Seizures

Mark Wahba

August 7, 2003

Statistics

• 10% of population will have 1 seizure in their lifetime

• 6% of population will have at least 1 afebrile seizure in their lifetime

• Incidence of epilepsy in the population is <1%

• 1% of ED visits is for seizures

Sub-presentations

• Status epilepticus• Febrile Seizures• Medical

management acute and chronic

Outline

• Definitions

• Classification of seizures

• Pathophysiology

• Clinical Features

• Postictal state

• Emergency Department Management

• Summary

Definitions

Seizure

• “clinical manifestation of excessive, abnormal cortical neuron activity” Rosen’s p.1445

• Not a diagnosis but a series of signs and symptoms

Epilepsy

• “recurring seizures without consistent provocation” Rosen’s p1445

Ictal

• “pertaining to, marked by, or due to a stroke or an acute epileptic seizure” Dorland’s Pocket Medical Dictionary 25th Ed. 1995 W.B. Saunders Company

Classification of Seizures

Primary and Secondary

• Primary seizure• Idiopathic/Genetic• Epilepsy

• Secondary seizure• aka reactive seizure• Response to certain

toxic, pathophysiologic, or environmental stress

• Not epilepsy

Generalized and Partial

• Generalized• Electrical activity

simultaneously involves both cerebral hemispheres

• Loss of consciousness

• Partial (Focal )• Electrical activity

limited to part of one cerebral hemisphere

Partial Seizure

• Partial with secondary Generalization• Starts partial then becomes generalized

• Complex Partial• Consciousness is

impaired

• Simple Partial• Consciousness is

maintained

Cryptogenic Seizure

• Thought to be secondary but identifiable cause found

Febrile Seizure

• Most common pediatric seizure

• 2-5% of children between 6mo -5years

• 20-30% have at least 1 recurrence

• Impt. to differentiate febrile seizure from seizure with fever

Pathophysiology

Pathophysiology

• Not completely understood

• Knowledge is from animal studies

• Electrical or pharmacologic stimulation applied to the brain cortex

Recruitment

• Generalized:• “when the initiating neurons’ abnormal,

increased electrical activity activates adjacent neurons and propagates until the thalamus and other subcortical structures are recruited” Rosen’s p.1446

Recruitment

• Partial:• Less recruitment and ictal activity does not

cross the midline

Why?

• Unclear

• Disruption of normal structure: congenital, maturational, acquired

• Disruption of local metabolic or biochemical function

Neurotransmitters

• acetylcholine-excitatory to cortical neurons

• gamma-aminobutyric acid (GABA)-inhibitory to cortical neurons

• changes in concentration of these NTs may produce membrane depolarization, then hyperpolarization, then recruitment

Why is consciousness altered?

• Ictal discharge reaches below the cortex

• Enters brainstem and effects the reticular activating system

Why does the seizure stop?

• hyperpolarization subsides

• electrical discharges terminate• “Due to reflex inhibition, loss of

synchrony, neuronal exhaustion, alteration of the local balance of ACH and GABA in favor of inhibition” Rosen’s p. 1446

How are seizures confirmed?

• Electroencephalography (EEG)

Clinical Features

Primary Seizures

Simple Partial

• Specific function of initiating neurons determines the clinical manifestation of the ictal event

Features

• motor

• somato-sensory• special sensory

• autonomic• psychic

• focal clonic movements

• paresthesias• visual, auditory,

olfactory, gustatory• sweating, flushing• sense of déjà vu,

fear

Complex Partial

• Impairment but not loss of consciousness

• Amnesia, but may be responsive during seizure

• Automatisms: lip smacking, swallowing

• Aura: taste, smell, visual

• Maintain high cortical functioning

Generalized Seizures

• Loss of consciousness

• No aura

• May have a vague prodrome or dysphoric state prior

• Convulsive or Non-Convulsive

Convulsive Generalized Seizures

• ‘Grand-Mal’

• generalized hypertonus

• “rhythmic, violent contractions of multiple, bilateral, symmetric muscle groups”

• posterior shoulder dislocation, # thoracic spine vertebral bodies

• transient apnea

• incontinence: urinary > fecal

• followed by postictal state, headache, drowsiness that may last for hours

Nonconvulsive Generalized Seizures

• Absence or ‘Petit mal’

• Myoclonic

• Tonic

• Atonic

Absence Seizures

• Begin in childhood

• Sudden cessation of normal, conscious activity

• dissociative state lasting secs to min

• sudden termination of such state

• No postictal state

Myoclonic and Tonic Seizures

• Sudden, brief muscle group contractions

• If entire body involved: ‘drop attack’

• No postictal state

Atonic Seizure

• Loss of muscle tone

• May cause ‘drop attack’

Clinical Features

Secondary seizures

Caused by Metabolic Derangements

Hypoglycemia

• Most common metabolic cause of seizure activity

• Plasma glucose level <45mg/dL or 2.5mmol/L

• Extremes of age particularly susceptible

Ketotic Hypoglycemia

• Most common cause of childhood hypoglycemia

• Small for age kids• “Episodes of symptomatic hypoglycemia

during periods of caloric deprivation or under provocation by a ketogenic diet” Rosen’s p.1448

• Hypoglycemia and ketonuria• Dietary management

Osmolar Disorders

• Hyponatremia Na<120mmol/l

• Rate of decline is factor

• Treat slowly: increase Na by 0.5mmol/h

• Treat with 3% NaCl only if seizing

Osmolar Disorders

• Hypernatremia Na>160mmol/l

• Usually due to dehydrating illness

• Correct slowly

others• Hypocalcemia, Hypoparathyroidism• Hypomagnesemia• Nonketotic Hyperosmolar Hyperglycemia• Uremic Encephalopathy in renal failure• Hypothyroidism• Thyrotoxicosis• High anion gap acidosis• Hypertensive Encephalopathy• Acute Intermittent Porphyria

Infectious Causes

Infectious Causes

• Independent of febrile mechanism

• Usually CNS infections

Meningitis

• 15-40% of pts will seize

• More common at extremes of age

• Partial seizures > general

Meningoencephalitides

• Usually partial motor

• Postictal paralysis common esp. with herpetic infections

• Presenting sign in 1/3 of cerebral abscesses

Other

• Neurocysticercosis: parasite in immigrants from Latin America

• Latent syphilis

• Primary HIV disease and its infections

Drugs and Toxins

Drugs and Toxins• Antimicrobials• Neuroleptics• Sympathomimetics• Anticholinergics:

tricyclics, antihistamines

• cocaine• amphetamines• PCP

• Withdrawal:alcohol, BZD

• Overdose: ASA,theophylline, INH, Li, phenytoin

• Insecticides• Rodenticides• hydrocarbons

Cocaine induced Seizures

• Fever

• Rhabdomyolysis

• Arrhythmias

• Rx: BZD

EtOH Associated seizures

• Overdose

• Withdrawal

• Must r/o other causes

• Rx: BZD

• “substitute for the GABA enhancing effect of ethanol in the CNS” Rosen’s p.1449

Trauma Associated Seizures

Early

• <1 week post injury

• Epi + Sub dural hematomas

• Intracerebral Hemorrhage

• SAH

Late

• >1week post injury

• 1 year after significant head trauma, incidence of seizures is increased 12 x

• Severity of head injury is directly proportional to likelihood of seizures

• 10-15% will develop post traumatic epilepsy

Malignancy Associated Seizures

Malignancy Associated Seizures

• Primary tumors or metastases

• Usually partial with secondary generalization

Vasculitic Associated Seizures

Vasculitic Associated Seizures

• Systemic Lupus Erythematosus

• Polyarteritis Nodosa

• Complex partial

Other Neurologic Causes

• Stroke: incidence of seizures 4-15%

• Incidence of epilepsy post stroke is 4-9%

• Aneurysm and AVM

• Migrainous activation of an epileptic focus

• MS - 5% of patients

• Neurofibromatosis: café au lait, axillary freckling

• Tuberous Sclerosis: ash leaf spots, adenoma sebaceum

• Sturge-Weber syndrome: facial port wine nevus

• Alzheimer’s Dementia

Gestational Seizures

Gestational Seizures

• Gestational epilepsy

• Hormonal and metabolic changes unmask underlying epilepsy

• Eclampsia

• Seizures, hypertension, proteinuria, edema, coma

Pseudoseizures

Pseudoseizures

• Functional• Not the result of abnormal CNS

electrical activity• “lower intelligence and have an

underlying anxiety or hysterical personality disorder” Rosen’s P.1450

• ED evaluation is difficult• Can co-exist with seizures

Post ictal state

Postictal State

• Decreased level of arousal and consciousness

• Amnesia

• Headache

• Minutes to hours

• Must monitor and investigate altered mental status after a seizure

• Airway, pulse oximetry, blood glucose, cardiac monitoring

• Monitor until recovery

Postictal Paralysis

• “Todd’s Paralysis”

• May follow generalized or complex partial

• Focal motor deficit

• Lasts up to 24h

• High likelihood of an underlying structural cause

Neurogenic Pulmonary Edema

• Common, but often subclinical feature of any CNS insult

• “centrally mediated sympathetic discharge and generalized vasoconstriction, coupled with increased pulmonary capillary membrane permeability” Rosen’s p.1451

• May appear like aspiration pneumonia• Ventilatory support if necessary

Emergency Department Management

http://www.seizurerobots.com/

Diagnosis

• Hx of ictal event, known or potential precipitants and exposures and PMHx

• Thorough Physical Examination

History taking

• 1. Hx of seizures?

• 2. If no, was the event witnessed?

Differential Diagnosis

• Syncope• Hyperventilation• Breath holding• Toxic state: DTs• Metabolic state:

hypoglycemia

• TIA• Narcolepsy• Movement disorders• Psychogenic illness

COLD

• Character-type of seizure

• Onset-when, what was pt doing

• Location-where

• Duration-how long

seizure

• Abrupt onset-no aura

• Brief duration-usually <120s

• Altered mental status

• Purposeless activity

• Unprovoked

• Postictal state

Previous Seizures

• Focus on:

• Anticonvusant level, med noncompliance, med change

• Drugs, etoh

• Drug-drug interactions

• Change in ictal pattern

• Cause for lowered seizure threshold

Physical Examination• Medic alert• Hypertension,

tachycardia, tachypnea• Tongue biting• Shoulder dislocation• Back pain• Urinary or fecal

incontinence• Neurocutaneous signs

Lab

• Stat glucose is vital• in neurologically N, healthy pt: little

value• Medically ill: labs• Anticonvulsant levels• Tox screen if suspicion of abuse• BHCG if eclampsia suspected• Meningitis or SAH: LP if no inc. ICP

Lab abnormalities

• Hypoglycemia- cause/effect?

• Lactic Acidosis

• Rhabdomyolysis

First time seizure

• Never assume it is idiopathic

• 46% will need admission

• Focus on medical, toxicologic, neurologic cause

First time seizure:CT scan in the department?

• if you suspect a ‘serious structural lesion’

Suspect a ‘serious structural lesion’?

• New focal deficit• Persistent altered

metal status• Fever• Trauma• Persistent headache

• History of cancer• Anticoagulant use• Suspicion or known

AIDS• Age > 40• Partial onset seizure• Increased ICP

First time Seizure

• Scan as an outpatient if:

• Complete recovery and no apparent cause of seizure found

• If follow up questionable: scan in ED

Recurrent Seizures

• Initial stabilization same• Most common cause is med noncompliance• Must measure anticonvulsant levels• Supratherapeutic levels of phenytoin and

carbamazepine may cause seizures• Be careful about giving loading dose before

checking a serum level• Hx and PE

Known or Recurrent Epilepsy:CT scan in dept?

• Same considerations as with first time seizure

• Also:

• Change in seizure pattern

• Prolonged post-ictal state

Management

Stabilization

• Monitored bed

• Oxygen

• Pulse oximetry

• Heart rate monitor, BP cuff

• IV access

Airway

• Anticipatory

• Gag reflex suppressed

• +/- vomiting

• Left lateral decubitus

• ?Bite block to prevent tongue biting and to allow suctioning

• +/- nasopharyngeal airway

Apneic or airway threat

• If O2 sat<90% or inability to protect airway

• Endotracheally intubate

• BZD for induction

• If trismus, may need neuromuscular blockade

Think:

• If seizure lasts longer than 5 minutes it is unlikely to stop

• should start thinking about status epilepticus

• Treat ASAP

stolen from Dr. S. Bernbaum

Drug Rx of SE

• Starting Rx ASAP has been correlated with a better response rate to drug Rx, and lower morbidity– Lowenstein DH, Alldredge BK

Neurology 1993 (43): 483-8• < 30 min - 80% stopped• > 120 min - < 40% stopped

but - retrospective review; • ? groups comparable

Reversible causes

• Hypoglycemia

• Isoniazid

• Eclampsia

• Dextrose

• Pyridoxine

• Magnesium

Medications

• First Line: Benzodiazepines IV• Directly enhance GABA-mediated neuronal

inhibition• affect both clinical and electrical

manifestations of seizures • Terminate seizure activity in 75-90% of pts• May cause hypotension and respiratory

depression

Lorazepam (Ativan)

• 0.1mg/kg/IV

• 1-2mg/min

• Up to 10mg

• Peds: 0.05mg to 0.1mg/kg IV

• Longer duration of seizure suppression

Diazepam (Valium)

• 0.2mg/kg IV

• at 2mg/min

• up to 20mg

• Peds: 0.2-0.5mg/kg IV/IO/ET or 0.5-1.0mg PR

• Works well rectally, endotracheally, interosseously

Midazolam (Versed)

• 2.5-5.0mg IV

• 0.2mg/kg IM

• Peds: 0.15mg/kg IV then 2-10ug/kg/min

• Works well IM

Second line

• anticonvulsants

Phenytoin (Dilantin)

• suppresses neuronal recruitment

• does not suppress electrical activity at the ictogenic focus

• No sedation or resp depression

• May cause hypotension if given rapid IV

• Takes 30min to infuse

Phenytoin

• 20mg/kg IV at <50mg/min

• Peds: 20mg/kg IV at 1mg/kg/min

• If pt subtherapeutic:

• May give loading dose IV or PO to boost serum levels

Fosphenytoin

• Phenytoin prodrug

• Water soluble

• May be administered quickly

• Better tolerated, more safe, more stable than phenytoin

• More difficult to monitor, delayed hypotension

Fosphenytoin

• 15-20 PE/kg at 100-150mg PE/min

• PE: phenytoin sodium equivalent

• Peds: not established

Phenobarbital

• third-line

• in pediatrics is second-line therapy

• CNS depressant decreases both ictal and physiologic cortical electrical activity

• anticipate: sedation and depression of respiratory drive and BP

Phenobarbital

• 20mg/kg IV at 60-100mg/min

• Ped: same

• May give as IM loading dose

Eclampsia

• Magnesium is not an anticonvulsant• 4-6g IV followed by 1-2g/h infusion with

hydralazine• Unexplained efficacy• BZD effective short term• Phenytoin may be efficacious-teratogenic• Should consult Obs/Gyn or have established

protocol

stolen from Dr. S. Bernbuam

Status Epilepticus• continuous or rapidly repeating seizures• no consensus on exact definition - “abn prolonged”

– “no recovery between attacks”– “20-30 min” --> injury to CNS neurons– more practical definition: since isolated tonic -

clonic seizures rarely last > few minutes ... consider Status if sz > 5 min or 2 discrete sz with no regaining of consciousness between

• vs. serial sz - close together - regained consciousness in between

stolen from Dr. S. Bernbaum

CNS damage can occur

• uncontrolled neuronal firing

• excess glutamate (exitatory NT)

• this sustained high influx of calcium ions into neurons leads to cell death (“excitotoxicity”)

Management of ‘Status’

• Valproate: PR, increases GABA conc.

• Valproate IV 25mg/kg in future

• Barbiturate Coma

Barbiturate coma• works well but suppresses all brainstem function• Neuro, ICU consults recommended: resp arrest,

myocardial depression, hypotension, dec ICP, dec cerebral perfusion

• phenobarbital 20mg/kg IV at 60mg/min• pentobarbital 10-15mg/kg IV load then 0.5-

1.0mg/kg/hr infusion• Need intubation and ventilatory support, cardiac

monitoring, invasive hemodynamic monitoring, +/- pressors = ICU

Midazolam and Propofol

• midazolam 0.2mg/kg bolus then 0.045mg/kg/h infusion

• propofol 1mg/kg bolus then 2mg/kg/h infusion

• Hypotension

• Intubation and ICU

Isoflurane Anaesthesia

• Final alternative in refractory status

• Anaesthesia involved

• BZD induction agent + lidocaine pretreatment

• ICU

Not moving = Not seizing?

• NO

• Visual manifestations of convulsive ictus are extinguished by neuromuscular blockade.

• Need electroencephalographic monitoring arranged

Disposition

• Individualized for pt.

• Home, home with GP follow, neuro consult in ED, neuro follow up

• Shouldn’t drive for 6 months

• Law varies from province to province

Summary

• Several types of and many causes for seizures

• History is important• First seizure likely needs imaging• Treat immediately• If seizure lasts >5min think status

epilepticus• “Sub” areas to consider: febrile seizures,

status epilepticus

References• Dorland’s Pocket Medical Dictionary 25th Ed. 1995 W.B.

Saunders Company• Neuroimaging in the emergency department patient presenting

with seizures, Neurology 47:26, 1996.• Rosen’s Emergency Medicine 5th edition, Marx et al. Mosby,

Toronto, 2002• Emergency Medicine Secrets 3rd Ed. Markovchick et al. Hanley

& Belfus, Philadelphia 2003• Seizures in the Emergency Department, Nicholl J.S. et al

http://www.emedicine.com/neuro/topic694.htm• Status Epilepticus, Stan Bernbaum MD CCFP-EM, May 31,

2001, http://www.calgaryhealthregion.ca/em/