Clinical Approach to Posttraumatic Epilepsy
As in any area of neurology, the diagnosis of PTE begins with the collection of a thorough history. Patients often will not volunteer certain incidences of head trauma (e.g., sports-related concussions or physical abuse with blows to the head), and these may only be elicited with focused questioning. Ascertainment bias is inevitable, but should not deter exploration of the circumstances of prior head trauma because the risk of PTE scales with the nature and severity of TBI. Witnesses may be able to provide valuable collateral history, such as the duration of loss of consciousness and occurrence of immediate convulsions. Drug intoxication and withdrawal can be associated with both head injury and seizures, and clinicians should be aware of these confounders. Once the history of head trauma is established, the possibility of seizures can be evaluated. Symptoms to screen for include premonitory aura, episodes of altered awareness or unresponsiveness, déjà vu or jamais vu, involuntary focal motor activity (e.g., clonic movements, hand and oroalimentary automatisms), dysphasia, olfactory or gustatory hallucinations, amnesia or periods of lost time, and unexplained nocturnal injuries or incontinence. In general, the presence of spells that are paroxysmal and stereotyped should raise high suspicion for seizures. Slow fluctuations in consciousness are often a prominent component of posttraumatic encephalopathy, but are not necessarily epileptic. Similarly, fleeting attentional lapses and cognitive changes that persist over long periods are unlikely to represent seizures. Psychogenic nonepileptic spells (PNES) are common after TBI, and are frequently mistaken for epileptic seizures. Gold-standard diagnosis of PNES requires continuous video-electroencephalography (cVEEG) monitoring.
A neurologic exam may reveal deficits referable to cerebral injury, complementing neuroimaging, and in some cases, obviating the need for it. In an acute setting, the exam should include evaluation for signs of skull fracture, level of consciousness, and focal motor or verbal deficits. Exam findings may help prognosticate long-term outcome after TBI, and a variety of clinical scoring systems have been developed in this regard.
The EEG findings in TBI are usually nonspecific, and epileptiform activity on EEG does not predict disability outcome or the development of PTE. Notwithstanding recent efforts to develop objective EEG-based criteria for classifying TBI severity, EEG traditionally has been regarded as adding little clinical value in patients with TBI. However, there is growing awareness that subclinical seizures, including nonconvulsive status epilepticus (NCSE), are relatively common after TBI and can only be detected by cVEEG. In one study of 87 pediatric patients who required intensive care unit (ICU) admission after TBI and were monitored by cVEEG, 42.5% had seizures and over one-third of these patients had subclinical seizures, mostly NCSE. Nonconvulsive seizures have been associated with hippocampal atrophy, so aggressive treatment is warranted. ICU management is often required for patients with moderate–severe TBI, and cVEEG should be considered for at least a subset of these patients to enable early detection and treatment of NCSE. In addition, some information from continuous EEG recordings, such as persistent impairment of α variability, may portend a worse prognosis after TBI.
Cranial imaging by computed tomography (CT) should be obtained urgently after moderate–severe TBI, and repeat CT is indicated for patients who develop seizures after initial imaging. In mild TBI, head CT prompted by posttraumatic seizures is often negative, but when positive, most commonly reveals intracranial hemorrhage, which may be devastating without urgent surgical intervention. Beyond the acute setting, the mainstay of neuroimaging for PTE is magnetic resonance imaging (MRI), which provides the most sensitive means of defining the extent and severity of brain injury. Conventional MRI sequences, including T1-weighted, T2-weighted, gradient-echo, and diffusion-weighted imaging, may identify parenchymal hemorrhages, extra-axial blood products, early ischemia, edema, and gliosis. Advanced MRI techniques, such as susceptibility-weighted imaging and diffusion tensor imaging, are more sensitive to microhemorrhages and white matter injury, respectively, and are being investigated for their potential to improve detection, to identify optimal treatments, and to predict outcomes. Other forms of neuroimaging—magnetoencephalography, single photon emission CT, positron emission tomography, and EEG coupled with functional MRI—are less prevalent in routine clinical practice, but may one day form the basis for a multimodal imaging-based approach to evaluating patients after TBI.
Diagnosis
As in any area of neurology, the diagnosis of PTE begins with the collection of a thorough history. Patients often will not volunteer certain incidences of head trauma (e.g., sports-related concussions or physical abuse with blows to the head), and these may only be elicited with focused questioning. Ascertainment bias is inevitable, but should not deter exploration of the circumstances of prior head trauma because the risk of PTE scales with the nature and severity of TBI. Witnesses may be able to provide valuable collateral history, such as the duration of loss of consciousness and occurrence of immediate convulsions. Drug intoxication and withdrawal can be associated with both head injury and seizures, and clinicians should be aware of these confounders. Once the history of head trauma is established, the possibility of seizures can be evaluated. Symptoms to screen for include premonitory aura, episodes of altered awareness or unresponsiveness, déjà vu or jamais vu, involuntary focal motor activity (e.g., clonic movements, hand and oroalimentary automatisms), dysphasia, olfactory or gustatory hallucinations, amnesia or periods of lost time, and unexplained nocturnal injuries or incontinence. In general, the presence of spells that are paroxysmal and stereotyped should raise high suspicion for seizures. Slow fluctuations in consciousness are often a prominent component of posttraumatic encephalopathy, but are not necessarily epileptic. Similarly, fleeting attentional lapses and cognitive changes that persist over long periods are unlikely to represent seizures. Psychogenic nonepileptic spells (PNES) are common after TBI, and are frequently mistaken for epileptic seizures. Gold-standard diagnosis of PNES requires continuous video-electroencephalography (cVEEG) monitoring.
A neurologic exam may reveal deficits referable to cerebral injury, complementing neuroimaging, and in some cases, obviating the need for it. In an acute setting, the exam should include evaluation for signs of skull fracture, level of consciousness, and focal motor or verbal deficits. Exam findings may help prognosticate long-term outcome after TBI, and a variety of clinical scoring systems have been developed in this regard.
The EEG findings in TBI are usually nonspecific, and epileptiform activity on EEG does not predict disability outcome or the development of PTE. Notwithstanding recent efforts to develop objective EEG-based criteria for classifying TBI severity, EEG traditionally has been regarded as adding little clinical value in patients with TBI. However, there is growing awareness that subclinical seizures, including nonconvulsive status epilepticus (NCSE), are relatively common after TBI and can only be detected by cVEEG. In one study of 87 pediatric patients who required intensive care unit (ICU) admission after TBI and were monitored by cVEEG, 42.5% had seizures and over one-third of these patients had subclinical seizures, mostly NCSE. Nonconvulsive seizures have been associated with hippocampal atrophy, so aggressive treatment is warranted. ICU management is often required for patients with moderate–severe TBI, and cVEEG should be considered for at least a subset of these patients to enable early detection and treatment of NCSE. In addition, some information from continuous EEG recordings, such as persistent impairment of α variability, may portend a worse prognosis after TBI.
Cranial imaging by computed tomography (CT) should be obtained urgently after moderate–severe TBI, and repeat CT is indicated for patients who develop seizures after initial imaging. In mild TBI, head CT prompted by posttraumatic seizures is often negative, but when positive, most commonly reveals intracranial hemorrhage, which may be devastating without urgent surgical intervention. Beyond the acute setting, the mainstay of neuroimaging for PTE is magnetic resonance imaging (MRI), which provides the most sensitive means of defining the extent and severity of brain injury. Conventional MRI sequences, including T1-weighted, T2-weighted, gradient-echo, and diffusion-weighted imaging, may identify parenchymal hemorrhages, extra-axial blood products, early ischemia, edema, and gliosis. Advanced MRI techniques, such as susceptibility-weighted imaging and diffusion tensor imaging, are more sensitive to microhemorrhages and white matter injury, respectively, and are being investigated for their potential to improve detection, to identify optimal treatments, and to predict outcomes. Other forms of neuroimaging—magnetoencephalography, single photon emission CT, positron emission tomography, and EEG coupled with functional MRI—are less prevalent in routine clinical practice, but may one day form the basis for a multimodal imaging-based approach to evaluating patients after TBI.
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