EM guidemap - Seizures in adults

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Introduction

Definitions and general principles

History Examination

Medical decision-making

Appendix
Introduction

- this guidemap is primarily focused on the clinical evaluation and management of generalized convulsive seizures in adults in an ED setting, and it does not focus any attention on the management of the other major types of seizure disorder eg. absence seizures, simple and complex partial seizures

- see the status epilepticus guidemap for more details on drug therapy for actively seizing patients
 
Definitions and general principles

Definition of a seizure

- a seizure is defined as a transient disturbance of normal neurological function caused by an abnormal brain neuronal discharge

Definition of epilepsy

- epilepsy is a clinical condition in which the patient suffers recurrent seizures

- idiopathic epilepsy, for which no specific cause can be established, accounts for ~ 75% of seizure disorders

- epilepsy is not referable to recurrent episodes of reactive seizures due to conditions like hypoglycemia, cocaine abuse and alcohol related/withdrawal seizures

Types of seizures

- a seizure can occur due to an identifiable neurological disorder, and it's then labelled symptomatic or provoked

- an acute symptomatic seizure is a seizure that occurs within one week of a neurological insult, while a remote symptomatic seizure is used to describe a symptomatic seizure that occurs > 1 week after a neurological insult that is known to predispose a person to epilepsy

- a seizure can be due to unknown causes in patients with no known neurological disorder, and it is then labelled cryptogenic or idiopathic or unprovoked

(* cryptogenic is the preferred term and recent ILAE guidelines discourage use of the term idiopathic for seizures of unknown etiology)

- reactive seizures can simply be due to electrical stimulation of the brain (electroconvulsive therapy), exposure to pro-convulsant drugs, profound metabolic disturbances, and direct blunt head trauma => therefore, reactive seizures are not always classified as true symptomatic seizures

(* there is no consistency in the use of the term reactive seizure, because some clinicians arbitrarily define some types of symptomatic seizures as reactive seizures, while other clinicians use the two terms interchangeably)

Classification of seizures

- two major types => generalized and partial

Generalized seizures

- generalized seizures can be primary, or secondary to another type of seizure (eg. complex partial seizure) which generalizes to involve the entire cerebral cortex

- primary generalized seizures start with a loss of consciousness  due to diffuse bilateral brain involvement; the loss of consciousness is profound and the patients are deeply unresponsive

- by definition, primary generalized seizures do not start with an aura

(* the presence of an aura suggests a secondary generalized seizure due to evolution of a focal seizure)

- primary generalized seizures are divided into two major types => convulsive seizures and non-convulsive seizures (absence seizures)

- there are 6 major types of generalized seizure => tonic-clonic (grand mal), absence (petit mal), tonic, clonic, myoclonic and atonic

(* although clonic and tonic and atonic and myoclonic seizures are motor-type seizures, they are sometimes classified as non-convulsive seizures and are grouped together with absence seizures; they are often seen in patients who also suffer from absence seizures)

Convulsive seizures

- tonic-clonic (grand mal) seizures represent the most frequent type of generalized convulsive seizure requiring emergent treatment in an ED

- a tonic-clonic seizure is typified by the grand mal seizure in which the patient suddenly loses consciousness and becomes stiff with generalized hypertonus (10 - 30 seconds) => symmetric, bilateral rhythmic muscle contractions of the face, trunk and limb muscles (30 - 60 seconds) => postictal state (decreased level of arousal and responsiveness) => slow recovery with variables degrees of lethargy and headache and myalgia

Absence seizures

- absence seizures are divided into two types => typical and atypical

- typical absence seizures are characterized by sudden behavioural arrest and unresponsiveness (blank stare) that may be accompanied by subtle eyelid blinking or facial clonus, and very rarely automatisms

(* complex partial seizures also produce automatisms, which are usually more complex and the whole seizure event usually lasts > 30 seconds with an additional element of postictal confusion)

- typical absence seizures usually last < 10 seconds and are not associated with an aura or post-ictal state

- atypical absence seizures usually last > 10 seconds, begin and end more gradually, and produce less marked altered LOC, and are more likely to be associated with tonic, clonic or myoclonic events

- absence seizures usually commence in childhood and do not persist beyond 20 years, and they are not common seizure-presentations in adults => if absence seizures occur in later life - search for metabolic (hypocalcemia, hyponatremia) or pharmacologic (benzodiazepine withdrawal) etiologies

- tonic seizures are characterized by sustained, non-vibratory contractions of the axial musculature usually involving flexion of the upper limbs and flexion or extension of the lower limbs + variable alteration of consciousness

- tonic seizures are usually abrupt in onset and usually last < 10 seconds and nearly always < 60 seconds, and often occur in clusters when awakening from sleep

- tonic seizures are poorly understood and are most common in Lennox-Gastaut's syndrome

- tonic seizures may mimic the tonic spasms seen in multiple sclerosis, or mimic decerebrate posturing or paroxysmal dystonia

- atonic seizures (drop attacks) are usually characterized by abrupt loss of muscle tone + variable LOC and they last a few seconds => may cause sudden, unexpected falls

- atonic seizures may be limited to the neck muscles => head drop; atonic seizures may be preceded by a few myoclonic jerks

Partial seizures

- partial seizures are focal seizures associated with electrical activity in one part of one cerebral hemisphere

- partial seizures may be simple (consciousness preserved) or complex (consciouness impaired)

- a simple partial seizure is not associated with any altered LOC and the pattern usually reflects the electrical discharge of a focus in the contralateral cerebral cortex

- about 50% of patients have abnormal CT scans

- the most common cause of simple partial seizures in children are congenital malformations and low-grade glioma; the most cause in young adults is mesial temporal sclerosis; the most common cause in elderly adults is cerebrovascular disease

- simple partial seizures may manifest with focal motor signs, somatosensory or special sensory symptoms, autonomic or psychic symptoms

- motor signs include focal clonic movements, tonic posturing, sudden movements of the eyes or head or body to one side (versions), or sudden arrest of movement or speech; the focal motor signs may occasionally spread to involve contiguous areas of the motor cortex (jacksonian march)

- sensory symptoms include somatosensory, visual, auditory, olfactory, gustatory or vertiginous symptoms

- autonomic symptoms include epigastric rising sensation, pallor, sweating, flushing, piloerection and pupilllary dilatation

- psychic symptoms include dysmnesic phenomena like deja vu and jamais vu, dreamy states, mental distortions of time and space, forced thinking, affective symptoms like fear or paranoia, or an abnormal sense of depersonalization or dissociation

- if a simple partial seizure progresses to a generalized convulsive seizure, the initial focal symptoms are referred to as an aura

- a complex partial seizure is a focal seizure that is associated with an impaired LOC and it's the most common type of acquired epileptic seizure in adults

(* LOC is impaired and not lost => the patient may appear awake, but is not in contact with others in the enviroment, and the patient does not respond normally to questions or instructions => the patient appears "out-of-touch" for 30 - 90 seconds)

- a complex partial seizure can evolve from a simple partial seizure, or there may be impaired LOC from the onset => the patient manifests an initial wide-eyed motionless stare or behavioural arrest of activity, which may be accompanied by automatisms (purposeless , coordinated, repetitive motor activities) eg. lip smacking, chewing, fidgeting hand movements or hand wringing, fiddling with clothes, snapping or tapping the fingers, repetitive verbal automatisms, and automatic behaviour (complex motor acts) +/- dystonic posturing of the contralateral limb

- the hallmark of complex partial seizures is the fact that the patient initially has impaired consciousness with decreased awareness of self and the enviroment, and also amnesia for the event afterwards

- the patient may still be able to perform complex motor acts during the complex partial seizure eg. driving an automobile, riding a bicycle, washing dishes

- a postictal state of confusion and disorientation is common for several minutes, and the patient may appear slightly confused or drowsy for hours thereafter

- a complex partial seizure can also evolve into a generalized convulsive seizure

- about 70% of complex partial seizures arise in the temporal lobe (mainly in the mesial temporal lobe); frontal lobe origin is less common, and parietal lobe and occipital lobe least common => the type of aura depends on the site of origin

- temporal lobe auras often begin with an epigastric rising sensation, fear, sense of unreality or deja vu or jamais vu or depersonalization/dissociation feelings, or olfactory or gustatory or auditory hallucinations; parietal lobe auras involve electrical sensations or paresthesias and occipital lobe auras may involve visual changes eg. colored lines, spots, shapes or temporary loss of vision or visual illusions (macropsia, micropsia, metamorphosia)

- frontal lobe complex partial seizures are more abrupt in onset and termination, shorter in duration (often < 30 seconds) and often involve bizarre motor movements from the onset (asynchronous limb movements, right-to-left head rolling, pelvic thrusting, bicycling movements, wild thrashing) accompanied by laughter/crying; they are not usually associated with an initial altered responsiveness or a postictal state; they are more prone to rapidly evolve into generalized seizures
 
History

- the history should first focus on establishing whether the "apparent" seizure event was a "true" seizure, and whether the patient has a previous history of similar seizures

- the major differential diagnosis of a generalized seizure is syncope, and a physician should seek clarifying information that helps distinguish a generalized seizure from a syncopal event

- pertinent questions include historical information about:-

Presence of premonitory symptoms

- some epileptic patients have vague, non-specific premonitory symptoms in the minutes-hours prior to the seizure (irritability, malaise, sense of foreboding, mood change, changes in appetite, dizziness, headache)

- vaso-vagal or postural syncope patients may have prolonged symptoms of lightheadedness ("graying out" or wooziness or dimness of vision) preceding the syncope if they are standing or sitting erect, or they may only develop lightheadedness immediately preceding the syncopal event

Presence of a preceding aura or purposeless movements

Was the episode preceded by localized sensory or motor or psychic phenomena?

How long did they last and were they "marching" in type?

Was the episode preceded by impaired consciousness with blank staring spells?

Were the blank staring spells associated with automatisms?

Did the state of impaired consciousness evolve into a state of total unconsciousness coincident with the onset of generalized convulsions?

- an aura does not always precede a seizure and its absence is not significant in excluding a seizure; however, the presence of an aura suggests a partial (focal) seizure that subsequently evolved into a generalized seizure

- patients with syncopal events due to postural or vaso-vagal syncope may have non-specific aural symptoms of lightheadeness ("near-syncope") immediately preceding the event +/- awareness of incipient syncope, while a patient having a true seizure may have sensory auras that are neurological in type (sensory symptoms - paresthesia, flashes of light; psychiatric symptoms - fear, bizarre olfactory or gustatory hallucinations; disturbances of memory - deja vu or jamie vu phenomena; autonomic symptoms - epigastric rising sensation; simple motor symptoms - eyelid or limb muscle twitching, or adversive eye movements; complex motor symptoms - fiddling with buttons or clothing, verbally repeating short phrases)

- a sensory aura usually only lasts a few seconds and longer lasting aural symptoms suggest the possibility of other disorders such as migraine (especially if the aural symptoms are "marching" in pattern and last longer than 30 seconds)

- purposeless movements (automatisms - blinking, lip smacking, finger fiddling) immediately preceding the generalized seizure suggests a simple or complex partial seizure that evolved into a generalized convulsive seizure

- the sequence of impaired consciousness evolving into a state of generalized convulsions with total loss of consciousness suggests the evolution of complex partial seizures => secondary generalized convulsive seizures

Abruptness of onset

Did the generalized seizure start abruptly without any aura?

- most generalized seizures start abruptly without any aura, and the sudden onset of tonic stiffening and/or clonic rhythmic movements may be the first manifestation of the seizure

- focal seizures that evolve into generalized convulsive seizures may produce focal myoclonic jerking (eg. unilateral twitching of a limb or face or eyelids) just prior to onset of the major generalized seizure

- some seizures start with versive eye or head movements towards the one side, or a "whooshing" vocalization cry due to a forced expiration following simultaneous contraction of the diaphragm and the abdominal muscles against a spasmodic glottis +/- upward deviation of the eyes +/- pupillary dilatation

- syncopal patients who develop syncopal seizures first "pass-out" and then develop spasmodic motor jerking; motor jerking is rarely seen at the exact moment of syncope onset

Duration of the seizure

How long did the muscle contractions last?

- the entire phase of tonic-clonic motor seizures usually lasts 90 - 120 seconds, and the seizure usually stops abruptly after a final tonic convulsion

- syncope can be associated with short-lived convulsions, and the syncopal seizures usually only last a few seconds (rarely > 30 seconds)

Pattern of the seizure

Did the patient have generalized stiffness and/or rhythmic muscle contractions?

Were all the limbs equally involved with synchronous muscle contractions, or were the muscle contractions asymmetric and/or asynchronous?

Did the patient bite his tongue or become incontinent of urine or stools?

- the history should include complete details about the seizure pattern:-  tonic vs tonic-clonic seizures, involvement of one or all 4 limbs, synchronous rhythmic jerking convulsions vs sporadic irregular jerking movements

- there are a variety of generalized seizure patterns (eg. tonic-clonic, pure tonic, pure clonic), and the "classic" generalized convulsive seizure pattern starts with a tonic phase that is followed shortly thereafter by a clonic phase => the tonic phase usually causes stiffening of the body for a variable period => rhythmic clonic movements of all 4 limbs +/- twiching of facial and eyelid muscles + pupillary dilatation

- syncopal seizures usually consist of irregular (non-rhythmical) jerking movements of one-or-more limbs rather than synchronous, rhythmical clonic movements of all 4 limbs (as seen in true generalized seizures)

- bizarre, purposeful or markedly asynchronous movements suggest psychogenic seizures (rarely frontal lobe complex partial seizures)

- tongue biting may occur during a generalized convulsive seizure and the tongue bite patterns are usually seen on the lateral borders of the tongue; tongue biting is far less common during a syncopal seizure and it is usually situated on the anterior tongue

- urinary incontinence is far more common during a true generalized seizure than a syncopal seizure, although incontinence of urine is not a consistent finding in any type of seizure

Rate of recovery, and presence and duration of a post-ictal state

Did the patient recover rapidly or slowly?

Did the patient remain confused or disoriented for many minutes after the motor seizure?

Did the patient become sleepy for minutes-hours after the event?

Was there any localized unilateral motor weakness (Todd's paralysis) after the event?

- the patient usually remains deeply unresponsive for many minutes after a true seizure, and a post-ictal state of impaired consciousness may last 20 - 30 minutes => sleepiness and confusion +/- post-ictal headache and myalgia may variably follow the immediate post-ictal period of "variably-deep" unresponsiveness

- the presence of Todd's paralysis suggests a true secondary seizure, rather than a syncopal seizure

- a syncopal seizure patient usually recovers consciousness rapidly (within 15 - 60 seconds) and the patient does not usually manifest disproportionate sleepiness or confusion in the post-ictal period

- both convulsive syncope and true generalized seizure patients have retrograde amnesia for the seizure-event, and an accurate recollection of the seizure-event suggests psychogenic seizures or some other convulsive-type disorder eg. strychnine poisoning or tetanus or myoclonic seizures

Precipitating factors

Was there an immediate precipitating event?

Any recent illness?

Any associated neurological symptoms?

Any recent head trauma or drug ingestion?

- epileptic seizures may be precipitated by photic stimuli (bright or flashing lights), loud music, strong emotions, intense exercise, hyperventilation or lack of sleep

- symptomatic seizures may be precipitated by an underlying metabolic abnormality (eg. hypoglycemia or hyponatremia) or drug intoxication (eg. theophylline, tricyclic antidepressants, cocaine) or drug withdrawal (alcohol- sedative-hypnotics), head trauma or an underlying neurological disorder (eg. degenerative neurological disorder or stroke or brain surgery)

- the presence of a headache preceding the seizure suggests a SAH, or ICH, or cerebral venous sinus thrombosis, or carbon monoxide poisoning

- the presence of anteceding/associated focal neurological signs suggests a CVA

- the presence of an antecedent febrile illness suggests meningitis, encephalitis, a brain abscess or a hyperpyrexia syndrome

- antecedent emotional distress suggests vaso-vagal syncope or psychogenic seizures; situational syncope is suggested by the nature of the immediate preceding event (eg. coughing, micturition, weightlifting, stretching)

History of previous seizures or "spells"

- similar previous generalized seizures strongly suggests epilepsy

- a history of brief "absences" (short-lived staring spells of blank inattention +/- brief automatisms) suggests simple partial seizures; "acting-out" or "out-of-touch" spells involving more elaborate behaviourisms suggest complex partial seizures; a history of unexplained injuries occurring during "blackouts" or sleep, or unexplained nocturnal enuresis or encopresis or tongue-biting suggests previous generalized seizures

Risk factors for seizures and any underlying medical problems

The most common risk factor for recurrent seizures in an epileptic patient is anticonvulsant medication non-compliance

- therefore, inquire about a previous history of epileptic seizures and the regularity of use of anticonvulsant medications

- some other risk factors for seizures include:-

Evidence of secondary injury

- injury can result from a fall if the seizure occurred when the patient was standing, and the pattern of injury cannot differentiate a generalized seizure from a syncopal event

- however, certain injuries strongly suggest a true generalized seizure eg. posterior shoulder or jaw dislocation
 

Differentiating seizure from syncope
Feature Syncope Seizure
Aura Absent Rarely present
Antecedent "dizziness" prior to event Sometimes present Absent
Color at onset of event Sometimes pale Sometimes florid/purple
Jerking movements Infrequent and short-lived (seconds) Common and long-lasting (1 - 2 minutes)
Pattern of convulsions Uncoordinated myoclonic jerks and twitches - after LOC Generalized tonic and/or clonic movements - coincident with LOC
Forced conjugate deviation of eyes or head Absent Sometimes present
Tongue biting - lateral Absent Common
Urinary incontinence Rare Common
Duration of event Seconds Minutes
Prolonged disorientation or sleepiness after event Absent-rare Present
Increase in serum CK or lactate Absent Present
Todd's paralysis Absent May be present

 
Examination

- pay strict attention to the vital signs and LOC after the seizure ceases

- a high temperature suggests the possibility of CNS infection or a hyperpyrexia syndrome (neuroleptic malignant syndrome, heat stroke, thyroid storm, sympathomimetic or anticholinergic drug intoxication); a mildly elevated temperature can be secondary to the generalized convulsions

- persistent hypertension suggests the possibility of hypertensive encephalopathy or a hyperadrenergic crises

- hypertension + bradycardia suggests an intracranial catastrophe producing a markedly increased ICP or a rapidly expanding posterior fossa lesion (eg. cerebellar bleed) compressing the medulla

- persistent tachycardia suggests a sympathomimetic or anticholinergic drug overdose, or a hyperadrenergic state (eg, thyroid storm, pheochromocytoma, MAOI interaction, neuroleptic malignant syndrome)

- temporary tachypnea and Kussmaul breathing may follow a seizure (due to the cumulative seizure-induced lacticacidosis); however, persistent tachypnea and Kussmaul breathing suggests an underlying metabolic acidosis (eg. DKA, ethylene glycol, methanol or cyanide poisoning)

- a failure of the LOC to progressively "lighten" after the seizure ceases suggests the possibility of non-convulsive status epilepticus, drug overdose, a metabolic coma, or intracranial pathology causing an increased ICP

- pupillary dilatation may occur during a seizure, but persistent  bilateral mydriasis after the seizure ends suggests anticholinergic or sympathomimetic drug overdose

- an unilateral, unresponsive mydriasis suggests a space-occupying supratentorial lesion and secondary transtentorial herniation (differential diagnosis of the "apparent" seizure = decerebrate posturing), or a SAH secondary to a leaking posterior communicating artery aneurysm, which has compressed the ipsilateral oculomotor nerve

- focal neurological signs could be due to Todds paralysis (secondary to the seizure), or be reflective of new or old intracranial pathology (eg. new or old stroke)

- check for skin, soft tissue and skeletal signs of primary or secondary trauma

(* posterior shoulder and jaw dislocations strongly suggest a seizure)

- clinical clues suggesting a specific underlying cause of seizures include:-

Medical decision-making

Actively seizing patient

- if the patient is actively seizing, the patient should be kept in the supine position and protected from further injury

- no attempt should be made to place a tongue blade or bite block in the patient's mouth to prevent the patient biting his tongue => the maneuver doesn't usually prevent tongue-biting and there is a considerable risk of iatrogenic injury

- passive oxygen administration by placing an oxygen mask over the patient's face (or via nasal cannulae inserted partway into pre-placed nasal airways) is advisable; however, bag-mask ventilation should be avoided because it increases the risk of gastric insufflation and secondary regurgitation and aspiration (ventilation of the lungs is not possible during the active seizure-phase anyway)

- if the patient starts to vomit immediately after the active seizure-phase, the patient should be placed in the lateral decubitus position to minimize the risk of aspiration

(* C-spine precautions should be maintained during turning if there is any chance of a cervical vertebrae fracture secondary to a fall)

A dextrostix should be rapidly performed to exclude the possibility of hypoglycemia

- empiric 50% glucose administration (2cc/kg) is advisable if the patient is hypoglycemic or if the dextrostix result is inconclusive; thiamine should always precede glucose if the patient is malnourished or an alcoholic

- if the patient seizes for longer than 2 minutes, an IV should be established => first-line anticonvulsant agents (benzodiazopines) should be administered if the generalized seizure persists for longer than 5 minutes => see the status epilepticus guidemap for more detailed information on anti-seizure drug use in actively seizing patients

- if the seizure last < 2 minutes => just observe the seizure and note whether there is any sign of seizure focality => focal seizures may mandate an emergency CT scan +/- long-term anticonvulsant therapy

- treat the underlying cause if the symptomatic seizures are secondary to an identified cause of seizures (eg. hypoglycemia, hyponatremia, hypocalcemia)

- treat the secondary complications of the seizure

- always consider, and manage, alternative causes of seizures/spells that can mimic generalized convulsive seizures

Differential diagnoses of spells/seizures

Features suggesting psychogenic seizures
  • only occur when people are present
  • asynchronous or out-of-phase or dramatic thrashing/flailing movements of the extremities
  • directed violence against other people may be present
  • violent (high-amplitude) side-to-side head or body movements
  • opisthotonic posturing
  • forward pelvic thrusting
  • geotropic eye movements or eyes always turned away from the examiner
  • intact corneal reflex and no pupillary dilatation
  • intact gag reflex
  • urinary incontinence and self-injury may rarely occur, fecal incontinence very rare
  • the patient may actively resist the examiner's attempts to open the eyes by lifting the upper eyelids
  • the patient may verbalize during the seizure
  • the patient is particularly responsive to gentle verbal suggestions encouraging "seizure-termination"
  • the patient is responsive to noxious stimuli eg. ammonia capsule held under the nose
  • serum prolactin levels do not rise and a metabolic acidosis does not occur
  • the patient can recall events occurring during the seizure
  • no post-ictal phase of unresponsiveness or confusion or lethargy
  • no positive response to anticonvulsant therapy

Seizure ceases spontaneously and the patient is alert with a normal neurological examination

- further management depends on whether the presenting seizure was a first-time seizure, or a recurrent seizure in an epileptic patient

Known seizure disorder

- if the seizure was a recurrent seizure in a patient with a known seizure disorder + seizure pattern is similar to previous seizures => only order serum anticonvulsant drug levels => administer an additional dose of anticonvulsant if the serum anticonvulsant level is sub-therapeutic

- a basic formula can be used to estimate the dose of required anticonvulsant

Dose of anticonvulsant (mg) = weight of patient (kg) x volume of distribution of the drug (L/kg) x [desired drug level - current drug level (mcg/ml)]

- volume of distribution for phenytoin and carbamazepine is 0.8, for phenobarbital 0.6, and for valproate 0.2

- if the patient's particular optimum serum drug level is unknown, reasonable target levels are the upper end of the usual therapeutic range => 15-20 mcg/ml for phenytoin, 15-40 mcg/ml for phenobarbital, and 70-100 mcg/ml for valproate

- if the serum anticonvulsant drug level is very low (eg. serum phenytoin level < 4mg/dl) => administer a full loading dose of the anticonvulsant (15-20 mg/kg phenytoin)

- IV loading can be performed with phenytoin, phenobarbital and valproate; alternatively, the oral loading dose can be spread out over a day eg. 400mg phenytoin every 2 - 4 hours

(* there is no universally agreed-upon approach to anticonvulsant drug loading => the disadvantage of giving the loading dose of phenytoin as a single oral loading dose is that it may induce nausea/vomiting and temporary neurotoxic effects eg. ataxia, nystagmus, somnolence; oral phenytoin loading at the appropriate daily maintenance dose, without a loading dose, will achieve a serum phenytoin level > 10 mg/L in 3 - 7 days; IV phenytoin loading will achieve therapeutic serum levels within minutes after completing the infusion; fosphenytoin is expensive and may only be appropriate in status epilepticus because there is a strong imperative to rapidly achieve therapeutic serum levels of phenytoin)

- if the seizure pattern is different to the usual pattern, or if the frequency of seizures has markedly increased => consult a neurologist and consider emergent neuroimaging +/- hospital admission

- if the seizure pattern is consistent with the usual pattern + serum levels of the appropriate anticonvulsant are in the therapeutic range => specific treatment may not be needed => patient can consult his neurologist electively for any necessary changes in drug therapy

-  if the seizure pattern is consistent with the usual pattern + serum levels of the appropriate anticonvulsant are in the sub-therapeutic range => consider whether there is an element of medication non-compliance, or whether other co-incidental factors may be at play eg. intercurrent illness, self-induction of liver enzymes, addition of other drugs that interfere with liver metabolism of the anticonvulsant, "bad" batch of anticonvulsant drugs, use of "out-of-date" or generic versions of the anticonvulsant drugs

First onset seizure

- there are no mandatory diagnostic or therapeutic imperatives if the patient has fully recovered from the seizure and the neurological examination is normal

- two minimalistic approaches with respect to diagnostic blood tests:- i) the only mandatory blood work is a serum glucose to exclude hypoglycemia in a patient with persistent altered LOC despite normal dextrostix testing or ii) a serum glucose + electrolytes + serum HCG in young females as a standard batch of tests (ACEP policy)

- some clinicians even order more comprehensive routine blood work(CBC, serum electrolytes, calcium, magnesium, BUN, Cr and liver function tests) in all first-onset seizure patients => other clinicians are more selective and only order comprehensive blood work if the patient is likely to have a metabolic abnormality (eg. history of renal or liver failure, CHF and chronic diuretic use, dialysis patient, malignancy and suspected hypercalcemia, previous thyroid or anterior neck surgery => suspected hypocalcemia)

- an urine drug screen is recommended if illicit drug use or an intentional drug overdose is suspected

- an ABG may be useful if an underlying metabolic acidosis is suspected, and a persistent anion gap acidosis suggests a methanol or ethylene glycol overdose, or carbon monoxide/cyanide/isoniazid/iron/salicylate poisoning

(* a lacticacidosis due to the motor convulsions usually normalizes within one hour of the seizure ending)

- if the patient is alert, rational and cooperative + high likelihood of patient-compliance + no recurrent seizure within 6 hours of seizure onset => arrange follow-up with a family physician or neurologist +/- arrange for an outpatient MRI and EEG while the patient is still in the ED

(* some neurologists think that an EEG is more sensitive if performed within 24 hours of a seizure => an early EEG may therefore routinely be warranted - prior to the patient been seen by the follow-up physician within a few days of the ED visit)

- there is no value in routinely doing an emergent CT scan in the ED setting, because a contrast MRI will still be required to be absolutely certain that there is no evidence of structural brain disease

Indications for performing an emergent CT scan in the ED

Indications for performing a LP in the ED Indications for performing an EEG in the ED Indications for consulation with a neurologist while the patient is in the ED ACEP guidelines for hospital admission Does the patient require to be treated with anticonvulsants as an outpatient?

- long-term anticonvulsant therapy is not required after the first seizure unless there is definite evidence of structural brain injury on neuroimaging (eg. CT scan)

(* focal seizures + normal CT scan  => it is questionable whether there is any need to initiate anticonvulsant therapy in the ED => the decision can be deferred to the patient's neurologist; positive structural lesion on CT scan eg. brain tumor => anticonvulsant therapy is indicated)

- the average risk of a recurrent seizure after the first onset seizure is 20 - 60%

(* the risk is 20% if the neurological examination is normal and the EEG is normal; the risk is higher if the patient has evidence of focal neurological disease + an abnormal EEG (60%) => however, the results of the EEG are not usually known at the time of ED presentation => the neurologist, at the time of outpatient follow-up, can decide whether to initiate outpatient anticonvulsant therapy based on a positive MRI and/or a positive EEG study; anxious patients may request anticonvulsant therapy pending performance of an outpatient EEG =>  anticonvulsant therapy can be prescribed and subsequently stopped if the EEG is normal)

- the risk of seizure recurrence is >70% if the patient has a history of two (or more) unprovoked seizures => anticonvulsant therapy is advisable after consultation with a neurologist => anticonvulsant drug loading can be performed by the IV or oral route

- the current recommendation for the treatment of epilepsy is monotherapy => common first-line drug choices for generalized convulsive seizures include phenytoin, carbamazepine and valproate; primidone and phenobarbital are sometimes also used as primary therapy; ethosuximide and valproate are used as first-line drugs for absence seizures

- newer drugs such as gabapentin, lamotrigine, topiramate, vigabatrin, and tiagabine are used as supplementary anticonvulsants for patients who do not respond to monotherapy with first-line drugs

- the patient should be advised not to drive an automobile until cleared by his family physician or neurologist, and to avoid operating dangerous machinery, working at heights or swimming (showering is recommended instead of bathing in a tub) => the patient should preferably be discharged with an accompanying responsible adult + with pre-arranged MRI/EEG and physician appointments
 
Appendix

 

Some causes of symptomatic seizures in adults
 Structural lesions
  • vascular lesion (aneurysm, AV malformation)
  • mass lesion (benign or malignant tumor)
  • traumatic brain lesion (including intraparenchymal, subarachnoid, subdural or epidural hemorrhage)
  • neurodegenerative diseases
  • congenital abnormalities
 Infection
  • meningitis
  • encephalitis
  • brain abscess
  • septic thrombophlebitis of cerebral vessels
 Metabolic disturbances
  • hypoglycemia/hyperglycemia
  • hypocalcemia/hypercalcemia
  • hyponatremia/hypernatremia
  • hypomagnesemia
  • hyperosmolar states
  • renal failure
  • liver failure
 Drugs and toxins
  • cocaine
  • amphetamines and other sympathomimetics
  • propanolol
  • phencyclidine/LSD
  • tricyclic antidepressants
  • theophylline
  • salicylates
  • antibiotics (penicillins)
  • INH, lithium
  • antihistamines, anticholinergic agents, antipsychotics drugs (haloperidol)
  • alcohol or sedative-hypnotic drug withdrawal
  • cyanide/carbon monoxide
  • strychnine, camphor, chlorinated hydrocarbons, organophosphate insecticides
  • local anesthetics - lidocaine, bupivacaine. procaine
  • general anesthetics - methohexital, ketamine, etomidate
  • hypo-osmolar parenteral solutions
 Miscellaneous
  • hypertensive encephalopathy
  • cerebral venous sinus thrombosis
  • dialysis dysequilibrium syndrome
  • vasculitis, TTP, porphyria, sickle cell disease, syphilis

 
Extensive list of drugs and toxins associated with seizures
Alcohols
  • ethanol
  • ethylene glycol
  • methanol
  • propylene glycol
Local anesthetics
  • bupivacaine
  • cocaine
  • lidocaine
  • procaine
  • tetracaine
General anesthetics
  • enflurane
  • etomidate
  • isoflurane
  • ketamine
  • methohexital
Antibiotics
  • cephalosporins
  • ciprofloxacin
  • gentamicin
  • imipenem/cilastin
  • isoniazid
  • metronidazole
  • nalidixic acid
  • norfloxacin
  • penicillins
Anticonvulsants
  • carbamazepine
  • ethhosuximide
  • phenytoin
  • valproic acid
Anticholinergics
  • atropine
  • cogentin
  • optic cyclopentolate
  • diphenhydramine
  • scopolamine
Cyclic antidepressants
  • amitryptyline
  • amoxapine
  • clomipramine
  • desmipramine
  • doxepin
  • imipramine
  • nortryptyline
  • protryptyline
  • trimipramine
Other anidepressants
  • bupropion
  • fluoxetine
  • marprotiline
  • mianserin
  • trazodone
Antifungals
  • amphotericin
  • miconazol
Antihistamines
  • astemizole
  • brompheneramine
  • chlorpheneramine
  • diphenhydramine
  • doxylamine
  • hydroxyzine
  • pyrilamine
Antineoplastics
  • bleomycin
  • busulphan
  • carmustine
  • chlorambucil
  • cisplatin
  • ctarabine
  • mechlorethamine
  • methotrexate
  • vinblastine
  • vincristine
Antiparasites
  • chloroquine
  • oxamniquine
  • purimethamine
Antivirals
  • acylocvir
  • amantidine
Asphyxiants
  • acetylene
  • butane
  • carbon dioxide
  • ethane
  • methane nitrogen
  • propane
 Cardiovascular agents
  • aprindine
  • digoxin
  • disopyramide
  • encainide
  • ergotamine
  • esmolol
  • flecainide
  • lidocaine
  • lorcainide
  • methyldopa
  • metoprolol
  • mexilitine
  • propafenone
  • propanolol
  • quinidine
  • tocainide
  • verapamil
Drugs of abuse
  • amphetamines
  • cocaine
  • lysergic acid
  • marijuana
  • methamphetamine
  • phencyclidine
Drug withdrawal
  • anticonvulsants
  • barbiturates
  • benzodiazepines
  • ethanol
  • others
Hypoglycemics
  • insulin
  • sulfonylureas
Hydrocarbons
  • acetone
  • benzene
  • camphor
  • ethyl ether
  • eucalyptus oil
  • methylene chloride
  • nitromethane
  • phenol
  • pine oil
  • toluene
  • tupentine oil
  • xylene
Immunosuppressives
  • azathioprine
  • cyclosporin
  • glucocorticosteroids
Inhalants
  • carbon monoxide
Insecticides
  • benzene hexachloride
  • carbamates
  • organophosphates
  • pyrethrins
  • rotenone
  • DEET
Metal chelators
  • deferoxamine
  • EDTA
  • penicillamine
Metals
  • aluminum
  • arsenic
  • bismuth salts
  • copper
  • iron
  • lead
  • mercury
Mushrooms
  • cyclopeptides
  • orellanine
  • monomethylhydrazine
  • muscimol-ibotenic acid
  • psilocybe
Neuroleptics
  • haloperidol
  • lithium carbonate
  • thiothixene
Neuromuscular blockers
  • atracurium
  • tubocurarine
NSIADs
  • ibuprofen
  • ketoprofen
  • mefanemic acid
  • naproxen
  • piroxicam
  • phenylbutazone
  • salicylates
 Opiods
  • alfentanil
  • fentanyl
  • meperidine
  • morphine
  • pentazocine
  • propoxyphene
  • sufentanil
Plants
  • akee (hypoglycins)
  • angel's trumpet (belladonna alkaloids)
  • azalea (gryanotoxin)
  • bleeding hearts (isoquiniline alkaloids)
  • carolina jasmine (gelsemium)
  • chinaberry
  • christmas rose (glycocides)
  • daffodil (narcissine, lycorine)
  • deadly nightshade (solanine alkaloids)
  • golden chain (quinolizidine alkaloids)
  • ground hemlock (taxus)
  • juniper (essential oils)
  • jimson weed (solanaceous alkaloids)
  • jerusalem cherry (solanine alkaloids)
  • mountain laurel (cytisine)
  • mistletoe
  • poison hemlock (conium maculatum)
  • rhododendron (grayanotoxin)
  • rhubarb (oxalic acid)
  • strychnine nux vomicus
  • tobacco (nicotine)
  • umbrella plant (essential oils)
  • water hemlock (cicutoxin)
  • yew (taxus)
Radiographic contrast media
  • diatrizoic acid
  • iopamidol
  • iothalamate
  • meglumine
  • metrizamide
  • metrizoate
Rodenticides
  • fluoroacetate
  • phosphorus
  • phosphine
  • strychnine
  • thallium
  • vacor
Skeletal muscle relaxants
  • baclofen
Sympathomimetics
  • albuterol
  • amphetamines
  • aminophenzole
  • caffeine
  • doxapram
  • ephedrine
  • etamivan
  • flurotyl
  • imidazolines
  • lobeline
  • methylphenidate
  • metrazole
  • phenylephrine
  • phenylpropanolamine
  • pseudoephrine
  • picrotoxin
  • prethcamide
  • terbutaline
  • theophylline
Vaccines
  • measles
  • pertussis
Miscellaneous
  • allopurinol
  • borates
  • cimetidine
  • colchicine
  • cyanide
  • cycloserine
  • dantrolene
  • disulfiram
  • ergonovine
  • ergot alkaloids
  • erythropoietin
  • famotidine
  • fluoride
  • hydrogen sulfide
  • levamisole
  • levodopa
  • levothyroxine
  • nicotine
  • pimozide
  • probenicid
  • prostagladins

Disclaimer: My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use.