neuro

• Voluntary movement
• Complicated/delicate movements
• Slight tension (when muscle is relaxed)

Cranial Nerves movements

• Muscle tone
• Controls gross autonomic mvts (walking)

• Maintains equilibrium
• Controls posture

• Pain
• Temp
• Crude Touch

• Vibration
• Proprioception
• Pressure
• Fine touch

nerve cell bodies

Located in the motor strip of the cerebral cortex and in several brainstem nuclei

synapse with motor nuclei in brainstem (cranial nerves) and spinal cord (peripheral nerves)

tracts crossover in the medulla of the brainstem and carry impulses to spinal nerves

motor impairment develops on the contralateral side

motor impairment develops on the ipsilateral side

• or cell bodies are called anterior horn cells
• LMN
• transmit impulses through anterior roots and spinal nerves to peripheral nerves which terminate at the neuromuscular junction
• Damage to LMN
• causes ipsilateral weakness and paralysis,
• decreased muscle tone
• and decreased or absent reflexes

70% of strokes occur anteriorly (anterior arteries in the Circle of Willis)

- progressive stuttering onset, weakness on contralateral side, numbness/paresthesias, gaze deviation toward infarcted hemisphere, Horner’s syndrome affected side, reflex changes, lethargy, stupor

• paralysis and decreased sensory of opposite leg and arm, apraxia, decreased opposite grasp reflex, absent spontaneity
• Anterior Communicating Artery

aralysis and decreased sensory of opposite arm weaker than leg, aphasia, agraphia, apraxia, confusion, gaze toward infarcted hemisphere

30% of strokes occur posteriorly

• Cranial nerve palsies, diplopia, vertigo,
• nausea/vomiting, dysarthria, perioral weakness,
• dysphagia,
• ipsilateral facial sensory and motor loss,
• contralateral hemiparesis, impaired consciousness, coma

• homonymous hemianopsia,
• memory deficit, visual hallucinations,
• sensory loss,
• CNIII palsy, paralysis of eye movements,
• contralateral hemiplegia, ataxia

• sudden, focal ischemia causing transient neurological deficits
• 80% usually last a couple of mins., but no more than 24 hr , resolves completely

• increases with age
• male > female
• called “warning sign” of impending stroke

• Embolism causing interruption of blood flow to certain part of brain
• cardia
• Non cardiac

Afib, rheumatic dz, valvular dz, infective endocarditis

atherosclerosis, inflammatory, lesions/tumor, polycythemia, sickle cell dz

ABCD2 - age, BP, Clinical features, duration, DM (3 or more admit)

• MRI (within 24hr of symptoms),
• CBC, CMP, lipid panel, cardiac enzymes, coags,
• consider carotid Doppler,
• CT angio,
• Cerebral arteriography (gold standard diagnostic and theraputic)

Goal to prevent stroke.

Anti-platelet – ASA, clopidogrel (Plavix), ASA/Dipyridamole (Aggrenox), Cilostizol (Pletal)

warfarin (Coumadin)

• control DM, control HTN, statins for hyperlipidemia, smoking cessation, healthy diet and exercise
• Surgery for focal carotid stenosis of >70-98%

• Ischemic and Hemorrhagic
• Abrupt/sudden onset, cell death due to inadequate blood flow in localized area, hemiparesis or monoparesis, sensory deficits, visual fields deficits, vision loss, diplopia, dysarthria or aphasia, ataxia, facial droop, nystagmus, decrease in level of consciousness

• caused by thrombotic or embolic
• Lacunar or Small-vessel (usually associated with uncontrolled HTN)
• Carotid or Large-artery (vertebrobasilar, cerebral arteries)
• Cardioembolic infarction (source of recurrent strokes)

• prior TIA/stroke, HTN, DM, hypercholesterolemia,
• increased blood viscosity, smoking,
• FH stroke, cardiac (rhythm, valve, muscle dz),
• excess alcohol

good history and PE, (serial neuro exams) determine time frame/onset of symptoms, determine ischemic vs hemorrhagic, rule out trauma, NIHSS

• CT = quick, evaluate acute bleed vs ischemic (90-95% sensitive SAH)
• MRI = takes time to get, good when looking for tissue changes (poor with hemorrhages)
• CBC, CMP, ECG, CXR, LP if suspect hemorrhage and imaging inconclusive, Blood cx if suspect infection, coags, cardiac enzymes
• Echocardiogram rule out valvular dz.

• ABC’s, supplemental oxygen, airway management,
• fibrinolytic therapy/antiplatelet agents,
• glycemic control, optimal blood pressure control

Given within 3 hours (4.5 hours) of stroke onset, given only after CT scan ruled out hemorrhagic stroke, should be given within 1 hour after arriving to the hospital, 18 yrs or older, do not give if >4.5 hours after onset of ischemic symptoms

Head trauma or prior stroke in previous 3 months, symptoms suggestive of subarachnoid hemorrhage, history of intracranial neoplasm, arteriovenous malformation, or aneurysm, recent intracranial or intraspinal surgery, increased risk for hemorrhage (anticoag meds INR>1.7), systolic BP >185 mmHg, diastolic BP > 110 mmHg

• inpatient in stroke unit if available, monitor O2, treat BP >185/110, prevent hyperthermia, early ambulation/PT, SC heparin, if surgical candidate carotid endarterectomy if stenosis >70%,
• Medical management = ASA 325 mg daily, Warfarin – target INR 2-3

less common than ischemic (15% of all strokes)

10% of bleeds)

HTN, noncompliance with meds, smoking, excess EtOH, younger than 55 yo

Intracranial aneurysms, AVM’s, neoplasms, coagulopathy (Coumadin), drugs (cocaine), HTN, ischemic infarction, Cerebral Venous Thrombosis

sudden, severe HA, then obtunded, marked elevated BP, maximum deficit at onset

(5% of bleeds)

for aneurysm rupture is smoking

• Trauma = 80% related to head injury
• Spontaneous = 20% related to aneurysms (in 40-70 yo) or AVM’s (in 20-40 yo)

• immediate severe headache “Worst headache of my life”, Thunderclap HA
• May have symptoms (sentinel event) in previous 30 days = warning leaks
• Photophobia
• N/V
• +/- focal neuro deficits
• +/- LOC

• Good history
• Labs: CBC, coags, CMP, ESR, toxicology
• LP: xanthochromia (yellowish color indicating bilirubin from breakdown of blood)

• CT = bleed/hemorrhage/hydrocephalus in first 24 hours
• MRI = ischemia, structural changes
• Cerebral angiography = identify source of bleed –
• ~~gold standard for surgical evaluation(pre-op)
• CT – bleed shows immediately

• directed to prevent re-bleed, hydrocephalus and cerebral vasospasm
• Manage: ABC’s, BP, fever, blood glucose level, electrolytes, agitation/seizures, intracranial pressure

• obliterate AVM’s - surgical removal or balloon, sclerosing agents, embolization
• obliterate aneurysm - surgical clipping, endovascular balloon angioplasty
• Treat hydrocephalus: surgical shunt placement

• bleed between dura and arachnoid membrane, common after trauma
• Presents with HA and confusion (patient can be lucid after impact and prior to symptoms developing)
• Concave lesion on CT scan, monitor with serial CT’s (worsening symptoms), supportive care, surgery in severe cases

• Dementia
• Progressive decline in intellectual function
• Usually an insidious onset with gradual progression
• Typically begins after age 60 (more prevalent in women because of longer life expectancy)
• Most common cause is primary neurodegenerative disease

Primary neurodegenerative disease

• Family history of dementia
• DM
• Vascular disease (ie stroke)
• History of significant head injury
• Smoking (2-4 fold increase)

• Short term memory loss
• Word finding difficulty
• Visuospatial dysfunction
• Executive dysfunction
• Apathy
• Apraxia

• results from pathology in the hippocampus
• Repeating questions or stories
• Diminished ability to recall details of recent conversations/events

• results from pathology in the temporoparietal jn left hemisphere
• Difficulty recalling names of people, places, objects
• Low-frequency words affected first – speak in a round-about-way, indirect way

• results from pathology in right parietal lobe
• Poor navigation, getting lost in familiar places
• Impaired recognition of familiar faces

• results in pathology in various areas; frontal lobe or basal ganglia or cerebral white matter
• Easy distractibility and Impulsivity
• Slowed processing speed
• Poor planning/organization

• results in pathology of frontal lobe or basal ganglia or cerebral wht. matter
• Indifference, separate from depression

• results from pathology of frontal or parietal lobes especially left parietal
• Loss of learned motor behaviors

• Executive dysfunction
• Apathy

Visuospatial dysfunction

Apraxia

Difficulty finding words

Short term memory loss

• new cognitive complaints
• – rule out cerebrovascular disease, tumor, other possible causes of decreased cognition

• MRI is preferred – evaluate for global or focal brain atrophy
• CT without contrast if MRI not available
• PET scan – with fluoro-deoxyglucose can help discriminate between Alzheimer’s and Frontotemporal pathology (but less sensitive after age 60-70)

B12, TSH/T4, RPR (if risk or suspicion of syphilis), CBC, CMP(glucose, electrolytes)

• Age related demntia (90%)
• Other

• (90%)
• Alzheimer’s disease
• Vascular dementia
• Dementia with Lewy Bodies (DLB)
• Frontotemporal dementia (FTD)

• (10%)
• Brain tumor
• Drug reactions
• Alcoholism / other addictions
• Depression
• Nutritional deficiencies

• Age at peak incidence in 60’s
• Prominent behavioral and personality changes:
• RELATIVE PRESERVATION OF MEMORY (different from Alzheimer’s)
• Associated with ALS

• Deficits in empathy, insight, executive function
• Disinhibited, impulsive behavior
• Hyperorality (inappropriate objects into mouth)

• Histologically indistinguishable from Parkinson – Parkinsonian motor features (usually confused with PD)
• Prominent visuospatial and executive deficits
• Fluctuating cognitive impairment
• Psychiatric disturbance; anxiety, VISUAL HALLUCINATIONS
• ONSET MORE RAPID THAN PD (within 12 months of motor symptoms compared to PPD where dementia occurs 4-5 yrs after motor symptoms)

• Single or multiple infarcts
• Mechanism – ischemia/thrombosis, or hemorrhage
• Symptoms depend on location of infarct
• STEPWISE OF PROGRESSIVE ACCUMULATION OF COGNIITIVE DEFICITS – dementia usually within 3 months of event
• Common co-morbidities:
• DM, HTN, CAD, PVD

• Most common age related (usually after 60) neurodegenerative dz. (risks doubles every 5 yrs)
• Positive family history in 50% of cases
• Progressive intellectual deterioration
• Executive impairement

• Senile plaques = extracellular deposits of beta-amyloid peptide surrounded by dystrophic axons
• Neurofibrillary tangles = intracellular accumulation of phosphorylated tau protein

• Short term memory impairment is early and prominent:
• Repetitive speech in conversation
• Difficulty remembering conversations, events, appointments
• Misplaced objects

• Decline in complex task performance
• Decline in problem solving ability
• Impairment in driving

• mild decline in memory/executive function
• +aphasia, apathy, depression

• moderate decline in memory/executive function
• +poor insight, agitation, psychosis

severe (ie. forget how to feed themselves)

• Treat symptoms early:
• Depression – SSRI (Paxil, Prozac, etc.)
• Insomnia – Trazodone (Desyrel) 25 – 100 mg qhs
• Moderate anxiety or restlessness – short acting benzodiazepine (Xanax, Ativan, etc.)
• Severe aggressive agitation – risperidone (Risperdal) 0.25 – 1.0 mg bid
• CHOLINESTERASE INHIBITORS
• GLUTAMATE RECEPTOR ANTAGONISTS

• for memory enhancement and to slow disease - increases acetylcholine (can take 6 wks for full effectiveness)
• Mild to Moderate symptoms: Donepezil (Aricept) 5-10 mg qd
• Rivastigimine (Exelon) 3-6 mg bid (less GI side effects) (Patch)

liver dz., PUD, severe COPD, bradycardia/SSS

• moderate to severe disease – decreases activation of NMDA receptors (N-methyl-D-aspartate) (can take months to see memory improvement/arrest progression)
• Memantine (Namenda) 5-10 mg bid

• severe, unilateral, localized in periorbital area and temple
• At least one of these: Ipsilateral lacrimation, nasal congestion, miosis/ptosis, eyelid/facial edema, restlessness/agitation
• More common in men (>30 yo) (occur at later age in women)
• Attacks can last 1 hr – 3 hrs and can occur 1 -6 times a day (commonly wakes people from sleep)

: attack phase lasting 1-4 months followed by cluster free period of 6 months to years duration

with a cluster free interval of <1 week in a 12 month period of time

• Oxygen 100% at 7-10 liters for 10-15 mins
• Sumatriptan (Imitrex) 6mg SC (max. of 12mg in 24 hrs. with at least 1 hr in between injections)
• (Contraindicated in CAD)
• Dihydroergotamine (DHE) (IV, SC, IM, nasal spray)

verapamil, Topiramate (Topamax), Divalproex (Topamax)

• Episodes vary - can last 4-72 hrs., frequency can be from once weekly to less that one per year
• Childhood = Male>Female
• Female>Male after menarche to mid-adult life

• Specific foods (aged cheese, red wine)
• Medications
• Family history (>80%)

• 1.Unilateral
• 2.Pulsating
• 3.Moderately severe.
• 4.Aggravated by physical activity

• 5
• Prodrome / Aura / (Early) HA / (Late) Resolution / Postdrome
• Without aura (common migraine) 80%
• With aura (classic migraine) – disturbance of neurological function prior to headache onset

drowsiness, talkativeness, hunger, depression, yawning, irritability, tension, nausea

• onset over a 5-20 min, last <1hr., visual MC: twinkling, geometric, hemianopsia
• Phase III: HA
• 60% one side, 40% bilateral, throbbing, N/V, aversion to light/sound, mvt. worse

pain improved, few symptoms remain; impaired concentration, fatigue nausea

“migraine hangover” fatigue, scalp tenderness

• Triptans: 5-HT-1 agnoists (during early/mild phase)
• Sumatriptan (Imitrex) SC 4-6 mg once, repeat once after 2 hrs if needed (max 12 mg in 24hrs.)
• Contraindicated in CAD, PVD, uncontrolled HTN
• Ergotamine tartate and caffeine (Cafergot) 1/100 mg (1-2 at start of HA the 1 every 30 mins as needed, max if 6 mg/day)
• Contraindicated in CAD, CVD

Topiramate, Valporic acid, Beta Blockers, Amitriptyline

bilateral, in frontal-occipital lobes or generalized, band-like pressure, muscular tightness or stiffness in neck

• Episodic – associated with stressful event
• Chronic – often recurring daily associated with contraction of muscles back of neck and scalp

poor posture, anxiety, depression, TMJ syndrome, dental dz, HTN, OA of cervical spine

• NSAIDs (motrin, advil) 400mg tid
• Naproxen sodium 500 mg bid

: SSRI’s, TCA

Loss of pigmented cells in substantia nigra that make and store dopamine

Tremor at rest, rigidity, bradykinesia, postural instability

poor enunciation of words, ocular abnormalities, depression (75%), dementia, sleep problems

unilateral minimal functional impairment (infrequent blinking)

bilateral without impairment of balance (lack of facial expression = “masked facies”)

bilateral, with instability and physically independent

Severe disability, can walk/stand without help but markedly incapacitated

heelchair or bedridden unless aided

• GOAL: to get more dopamine to the brain
• Surgery: deep Brain stimulator-if meds fail
• Dopamine agonist
• Levodopa/carbidopa
• COMT inhibitor
• Mao-B, anticholinergics
• 2nd line: antiviral

Parkinsons initial therapy, may delay need for levodopa

Pramipexole (Mirapex), Ropinirole (Requip), Patch Rotigotine (Neupro)

• 40-50% improvement in motor function –
• GOLD STANDARD

• taken with levodopa (blocks breakdown of levodopa)
• PD med

Entacaptone)

• used in late stage,
• blocks enzyme in brain that breaks down levodopa (boost effects of Sinemet)

Elderpryl/Carbex (Selegiline) –

Benzotropine (Cogentin), Trihexphenidyl (Artane):

decrease acetylcholine which controls movement

reduced motor fluctuations, used in mild, early PD

• unknown cause
• Advanced age is a risk factor, if genetically predisposed onset can be younger age
• Emotional stress enhances symptoms
• SMALL AMOUNTS OF ALCOHOL IMPROVE SYMPTOMS

• involuntary, rhythmic, oscillatory movement
• can present as resting tremor, action tremor, or intention tremor
• spreads proximally, does not reduce life expectancy
• Head tremor more common in women

• Propranolol, Primidone,
• clonazepam (Klonopin), carbamazepine (Tegretol)
• Surgery: Thalamotomy – ablative
• Deep Brain stimulator – non-ablative

• autoimmune d/o = pure motor syndrome
• blocked neuromuscular transmission at acetylcholine receptor
• Occurs typically 20-40yr : females peak in 3rd decade, males peak in 5th-6th decade

• Muscular Weakness: onset mild, intermittent over years, worse in the evening
• PTOSIS(25%)
• DIPLOPIA 25% Dysphonia
• PROXIMAL LIMB WEAKNESS; Facial weakness
• Fatigue on chewing; Neck weakness
• Dysarthria (10%); Dysphagia (10%)
• RESPIRATORY WEAKNESS

• Tensilon Test (edrophonium):
• Other test: EMG,
• immunoprecipitation assey (80-90% show antibodies in serum)

Diagnostic – grip strength improves within 30 secs.

• Anticholinesterase therapy:
• IMMUNO SUPPRESSANT THERAPY
• Surgical: Surgical: Thymectomy (not for very old or very young)

• Mestinon (Pyridostigmine bromide)
• Prostigmin (Neostigmine)

• Prednisone
• Azathioprine (Imuran)
• Cyclophosphamide (Cytoxan)
• Plasmaphoresis
• IVIG

• autoimmune d/o, demyelination of peripheral nerves
• Early signs paresthesias of hands and feet
• Usually in ASCENDING WEAKNESS/PARALYSIS OF LIMBS (moves distal to central)
• Gait affected, back and leg pain common, RESPIRATORY MUSCLE PARALYSIS (30% if untreated)

50-70% of cases follow infection (Campylobacter jejuni enteritis), viral URI or surgery

• Creatinine Kinase elevated (2-5 fold), LP (CSF)=elevated proteins, normal WBC
• Electrophysiology – marked slowing of conduction

• IVIG, Plasmaphoresis,
• symptomatic/supportive treatmen
• hospitalize for cardiopulmonary support (when needed)

unilateral paralysis/weakness of facial muscles (supplied by CN7)

• Herpes zoster, Lyme dz.,
• sarcoidosis, Guillian-Barre, MS, DN, cancer, trauma,
• viral infection
• Most common over age 30

• acute onset, unilateral total or partial paralysis of face muscles,
• numbness, ptosis, decreased nasolabial fold
• Ipsilateral; loss of taste,
• ear ache, inadequate tear production, loss of corneal reflex

• most resolve spontaneously (10% may have permanent disfigurement)
• Oral corticosteroids or prednisone, (eye patch)
• Start tx immediately for better outcomes
• (if patient presents with complete paralysis – less likely to have full recovery
• if complete paralysis at day 5 refer to neurologist

• Diabetes is the most common cause
• can affect any peripheral nerve
• Associated with hyperglycemia, nerve infarct, vascular insufficiency

• “Stocking/glove” presentation:
• common in toes/distal feet (later in hands)
• Tingling, burning,
• abnormal pain and temp. sensation,
• reduced vibratory sensation, Achilles reflex

nerve conduction studies

• uremia, EtOH, vasculitis
• B12 deficiency, hypothyroidism, amyloidosis

• tight control of serum glucose! Multiple agents are used for management
• Tricyclic antidepressants – amitriptyline, nortriptyline
• Anticonvulsants – carbamazepine (Tegretol), Gabapentin (Neurontin)
• Pain management – lidocaine patch, tramadol (Ultram)

• inflammatory process, multifocal demyelinization of the white matter in brain and spinal cord, unknown cause; autoimmune theory triggered by genetic susceptibility vs viral (EBV)
• More common in women – 16 to 40 years of age, caucasian/European decent
• Course – New neurologic symptoms in young person intermittent, progressive

• Multiple and varied neurologic signs/symptoms
• Ataxia +Babinski sign Clumsiness
• Fatigue Hand paralysis (tingling) Blurred vision in one eye (retrobulbar neuritis)
• Loss of position and vibration sense Clonus
• Sphincter disturbance urinary urgency/hesitancy

(initial episode): weakness, numbness, tingling, unsteadiness

• an interval of months to years after initial episode before new or recurring symptoms (acute relapses) followed by recovery (resolution of inflammation, myelin repair)
• Exacerbations may be triggered by infection, pregnancy

Infection and pregnancy

• relapses with incomplete remission, does not return to baseline, steady deterioration
• Optic atrophy, nystagmus, dysarthria, pyramidal, sensory, cerebellar deficits

• (less common) symptoms are steadily progressive from the onset
• Disability occurs at early stage

• MRI (more sensitive than CT) – shows many plaques – DAWSON’S FINGERS
• Visual evoked response (VER) – abnormal in 75-97% of MS cases
• CSF: elevated protein (especially after acute relapse) (myelin basic protein from destruction)
• Elevated IgG and discrete bands of IgG (oligoclonal bands)
• Glucose usually normal
• *Clinically definite disease is made in patients with relapsing/remitting MS and at least
• 2 lesions involving different areas of the CNS white matter

• Corticosteroids - Methyprednisolone - for acute attacks
• IVIG may control relapses

• reduces frequency of relapses, may delay disability
• Interferon-B 1a (Avonex, Rebif, Betaseron) or Interferon –B 1b (Betaseron/Extavia)
• Natalizumab (Tysabri®) - immunomodulator
• Fingolimod (Gilenya®)
• Novantrone (Mitoxantrone) - immunosuppressant

• Spasticity – Bacolfen
• Neuropathic pain – gabapentin
• Chronic fatigue - amantadine

• transient disturbance of cerebral function due to abnormal paroxysmal neuronal discharge in the brain
• increase risk of sudden death by 5-11 fold

seizure then consciousness the seizure again

further convulsions without consciousness between attacks

• idiopathic (no cause no neurological abnormality)
• Pediactric age group – congenital abnormalities or prenatal injury

• febrile,
• metabolic (EtOH, drugs, uremia, hypoglycemia),
• trauma, neoplasm,
• vascular (infarct, ischemia, AVM’s),
• infectious (reversible, meningitis/encephalitis)

• PARTIAL: simple & complex
• Generalized: absence, tonic-clonic

affects only part of the brain

• no LOC, isolated tonic OR clonic activity,
• transient altered sensory perception, ]’
• march/spread down extremity (Jacksonian March),
• light flashes, buzzes, déjà vu, illusions

• no LOC, characterized by aura, N/V,
• will not remember all or part of seizure,
• focal tonic or clonic activity, automatism (lip smacking, chewing, stroking, rubbing hands), last 1-3 mins, often confused after, it takes 5-10 mins to come around

affects entire brain

• Generalized seizure
• misses words in conversation,
• brief impairment (<20 sec) patient usually unaware,
• impaired consciousness “blank stare”,
• mild tonic or clonic or atonic components,
• starts in childhood stops by age 20, but can progress to other types of seizures

• this is what we think of as epilepsy
• tonic phase - lasts <1min. = sudden LOC, falls to floor, may “cry out”, may bite tongue
• clonic phase – jerking or convulsing, grunting, pale/cyanotic lasts 2-3 mins., then flaccid coma consciousness sleep postictal period

HA, confusion, drowsiness, nausea, muscle soreness - lasts mins. to hours

: all muscles go stiff, patient becomes rigid then falls, very short period, recovers quickly

all muscles go limp/floppy, patient falls usually forward, “drop attach”, recovers quickly

muscle jerk, arms and legs briefly jerk (like when we fall asleep)

• Imaging MRI (more sensitive than CT), order if new onset seizure, if focal neurologic signs/symptoms, if EEG shows focal disturbance, if progression of symptoms
• CBC, CMP, Calcium, Magnesium, CSF(if acute setting, new onset seizure)
• EEG – standard or 24 hr -72 hr ambulatory monitoring

• Antiepileptic Drugs (AED’s) = First Generation : Phenytoin (Dilantin), Carbamazepine (Tegretol), Valproate/Valproic acid (Depakote), Phenobarbital (Luminal)
• Second Generation: Levatiracetam (Keppra), Gabapentin (Neurontin), Lamotrigine (Lamictal), Topiramate (Topamax), Pregabalin (Lyrica)

• epileptic seizure that last >30 mins. or absence of full recovery of consciousness between seizures, cardiac and respiratory changes, cerebrovascular changes, postictal findings
• Is life threatening, can cause permanent brain damage due to hyperthermia, circulatory collapse

• : febrile convulsions,
• acute or chronic CNS injury
• , intoxication, idiopathic

• rapid control of seizure is critical to survival – ABC’s
• LORAZEPAM (Ativan) IV or Diazepam (Valium) IV and Phenytoin (Dilantin)
• If persist after 5 mins. Add Fosphenytoin (Cerebyx)
• If seizure persist/refractory status – ICU - induce drug coma Phenobarbital (Luminal) or Propofol (Diprivan)
• Once seizure controlled – prophylactic therapy

• Appearance: Clear (normal)
• Opening pressure: 10-20 cm H 2 O
• White cell count: 0-5 cells/µL (< 2 polymorphonucleocytes [PMN]);
• (normal cell counts do not rule out meningitis or any other pathology)
• Glucose- CSF:Serum glucose ratio: 0.6 (>60% of serum glucose)
• Protein level: < 45 mg/dL (0.45 g/L)

• Appearance: Clear, cloudy, or purulent (turbid)
• Opening pressure: Elevated (>30 cm H 2 O)
• WBC count: >100 cells/µL (>90% PMN); partially treated cases may have as low as 1 WBC/µL
• Glucose – CSF:serum ratio: decreased 0.4 (< 40% of serum glucose)
• Protein level: Elevated (>50 mg/dL)
• Consider additional tests: CSF Gram stain and cultures, blood cultures, CSF bacterial antigens, CSF polymerase chain reaction (PCR), others depending on clinical findings

• Appearance: Clear
• Opening pressure: Normal or mildly elevated
• WBC count: 10-1000 cells/µL (lymphs but PMN early)
• Glucose – CSF:serum ratio: >0.6 (>60% serum glucose, may be low in HSV infection)
• Protein level: normal or slightly elevated (>50 mg/dL)
• Consider additional tests: CSF Gram stain and cultures, blood cultures, CSF bacterial antigens, CSF PCR (eg, herpes simplex virus [HSV], varicella-zoster virus [VZV])

• Appearance: clear or opalescent (fibrin web)
• Opening pressure: often elevated
• WBC: 10-500 lymphocytes
• Glucose – CSF:serum ratio: decreased <0.4 (20-40%)
• Protein: increased but usually <500mg