Continue to Carry This Condition Epilepsy

DEFINITIONS

An epileptic seizure is a "transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain."¹ Epilepsy is a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures and by the neurobiological, cognitive, psychological, and social consequences of this condition.¹ The widely accepted operational definition of epilepsy requires that an individual have at least two unprovoked seizures on separate days, generally 24 hours apart. An unprovoked seizure refers to a seizure that occurs in the absence of an acute brain insult or systemic disorder.² This nosology is based on the observation that while a single unprovoked seizure is often an isolated event that does not recur during an individual's lifetime, two unprovoked seizures rarely occur in isolation and are associated with high risk of the individual experiencing more seizures. In some cases, such as when the seizure occurs in the setting of a potentially epileptogenic brain insult such as an episode of encephalitis or a traumatic brain injury (TBI), it is possible to recognize the specific form of epilepsy at its earliest presentation. In such cases, the diagnosis of epilepsy can be made after the very first unprovoked seizure.² Based on its definition, epilepsy is not a single disorder but rather a syndrome or syndromes. Different forms of epilepsy syndrome(s) have different causes, different manifestations, different implications for short- and longterm management and treatment, and different outcomes.

Post-traumatic epilepsy (PTE) refers to epilepsy that develops after TBI. Most investigators agree that PTE is to be distinguished from repeated seizures in the early stage following TBI, while the brain is acutely traumatized, inflamed, and metabolically disrupted. Therefore, a common set of definitions adopted by many researchers is the following: (1) immediate seizures, usually defined as those occurring within 24 h after injury; (2) early seizures, which occur less than 1 week after injury; and (3) late seizures, which occur more than a week after injury. Since the risk of recurrence after a single late post-traumatic seizure is over 70%, most investigators consider a single late post-traumatic seizure as being sufficient for the diagnosis of PTE.³ Although these are the most widely accepted definitions, there is controversy. Some narrow the definition of immediate seizures to those occurring at impact or within minutes of the injury, classifying seizures occurring hours after trauma as early seizures. Others extend the time of early seizures to as long as 30 days after the injury.

Another set of considerations related to PTE is the severity of head trauma. A variety of classifications of TBI severity exist, but most investigators currently use the following schema: (1) mild TBI, characterized by loss of consciousness less than 30 min, post-traumatic amnesia less than one hour, and normal neuroimaging; (2) moderate TBI, characterized by loss of consciousness more than 30 minutes and less than 24 hours, post-traumatic amnesia between 1 and 7 days, with or without abnormal neuroimaging; and (3) severe TBI, characterized by loss of consciousness greater than 24 hours, post-traumatic amnesia more than 7 days, usually with abnormal neuroimaging such as contusion, cerebral hematoma, or extra-axial hematoma.³ This nosology, while robust and usually easily applied, has many limitations, foremost among them the fact that it does not take into account findings from modern neuroimaging studies.

EPIDEMIOLOGY

The prevalence of epilepsy in the general United States population is estimated at 0.5%–2%, and the cumulative incidence of PTE ranges widely, from 2% to over 50% depending on injury severity (Tables 14.1 and 14.2).⁴ Studies on hospitalized TBI patients report a cumulative incidence of 5%–7%,⁵ and the risk of PTE is as high as 53% in a military series that included penetrating head injuries.⁶ ^, ⁷ In a large population-based study done out of Rochester, Minnesota, head trauma was identified as the cause of epilepsy in 6% of the population (see Figure 14.1).⁸ There are important differences among age groups. Of cases where the cause of epilepsy could be identified, trauma is the cause of epilepsy in almost 30% of individuals who develop seizures between ages 15 and 34 years, whereas it is a cause in approximately 14% in children younger than 14 years and 8% in adults older than 65 years.⁸ About 4% patients who were seen at a specialized epilepsy center reported a history of moderate to severe head trauma.⁹

TABLE 14.1

Frequency of Post-Traumatic Epilepsy (PTE) Stratified by Injury Severity in Civilian Populations

TABLE 14.2

Frequency of Post-Traumatic Epilepsy (PTE) Stratified by Injury Severity from Select Military Series

FIGURE 14.1

Proportion of incidence cases of epilepsy by etiology in Rochester, Minnesota, 1935–1983. (From Hauser W.A. et al., Epilepsia, 1993;34:453–468. With permission.)

Early seizures occur in 2%–17% of all patients with head injuries, being more common in children than adults, and correlated with the distribution of head-injury severity.⁴ ^, ¹⁰ The frequency of early seizures after severe head injuries is typically higher (10%–15% for adults; 30%–35% for children).⁴ ^, ¹⁰ Of the seizures that occur within the first week of trauma, about 50% occur within the first 24 hours.¹¹ Of the seizures that occur within the first 4 weeks of injury, about 10% occur within the first week.⁴ Clinically apparent early seizures with typical convulsive features are likely the tip of the iceberg, and the use of continuous electroencephalography (EEG) monitoring reveals that nonconvulsive seizures are much more common than convulsive seizures in the first week after severe TBI.¹² The clinical significance of nonconvulsive seizures identified through continuous EEG monitoring remains a topic of investigation. While they are associated with poor outcome, it is unclear whether aggressively treating them improves recovery.

The cumulative incidence of late seizure over 30 years after TBI is 2% for mild injuries, 4% for moderate injuries, and over 15% for severe injuries.¹³ The incidence was about 5% in people hospitalized with TBI.¹⁴ In the setting of severe head trauma with cortical injury and neurologic sequelae, the incidence of PTE increases reaches over 50%, particularly if the dura is penetrated.¹⁵ Late seizures can have a very long latency period but usually start in the first few years after injury.¹⁶ ^, ¹⁷ About 40% start within the first 6 months of injury, 50%–60% within the first 12 months, and approximately 80% of first late seizures occur within 2 years of the injury. The risk of incident late seizure decreases with time and reaches background risk for the population at 10–15 years after the head injury.¹³ ^, ¹⁸ Up to 86% of TBI survivors with a first posttraumatic seizure will have a second within 2 years, providing the rationale for making the diagnosis of post-traumatic epilepsy after a single late post-traumatic seizure. A certain percentage of PTE cases remain refractory to antiseizure medications.⁴

RISK FACTORS

Risk Factors for Early Seizures

Risk factors for early seizures include younger age (especially <5 years), acute intracerebral hematoma, acute subdural hematoma, diffuse cerebral edema, intracranial metal fragment retention, focal neurologic deficits, depressed/linear skull fractures, and loss of consciousness (LOC)/amnesia for >30 minutes.⁴ Early seizures may be a weaker predictor for PTE in children; the portion of children with early seizure who have late seizures is less than one-fifth in children and may be as low as one-tenth.¹⁹ On the other hand, about 3% of patients with no early seizures develop late PTE; this number is 25% in those who do have early PTS, and the distinction is greater if other risk factors for developing PTE are excluded.²⁰

Risk Factors for Late Seizures

Factors that increase the risk of late post-traumatic seizures are age at injury >65, the presence of early post-traumatic seizures (in adults), subdural hematoma, brain contusion, premorbid chronic alcoholism, penetrating head injury, retained metal fragments in brain, depressed skull fracture, focal neurological deficits, degree of loss of brain tissue, and severity of injury (Table 14.3).⁴ ^, ⁷ ^, ¹³ ^, ²¹

TABLE 14.3

Risk Factors for Epileptic Seizures and Epilepsy after Nonmissile Head Trauma

A population-based study in Olmsted County, Minnesota, found that the relative risk of late seizures was 12.7% in the first year, 4.4% during the next 5 years, and 1.4% thereafter.²² The head-injured victims were divided into groups with respect to severity of injury.¹³ ^, ²² Those with a severe head injury (brain contusion, intracerebral or intracranial hematoma, or 24 hours of unconsciousness or amnesia) had a risk factor of 7.1% within the first year after injury and 11.5% in 5 years with an overall incidence ratio of 17.0. Those with a moderate head injury (skull fracture or 30 minutes to 24 hours of unconsciousness or amnesia) had a risk factor of 0.7% within the first year and 1.6% within 5 years with an overall incidence ratio of 2.9. Those with a mild head injury (shorter periods of unconsciousness or amnesia) had a risk factor of 0.1% within the first year and 0.6% within 5 years with an overall incidence ratio of 1.5. Recent data suggest that genomic information (e.g., haptoglobin genotypes, apolipoprotein E levels) may be helpful in predicting an individual's risk for PTE as a possible genetic predisposition has been observed.²³ ^, ²⁴

Genetic Factors

Of note, not every patient with clinical risk factors for PTE goes on to develop PTE, and this variability in occurrence may be attributable to genetic variation in genes involved in the epileptogenic process. According to Jennett,²⁰ the incidence of a family history of epilepsy in patients with closed head trauma who develop late seizures is 6%–17%, compared with only 3%–4% in those who do not. Furthermore, the risk for late epilepsy is greater and the latency between head injury and the first late spontaneous seizure is shorter for patients who experience early reactive seizures. These findings strongly suggest that innate, presumably genetically determined, predisposing factors contribute to the development of PTE. That a family history of epilepsy may not be a significant risk factor for late epilepsy following penetrating head injuries could indicate that genetic influence is relatively weak compared with the effects of very extensive intracranial trauma.²⁵ Although advances in genetics have now revealed numerous susceptibility genes, predominantly involving ion channels and GABA receptors, which appear to play an important role in the manifestation of acquired epilepsy in humans,²⁵ relatively little has been conclusively established about genetic susceptibility to PTE.

Although there have not been any genome-wide allelic association studies designed to identify genetic variants associated with PTE, several candidate genes have been studied using allelic association. Inheritance of the apolipoprotein E (ApoE) epsilon 4 allele is associated with increased risk of Alzheimer's disease, progression to disability in multiple sclerosis, and poor outcome after traumatic brain injury. Diaz-Arrastia et al.²⁶ prospectively collected DNA samples from 106 patients in a neurocritical care unit who had suffered severe traumatic brain injury. Six months after injury, 22 patients (20%) had at least one later post-traumatic seizure. The relative risk of late post-traumatic seizures for patients with the epsilon 4 allele was 2.41 (95% confidence interval). In the other recent retrospective study, Miller et al. invested ApoE genotype in 322 adult Caucasians with a severe TBI.²⁷ Although no statistical associations were found, two out of the four individuals (50%) with the E4/E4 had late post-traumatic seizures. Sample size calculations indicate that over 2000 individuals would be needed to have a cohort large enough to definitively evaluate the E4/E4 genotype in relation to PTE.²⁷

C677T variant in the methylenetetrahydrofolate reductase (MTHFR) enzyme is a biologically plausible genetic risk factor for seizure or epilepsy. This variant is associated with elevated homocysteine levels, and homocysteine is recognized to lower seizure thresholds and has been used as a proconvulsant in animal epilepsy models.²⁸ ^– ³⁰ Homozygote TT genotype may be overrepresented in epilepsy patients.³¹ ^, ³² Scher et al. genotyped C677T in a military cohort and found that the odds of epilepsy were increased in subjects with the TT versus CC genotype (adjusted OR = 1.57).³³ Adenosine A1 receptors (A1AR) are located on neurons in regions susceptible to both seizures and TBI (e.g., hippocampus, cortex) and are spatially associated with NMDA receptors.³⁴ A1AR activation influences the extent of status epilepticus in both ex vivo and in vivo seizure models.³⁵ Importantly, profound PTE, leading to lethal status epilepticus, occurs in A1AR knockout (KO) mice when subjected to the controlled cortical impact (CCI) model of experimental TBI.³⁶ Tagging single nucleotide polymorphisms (tSNPs) analysis in the A1AR gene in 206 subjects with severe TBI demonstrated that genetic variability within the rs3766553 and the rs10920573 regions are associated with increased susceptibility for post-traumatic seizures. Subjects with both risk genotypes had a 47% chance of late post-traumatic seizures.

MECHANISM

Epileptogenesis is defined as the development and extension of tissue capable of generating spontaneous seizures, including development of an epilepsy condition and progression after the condition is established.²⁵ ^, ³⁷ ^, ³⁸ TBI can produce both focal and diffuse insults to the brain, and both mechanisms often coexist in given patients. Focal insults such as contusions or intracranial hematomas result in cicatrix in the cortex or subcortical regions, and the neighboring neural tissue experiences inflammation, gliosis, and ultimately neuronal sprouting and neurogenesis. These secondary tissue responses are believed to be the initiating events in a cascade of processes that result in epileptogenesis. However, the exact underlying pathophysiologic epileptogenic process is not clearly understood after brain trauma.

Immediate post-traumatic seizures likely occur because the impact from the injury stimulates brain tissue that has a low threshold for seizures when stimulated.³⁹ Early post-traumatic seizures can be the result of the secondary effects of the head trauma such as cerebral edema, intracranial hemorrhage, cerebral contusion or laceration, alterations in the blood–brain barrier, changes in extracellular ions, excessive release of excitatory neurotransmitters such as glutamate, damage to tissues caused by free radicals, and changes in the way cells produce energy.³⁹ ^, ⁴⁰ Late seizures are thought to indicate permanent changes in the brain's structure that are thought to result from neuronal and synaptic loss, aberrant sprouting, and rewiring.

Enhanced excitatory connectivity and decreases in GABAergic inhibition are important mechanisms underlying injury-induced epileptogenesis in many animal models and in humans. Sprouting of excitatory axons and establishment of new synapses is a ubiquitous epileptogenic response to cortical injury.⁴¹ The partially isolated neocortical island with intact pial circulation ("undercut") is an established in vivo and in vitro model for development of chronic post-traumatic hyperexcitability and epileptogenesis.⁴² This model provides a high yield of animals with epileptogenic cortex that may be studied in vitro.⁴³ ^, ⁴⁴ In this model, the treatment with tetrodotoxin (TTX) during a critical period early after lesion placement can prevent epileptogenesis.⁴¹ The immunocytochemical experiments show that such treatment markedly attenuates histologic indices of axonal and terminal sprouting and presumably associated aberrant excitatory connectivity.⁴² Another finding in the undercut model is a decrease in spontaneous inhibitory events. This is accompanied by regressive alterations in fast-spiking y-aminobutyric acid (GABA) ergic interneurons, including shrinkage of dendrites, marked decreases in axonal length, structural changes in inhibitory boutons, and loss of inhibitory synapse on pyramidal cells.⁴² A potential underlying mechanism is loss of trophic support from brain-derived neurotrophic factor (BDNF) released by pyramidal neurons acting on interneuronal TrkB receptors.⁴¹

In summary, there are many processes initiated by cortical injury that are ongoing in parallel. Each of them, or combinations of several, might well be important contributors to epileptogenesis and targets for prophylaxis.

CLINICAL PRESENTATION

Post-traumatic seizures may present anywhere in the spectrum, including partial seizure without alteration of consciousness, partial seizure with alteration of consciousness, and symptomatic and secondarily generalized seizures. However, primary generalized seizures, such as absence seizures, are not thought to be caused by head injury.⁴⁵ ^, ⁴⁶

The temporal lobes are the most common site for late post-traumatic seizures.⁹ ^, ⁴⁷ Temporal lobe seizures are associated with an aura approximately two-thirds of the time. The auras can be 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). As the seizure evolves, alteration of consciousness may occur and patients may stare and be unresponsive, and may also have stereotyped behaviors such as chewing, lip smacking, or grunting, as well as automatisms such as self-polishing or fumbling with their clothes. Secondarily generalizations are relatively rare with seizures of temporal lobe onset.

The frontal lobe is the second common site for post-traumatic epilepsy.⁹ ^, ⁴⁷ Auras are rare in frontal lobe epilepsy. Typical behaviors during frontal seizures include hyperkinetic motor movements, bicycling, hip thrusting, thrashing about, and asymmetric tonic posturing. Secondarily generalizations are common with frontal lobe onset seizures.⁹

Seizures arising from other lobes are less common.⁴⁷ Seizures starting in the occipital lobes are often associated with elementary visual hallucinations, such as seeing bright lights, zigzagging colored lines, or kaleidoscopic shapes. Seizures starting in the more rostral parts of the occipital lobe and occipitotemporal junction are often associated with formed visual hallucinations. Seizures starting in the parietal lobes are often associated with a vertiginous aura, and if they arise near the postcentral gyrus, then elementary sensory symptoms are experienced, which can be painful.

Any partial onset seizure can secondarily generalize. Secondarily generalized tonic–clonic seizures are characterized by tonic extensor posturing of the arms and legs, followed by rhythmic clonic movements of the arms, legs, and trunk. Generalized tonic–clonic seizures (GTCs) are often associated with transient apnea, vomiting, tongue biting, and sphincter incontinence. Partial seizures with alteration of consciousness and secondarily generalized seizures are characterized by a postictal period, during which the patient is obtunded and difficult to arouse. This stage usually lasts a few minutes but 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 seizure, particularly GTCs.

PHYSICAL EXAMINATION

No specific findings are noted on physical examination and the neurological examination of patients with PTE may be nonfocal. However, if present, focal neurological findings may correlate neuroanatomically with the traumatic brain lesion, which may be in the epileptogenic zone. If the patient can be examined immediately after a seizure, finding a focal neurologic deficit that later resolves (Todd's paralysis) is often very helpful for localizing the site of seizure onset.

DIAGNOSTIC EVALUATION

The differential diagnosis for post-traumatic spells needs to include PTS/PTE, concussive convulsions, psychogenic nonepileptic seizures (PNSs) (e.g., pseudoseizures), syncope (e.g., concussive syncope), confusional states (i.e., delirium), acute memory disorders (i.e., fugue state), dizziness, and imbalance. Concussive convulsions are not actual PTS and are not predictive of post-traumatic epilepsy.⁴⁸ They are thought to result from temporary loss of brain function rather than from structural damage and are usually associated with a good outcome.⁴⁹ PNS are seizure-like episodes that may occur after head injury, but video EEG (VEEG) monitoring, which is often required to definitively make the diagnosis, shows that the nature of the seizures is psychogenic rather than epileptic. Features that distinguish PNS from epileptic seizures on VEEG monitoring include lack of stereotypy in semiology and duration of the seizures, lack of scalp EEG correlate to the events, and atypical evolution of the behaviors, such as start-and-stop phenomena. In patients with moderate to severe traumatic brain injury referred to a Comprehensive Epilepsy Center for evaluation of refractory PTE, about 30% were found to have been misdiagnosed and have psychogenic attacks.⁴⁶ This percentage is similar to patients with epilepsy after nontraumatic etiologies. Therefore, if atypical features and seizures continue despite treatment, the diagnosis should be verified by VEEG rather than assuming the patient has PTE.

LABORATORY STUDIES

In patients hospitalized after a recent head injury, investigation of a seizure should focus on determining whether an intracranial bleed or a change in clinical condition (e.g., hyponatremia) caused the seizure. Acutely injured patients whose sensorium fails to return to normal after a seizure should be evaluated with EEG. For patients in otherwise stable condition whose serum electrolytes are within the normal range and whose neurologic findings are the same as those before the seizure, further laboratory studies are not needed. Some academic centers perform continuous VEEG monitoring routinely in patients who are comatose or stuperous after TBI, and routinely find that up to 20% have unrecognized nonconvulsive seizures.⁵⁰ ^, ⁵¹

In a patient presenting months or years after the injury, the usual investigations that are applicable for evaluation of first epileptic seizure should be performed (i.e., electrolytes, liver function test, urine drug screen). EEG is very helpful for differential diagnosis. An interictal EEG showing epileptiform discharges (spikes or sharp waves) has a specificity of >97% for epilepsy. However, the sensitivity of interictal EEG is low, in the range of 30%–50%. VEEG monitoring may help in narrowing the differential diagnosis, in localizing seizure foci and in prognosticating their severity, and in predicting relapse before anticonvulsant medication is withdrawn. VEEG evaluation should be considered in every patient with frequent, disabling spells who has not responded to appropriate antiepileptic medications.

RADIOGRAPHIC ASSESSMENT

Patients with a TBI and a seizure should be imaged with a CT scan immediately, and the study should be repeated if the condition of the patient does not improve or worsens (e.g., acute change in mental status). CT is less sensitive but more accessible and less expensive than MRI and should be able to depict all pathology (intracranial bleed, midline shift) that needs urgent intervention. Brain MRI is the study of choice for nonacute evaluations of PTS/PTE. Findings on certain sequences may convey important information relating to recent seizure or epileptogenic focus. Fluid attenuated inversion recovery (FLAIR) may show diffuse axonal injury (DAI), contusion, blood, edema, or encephalomalacia. Gradient echo (GRE) and susceptibility-weighted imaging (SWI) is more sensitive than CT and conventional MR techniques for demonstrating microhemorrhages resulting from shear injury. Diffusion tenor imaging (DTI) appears to be very sensitive for identifying disruption in white matter tracts, but its use is still primarily investigational. Of note, diffusion-weighted imaging (DWI) and FLAIR can demonstrate transient abnormalities after a seizure that later disappears, and does not necessarily reflect structural injury.

TREATMENT

The occurrence of PTS significantly worsens functional outcome, and prevention of PTS is an important goal.⁵² Prophylaxis treatment with antiseizure drugs is often initiated as soon as possible after moderate to severe TBI.¹⁶ A landmark study indicates that antiseizure medication (e.g., phenytoin) given within a day of injury prevents early seizures (within the first week of injury) but not late post-traumatic seizures or post-traumatic epilepsy.⁵³ Prophylactic treatment with antiepileptic drugs (AEDs) also does not improve functional outcome from TBI. There is also the suspicion that prophylactic use of AEDs over a long period is associated with an increased risk for seizures. For these reasons, AEDs are commonly used for a short time after head trauma to prevent immediate and early, but not late, seizures.⁵⁴ Thus, the use antiseizure drugs for prophylaxis during the first week, while a widespread practice, is an option and not a guideline. No treatment is established to prevent the development of epilepsy.⁵⁵ However, medications may be given to repress more seizures if late seizures do occur. In children, AEDs may be ineffective for both early and late seizures.⁵ 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

In those with a single unprovoked seizure, the decision whether to begin antiepileptic drug treatment depends on the risk of the individual for developing further seizures. For those with early PTS, the recommendation is that antiepileptic drugs should be started promptly and continued for a few weeks. Acutely, lorazepam, diazepam, fosphenytoin, sodium valproate, and levetiracetam are the drugs of choice and usually effective in stopping an ongoing seizure. In most cases, administering the medication via the intravenous (IV) route is desirable, as the patient is still in the recovery stage from the head injury. Chronically, one first or second generation antiepileptic medication can be used. Typically, the second generation medications are just as efficacious and better tolerated (fewer drug–drug interactions and side effects). No known randomized controlled studies have been performed to prove that one is better than the other. Phenytoin is widely used, but it seems to increase the risk of impairing cognitive function.⁵⁶ Levetiracetam is better tolerated and there is evidence that it is equivalently effective as phenytoin after craniotomy and in severe TBI.⁵⁷ ^, ⁵⁸ The dosage prescribed should lead to a therapeutic blood level. If control is not achieved, the dose is increased until the patient has toxic side effects. The dosage is then decreased just enough to prevent toxicity. If seizure control is not achieved with one drug, a second drug is added. For those with late PTS, because of the high risk of seizure recurrence after a first late PTS, chronic use of AEDs is recommended after even a single late seizure. The choice of antiepileptic medications is the same as noted earlier.

ONGOING CARE

Regular medical follow-up should be performed to review seizure control, medication side effects, and neurologic/neuropsychological assessment. Once a therapeutic medication regime 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 antiepileptic therapy, which if done should occur gradually over a period of several months. Factors such as the presence of focal neurologic deficits, CT evidence of structural brain disease, and persistent EEG abnormalities increase the risk of recurrence after tapering antiepileptic drugs, even after a prolonged period of seizure control while on medications. These factors should be assessed and used to inform the decision of whether to stop medication. If seizures remain intractable, then consultation with a neurologist or referral to an epilepsy center may be needed to confirm the diagnosis of PTS/PTE or for consideration further management, such as possible surgical therapy.

Surgical treatment may be an option for PTE refractory to medication. The aim of resective epilepsy surgery is to identify and remove the epileptogenic focus. This is sometimes more difficult in cases of PTE than in other types of epilepsy and may require intracranial EEG evaluation. Other surgical options may include implantation of a vagus nerve stimulator (Cyberonics), a responsive neurostimulator (NeuroPace), or a deep brain stimulator (Medtronic), some of which are experimental at the moment.

TREATMENT CONTROVERSIES

Prophylactic treatment of PTE has been common practice for many years and remains an issue of controversy. The theory that an antiepileptic medication prevents the epileptic foci from developing has been disproven for drugs that have been rigorously studied. As there remains a significant risk to developing epilepsy after severe head trauma, it remains common practice to initiate prophylactic antiepileptic therapy. However, since prevention of early seizures does not translate into improved neurologic recovery, the use of prophylactic medications during the first is optional.

Another area of controversy is whether treatment is useful in patients who experienced early PTS. There is little high-quality evidence to provide therapeutic guidance in this situation. Although an early PTS is not associated with such a high risk of recurrence that it is equivalent to PTE, most neurologists treat with antiepileptic drugs for several weeks to several months, and taper the medications off slowly if no late PTS is noted.

ADDITIONAL CONSIDERATIONS

Patients must be warned to exercise caution during bathing, swimming, and climbing heights. They should never be alone during these activities. In all situations, appropriate steps should be taken to ensure the safety of the person if a seizure occurs. Patients must also be counseled about the limitations in obtaining a driver's license, based on the laws in their state of residence. Psychological problems related to social isolation and the stigma of epilepsy are common and must be addressed. Consultation with psychiatrists, counselors, and social workers is very important in the management of post-traumatic epilepsy. The medical/legal aspect is an important issue in cases of PTE, as some patients pursue legal actions against various authorities and individuals responsible for the circumstances of the accident. Clinicians are often asked to estimate the risk of a patient developing PTE in the future as a result of sustained brain injury. This is a difficult task and should be left to an experienced senior specialist.

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