Classification

     Posttraumatic seizures, also called posttraumatic epileptic seizures, are single or recurrent seizure episodes in a patient with closed or penetrating TBI. Posttraumatic seizures reflect a temporary physiologic dysfunction of the brain, and are therefore seizures that cannot be attributable to another obvious cause, such as anoxia, metabolic abnormalities, mass-occupying lesions, including hemorrhage, recreational drugs, and medications, such as antipsychotic agents, tricyclic antidepressants, bromocriptine, and amantadine. They are categorized by:

• Time of onset
  • Early posttraumatic seizures occur within the first week following injury and can be further classified as
    • Immediate seizures, which occur within the first 24 hours postinjury
  • Late posttraumatic seizures occur after the first week

• Pattern of onset - TBI patients frequently have multiple foci of cerebral injury and > 1 type of seizure
  • Partial or focal seizures - originate in a localized area of one cerebral hemisphere and are either:
    • Simple partial, in which consciousness is maintained during the seizure, or
    • Complex partial, in which consciousness is impaired
  • Generalized seizures - convulsions are bilaterally symmetrical in origin without local onset, such as the grand mal seizure

• Etiology
  • Primary or idiopathic, when etiology is unknown and unsuspected
  • Secondary or symptomatic, when seizures are of known or suspected etiology
    • Temporal lobe epilepsy includes simple, partial seizures characterized by autonomic, psychic, and/or sensory phenomena
    • Orbitofrontal lobe epilepsy includes complex, partial seizures characterized by motor arrest followed by buccal automatisms, confusion, amnesia, sexual automatisms, kicking, screaming, and thrashing episodes. (Some patients, particularly those with mild TBI, also exhibit similar cognitive impairment and behavioral symptoms without concurrent seizures)

     Nonepileptic seizures, also called pseudoseizures or psychogenic seizures, are episodes that resemble posttraumatic or epileptic seizures, but are not associated with a physiologic dysfunction of the brain. They include nonstereotypic, asynchronous limb thrashing and head turning, and may coexist with epileptic seizures in TBI patients, particularly patients with milder injuries, other conversion disorders, and psychiatric histories. Nonepileptic seizures must be distinguished from posttraumatic (epileptic) seizures by video EEG monitoring.

Incidence

• Risk: 1.5 after mild TBI, 2.9 after moderate TBI, and 17.2 after severe TBI (Annegers & Coan, 2000)

• Onset: 50-66% of seizures begin within the first 12 months postinjury, and 75-80% within the first 2 years postinjury

• Recurrence:
  • Seizure onset after the first week postinjury is associated with recurrence
  • 25% of patients who experience seizure suffer a total of 2-3 seizures

• Risk factors:
  • History of alcohol abuse, alcoholism, and epilepsy
  • Intracranial hemorrhage, particularly subdural hemorrhage and those with satellite intracerebral hematoma
  • Severe closed head injuries and penetrating injuries of greater extent, with prolonged posttraumatic amnesia or coma, and those with posttraumatic porencephaly and increased volume of brain tissue loss visualized on CT
  • Focal neurologic deficits, depressed skull fractures, cerebral contusions observable with CT, and retained bone or metal fragments, specifically in decreasing order, biparietal contusions, dural penetration with bone and metal fragments, multiple intracranial operations, multiple subcortical contusions, subdural hematoma with evacuation, midline shift greater than 5mm, or multiple or bilateral cortical contusions (Englander, et al 2003)
  • Dilation of the subarachnoid space and ventricular system, cortical atrophy, porencephalic cysts, and gliotic foci in the frontotemporal region, observable on MRI

Complications

• Status epilepticus is rare and usually due to another cause, such as withdrawal from an anticonvulsant drug or acute systemic or neurologic injury, such as stroke, but is associated with a significant risk of death, also usually due to the precipitating disorder

• Recurrent posttraumatic seizures may affect functional status and cognition

Causes

• Iron released from hemoglobin, as a result of contusion or laceration, and sequestered as hemosiderin, may cause focal epileptiform discharges by initiating lipid peroxidation, damaging cell membranes, and inhibiting neuronal Na-K adenosine triphosphatase

• Collateral axonal sprouting during recovery may cause the development of seizure foci

Diagnosis - To determine if a true posttraumatic seizure disorder exists:

• Experienced staff can make the diagnosis from clinical observations
• EEG is the single most informative laboratory test, although the absence of EEG abnormalities does not exclude the presence of seizure disorder
• Serum prolactin measurement is:
  • Reliable for generalized tonic-clonic seizures and many complex partial seizures, following which serum prolactin levels are elevated within 20-40 minutes
  • Not reliable for nonepileptic seizures, simple partial seizures, or complex partial seizures of frontal lobe origin
  • May help confirm suspicion of an underlying epileptic disorder
• Long-term EEG monitoring is effective and clinically valuable, including:
  • 24 hour - 2 day ambulatory cassette monitoring, which still may miss genuine epileptic phenomena
  • Inpatient telemetry with video monitoring, which is the most reliable diagnostic tool for posttraumatic seizures

Drug Therapy - usually begins after the first seizure, when the benefits of avoiding a second seizure (based on a patient's risk for relapse) outweigh the risk of antiepileptic drug toxicity, with the drug best suited to the type of seizure, route and frequency of administration, and potential and actual side effects

• Partial onset and generalized tonic-clonic seizures are usually treated with carbamazepine, with phenytoin as the second choice, or with phenobarbital
  • Refractory partial seizures may be treated with gabapentin as an add-on therapy, particularly in patients with hepatic disease, since it has low inherent toxicity
  • Refractory partial and idiopathic generalized seizures may also be treated with lamotrigine (Lamictal) as an add-on therapy, since it is usually well tolerated
• Generalized, secondarily generalized, or multifocal onset seizures are usually treated with valproate
• Adverse effects of anticonvulsants include leukopenia, thrombocytopenia, rashes, hirsuitism, gingival hyperplasia, weight gain, elevated hepatic enzymes, memory and cognitive impairment, and impaired neurologic recovery
• Duration of treatment is usually 1 year after the last seizure, but seizures can recur during the withdrawal period and the first year of withdrawal, particularly in patients with a history of more frequent or generalized tonic-clonic seizures, abnormalities on pre-withdrawal EEG's, and treatment with > 1 antiepileptic drug