Test of choice* also notes signs of mass effect: cerebral edema, midline shift, and
         tissue compression
Concussion
    o    *Does not sustain a structural alteration to the brain after blunt trauma*
    o    Brief LOC <30 min

     o     Type of Mild TBI
     o     Sx: transient confusion, disorientation, memory loss, problems w/ concentration, and/or seizure
     o     Post concussive syndrome: ( 30% pts) HA, N/V, memory loss, blurred vision



Contusions- post-traumatic lesions in the brain in which high density changes(blood), and low density changes(edema) are
present



Skull Fractures
     o    *MC temporal bone*
     o    Moderate/severe TBI
     o    Basilar skull fx- presents w/ CSF otorrhea, rhinorrhea, and hemotympanum(blood behind tympanic), *raccoon
          eyes, and battle sign(behind mastoid)*



Epidural   Hematoma
    o       Arterial bleeds that tend to become larger rapidly
    o       MCC linear skull fx to the *middle meningeal artery*(MC)
    o       Classic H&P: pt. has trauma loses consciousness lucid interval(very awake) rapid neurological dysfunction
    o       CT scan: *biconvex shape*
    o       Tx: burr hole(trephination)



Subdural   Hematoma
    o      Venous origin
    o      Increased incidence with age and alcohol use due to brain atrophy
    o      CT scan: *crescent shape*
    o      Tx: burr hole(trephination)



Subarachnoid Hematoma
    o   Etiology: trauma or Berry aneurysm
    o   S/S: “worst headache of my life,” sudden onset of severe HA, sentinel HA hours to months before rupture(berry
        aneurysm), *meningeal irritation: nuchal rigidity, vomiting, and photophobia. (DO NOT confuse w/ meningitis)

     o     Dx: *CT scan w/o contrast always first*, if negative and still suspecting do lumbar puncture(xanthochromia)
     o     Tx: anti-hypertensive meds, surgically clip



Diffuse Axonal injury
     o   Pathophys: neuronal injury in subcortical gray matter or brainstem as a result of severe rotation/deceleration. 90%
         pts. will remain in persistent vegetative state
     o   You will have *“shearing”*- bkdwn of overall communication among neurons in brain
     o   H&P: severely depressed consciousness, neurological dysfunction or coma
     o   Dx: CT scan will be normal most of the time, may show punctuate hemorrhages



Treatment for Increased ICP
    1. ICP probe- inserted into subarachnoid space if GCS <9, or prolonged deep sedation
    2. Reverse Trendelenburg position- elevation of head to 20-30 degrees
    3. Hyperventilation- increases systemic BP by vasoconstriction
    4. Mannitol for brain edema (osmotic diuretic)
    5. Decompressive craniectomy- part of skull removed to expand dura


Cx of TBI: MC Cranial nerve injuries: I, IV, VII, VIII(1,4,6,8)
Headaches (Kruger)
Migraine HA
    o    Etiology: MC serotonin depletion, dopamine, norepinephrine
    o    Pathophys: You will have an initial phase of vasoconstriction, followed by vasodilation in phase 2
    o    Clinical Manif: *unilateral moderate/severe HA that is *frontotemporal and periocular*, can be bilateral though
               o   Prodromal symptoms can occur which are warnings such as mood disruptions, hunger/food cravings,
                   occur before aura

              o    Fully reversible aura(MC visual) seen in *Classic migraine* due to phase I vasoconstriction


              o    *Common Migraine (MC)* NO aura


              o    HA is throbbing or pulsatile in nature, assoc. w/* nausea, vomiting, photophobia, phonophobia,* vertigo;
                   pt will want to be in quiet room


    o    Tx: Moderate/Severe: 5HT-1 receptor agonists(triptan class)
             Prophylaxis: tricyclic antidepressants(amitriptyline) first line
                             Second line: calcium channel blockers


Types of Migraine
    A. Basilar migraine- occipital HA, visual changes, vertigo, decreased hearing, *LOC*, ataxia, *bilateral paresthesias*



    B.   Status migranosus- persistent migraine that does not resolve spontaneously



Tension HA
    o    *MC type of chronic recurrent HA

    o    Clinical Manif: *bilateral bifrontal-occipitonucchal location* that worsens throughout the day
               o   Pressing, *non pulsatile*, tightening, band like quality; NO aura or prodrome
               o   No nausea or vomiting, may have photophobia and/or phonophobia
               o   *Neck stiffness, furrowed brow, tense masseter muscles, and poor posture*



    o    Tx: acute- NSAIDs
             chronic- use same meds as migraine



Cluster HA
     o   Etiology: suspected hypothalamic hormonal influences, pain generated at level of pericarotid and cavernous sinus
         complex


    o    Clinical Manif: recurrent brief attacks of sudden, severe *unilateral periorbital and temporal pain*
               o   NO aura; Pain is penetrating, piercing, stabbing, exploding quality in their eye
               o   *Pt is restless, appear desperate, rock, pace, bang their heads, and can become suicidal*
               o   Ipsilateral lacrimation, miosis, rhinorrhea, ptosis
               o   Pain occurs few hours after pt. goes to bed
               o   Assoc. w/ Horner’s syndrome- ptosis, miosis, and anhydrosis



    o    Tx: acute- oxygen therapy, Sumatriptan(DOC)*
            Prophylaxis- verapamil(DOC)*


DDx of HA
    A. Hypertensive HA: throbbing/pulsating, occipital ; SBP>180, DBP>110

    B.   Brain abscess: best test is MRI*

    C.   Temporal arteritis: severe scalp or temporal pain in elderly Dx: palpable tender temporal artery
Brain Tumors (Podd)

Adults: located supratentorial

Children: located infratentorial


MC they are metastatic from another region
Metastatic etiology: Lung(MC), breast, melanoma, renal, colon


Primary etiologies
    o    Von Recklinghausen’s Dz(Chromosome 17 affected(17 letters)) (neurofibromatoma)


     o    Bilateral vestibular schwannomas



Sx: mental status changes, new onset seizures, HA that is ipsilateral, visual disturbances

Signs: papilledema, Babinski sign present, positive Romberg, positive pronator drift, Decorticate/Decerebrate positioning




Site-specific manif:
     o    Frontal: hemiplegia, defective memory, impaired judgment, and personality or mental changes


     o    Parietal: speech disturbances, agraphia


     o    Occipital: hemianopsia, visual


     o    Temporal: hearing losses


     o    Posterior fossa(cerebellum): ataxia, coordination



Types:
    1.    Metastatic Carcinoma
              o    higher prevalence than primary tumors
              o    highest in those aged 35-70



     2.   Primary   Cerebral Lymphoma
              o      B-cell malignancy that occurs in *immunocompromised states* and assoc. w/ EBV
              o      *CT and MRI will show ring enhancing lesions*
              o      Tx: glucocorticoids for EBV, high dose methotrexate



     3.   Glioblastoma multiforme
               o    a grade IV astrocytoma, MC adult primary intracranial neoplasm and most aggressive



     4.   Medulloblastoma
             o     MC in children and occur in posterior fossa, as well as 4th ventricle
Cerebral Palsy(Sanassi)
    o   Caused by *non-progressive(nonchanging) brain lesions*

    o    Age of onset: fetal or neonatal period up to age 3

    o    Etiologies/Risk Factors: long menstrual cycle, maternal thyroid disorder, maternal mental retardation, *intrauterine
         growth retardation(MCC during pregnancy)*, intracranial hemorrhage of infant, kernicterus due to Rh
         incompatibility

    o    Sex: M>F
    o    Types:
              1. Spastic(MC)*: spasticity, hyperreflexia, clonus, and positive babinski


                        a)   Spastic hemiplegia- one side of the body; UE>LE; have normal IQ and *walk on tiptoes.*
                             Affects *middle cerebral artery*


                        b)   Spastic diplegia- bilateral LE>UE; normal IQ w/ *scissor gait*


                        c)   Spastic quadriplegia- all 4 extremities; moderate/severe mental retardation



              2.   Dyskinetic: extrapyramidal signs(basal ganglia) characterized by abnormal movements; hypertonicity;
                   slow writhing movements,drool etc.


    o    Hx: *early hypotonia for first 6 mo.- 1 yr of life, then followed by spasticity*

    o    Dx: *MRI* of brain- Dx of choice for older children; US in early neonatal; CT scan(ICH)
    o    Tx: Benzodiazepines(Valium) for spasticity; dyskinetic- anticholinergic, dopaminergic drugs


Muscular Dystrophy(Senassi)
Duchenne’s Muscular Dystrophy
    o   X-linked condition involving replacement of muscle with fibrofatty tissue; M>F

    o    Clinical Manif:
               o   Age (0-4)- dystrophy progressively worsens, walking is delayed and begins at 18 months and significant
                   droop will be present in one of the legs at 18 months.

              o    At 1-2 yrs. Calf enlargement is present due to replacement w/ fat; will have a wide based gait and
                   lumbar lordosis

              o    Must use Gower’s maneuver to get up

              o    Age (4-8)- loss of knee flexion and extension

              o    Age (8-12)- worsening contractures and weakened quads leads to loss of stand/walk

              o    Age (12-older)- gain of weight, pulmonary dysfunction worsens, scoliosis develops(90%)


    o    Dx: CK levels from 7000-15,000 w/ clinical manif. most likely diagnostic
             If have high CK and negative DNA analysis(dystrophin), next step is *muscle bx*
    o    Tx: genetic counseling

Becker Muscular Dystrophy
    o   BMD progresses much slower than DMD and is less severe
    o   Clinical Manif:
              o   Delayed gross motor milestones(walking, running, jumping, stair climbing is difficult)
              o   Increase in falls, toe walking, difficulty in rising from floor
              o   *Proximal muscle weakness*
              o   *Dilated cardiomyopathy is first sign of dz later in life*
              o   Progressive symmetric muscle weakness and atrophy w/ pseudohypertrophic calves


    o    Dx: Serum CK (5-100 times the norm)
              Dystrophin gene deletion analysis shows specific axon deletions
              Muscle bx
Movement Disorders (Kruger)
Dyskinesia


    1.   Corticospinal(pyramidal) tracts
              o    influence *voluntary* motor neurons of *distal muscles of extremities*
              o    upper motor neuron lesion(cerebral cortex)- affect the contralateral side
                          i. spasticity and hyperreflexia, +Babinski accompanies this lesion
                         ii. affects group of distal muscles; *flexors of arms, extensors of legs*


              o    lower motor neuron lesion(ventral spinal cord)- affect the ipsilateral side
                         i. weakness, flaccid paralysis, fasciculation, and hyporeflexia
                        ii. affects individual distal muscles



    2.   Basal Ganglia(extrapyramidal tracts)
             o    cause most of movement disorders; controls involuntary movemen, *rigidity*
             o    No real weakness or reflex changes; *affects flexors and extensors of 4 limbs*



Tremor
    o    *MC movement disorder*, alternating involuntary movement caused by repetitive contraction/relaxation


    o    Essential tremor- slow tremor; affects hands, head, voice, usually unilateral Tx: alcohol, benzos


    o    Resting tremor- maximal at rest i.e: Parkinson’s dz


    o    Intention(kinetic) tremor- maximal during voluntary or purposeful movement toward target


Chorea- brief, rapid, jerky, involuntary movements of *distal extremities* and face, may merge into purposeful acts that
mask their disorder


Athetosis- writhing mvmts, often w/ alternating postures of *proximal limbs* that blend into a flowing stream of mvmt.
Slow, involves hands, fingers, and forearms are contracted. Chorea and athetosis can occur together called choreoathetosis.


Dystonia- sustained abnormal postures and muscle contractures; ex: spasmodic torticolous(neck stuck to shoulder), pt. may
become “twisted into grotesque fixed postures” Tx: anticholinergics, botulinum toxin



Tourette’s Syndrome
    o     Sx occur at age 7, assoc. with OCD and ADD
    o     Tics that are truly involuntary and suspected to occur in response to an external cue
    o     Clinical Manif:
                o   Simple tics(MC facial tics, then neck/shoulder)
                o   Coprolalia- yelling of bad words; vocal tics such as grunting, barking

              o    Relaxation lessens tics, may be suppressed voluntarily but will be followed by intense expr.
              o    At most severe: copropraxia(obscene gestures), animal sounds, talking in different accents


    o    Tx: neuroleptics, benzos



Hemiballismus
   o     Considered severe form of chorea; unilateral continuous proximal limb flinging mvmts
   o     Caused by lesion, usually infarct, in contralateral subthalamic nucleus(basal ganglia)
   o     Usually self-limited; Tx: dopamine depleting agents
Drug-Induced Movement Disorders

    o    MCC by neuroleptics which block dopamine CNS receptors

    o    Parkinsonian-like sx- including resting tremor, bradykinesia, rigidity, and postural instability
              o   Tx: remove offending drug, anticholinergics(amantadine)


    o    Tardive Dyskinesia- involuntary facial and tongue mvmts, and choreoathetoid mvmts


    o    Neuroleptic malignant syndrome- muscular rigidity, fever, tremor, AMS, autonomic instabil.


Restless Leg Syndrome- Tx: dopamine agonists, benzodiazepenes



Huntington’s Disease
    o    Gradual onset and sow progression leading to disability and death
    o    Pathophys: abnormality in chromosome 4 causing accumulation of protein huntingtin
    o    Death of GABA/neurotransmitters which increases dopamine activity

    o    Clinical Manif:
               o   Chorea- MC finding will lead to dystonia and Parkinsonian features and then akinetic
               o   *Triad: dementia, behavioral changes(depression), and involuntary movements*




    o    Dx: *On CT or MRI measure the bicaudate diameter* best test

    o    Tx: symptomatic treatment: benzos(choreoathetosis), SSRIs(depression), dopamine agonists



Parkinson’s Disease
     o   Gradually progressive neurodegenerative disorder of basal ganglia(loss of dopamine)
     o   Etiology- idiopathic but can come after encephalitis


    o    S/S:
                o   *Unilateral pill-rolling resting tremor*
                o   Shuffling gait, arms do not swing, and feet drag, have difficulty turning
                o   Drooling, Bradykinesia, cog wheel or *lead pipe rigidity*(constant resistance to ROM)
                o   Kinesia paradoxica- pt. may rise suddenly and walk normally



    o    Dx: Hx is very imp.

    o    Tx: *L-Dopa + Carbidopa(DOC)*, early tx- amantadine(anticholinergic)
Multiple Sclerosis (Kruger)
    o    Demyelinating autoimmune CNS disease
    o    Risk is 5x higher if lived in temperate climates <age 15 than in tropics

    o    Pathophys: slower conduction speed causing conduction delay, *incr. body temp. makes it worse*
    o    *Lesions often involve the optic nerve and white matter of the cerebellum, brainstem, basal ganglia, and spinal
         cord*


    o    Clinical Manif: ≥2 epis. of sx + ≥ 2 signs; episodes must last greater than 24 hrs.
               1. *Sensory loss*- early complaint and MC initial finding; loss of vibratory sense

              2.   Motor dysfx- spasticity, muscle cramping, Babinski’s sign, UMN dysfx., aphasia

              3.   Autonomic dysfx- bowel and bladder incontinence, and sexual dysfx, constipation
              4.   Cerebellar dysfx- ataxia of trunk or limb, dysarthria, *intention tremor*

              5.   Mental status- difficulty w/ attention span, concentration, memory or judgment(adv. Dz)

              6.   Lhermitte sign- not specific for dz; neck flexion results in electric shock to extremities

              7.   Optic neuritis- 50% of all pts w/ this have MS; visual blurring, flashes of light, decreased acuity,
                   discomfort moving the eye

              8.   Bilateral internuclear ophthalmoplegia- lesions in median longitudinal fasciculus resulting in adduction
                   defecits in each eye and nystagmus upon abduction of both eyes



    o    Categories of MS:

              1.   Relapsing-remitting MS- acute exacerbations lasting weeks to months w/ gradual full or partial
                   remissions; first experienced at age 20-40; after it happens again it is dx.


              2.   Primary progressive MS- MC after age 40; gradual decline, accumulated disability w/o remission


              3.   Secondary progressive MS- >50% w/ RR-MS enter this stage of continuous deterioration in first 10 yrs
                   and all pts by 25 yrs. Can aquire new sx


              4.   Progressive Relapsing MS- primary progressive MS w/ addition of sudden episodes of new sx or
                   worsened existing ones; *quickest and worst*




    o    Dx: *MRI of head w/ gadolinium-* best technique b/c plaques are enhanced w/ gadolinium
              CSF analysis- if dx is uncertain; oligoclonal bands(IgG) and increased myelin basic protein(MBP)



    o    Tx: acute exacerbations(optic neuritis, general MS)- IV methylprednisolone
             Relapsing-remitting MS- beta interferon, and glatiramer acetate(synthetic MBP)
            * Natalizumab*
Amyotrophic Lateral Sclerosis(Kruger)
   o   *Affects both UMN and LMN which is specific for this dz* only voluntary muscles

    o    Pathophys: Sporadic ALS due to *increased levels of glutamate* in body causing excitatory mechanisms leading to
         neuronal death and nerve cell degeneration

    o    S/S:
                o   Early sx include difficulty swallowing, and facial paresis- drooling, talking deficiency
                o   Bilateral limb weakness with atrophy of muscle groups *(distal to proximal)*
                               Fasiculations(LMN) and cramping(UMN), wrist or foot drop

                o   LMN depressed reflexes, and UMN hyperreflexia

                o   Unexplained weight loss- cachexia(wasting of muscle)
                o   Bulbar ALS- speech, chewing and swallowing w/ psychological sx will have worser px

                o   Respiratory muscles and vocal cords are affected late

                o   Classic signs: asymmetric muscle weakness, increased tone, hyperreflexia, fasciculation, muscle
                    atrophy*




    o    Dx: MRI of brain- to R/O differentials, nerve conduction studies, muscle bx, forced vital capacity(compare w/
         baseline of pt)


    o    Tx: *Riluzole* (DOC)




Sleep Disorders (Leshinski)

NREM and REM alternate w/ an average of 90 min of 4-5 cycles


Stage I: alert and relaxed, falling asleep, easily aroused, sudden muscle contractions and hallucinations

Stage II: NREM, brain waves slower, may forget where you are, sleep spindles and K complexes

Stage III + IV: deepest and most restorative sleep, delta waves will be present, bed wetting, night terrors

Stage V: REM, dreams occur here, brain activity increases again


I. Insomnia
     o   Inability to reach Stage IV of sleep, leads to being tired during the day
     o   Can be due to depression, caffeine, stress, pain etc
     o   Dx: polysomnography
     o   Tx: Zolpidem and Zaleplon



II. Sleep Apnea


    o    Tx: Nasal CPAP if severe



III. Narcolepsy
      o   Abrupt transition to REM sleep, excessive daytime sleepiness most often in boring situations
      o   Tx: Methylphenidate(Ritalin)
Seizure Disorders (Kruger)
    o   Seizures occur because focal point(excitation) overcomes the inhibitory actions of GABA receptors

     o   Can occur w/ or w/o alteration in consciousness

     o   Temporal lobe- psychic phenomena(hallucinations), taste manifestations(butter, salt, rubber) and smell; Occipital
         lobe- visual disturbances; Parietal lobe- sensory disturbance(numbness/tingling)

     o   Epilepsy- 2 or more recurrent seizures


     o   Etiology: hypo/hyperglycemia, uremia, mass lesions in brain, non-compliance anticonvulsants(MCC in epileptic
         pts), withdrawal of drugs, stroke (elderly MC)


     o   Dx: EEG, MRI, non contrast CT


     o   Tx: Partial seizures- carbamezepine, Absence seizures- ethosuximide, tonic-clonic- valproic acid


Types of Seizures:
1. Partial Seizure- seizure focus located in one area of cerebral cortex, and will only affect one hemisphere

         a.   Simple:
                    i. Brief w/ no alteration of consciousness
                   ii. Manif: paresthesias, muscle spasm, mood changes, déjà vu, mild hallucination
                  iii. Lasts few sec.- min.; if ≥30 min called *simple partial status epilepticus*

                   iv.   Jacksonian seizures- inv. muscle groups, one limb or one part of body in distal to proximal fashion,
                         sensory then motor


         b.   Complex:
                   i. *Alteration of consciousness is present*
                  ii. Lasts for 60-90sec. followed by brief *postictal confusion(after seizure)*, and HA
                 iii. Manif: mvmt & speech change, confusion(after), hallucinations, automatisms(repet. mvmts such as
                       lip smacking, chewing, pacing)
                 iv. Pt is unresponsive to verbal command and resistant to physical manipulation
                  v. Precedent aura may be present (odor/taste) (signs of shift from simple to complex)


         c.   Secondarily generalized: often begins w/ aura evolves from complex to generalized tonic-clonic


2.   Generalized Seizure- affects both cerebral hemispheres, *ALWAYS results in LOC*

         a.   Absence:
                    i. brief episodes(<30sec) of impaired consciousness, sudden immobility & blank stare
                   ii. No aura or postictal confusion, few or no automatisms
                  iii. Precipitated by phonic stim. , and hyperventilation
                  iv. Dx: *EEG- 3.5Hz spike and slow wave complexes*


         b.   Myoclonic- *Dx: EEG- fast polyspike and slow wave complexes*


         c.   Tonic-clonic:
                     i. bilateral, symmetric contraction for several seconds, *pt falls in trunk and limb exten.*
                    ii. lasts for about 10-30 sec; may develop perioral cyanosis, and drooling
                   iii. pt becomes flaccid w/ prolonged postictal confusion; aura may precede seizure
                  iv. urinary and bowel incontinence; Todd’s paralysis(temporary) lasts <48hrs after


3.   Status epilepticus
          a. Any seizure that lasts ≥30min or repetitive generalized seizures w/o return to consciousness
          b. Clinical Manif:
                     i. Increased catecholamine secretion, pupil dilation, hyperthermia, lactic acidosis,
                        hyperglycemiahypoglycemia, hyperkalemia, acute tubular necrosis, postictal findings
          c. Tx: Lorazepam *DOC*, 2nd line phenytoin, 3rd line Phenobarbital
Vascular Emergencies (Leshinsky)
Transient Ischemic Attack
    o    Temporary ischemic disturbance in cerebral blood flow; *neurologic deficit that resolves in 24 hrs*
    o    Clinical Manif: loss of speech(temporary), weakness to contralateral extremity, amaurosis fugax(temp loss of vision
         in ipsilateral eye), dizziness, diplopia, drop attack


    o    Dx: initial test: CT w/o contrast to R/O hemorrhagic properties then CT w/ contrast

    o    Tx: Heparin, coumadin, aspirin, plavix(antiplatelet)

    o    Cx: stroke


Ischemic Stroke
     o   Obstruction by thrombus or emboli
     o   Ischemic penumbra- area of minimal profused cells that can return to normal

    o    Dx: CT w/ contrast or MRI w/ contrast

    o    Tx: Heparin, thrombolytics only if viable brain tissue can be salvaged, antiplatelets


I: Large vessel thrombotic stroke


    o    located in internal carotid and cerebral arteries, as well as basilar and vertebral arteries

    o    Middle cerebral artery: *MC* contralateral hemiplegia to face/arm, homonymous hemianopsia of contralateral
         visual field in both eyes, aphasia and apraxia(cannot learn)

    o    Anterior cerebral artery: hemiplegia to foot, leg, or toes, difficulty in decision making, incontinence

    o    Posterior cerebral artery: homonymous hemianopsia of contralateral visual field(both eyes), loss of central vision,
         alexia(inability to read), anomic aphasia(difficulty naming), loss of sensory senses

    o    Vertebral and Basilar artery: diplopia, vertigo, dysphagia, ipsilateral loss of facial pain



II: Small Vessel stroke Lacunar infarct
     o    Located in deeper noncortical parts of the brain or brain stem; Risks: HTN, DM

    o    Clinical Manif: contralateral motor hemiplegia(face,arms, legs) or pure sensory hemiplegia(numbness, face, arm,
         leg), ataxic hemiparesis(weakness of lower limb, +Babinski)



III: Cardiogenic Embolic Stroke
      o   A thrombus from heart travels to brain; *MC to middle cerebral artery*
      o   Hx: rapid onset of paresis, neurologic deficit w/ cardiac condition

    o    Dx: CT; carotid Doppler and US for carotid stenosis, and echocardiogram for valve dysfx



Hemorrhagic Stroke
   o    rupture of blood vessel and hemorrhage into brain tissue
   o    Risks: HTN, AV malformation
   o    Location: *MC* basal ganglia
   o    Vomiting and HA on onset; flaccidity leading to spasticity, can progress to coma and death



I: Cerebral Anuerysm(Berry)
     o    Rupture will lead to subarachnoid hemorrhage; If not ruptured yet will be asymptomatic
     o    Once it ruptures it will cause: cerebral edema, compression of brain contents, herniation, incr. ICP
     o    Clinical Manif: severe HA, collapse and LOC, Nuchal rigidity, photophobia, fever, HTN


    o    Dx: CT w/o contrast, LP only if CT negative(xanthochromia), cerebral angiography
    o    Tx: surgery, anti-hypertensives
CNS Infections and CSF Analysis (Senassi)

CSF Analysis: Tube #1 to chem. lab (glucose, protein), Tube #2 to heme lab (cell count), Tube #3 to to microbio &
immuno lab (gram stain, culture), Tube #4 hold if other studies needed.

Opening pressure: Children (10-100 mm H2O), >8 y.o.                  Glucose- 2/3 the concent. of blood glucose
(60-200 mmH2O), Obese (<250 mmH2O), intracranial                             ↓ in presence of bacteria, WBCs, funal infx, or
HTN (>250 mmH2O)                                                              malignant cells
        ↑ in: tumors, infx (bacterial), hydrocephalus
         (accumulation of CSF), bleeding.                            Protein- small amount is normal
        ↓ in: dehydration, shock, leakage of CSF                             ↑ with meningitis, brain abscess, CNS tumors,
                                                                               MS, Guillain-Barre Syndrome, syphilis.
Color                                                                         ↓ in protein is not significant.
         Supernatant- clear & colorless
         Xanthochromic (yellow, orange or pink)-                    Gram Stain: acid fast (TB), India ink (cryptococcus),
          presence of bilirubin or breakdown of RBCs due             Wright/ Giemsa stain (toxoplasmosis), Wet preparation
          to bleeding                                                (protozoan/ helminthic infx)
         Green- bilirubin or infx.
                                                                     Culture: absence of growth doesn’t r/o an infx
Turbidity (cloudy)- presence of WBCs, RBCs, bacteria or              Lactic acid
↑ protein                                                                     ↑ w/ bacterial or fungal meningitis
                                                                              normal or slightly elevated w/ viral meningitis
Viscosity- if more viscous than H2O: malignancy or
meningitis                                                           LDH (Lactate dehydrogenase)- differentiates btw
                                                                     bacterial & viral meningitis, ↑ w/ leukemia or stroke
Tumor markers- carcinoembryonic antigen (CEA), a-
fetoprotein (AFP), hCG.                                              CRP (C-reactive protein)- ↑ w/ inflammation & bacterial
                                                                     meningitis


CSF Infections- combination of fever, HA, & neurological s/s (AMS, focal weakness, meningeal signs) treated as CSF infx
until proven otherwise.
         Lumbar puncture: required if any 2 of the 3 are present: fever, HA, AMS
         CT scan required prior to LP to avoid brain herniation

Meningitis (Bacterial)


     Etiology + TX:
         TX is empiric (Abx’s +/- steroids) if LP cannot be done within 30 mins of ED admission

         Neonates (<1 month): Strep. group B. Tx: Ampicillin + cefotaxime OR gentamicin. Add Acyclovir for HSV

         Children (1 month-7 y.o.): H. flu (50%), Strep. pneumo (13%), N. meningitides. Tx: Cefotaxime or Ceftriaxone, +
          Vancomycin (if DRSP).

         Adults (7-50 y.o.): Strep. pneumo (30-50%), Listeria monocytogenes (5%). Tx: Cefotaxime or Ceftriaxone plus
          vancomycin, +/- Rifampin.

         Older Adults (>50), immunocomp, & Alcoholics: Strep. pneumo




     Clinical Features:

         Triad: fever, AMS, nuchal rigidity.
         HA(more severe lying down), high fever w/ chills, N/V, photophobia, seizures
         stiff/painful neck, maculopapular rash w/ petechiae(N. mening), vesicular lesions(HSV), ↑ ICP, cranial nerve palsies
         Kerning’s sign- inability to fully extend knees when pt supine and hips flexed.

         Brudzinski’s sign- flexion of legs and thighs that is brought on by passive flexion of neck.



         Dx: *LP- (bacterial) cloudy CSF consistent w/ pyogenic leukocytosis, low glucose, high protein

         Prevention: *MCV4 (Meningococcal conjugate vaccine), MPSV4 (meningococcal polysaccharide vaccine).
Meningitis (Viral/ Aseptic)

         Etiology: Enterovirus (85%), HSV, Echovirus, coxsackievirus B (children <3 y.o.)

         Transmission: hematogenous, neural penetration (HSV).

         ss: constitutional for 48 hrs, low grade  high-grade fever, severe HA, photophobia (less severe), seizures,
          pharyngitis, zoster eruption, viral exanthems.

         DX: LP (↑ mononuclear cells, lymphocytic pleocytosis, protein and glucose norm), head CT, EEG (if encephalitis).


         Tx: supportive, HSV (IV acyclovir), HIV meningoencephalitis (anti-HIV therapy), CMV (IV Ganciclovir).


Meningitis (Fungal)

         Opportunistic in immunicomp (HIV/AIDS, malignancy, organ transplantation, alcoholism)

         Etiology: Cryptococcus neoformans
         Dx: India ink stain (capsular Ag in CSF)
         Tx: Fluconazole (mild), Amphotericin B (severe).


Meningitis (Noninfectious)
         Metastasis to meninges (malignant meningitis)
         Drugs (NSAIDs, abx’s, IV Ig)
         inflammatory conditions (sarcoidosis, SLE, systemic vasculitis disorders)


Viral Encephalitis
         diffuse inflammation of the brain parenchyma

         Etiology: Arbovirus(MCC, West Nile, St. Louis Encephalitis, California Virus, Eastern Equine Encephalitis, Western

          Equine Encephalitis, Japanese Virus encephalitis), HSV, measles, mumps, rubella, influenza etc.


         Pathophysiology: transmission is human-to-human or reactivation of HSV. Virus replicates ouside CNS & enters
          CNS hematogenously, or by traveling along neural (HSV, VZV) and olfactory (HSV) pathways)  invades grey
          matter

         s/s: Prodrome (HA, malaise, myalgias, signs and sx of meningitis but less intense)

               o      Altered sensorium, including confusion, delirium, disorientation, hemiparesis, cranial nerve lesions and
                      seizures can be present, behavioral or personality changes, AMS, skin lesions (if HSV in neonates).

         Dx: 1. head CT  2. LP: lymphocytosis w/ normal glucose(similar to viral meningitis), PCR for DNA HSV, HSV
          culture.


         Tx: supportive, IV acyclovir (if HSV, VZV, CMV), IV foscarnet (HIV), if ↑ ICP (dexamethasone, diuretics)


Brain Abscess
        Etiology: s. aureus, strep, pseudomonas.
        pathophys:
              o    *Contigious spread: otitis media, dental infx, mastoiditis, sinusitis.

               o      Hematogenous spread: multiloculated, endocarditis, severe lung infx, skin or abdominal infx, IVDA, HIV
               o      Trauma: open skull fractures, cx of intracranial surgery, bullets, foreign body

         s/s: Triad: fever, HA (severe on the side of abscess), focal neurologic deficit. AMS (cerebral edema).

               o    Rupture of abscess = sudden worsening HA + meningismus
         Dx: ↑ ESR & CRP, LP (nonspecific, unless abscess ruptures, head CT before LP), CT w/ contrast (quick dx), MRI
               (for dx & follow up).

         Tx: abscesses <2.5 cm respond to Abx’s

               o      Surgical excision or drainage + Abx’s (6-8 weeks)
               o      If multiple abscesse or abscesse in delicate areas: repeated aspirations w/ high-dose Abx’s.
Myasthenia Gravis
    Etiology:
                 Autoimmune disorder, Can occur at any age; *MC- 20-30 in women & >60 in males

    Pathophysiology:
                *Auto-antibodies to Ach receptors* which prevent Ach from binding to the ACH receptor protein  no
                 binding sites for Ach  muscular weakness throughout body
                Often associated with a Thymoma (Thymus is responsible for immune development in childhood)
                 Thymoma’s are postulated to create auto-antibodies
                *Pt can have other autoimmune Dz’s: thyroditis, SLE, rheumatoid arthritis

    Signs/ Symptoms:
                Exacerbated by: stress, infection, premenstrual, pregnancy, pos-partum
                *MC initial: EOM weakness (asymmetrical), ptosis, diplopia, blurred vision
                *Weakness exacerbated/progressed by excertion, continuous activity & worsened throughout day*
                Other symptoms: difficulty chewing & swallowing; weakness in *limbs (proximaldistal) & trunk are
                 LESS common than in the face, *weakness of neck muscles (flexorsextensors)
                3 unaffected areas: pupils, sensation, DTRs
                Myasthenic Crisis- respiratory muscle weakness, immediate intubation needed

    Diagnosis:
                 clinical (initially): signs of progressive weakness w/ continued activity
                 thyroid function test (to r/o hyperthyroidism, M.S)
                 *chest CT (to r/o thymoma)
                 *auto-Ab’s (80% sensitive): false(+): thymoma, Lambert-Eaton syndrome, SCLC (small cell lung ca)
                 *SFEMG (Single-fiber Electromyography)
                 *Edrophonium Test (Tensilon): Edrophonium or neostigimine is ACE-I more ACH marked
                  improvement in muscle strength

    Treatment:
            1.    *Pyridostigmine or Neostrigmine (AchE enzyme inhibitors--> increased ACH)
            2.    Thymectomy (resolution of disease in 70-80% of PTs)
            3.    If ACH-I & thymectomy fail: steroids and/or immunosuppresants (if steroids fail, Azathoprine,
                               cyclosporine)
             4.   If all fail or if myasthenic crisis plasma phoresis ( remove auto Ab’s) OR administed Ig




Lambert-Eaton Disease (Myasthenia Syndrome)

    Pathophysiology:
                auto-Ab’s to pre-synaptic Ca channels (responsible for ACH release)  limited ACH released w/ 1
                 contraction
                Repeated muscle stimulation leads to excess accumulation of ACH stronger contraction of the muscle
                 (as opposed to Myasthenia gravis=destruction of Ach receptors)

                 *strongly associated w/ small cell lung cancer

    Treatment:
                 Plasmaphoresis & steroids
                 Variable responsible to cholinesterase inhibitors

				
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