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
Outline
• Definitions
• Classification of seizures
• Pathophysiology
• Clinical Features
• Postictal state
• Emergency Department Management
• Summary
Seizure
• “clinical manifestation of excessive, abnormal cortical neuron activity” Rosen’s p.1445
• Not a diagnosis but a series of signs and symptoms
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
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
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
• 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
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
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
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
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
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• Antimicrobials• Neuroleptics• Sympathomimetics• Anticholinergics:
tricyclics, antihistamines
• cocaine• amphetamines• PCP
• Withdrawal:alcohol, BZD
• Overdose: ASA,theophylline, INH, Li, phenytoin
• Insecticides• Rodenticides• hydrocarbons
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
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
• Primary tumors or metastases
• Usually partial with secondary generalization
Vasculitic Associated Seizures
• Systemic Lupus Erythematosus
• Polyarteritis Nodosa
• Complex partial
• 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 epilepsy
• Hormonal and metabolic changes unmask underlying epilepsy
• Eclampsia
• Seizures, hypertension, proteinuria, edema, coma
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
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
Diagnosis
• Hx of ictal event, known or potential precipitants and exposures and PMHx
• Thorough Physical Examination
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
First time seizure
• Never assume it is idiopathic
• 46% will need admission
• Focus on medical, toxicologic, neurologic cause
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
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
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
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
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/