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Leah D. Polidario
• Paroxysmal disorder caused by sudden
excessive electrical discharge in the cerebral
cortex or its underlying structures
• Occurs in 5 to 10% of the population
• Clinical manifestations can range from
dramatic to subtle
• Recurrent seizures due to an underlying cause
• 0.5 to 1% of population
Table 369-1 Classification of Seizures
1.Focal seizures
(Can be further described as having motor, sensory, autonomic,
cognitive, or other features)
2.Generalized seizures
1. Absence
2. Typical
3. Atypical
4. Tonic clonic
5. Clonic
6. Tonic
7. Atonic
8. Myoclonic
3. May be focal, generalized, or unclear
Epileptic spasms
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 ( approx. 30 sec.) with intermittent
relaxing and tensing of muscles
• absence (petit mal) :
– transient lapse of consciousness w/o loss of
postural tone
• Myoclonic (infantile spasms & juvenile
myoclonic epilepsy) :
– sudden brief contraction
Partial or focal seizures :
– involves discrete areas, implies a focal, structural
• simple:
– without impairment of consciousness; may be motor,
sensory, or autonomic
• complex:
– with impairment of consciousness +/- automatisms or
psychogenic features
• Partial with secondary generalization:
– starts focal, becomes diffuse
Differential Diagnosis
• Syncope :
– lacks true aura (altho' patient may describe feeling
unwell w/ diaphoresis, nausea, and tunneling of
vision), motor manifestation <30 sec (convulsive
activity <10 sec may occur with transient cerebral
hypoperfusion), and without postictal
disorientation, muscle soreness, or sleepiness;
skin pallor & clamminess support syncope
• Psychogenic seizure :
– may see side-to-side head turning, asymmetric
large amplitude limb movements, diffuse
twitching w/o LOC, crying/talking during event
• Other :
– metabolic disorders (eg; alcoholic blackouts,
– Migraines
– narcolepsy
– nonepileptic myoclonus
• Alcohol withdrawal, illicit drugs, meds (eg;B-
lactams, mmeperidine'antidep., clozapine
• Brain tumor or penetrating trauma
• Cerebrovascular disease, incldg subdural
hematomas, hypertensive encephalopathy
• Degenerative disorders of the CNS (eg,
• Electrolyte (hyponatremia) & other metabolic
(eg, uremia, liver failure, hypoglycemia)
Clinical Manifestations
• Aura (sec to mins) :
– premonition consisting of abnormal smells/tastes,
unusual behavior, oral or appendicular
• 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 neurological deficits
("Todd's paralysis")
• Status Epilepticus :
– continuous tonic-clonic seizure > 30 mins, or
repeated seizures such that there is no resolution
of postictal periods
– Complications include neuronal death,
rhabdomyolysis, and lactic acidosis
• Nonconvulsive status epilepticus:
– alteration of awareness (ranging from confusion to
coma) w/o motor manifestations
– Dx with EEG
Clinical Evaluation
• Seizure: patient usually w/o recollection, must
talk to witnesses
– unusual behavior before seizure (ie, aura)
– type and pattern of abnormal movements, incldg
head turning & eye deviation (gaze preference
away from seizure focus)
– loss of responsiveness
• HPI: recent illnesses/fevers, head trauma
• PMH: prior seizures or (+) family, prior
meningitis/encephalitis, prior strokes or head
• Medications, alcohol, and illicit drug use
• General physical exam should include the skin,
looking for neuroectodermal disorders (eg,
neurofibromatosis, tuberous sclerosis) that are
associated with seizures
• Neurological exam should look for focal
abnormalities----underlying structural
Diagnostic studies
• Laboratory:
– full electrolytes; BUN, Cr, Glc, LFTs, tox screen,
medication levels
– frequent seizures:
• can confirm by demonstrating repetitive rhythmic activity
(gen seizures will always have abnormal EEG; partial seizures
may not)
– infrequent seizures: may show interictal epileptiform
activity (eg, spikes or sharp waves), but such patterns
seen in up to 2% of normal population
– sleep deprivation increases the yield of EEG; video
monitoring may help w/ psychogenic seizures
• MRI to r/o structural abnormalities:
– inc sensitivity w/ fine coronal cuts of frontal &
temporal lobes
• Lumbar puncture (after ruling out space-
occupying lesion):
– if suspecting meningitis or encephalitis and in all
HIV (+) patients
• Treat underlying causes, incldg CNS infections,
intoxication, or withdrawal, etc.
• Antiepileptic drug (AED) therapy
– usually reserved for pts w/ underlying structural
abnormality or an idiopathic seizure plus :
– (1) status epilepticus on presentation
– (2) focal neurological exam
– (3) postictal Todd's paralysis
– (4) abnormal EEG
• For pts w/ infrequent seizures, early (vs. delayed)
intervention with AED inc time to seizure
recurrence, but has no effect on long-term
seizure-free status
• Generalized tonic-clonic:
– valproic acid, phenytoin, topiramate, lamotrigine
• Partial (w/ or w/o sec. generalization) :
– carbamazepine, ooxcarbazepine, lamotrigine,
phenytoin, valproic acid
• Absence:
– ethosuximide, valproic acid
• Secondary Agents:
– Leviteracitam, gabapentin, clonazepam,
• Introduce gradually, monitor carefully
• May consider withdrawal if seizure-free
(typically for at least 1 year) and normal EEG
• Individual state laws mandate seizure-free
duration before being allowed to drive
Status Epilepticus
• Place patient in semiprone position to dec risk of
• Oral airway or if prolonged, endotracheal
• IV access, start normal saline infusion
• STAT labs including gluc, Na, Ca, serum & urine
toxicology screen, anticonvulsat levels
• Thiamine (100 mg IV) prior to dextrose to prevent
exacerbaton of Wernicke's encephalopathy
• Dextrose (50 g IV push)
• Na or Ca repletion as needed
• Thank you…
• & &
• Happy Weekend
Happy Weekend