NEUROLOGY
SEIZURES
Definitions (NEJM 2003;349:1257; Epilepsia 2010;51:676)
• Seizure = abnormal, paroxysmal, excessive discharge of CNS neurons; occurs in 5–10% of the population; can range clinically from dramatic to subtle
• Epilepsy = recurrent unprovoked seizures; 0.5–1.0% of population
• Generalized seizures (involves brain diffusely)
Tonic-clonic (grand mal): tonic phase (10–20 sec) with contraction of muscles (causing expiratory moan, cyanosis, pooling of secretions, tongue biting) → clonic phase (~30 sec) with intermittent relaxing and tensing of muscles
Absence (petit mal): transient lapse of consciousness w/o loss of postural tone, usu pedi
Myoclonic (infantile spasms & juvenile myoclonic epilepsy): sudden, brief contraction
• Focal (partial) seizures (involves discrete brain area, implies a structural lesion)
Simple (w/o Δ MS) vs. complex (w/ Δ MS): motor, sensory and/or autonomic
Focal with secondary generalization: starts focal, becomes generalized
Differential diagnosis
• Syncope (Lancet Neurol 2006;5:171)
• Nonepileptic seizure (NES, aka “psychogenic”): may see side-to-side head turning, asymmetric large-amplitude limb movements, diffuse shaking w/o LOC, and crying or talking during event
• Other: metabolic disorders (eg, alcoholic blackouts, hypoglycemia), migraine, TIA, transient global amnesia, narcolepsy (cataplexy), nonepileptic myoclonus, tics, asterixis
Etiologies (varies strongly by age)
• Alcohol withdrawal, illicit drugs, meds (eg, β-lactams, bupropion, tramadol, metronidazole, meperidine, CsA, antidep., clozapine can lower seizure threshold)
• Brain tumor or penetrating trauma
• Cerebrovascular disease, including subdural hematomas, hypertensive encephalopathy
• Degenerative disorders of the CNS (eg, Alzheimer’s)
• Electrolyte (hyponatremia) & other metabolic (eg, uremia, liver failure, hypoglycemia)
• Idiopathic (in ~60%)
Clinical manifestations
• Aura (sec to mins): premonition with paresthesias, focal motor contractions, abnormal smells/tastes, fear, depersonalization, déjà vu, autonomic changes, automatisms
• Ictal period (sec to mins): tonic and/or clonic movements of head, eyes, trunk or extrem.
• Postictal period (mins to h): slowly resolving period of confusion, disorientation, and lethargy. May be accompanied by focal neurologic deficits (Todd’s paralysis).
• Status epilepticus: continuous tonic-clonic seizure ≥30 min or repeated seizures w/o resolution of postictal encephalopathy. Complications include neuronal death, rhabdomyolysis and lactic acidosis.
• Nonconvulsive status epilepticus: alteration of awareness (ranging from confusion to coma) w/o motor manifestations of seizure. Dx with EEG.
Clinical evaluation
• Seizure: patient usually w/o recollection, must talk to witnesses
unusual behavior before seizure (ie, an aura)
type & pattern of abnl movements, incl. head turning & eye deviation (gaze preference usually away from seizure focus)
loss of responsiveness
• HPI: recent illnesses/fevers, head trauma, sleep deprivation, medication compliance
• PMH: prior seizures or 
FHx, prior meningitis/encephalitis, prior stroke or head trauma
• Medications, alcohol and illicit drug use
• General physical exam should include the skin, looking for neuroectodermal disorders (eg, neurofibromatosis, tuberous sclerosis) that are a/w seizures
• Neurologic exam should look for focal abnormalities → underlying structural abnormality
Diagnostic studies (Neurology 2007;69:1996)
• Laboratory: full electrolytes, BUN, Cr, glc, LFTs, tox screen, medication levels
• EEG: during seizure can capture repetitive rhythmic activity (generalized seizures will typically have abnl EEG; partial may not); interictal EEG normal in 50% of Pts w/ epilepsy, and interictal epileptiform activity (spikes or sharp waves) seen in only 25% of Pts w/ epilepsy but up to 2% of normal population; sleep deprivation and repeated studies ↑ dx yield of EEG; video monitoring may help w/ nonepileptic seizures
• MRI to r/o structural abnormalities; ↑ Se w/ fine coronal imaging of frontal & temporal lobes
• LP (if no space-occupying lesion on imaging): if suspect meningitis (eg, fever, ↑ WBC, nuchal rigidity) or encephalitis and in all HIV Pts
Treatment (Lancet 2006;367:1087 & 2007;369:1000, 1016; NEJM 2008;359:166)
• Treat any underlying causes, including CNS infections, intoxication, withdrawal, etc.
• Antiepileptic drug (AED) therapy is usually reserved for Pts w/ underlying structural abnormality or an idiopathic seizure plus (i) status epilepticus on presentation, (ii) focal neurologic exam, (iii) postictal Todd’s paralysis or (iv) abnormal EEG
• After 1st unprovoked sz, if EEG and MRI nl → 65% sz-free at 5 y (Lancet Neurol 2006;5:317)
• For Pts w/ infrequent seizures, early (vs. delayed) intervention w/ AED ↑ time to seizure recurrence, but has no effect on long-term seizure-free status (Lancet 2005;365:2007)
• AED choice dependent on type of seizure, side effects, cost, mechanism of elimination (if hepatic or renal insufficiency), teratogenesis and drug interactions
• Introduce gradually, monitor carefully
• May consider withdrawal if seizure-free (typically for at least 1 y) and normal EEG
• Individual state laws mandate seizure-free duration before being allowed to drive
Status epilepticus (consult neurology)
• Place Pt in semiprone position to ↓ risk of aspiration
• Oral airway or, if prolonged, endotracheal intubation
• IV access, start normal saline infusion
• STAT labs including glc, Na, Ca, serum & urine toxicology screen, anticonvulsant levels
• Thiamine (100 mg IV) prior to dextrose to prevent Wernicke’s encephalopathy
• Dextrose (50 g IV push)
