Neurology Step Up to Medicine Flashcards
reversible ischemic neurologic deficit
same as TIA but sx last longer than 24 hours, but resolve w/in 2 weeks
evolving stroke
stroke with worsening sx
completed stroke
stroke in which maximal deficit has occured
TIA
transient neurological deficit that lasts from minutes to no more than 24 hours (usually resolves w/in 30 min)
MCC of TIA
embolic
- can also be due to transient hypotension in the presence of severe carotid stenosis (> 75%)
what is the relationship between TIA and risk for stroke
risk of stroke in pt with previous TIA is about 10% per year with a 30% 5-year stroke risk
most impt RF for stroke
age
HTN
RFs for stroke in younger pts,
OCP use
hypercoagulable states - protein C/S deficiency, antiphospholipid syndrome
vasoconstrictive drug use - cocaine, amphetamine
polycythemia vera
sickle cell dz
MC origins of embolus in embolic stoke
heart - mural thrombus
internal carotid artery
aorta
paradoxical
artery most commonly affected by atherosclerosis in brain
middle cerebral artery
what structures does a lacunar stroke affect?
basal ganglia
thalamus
internal capsule
brain stem
main predisposing factor for lacunar strokes
HTN
how do you evaluate the source of embolic stroke?
- echo
- carotid doppler
- ECG/Holter monitoring
Most common location of stroke and assoc. findings
MCA
- contralateral hemiparesis/hemisensory loss
- aphasia (dom. hemisphere)
- apraxia, CL body neglect and confusion (non-dom. hemisphere)
signs/symptoms of a TIA of the carotid system
- temporary loss of speech, paralysis/paresthesias of CL extremity, clumsiness of one limb
- amaurosis fugax
amaurosis fugax
transient, curtain-like loss of sight in ipsilateral eye due to microemboli to the retina
signs/sx of Vertebrobasilar TIA
decreased perfusion of posterior fossa leading to:
- dizziness, double vision, vertigo
- numbness of ipsilateral face and CL limbs
- dysarthria, dysphagia and hoarseness
- projectile vomiting
- headaches
- drop attacks
subclavian steal syndrome
caused by stenosis of subclavian artery proximal to origin of vertebral artery - exercise of left arm causes reversal of blood flow down ipsilateral vertebral artery to fill subclavian aa distal to stenosis -> get signs of vertebrobasilar arterial insufficiency
sx. of subclavian steal syndrome
- BP differential in arms (left arm < right arm, decreased pulse in left arm)
- neuro deficits
- UE claudication
- presyncope/syncope
classic presentation of thrombotic stroke
pt awakens from sleep with neurological deficits
classic presentation of embolic stroke
onset is very rapid (w/in seconds) and deficits are maximal initially
four major syndromes of lacunar stroke
- pure motor stroke (IC)
- pure sensory stroke (thalamus)
- ataxis hemiparesis (incoordination ipsilaterally)
- clumsy hand dysarthria
deficits seen in ACA stroke
contralateral lower extremity
hemiparesis/hemisensory loss
urinary incontinence
deficits seen in MCA stroke
aphasia- dominant side
contralateral hemiparesis: upper extremity/face
hemineglect- nondominant
homonymous hemianopia w/ macular sparing
deficits seen in vertebrobasilar stroke
ipsilateral: ataxia, diplopia, dysphagia, dysarthria and vertigo
contralateral: homonymous hemianopia (basilar-PCA lesions)
what is the first test you order if pt presents with stroke symptoms
non-contrast CT scan
- R/O hemorrhage
- ischemic strokes appear darker on CT scan
what is the definitive test for dx. stenosis of vessels of head/neck and aneurysms
magnetic resonance arteriogram
what are the uses of head CT in the ED?
- diff ischemic vs. hemorrhagic stroke
- identifies > 95% of SAH
- identifies abscesses/tumors
- identifies epidural and subdural hematomas
who should be screened with a carotid duplex study?
patients with:
- carotid bruit
- peripheral vascular dz
- coronary artery dz
what are the tests that should be ordered with pt presents to ED with symptoms of acute stroke?
- non contrast head CT
- EKG, CXR
- CBC, platelet count, PT/PTT, electrolytes, glucose
- bilateral carotid USG
- ECHO
if a young pt (< 50 yo) presents with stroke, what should you look for?
vasculitis, hypercoagulable state and thrombophilia
indications for tPA
within 3 hours of symptom onset
contraindications to tPA
- if time is unknown or > 3 hours
- uncontrolled HTN
- bleeding disorder
- tx with anticoagulants
- hx of recent trauma/surgery
if giving pt tPA, what should be BP level be maintained at?
< 185/110 mmHg
if pt presents after 3 hours of sx onset what drug is indicated?
Aspirin
- clopidogrel or ticlopidine if pt cannot take aspirin due to allergy or intolerance
role of anticoagulants in stroke tx.
heparin/warfarin have not been proven to have efficacy - therefore, not given in acute setting
- unless stroke is due to emboli from a cardiac source
under what conditions do you give anti-hypertensives in stroke pt?
- BP is > 220/120 or MAP > 130 mmHg
- pt has signifcant medical indication for it i.e. acute MI, aortic dissection, CHF, hypertensive encephalopathy
- pt is receiving thrombolytic therapy
indications for carotid endarterectomy
if pt is symptomatic and has carotid stenosis > 70%
Main causes of intracerebral hemorrhage
HTN - sudden increases ischemic stroke amyloid angiopathy anticoagulant/antithrombolytic drugs brain tumors AV malformations
MC locations of intracerebral hemorrhage
basal ganglia (MC)
pons
cerebellum
cortex
CF of intracerebral hemorrhage
abrupt onset of a focal neuro deficit that worsens steadily over 30-90 min with altered LOC, headache, vomiting and signs of ICP
pupillary findings in ICH and their level of involvement..(3)
pinpoint = pons
poorly reactive = thalamus
dilated = putamen
threshold for BP treatment in ICH
give antihypertensive if BP is > 160-180/105 mmHg
DOC for BP management in ICH
nitroprusside
should you use steroids to reduce ICP in ICH?
no..use of steroids can be harmful in hemorrhage
causes of SAH
- ruptured berry aneurysm
- trauma
- AVM
common sites of SAH
- junction of anterior comm. aa with ACA
- junction of posterior comm. aa with ICA
- bifurcation of MCA
CF of subarachnoid hemorrhage
sudden, severe excruciating headache in absence of focal neuro deficits
transient LOC
vomiting
meningeal irritation, nuchal rigidity and photophobia
retinal hemorrhages
diagnostic test of choice for SAH
non contrast CT scan of head
if CT scan is non-equivocal in dx of SAH, what test should you do?
Lumbar puncture
- unless there is papilledema in which case repeat the CT scan
gold standard for diagnosis of SAH
xanthochromia on LP
- results from RBC lysis; implies blood has been in CSF for several hours and that it is not due to traumatic tap
once SAH is diagnosed, what test do you order?
cerebral angiogram
- definitive study for detecting site of bleeding and for surgical clipping
complications of SAH
- rebleeding
- vasospasm
- seizures
- communicating hydrocephalus
- SIADH
what drug is used to reduce incidence/infarction due to vasospasm in SAH?
CCB - nifedipine
medical therapy of SAH
- bed rest in quiet dark room
- stool softeners
- analgesics
- IVF for hydration
- BP meds (lower gradually)
major pathophys of Parkinsons dz
loss of DA-containing neurons located in the pigmented substantia nigra and the locus ceruleus in the midbrain
CF of Parkinson’s dz
- pill rolling tremor at rest (worse w/ emotional stress)
- cogwheel rigidity
- bradykinesia
- postural instability
- masked facies, decreased blinking
- dysarthria and dysphagia, micrographia
- dementia later in dz
- autonomic dysfunction - orthostatic hypotension, increased sweating
- personality changes
Shy-Drager syndrome
Parkinsonian symptoms AND autonomic insufficiency
widespread neurological signs (cerebellar, pyramidal, LMN)
most effective drug for tx of parkinsonian symptoms
carbidopa-levodopa (Sinemet)
side effects of sinemet
- dyskinesias (involuntary, choreic movements) can occur after 5-7 years of therapy
- NV, anorexia
- HTN
- Hallucinations
what DA-R agonists are used in tx of Parkinsons?
bromocriptine
pramipexole - MC used
what are DA-R agonists esp. useful for in tx of PD?
- sudden episodes of hesitancy or immobility (“freezing”)
- can control initial symptoms and delay need for levodopa for many years
Selegeline
MOA-B inhibitor (increases DA activity and reduced levodopa metabolism); used as an adjunctive agent in tx of PD, usually in early dz
amantadine
antiviral agent used to tx. early or mild parkinsons disease
what anticholinergic drugs can be used in tx of Parkinsons
trihexiphenidyl
benztropine
what is the major benefit of anticholinergic drugs as tx of PD?
mostly help with tremor symptoms
what antidepressant can be used to tx both Parkinsonian symptoms and depressive symptoms of PD?
amitryptiline
- both anticholinergic and antidepressant
what are indications for deep brain stimulation as tx of PD?
if pt is unresponsive to medications OR pt develops severe dz before age of 40
progressive supranuclear palsy
degenerative condition of brain stem, basal ganglia and cerebellum that causes bradykinesia, rigidity, cognitive decline and opthalmoplegia; it does not cause tremor
does tremor or bradykinesia as the major symptom impart better prognosis in PD
tremor
what medications cause parkinsonian side effects
- neuroleptics - chlorpromazine, haloperidol, perphenazine
- metoclopramide
- reserpine
pathophys of Huntingtons chorea
AD mutation on Xm4 causing extended triple repeat (CAG) leads to loss of GABA-producing neurons in striatum
what should you always keep in mind in a young patient who develops a movement disorder?
Wilson’s disease
CF of Huntington’s chorea
- chorea
- altered behavior - irritability, personality changes, antisocial behavior, depression, psychosis
- progressive dementia
- unsteady and irregular gait
- incontinence
diagnosis of Huntington’s
MRI will show atrophy of head of caudate; DNA testing confirms the diagnosis
Tx of Huntington’s
supportive
- DA blockers may improve psychosis and chorea
- anxiolytics/antidepressants may be necessary
coarse, action tremor aka intention tremor is due to lesion in…
cerebellum
features of essential tremor
fine tremor that occurs with certain postures (arms outstretched) or certain tasks (handwriting); improved by alcohol consumption
assoc. features with a cerebellar tremor
ataxia
nystagmus
dysarthria
assoc. features with an essential tremor
vocal tremulousness
head tremor
characteristic tremor seen in Parkinsons
resting, pill-rolling tremor that is improved by actions
tx for essential tremor
propranolol
general characteristics of ataxia
gait instability
loss of balance
impaired limb coordination
acquired causes of ataxia
alcohol intoxication vit B12 or thiamine deficiency cerebellar infarction/neoplasm demyelinating disease tertiary syphillis (tabes dorsalis)
Friedrich’s ataxia
AR dz that presents in young adulthood with ataxia, nystagmus, impaired vibratory sense and proprioception
ataxia telengiectasia
AR dz that presents by childhood with ataxia, nystagmus, impaired vibratory and position sense as well as telengiectasias; pts have increased risk of cancer
potentially reversible causes of dementia
hypothyroidism neurosyphillis vit B12/folate/thiamine deficiency medications normal-pressure hydrocephalus depression subdural hematoma
Binswanger’s dz
insiduous onset dementia due to diffuse subcortical degeneration, MC in pt with long standing HTN and atherosclerosis
cortical dementia
Cortical dementia is atrophy of the cortex which affects ‘higher’ functions such as memory, language, and semantic knowledge
subcortical dementia
subcortical dementia affects mental manipulation, forgetfulness, and personality/emotional changes.
CF of normal pressure hydrocephalus
triad of dementia, gait ataxia and urinary incontinence; normal CSF pressure with dilated ventricles
risk factors for Alzheimer’s dementia
- increased age
- family history
- Down Syndrome
- genes - Xm 21, 14 and 19 involved
senile plaque
focal collection of dilated, tortuous neuritic processes surrounding a central amyloid core (amyloid beta protein)
neurofibrillary tangle
bundles of neurofilaments in cytoplasm of neurons; denote neuronal degeneration
how do you diagnose Alzheimer’s disease?
CLINICAL diagnosis
- CT or MRI showing cortical atrophy with enlarged ventricles supports the diagnosis
first line tx of Alzheimer’s dementia
cholinesterase inhibitors i.e. donepezil, galantamine, rivastigmine
relationship between vitamin E intake and Alzheimers
study showed that megadoses of vitamin E (2000 IU/day) slowed disease progression and preserved function in pts with moderately severe dementia
relationship between hormone replacement therapy and Alzheimers
hormone replacement therapy is associated with lower risk of developing Alzheimers
CF of Lewy Body Dementia
visual hallucinations
Parkinsonian symptoms
fluctuating mental status
pts are sensitive to adverse effects of neuroleptic agents
anticholinesterase medications are indicated only for what two kinds of dementia?
Alzheimers and Lewy Body dementia
arousal relies on…
intact reticular activating system in BS
cognition relies on…
intact cerebral hemispheres
which medications/drugs can precipitate delirium?
TCAs corticosteroids anticholinergics hallucinogens cocaine benzodiazepines narcotics
what test should be performed in any febrile, delirious patient unless contraindications?
lumbar puncture
if asymmetry is noted on motor exam in a comatose patient….
mass lesion is likely the cause
- metabolic of systemic causes would not cause asymmetric motor abnormalities
what can cause an abnormal pupillary light reflex in comatose patient?
structural intracranial lesions
drugs - morphine, atropine
anoxic encephalopathy
recent eye drops
what can cause bilateral fixed, dilated pupils in a comatose pt?
severe anoxia
what can cause unilateral, fixed and dilated pupil in comatose pt?
CN III palsy (uncal herniation)
what can cause pinpoint pupils in a comatose pt?
narcotics
intracerebral hemorrhage
if pupils are round and symmetrically reactive to light in comatose pt…
midbrain is intact and not cause of coma
anisocoria (asymmetric) pupils in comatose pt is a sign of
uncal herniation
locked in syndrome
mimics coma bc pt is completely paralyzed (muscles for blinking, vertical eye movements and breathing intact); pt is fully aware of their surroundings and pain
lesion that causes locked in syndrome
infarction or hemorrhage of ventral pons
criteria for dx of brain death
- irreversible absence of brain/brainstem function - unresponsiveness, apnea despite oxygenation/ventilation and no brainstem reflexes
- no drug intoxication or metabolic condition
- core body temp > 32 C
- clinical evidence or imaging study to suggest reason
- repeat exams or EEG shows isoelectric activity
classic location of plaques in MS
angles of lateral ventricles
commonly involved tracts in MS
pyramidal and cerebellar pathways
medial longitudinal fasciculus
optic nerve
posterior columns
clinically definite MS
two episodes of symptoms
two lesions on imaging
lab-supported definite MS
two episodes of sx
atleast one white matter lesion on imaging
oligoclonal bands in CSF
probable MS
two episodes of sx and either one white matter lesions OR oligoclonal bands
MC initial presentation of MS
transient sensory deficits - decreased sensation or paresthesias in upper or lower limbs
MC complaint of MS pts
fatigue
what kinds of motor sx are seen in MS
weakness - pyramidal tract involvement
spasticity - leg stiffness (may affect pts ability to walk / balance)
CF of optic neuritis as seen in MS
monocular vision loss with pain on movement of eyes; central scotoma and decreased pupillary light reflex
internuclear opthalmoplegia
lesion in MLF resulting in ipsilateral medial rectus palsy on attempted lateral gaze (Adduction defect) and horizontal nystagmus of abducting eye
what factors increase the chance of severe disability in MS pt
- frequent attacks early in dz
- onset at older age
- progressive course
- early cerebellar or pyramidal involvement
diagnostic test of choice for MS
MRI
- the number of lesions is not proportional to disease severity or progression
LP finding in MS
oligoclonal bands of IgG
how can evoked potentials be applied to MS diagnosis
measure speed of nerve conduction w/in the brain; newly remyelinated axons will conduct sensory impulses more slowly
Tx of acute MS attack
high dose IV steroids
- oral steroids dont work
- dont affect MS course or outcome
tx option for steroid-refractory acute demyelinating attacks
therapeutic plasma exchange
what drug has shown to reduce relapse rates in MS?
Interferon
- should be started early in course of disease before disability becomes irreversible
what kind of tx can be used for rapidly progressive disease in MS?
non-specific immunosuppressive therapy with cyclophosphamide
symptomatic tx of muscle spasticity in MS
baclofen or dantrolene
symptomatic tx. of neuropathic pain in MS
carbamazepine or gabapentin
main CF of Guillain-Barre syndrome
rapidly ascending symmetric weakness/paralysis of all 4 extremities that frequently progresses to involve facial, bulbar and respiratory muscles; sphincter control and mentation are generally preserved
CSF analysis in pt with Guillain-Barre syndrome
elevated protein, but normal cell count
nerve conduction studies in Guillain-Barre syndrome
decreased motor nerve conduction velocity
Tx of Guillain-Barre syndrome
- monitor pulmonary function
- IV immunoglobulin - if pt has sig weakness
- plasmapheresis - may reduce severity
- do NOT give steroids
what is Guillain Barre syndrome
inflammatory demyelinating polyneuropathy that affects motor nerves; usually preceded by viral or mycoplasmal infection of upper respiratory or GI tracts
what common infections lead to Guillain Barre
camplyobacter jejuni, CMV, hepatitis, HIV
non infectious causes of Guillain Barre
Hodgkins disease
lupus
after surgery
after HIV seroconversion
pathomechanism of Myasthenia Gravis
autoantibodies directed against the nAch-R of NMJ leading to reduced post-synaptic response to Ach, resulting in significant muscle fatigue
what muscles are most affected in Myasthenia Gravis
skeletal mm that are stimulated repeatedly i.e. extraocular mm
MC initial symptoms of Myasthenia
ptosis, diplopia and blurred vision
which cranial muscles are involved in Myasthenia
extraocular mm
eyelids (ptosis)
facial muscles (diff chewing, weakness, slurred speech)
main CF in Myasthenia gravisi
skeletal mm weakness that gets worse with activity (worse at end of day) and improved with rest; sensation and reflexes are preserved
myasthenic crisis
acute exacerbation of MG; medical emergency with diaphragmatic and intercostal mm fatigue leading to respiratory failure; usually starts with bulbar weakness, which can lead to dysphagia or upper airway obstruction
causes of myasthenic crisis
concurrent infections
surgery
pregnancy/childbirth
medications: antibiotics (aminoglycosidies, erythromycin, azithromycin), cardiac drugs (BB, procainamide, quinidine, Mg2+)
indications for elective intubation in myasthenic crisis
if VC is < 20 ml/kg or maximal inspiratory force (MIF) is less than - 30 cmH20
Tx of myasthenic crisis
withdrawal of anticholinesterases for few days
mechanical ventilation
plasmaphoresis»_space; IVIG
diagnostic test of choice for Myasthenia
Ach-R antibody test
what does EMG show in Myasthenia
decremental response to repetitive stimulation of motor nerves
Edrophonium (Tensilon) test
AchE medications cause marked improvement of symptoms
Tx. approach to Myasthenia gravis
- AchE inhibitors - pyridostigmine (symptomatic benefit)
- use steroids if pt has poor response
- third line: azathioprine and cyclosporine - Thymectomy
- symptomatic and complete remission in many pts - Plasmaphoresis or IVIG in acute exacerbations
medications that exacerbate Myasthenia Gravis
antibiotics - aminoglycosides, tetracyclines, macrolides
B-blockers
antiarrhythmics - procainamide, quinidine, lidocaine
main CF of Duchenne Muscular dystrophy
progressive muscle weakness that is symmetric and begins in childhood; promixal muscles are primarily affected (pelvic girdle)
Gower’s manuever
patient uses hands to get up from floor because the weakness in the proximal LE mm makes it difficult to rise w/o support
dx of Duchenne muscular dystrophy
serum CPK elevated
DNA testing has replaced muscle biopsy
tx of Duchenne muscular dystrophy
- Prednisone - can increase mm strength and function; use in boys > 5 yo whose motor skills are declining
- Surgery to prevent progressive scoliosis
central cavitation of cervical cord due to abnormal collection of fluid w/in spinal parenchyma
syringomyelia
what is syringomyelia associated with
Arnold Chiari malformation
- other causes: trauma, infection, tethered cord, intramedullary tumors
CF of syringomyelia
bilateral loss of pain and temp over shoulders (cape like distribution), preservation of touch, thoracic scoliosis and mm atrophy of hands
causes of spinal hemisection
crush injury to one side
trauma - stab, fracture
tumors
abscesses
CF of Brown Sequard syndrome
C/L loss of pain and temp (spinothalamic)
I/L hemiparesis (corticospinal)
I/L loss of position/vibration (DCML)
what is transverse myelitis
rare condition affecting tracts across the horizontal aspect of spinal cord at a given level, most commonly thoracic spine
CF of transverse myelitis
LE weakness/paralysis
sensory loss below lesion
back pain
sphincter disturbance
diagnostic study of choice for tranverse myelitis
MRI with contrast
tx of transverse myelitis
high dose steroids
- evidence supporting its use is equivocal
Horner’s syndrome results from…
interuption of cervical SNS nerves; can be either PRE (central lesions) or POST (distal to superior cervical ganglion)
CF of Horner’s syndrome
ipsilateral ptosis, miosis and anhydrosis
causes of Horner’s syndrome
idiopathic Pancoasts tumor internal carotid dissection brainstem stroke neck trauma (cervical spinal injury)
what does poliovirus affect
anterior horn cells and motor neurons of spinal cord and brain stem; LMN involvement
CF of poliomyelitis
- asymmetric mm weakness (leg»_space; arm)
- absent DTRs
- flaccid, atrophic mm
- normal sensation
vertigo
disturbance of vestibular system characterized by sensation of spinning or hallucination of movement
features of central vertigo
- gradual onset
- concurrent neuro findings (brainstem)
- look for CV risk factors in pt
- accompanying nystagmus
- no refractoriness
features of peripheral vertgio
- acute onset
- head position has strong effect
- NV
- tinnitus/hearing loss
benign positional vertigo
vertigo is experienced in certain positions/positional changes; lasts a few moments and is more common among pts > 60 yo
tx of benign positional vertigo
meclizine
- usually resolves w/in 6 months
Meniere’s disease
triad of vertigo, tinnitus and hearing loss
tx. of Meniere’s disease
sodium restriction
diuretics
what CF can be seen with an acoustic neuroma
ataxia, gait unsteadiness, nystagmus, hearing loss and tinnitus
causes of central vertigo
MS - demyelination of vestibular pathways
vertebrobasilar insufficiency
migraine-associated vertigo
syncope
transient LOC/postural tone secondary to acute decrease in cerebral blood flow
cardinal features of syncope due to cardiac cause
sudden syncope without any prodromal symptoms i.e. the pt hits the floor
causes of cardiac syncope
arrhythmias
obstruction of blood flow
massive MI
characteristic features of vasogenic syncope
preciipitating factors including emotional stress, pain,fear, extreme fatigue or claustrophobic situations with premonitory sx such as pallor, diaphoresis, lightheadedness, nausea, dimming of vision, roaring in ears
what test can reproduce the sx of vasogenic syncope
tilt table test
tx of vasogenic syncope
assume supine position, elevate legs
B-Blockers
Disopyramide
causes of orthostatic hypotension syncope
ganglionic blocking agents diabetes old age prolonged bed rest vasodilators/diuretic use
what are you worried about if syncope happens with exertion
assess for potentially life threatening hypertrophic cardiomyopathy or aortic stenosis
tx of orthostatic hypotension syncope
increased sodium intake and fluids
fludrocortisone
what type of stroke can cause syncope
if it involves vertebrobasilar system “drop attacks”
San Francisco syncope rule
high risk of adverse outcomes due to syncope if:
- hx of dyspnea or CHF
- sys. BP < 90
- decreased hematocrit
- abnormal ECG
who should be admitted with syncope?
- older pt > 60-70 yo
- sig cardiac RFs
- recurrent syncope
- serious underlying illness
metabolic causes of seizure
hyponatremia, water intoxication hypo/hyperglycemia hypocalcemia uremia thyroid storm hyperthermia
mass lesions that can cause seizures
tumors - primary and mets
hemorrhage
what “missing drugs” can cause seizures
noncompliance w/ anticonvulsants
acute w/d from alcohol, BDZs and barbiturates
misc causes of seizures not covered by 4 M’s and Is
pseudoseizures
eclampsia
hypertensive encephalopathy
Intoxications with what substances can cause seizure
cocaine lithium lidocaine theophylline metal poisoning - lead, mercury CO poisoning
4 I’s that cause seizures
Intoxications
Infections
Ischemia
Increased ICP
simple partial seizure
consciousness remains INTACT, seizure remains localized, may involve transient unilateral tonic-clonic movement
complex partial seizure
consciousness is impaired with postictal confusion; automatisms are common, pt may become aggressive if restrained and olfcatory/gustatory hallucinations present
generalized seizure
loss of consciousness and involve disruption of electrical activity in entire brain
DOC for partial seizures
phenytoin and carbamazepine
typical course of grand-mal seizure
bilaterally, symmetric w/o focal onset
- sudden LOC, pt drops
- tonic: rigid with extension of all 4 extremities
- clonic: musculature jerking (30 sec)
- pt becomes flaccid and comatose before regaining consciousness
- usually postictal confusion and drowsiness
typical features of petit-mal (absence) seizure
usually in school aged children; pts disengage from current activity and stare into space - impaired consciousness but no loss of postural tone or continence and no postictal confusion
lab values to check immediately in unfamiliar, seizing patient
serum calcium
serum sodium
serum glucose
BUN
what is most impt test for pt with known epilepsy who has a seizure
anticonvulsant levels
what is status epilepticus
prolonged, sustained LOC with persistent convulsive activity in seizing pt; medical emergency with high mortality
causes of status epilepticus
poor compliance w/ meds alcohol withdrawal neoplasm metabolic disorder drug overdose
management of status epilepticus
establish airway IV diazepam IV phenytoin 50 mg dextrose - resistant cases: IV phenobarbital
