Posttraumatic Seizures

Kan Ding and Ramon Diaz-Arrastia

GENERAL PRINCIPLES

Definition

A seizure (sz) is an abnormal excessive synchronous discharge of cortical neurons that can result in clinical manifestations such as sensations, alteration in behavior or consciousness, and/or body movements.

• Subclinical sz—“nonconvulsive sz”; sz activity seen on electroencephalogram (EEG) with no overt clinical features

• Simple partial sz (SPS)—focal sz without impairment of consciousness or awareness (i.e., intact memory)

• Complex partial sz (CPS)—focal sz with impaired attention, awareness, and/or consciousness (i.e., impaired memory)

• Generalized tonic–clonic sz (GTCS)—generalized tonic–clonic movements of the extremities associated with loss of consciousness (LOC); can be primarily generalized or secondarily generalized (from SPS or CPS)

A posttraumatic sz (PTS) refers to a sz after traumatic brain injury (TBI)

• Immediate szs or “concussive convulsions” are acute symptomatic szs that occur within 24 hours of TBI; not predictive of posttraumatic epilepsy (PTE) [1]

• Early PTS are acute symptomatic szs occurring within 1 week after TBI

• Late PTS occur more than 1 week after TBI

PTE refers to a disorder of recurrent, unprovoked, late PTS. The recurrent rate after a single late PTS is over 70%, so a single late PTS is sufficient for the diagnosis of PTE [1].

Epidemiology

• The prevalence of PTS in the United States is 2% to more than 50% depending on cohort and injury severity [2,3].

• About 80% of first PTS occur within 2 years, 50% to 60% within 1 year, and 40% within 6 months of TBI [4].

• Early PTS occur in 2% to 17% of all patients with brain injuries, are more common in children, and correlate with TBI severity [2].

• The cumulative incidence of late PTS in the first 30 years after TBI is 2% for mild injuries, 4% for moderate injuries, 20% for severe closed head injuries, and more than 50% if the dura is penetrated [5,6]. The cumulative incidence of epilepsy in the general population is approximately 1.5% [4].

Pathophysiology

• Physiological mechanisms causing szs after TBI are not completely understood [7,8,9].

• Both focal and diffuse brain insults often coexist in TBI patients. Focal insults (contusions or intracranial hematomas) result in neighboring neural inflammation, gliosis, sprouting, and neurogenesis, which are felt to result in epileptogenesis [10]. Diffuse insults can result in injury to susceptible brain regions, such as the hippocampus. Injury can lead to atrophy and sclerosis; up to one-third of PTE is of temporal lobe origin [10].

DIAGNOSIS

Risk Factors

• For early PTS—younger age (especially less than 5 years), acute intracranial hemorrhage (ICH), acute subdural hematomas (SDH; in children), diffuse cerebral edema (in children), metal fragment retention, neurological deficits, depressed or linear skull fractures (in adults), and LOC or amnesia for greater than 30 minutes [2].

• For late PTS—age greater than 65 years, early PTS (in adults), SDH, brain contusion, alcoholism, penetrating injury, retained metal fragments, depressed skull fracture, posttraumatic amnesia greater than 24 hours, neurological deficits, brain tissue loss, and severe TBI with initial Glasgow Coma Scale (GCS) less than 8 [2,4,12] (see Engel under Additional Reading).

• The relative risk of late PTS is 13% in the first year and decreases with time and reaches the baseline value for the population at 10 to 15 years after the brain injury [4].

• A single late PTS has a 65% to 90% chance of progressing to PTE.

• The likelihood that PTE will go into remission is lower if PTS are frequent in the first year after TBI, if PTS onset is greater than 4 years after TBI, or if there is ICH [12–14] (see Engel under Additional Reading).

• The effect of genetic variation is unclear in posttraumatic epileptogenesis.

Clinical Presentation

• PTS may present as subclinical sz, focal sz with or without impaired consciousness (majority), symptomatic and secondarily generalized sz, or even as primary generalized szs (up to 5%) but not as generalized absence sz [12,13,15,16] (see Diaz-Arrastia under Additional Reading).

• Any focal onset sz (SPS or CPS) can secondarily generalize; more common with frontal than temporal lobe origin sz.

• Typical symptoms associated with SPS by location of sz origin:

Frontal lobe—rare auras; clonic or tonic posturing of body parts

Temporal lobe—autonomic (abdominal discomfort, nausea, abdominal rising feeling), psychic (fear or sense of impending doom, anxiety, feelings of déjà vu or jamais vu), or olfactory and gustatory hallucinations (usually of an obnoxious smell or taste)

Parietal lobe—vertiginous aura, elementary sensory symptoms (which can be painful)

Occipital lobe—elementary visual hallucinations (bright lights, zig-zagging colored lines, or kaleidoscopic shapes), formed visual hallucinations

• Typical symptoms associated with CPS by location of sz origin:

Frontal lobe CPS—hyperkinetic motor movements, bicycling, hip thrusting, thrashing, and asymmetric tonic posturing

Temporal lobe CPS—staring, unresponsiveness, automatisms (i.e., stereotyped behaviors such as chewing, lip smacking, self-polishing movements of fumbling with their clothes), or dystonic posturing of the extremities

• GTCS are characterized by tonic extensor posturing of the arms and legs, followed by rhythmic clonic movements of the arms, legs, and trunk. GTCS are often associated with transient apnea, vomiting, tongue biting, and sphincter incontinence.

• After a CPS or GTCS, there may be a postictal period (typically lasting less than 10 minutes), during which the patient is obtunded and difficult to arouse. Even after regaining consciousness, patients are often confused and amnestic for up to several more hours. Patients often report headaches, dizziness, and sleepiness after a sz, particularly GTCS.

• Subclinical szs are common after prolonged clinical convulsive sz or in critically ill patients. Unexplained prolonged postictal confusion should raise the concern for subclinical sz.

Physical Examination

• Neurological findings, if present, may correlate with the epileptogenic zone.

• Immediately after a sz, transient focal neurological deficits (i.e., weakness that later resolves [“Todd’s paralysis”] or aphasia) are often helpful in localizing sz origin.

Diagnostic Evaluation

• Differential diagnosis includes psychogenic nonepileptic szs (PNES) (i.e., “pseudoseizures”), syncope (e.g., concussive syncope), confusional states (i.e., delirium), acute memory disorders (e.g., fugue state), dizziness, and imbalance.

• In patients with moderate-to-severe TBI with refractory spells, about 30% were misdiagnosed as having PTE but actually had PNES [17]. Therefore, if atypical features are present and szs continue despite treatment, the diagnosis of PTE should be verified by video electroencephalogram (VEEG).

Laboratory Studies

• Serum tests: chemistry panel, liver function tests, urine drug screen, and antiseizure medication (ASM) serum level, if appropriate.

• Routine scalp EEG: a single 30-minute interictal (between sz) EEG has a low sensitivity (30%–50%, which approaches 80%–85% with serial EEGs) for capturing epileptiform activity. However, if captured, epileptiform discharges (spikes or sharp waves) are greater than 97% specific for epilepsy. An EEG after sleep deprivation or after a sz may increase the yield of detecting epileptiform discharges.

• Inpatient Epilepsy Monitoring Unit (EMU) evaluation with VEEG monitoring should be considered if szs are disabling and do not respond to appropriate ASMs.

• VEEG monitoring is required for the diagnosis of subclinical sz. 24-hour VEEG recording generally is required to rule out subclinical sz in noncomatose patients and 48-hour VEEG recording for comatose patients [11].

• Prolonged ambulatory EEG monitoring is less expensive than inpatient VEEG, and may be of value, but the lack of video recordings to correlate with EEG findings significantly limits the sensitivity and specificity.

Radiographic Assessment

• Patients who present with an acute TBI and a sz should be imaged with a computed tomography (CT) scan immediately and the study should be repeated if the condition of the patient does not improve or worsens.

• Head CT is more accessible and cheaper than magnetic resonance imaging (MRI) and is usually able to depict acute pathology (i.e., intracranial bleed) that needs urgent intervention.

• Brain MRI is the study of choice for nonurgent evaluation of PTS or PTE. Transient diffusion weighted imaging (DWI) and/or fluid-attenuated inversion-recovery imaging (FLAIR) changes may occur with recent sz activity and do not reflect structural injury.

TREATMENT

Guiding Principles

• Prophylaxis with AEDs is often initiated as soon as possible after moderate-to-severe TBI [18]. ASMs (i.e., phenytoin, levetiracetam) given within a day of injury prevent early PTS but not late PTS or PTE [3,6,15]. Chronic prophylactic use of ASMs is possibly associated with an increased risk for PTS. For these reasons, ASMs are widely recommended for a short time after head trauma (7 days) to prevent early but not late PTS (see Temkin under Additional Reading).

• Late PTS or PTE worsens functional outcome after TBI significantly, and therefore prevention of PTS is an important goal [11]. However, no treatment is established to prevent the development of epilepsy (e.g., antiepileptogenesis). ASMs may repress sz if late PTS or PTE do occur.

• In children, ASMs may be ineffective in preventing both early and late PTS.

• Treatment of PTE does not require hospitalization, but admission may be needed for the treatment of status epilepticus or for VEEG to assist in the diagnosis.

Initial Management

• PTS prophylaxis—See Guiding Principles.

• In those with a single unprovoked sz, the decision whether or not to begin AEDs depends on the risk of developing further szs (see “Risk Factors” section).

• Early PTS

The recommendation is that early PTS should be treated promptly. Acutely, benzodiazepine (i.e., lorazepam, diazepam, and midazolam), phenytoin/fosphenytoin, sodium valproate, and levetiracetam are the drugs of choice and are usually effective in stopping an ongoing sz. There is little data on how long to continue therapy, but many continue ASMs for a few weeks to months, especially in those with moderate-to-severe TBI.

One ASM can be started based on the comorbidity and side effect profile. Table 46.1 is the summary of commonly used ASMs. No randomized controlled studies have been performed to prove that one is better than the other for PTS. Phenytoin probably should be avoided, because it increases the risk of impairing cognitive function, and may adversely impact neural plasticity. Levetiracetam is better tolerated and just as effective as phenytoin in TBI.

If sz control is not achieved with one drug, changing to a second or even a third ASM may be required to achieve sz control.

• Late PTS

The risk of sz recurrence after a first late PTS is high; chronic use of ASMs is recommended in these individuals. The choice of ASMs is the same as mentioned earlier.

• PTE—The choice of ASMs is the same as mentioned earlier.

TABLE 46.1 Summary of Antiseizure Medications

Ongoing Care

• Regular follow-up (at least yearly) should be performed.

• Once a therapeutic medication regimen is achieved, the individual is typically maintained on the same dosage for a period of 2 years. After 2 years, the individual should be evaluated for the possibility of withdrawal from the antiseizure therapy.

• Factors such as the presence of focal neurological deficits, CT or MRI evidence of structural brain disease, and persistent EEG abnormalities increase the risk of recurrence.

• If szs become intractable, referral to an epilepsy specialist may be indicated, and consideration may need to be given to interventional approaches such as placement of a neurostimulator or epilepsy surgery.

Additional Considerations

• Patients must be warned to exercise safety precautions during swimming, and climbing heights. They should never be alone during these activities. Tub baths are dangerous in patients with epilepsy, and showers are recommended.

• Patients must also be counseled about limitations in driving based on the laws in their states or countries of residence.

• Psychological problems related to social isolation and the stigma of epilepsy must be addressed. Depression is also a common comorbidity. Consultation with psychiatrists, counselors, and/or social workers should be considered when these issues are identified.

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