Post-Traumatic Seizures

Date Published: July 10, 2020

Overview

Definition

Seizure

A seizure is defined as a discrete clinical event that reflects temporary physiologic dysfunction of the brain characterized by excessive and hypersynchronous discharge of cortical neurons. ¹

Post-Traumatic Seizure

A post-traumatic seizure (PTS) is an initial or recurrent seizure episode not attributable to another obvious cause after penetrating or non-penetrating traumatic brain injury (TBI). The term post-traumatic seizure is preferred over post-traumatic epilepsy because the former encompasses both single and recurrent events. ¹

Post traumatic seizures are classified as:

Immediate PTS

A seizure due to TBI occurring within the first 24 hours of injury.

Early PTS

A seizure due to TBI occurring within the first week of injury.

Late PTS

A seizure due to TBI occurring after the first week of injury.

Post-Traumatic Epilepsy

Post-Traumatic Epilepsy (PTE) is a disorder characterized by recurrent late seizure episodes not attributable to another obvious cause in patients following TBI. The term should be reserved for recurrent, late post-traumatic seizures.

Prevalence

PTS

PTS develop in 5% to 7% of hospitalized patients with TBI ²
Higher prevalence on rehabilitation units (as much as 18%), which likely reflects increased injury severity and the presence of a higher number of risk factors in this population ^3-7

Of PTS that occur post moderate-to-severe TBI, the incidence rates are as follows:

Immediate PTS: 0.4%^8,9
Early PTS: 0.5% to 22%^9-11
Late PTS: 4% to 88.7%^8,9,12,13
Late PTS are the most common

Most common seizure types in order: ¹⁴

Focal onset impaired awareness seizure
Focal seizure
Generalized seizure

PTE

PTE develops in 10% to 25% of individuals with moderate-to-severe TBI ¹⁵

Etiology

Structural	Hydrocephalus Space occupying lesions (e.g., hemorrhage, abscess – more common in penetrating injuries)
Metabolic	Electrolyte abnormalities (Na, Mg, Ca) Hypoglycemia Uremia Hepatic encephalopathy Hypoxemia
Infectious	Sepsis/fever Encephalitis Meningitis
Illicit Substances	Alcohol Cocaine Ecstasy Amphetamines (rare with therapeutic doses) Caffeine (high doses)
Medications	Tricyclic antidepressants Clozapine Antibiotics (penicillins, imipenem, fluoroquinolones, cephalosporins) Bupropion Opioids Abrupt withdrawal of sedative hypnotics (benzodiazepines, barbiturates)

^16,17

Risk Factors

Patient Factors

Increased age
Chronic alcohol use
Family history of seizures
Previous head injuries
Other concomitant injuries/comorbid conditions

Injury Characteristics

Penetration of dura with retained metal and bone fragments ¹⁸
Depressed skull fracture ²
Cortical contusions (multiple > single, bilateral > unilateral)¹⁸
Subcortical contusions (multiple > single) ¹⁸
Focal neurological deficits
Intracranial hemorrhage (intracerebral, epidural and subdural hemorrhages) ²
Increased injury severity: GCS<10, prolonged post traumatic amnesia or prolonged coma²
Midline shift and cisternal compression on CT scan ¹⁸

Treatment Related

Subdural hematoma with surgical evacuation ¹⁸
Ventriculostomy ¹⁸
Performance of multiple neurosurgical procedures ¹⁸

Clinical Features

Aura (e.g., rising epigastric sensation, déjà vu)
Focal signs (e.g., head turn)
Automatisms
Involuntary movements (e.g., tonic clonic)
Tongue biting
Urinary incontinence
Staring
Loss of awareness/consciousness
Post-ictal confusion and agitation
Some patients may present non-specifically with a gradual deterioration in cognitive, behavioural or overall functioning

Assessment

History

Relevant TBI History

Mechanism of (cause, injury, injury location, severity, time since injury, surgical history. markers, medications)

Circumstances and Characteristics of Event

Collateral history from someone who witnessed one or more events is essential.

Obtain description of:

Physical observations (e.g. body stiffening, limb jerking, staring, unresponsiveness, automatisms – swallowing, chewing, lip smacking, plucking at clothing or objects)
Order in which events occurred
Overall duration of the event

Inquire as to whether the individual experienced a subjective aura (e.g. epigastric rising sensation, unpleasant olfactory sensation, palpitations, déjà vu or jamais vu, fear, somatosensory changes, hallucinations).

Ask about post-ictal symptoms including anterograde amnesia, confusion, fatigue, somnolence, sore limb muscles, aphasia.

Review comorbidities, medications (including over the counter agents and supplements), substance use history

Objective Observations

Objective signs of seizure may include oral lacerations, tongue biting, urinary incontinence, posterior shoulder dislocation, other injuries (contusions, wounds, fractures, abrasions).
Complete review of systems (especially constitutional symptoms of fever, chills or neck rigidity)

Physical Exam

General appearance
Vital signs
Head & neck: inspect for scalp/facial lacerations, oral lacerations
Cardiovascular: orthostatic vital signs, cardiac auscultation
Abdomen: stigmata of liver disease
Nervous system: focal neurologic deficits, cognitive deficits
Musculoskeletal system: fractures, posterior shoulder dislocation, nuchal rigidity

Diagnostic Testing

The gold standard for diagnosis is continuous video electroencephalography¹⁹

Laboratory Investigations

A detailed history and physical examination can guide further investigations in an effort to rule out potential causes

Complete blood count
Comprehensive metabolic panel including electrolytes, extended electrolytes, blood glucose, renal function, liver function, and thyroid function
Urine toxicology screen
Alcohol level
- Lumbar puncture if meningitis is suspected
CT or MRI head to rule out structural causes (e.g. hydrocephalus, hemorrhage)

Diagnosis

All patients presenting with seizure should undergo EEG
Comatose patients with a TBI should undergo continuous EEG to rule out nonconvulsive seizures ²⁰

Differential Diagnosis

Seizure due to metabolic abnormalities (hyper- or hypoglycemia) or hypoxia
Encephalomyelitis
Meningitis
Drug intoxication/withdrawal
Tremors
Psychogenic non-epileptic seizures
Presyncope/syncope
Stroke
Migraine
Movement disorder

Complications

Status epilepticus can be defined as either more than 5 minutes of continuous seizure activity or two or more sequential seizures without full recovery of consciousness between seizures. Status epilepticus is a serious complication of PTS that can contribute to the development of additional neurological damage; fortunately, this is a rare occurrence, affecting only 0.16% of individuals hospitalized with TBI.²¹

While the consequences of a single late post traumatic seizure are generally minimal, increased seizure frequency and severity is associated with increased mortality and morbidity through the following mechanisms:

Accidental injury
Hospitalization ²²
Negative impact on neurological recovery ^23,24
Decreased Cognitive and behavioural disorders ²³
Psychological effects (e.g. depression, anxiety)
Deterioration in Overall Functional Status
Loss of independence (e.g. driving license suspension) ²⁵
Difficulty with social integration ²⁵

It is important to note that, in Ontario, it is mandatory to report any individual who has experienced a seizure to the Ministry of Transportation.

Management

Non-pharmacological Interventions

Lifestyle Modifications (ketogenic diet, appropriate sleep schedule, exercise, avoid caffeine/drugs/alcohol)

Pharmacological Interventions

Prophylaxis of Early Post-Traumatic Seizures

Antiepileptic drugs are recommended during the 1st 7 days post TBI for individuals with moderate to severe TBI with significant PTS risk factors.
In this scenario, where the incidence of PTS is relatively high, the goal is to prevent PTS during a time when the brain is susceptible to secondary injury.
While it is important to prevent PTS, this must also be balanced against the risk of adverse effects associated with the use of antiepileptic drugs.
There is no evidence that antiepileptic drug prophylaxis prevents late PTS and therefore these medications should not be continued beyond 7 days post injury for this purpose ²⁶

Intervention	Effect	Level of Evidence
Phenytoin (Dilantin) compared to placebo	+	1b Phenytoin decreased the risk of early seizures compared to controls ²⁷
Carbamazepine compared to placebo	+	4 Carbamazepine decreased the risk of early seizures compared to controls ²⁷
Valproate compared to phenytoin	C	1a Valproate is no more effective than phenytoin in reducing early PTS. Therefore it can be assumed it also decreases the risk of early seizures.
Levetiracetam (Keppra) compared to phenytoin	C	1b Levetiracetam is no more effective than phenytoin in reducing early PTS. Therefore it can be assumed it also decreases the risk of early seizures.
Lacosamide compared to phenytoin	C	3 Lacosamide is no more effective than phenytoin in reducing early PTS. Therefore it can be assumed it also decreases the risk of early seizures.

Treatment of Active Seizures

Case series have shown midazolam administered intramuscularly stops seizure activity when other benzodiazepines have failed.

Intervention	Effect	Level of Evidence
Midazolam	+	4 May reduce seizure activity

Treatment of Late PTS

Antiepileptic drugs are indicated for the treatment of late PTS.
Antiepileptic drugs may cause serious side effects including: cognitive impairment, somnolence, behavioural disturbance, weight gain, weight loss, rash, hepatotoxicity as well as electrolyte and hematologic abnormalities.
Within the TBI population, valproic acid, lamotrigine and levetiracetam are often preferred as they are less likely to negatively impact neurorecovery or worsen post traumatic symptoms of cognitive impairment and somnolence; however, phenytoin has been evaluated over the long-term.

Intervention	Effect	Level of Evidence
Phenytoin	C	C Mixed evidence pertaining to effectiveness in reducing PTS long-term.

Miscellaneous Treatments for Post-Traumatic Seizures

Glucocorticoids and phenobarbital do not provide effective prophylaxis of post-traumatic seizures.
Methylphenidate may help to reduce seizure recurrence in some patients but the level of evidence is very low level.

Intervention	Effect	Level of Evidence
Glucocorticoids (Dexamethasone)	-	C Not effective in reducing seizure activity. May put patients at higher risk of late seizure development. Does not reduce rate of seizures.
Phenobarbital	-	1b Does not reduce the rate of seizures
Methylphenidate	+	4 May be effective in reducing rate of seizure recurrence in some patients

Surgical Interventions

Neurosurgical brain tissue resection (i.e., corpus colostomy, temporal lobectomy)
Resecting the seizure focus, when it can be localized, reduces the recurrence of post traumatic seizures.

Intervention	Effect	Level of Evidence
Surgical resection	+	4 Can be effective in a subgroup of TBI patients where the seizure focus can be localized
Vagus nerve stimulator	+	4 Reduced seizure frequency in those with partial onset seizures

Algorithm

PTS Algorithm

Resources

INESSS-ONF Clinical Practice Guidelines

Seizures

ERABI Module

Post-Traumatic Seizure Disorder Following Acquired Brain Injury

ERABI Guidebook

Post-Traumatic Seizures Following Acquired Brain Injury

References

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