Pφ

Seizures result from a paroxysmal high-voltage electrical discharge of hyperexcitable neurons within an epileptogenic focus. Different mechanisms have been hypothesized to explain generalized seizures, including (1) an abnormal response of hyperexcitable cortical neurons to a normal thalamic input, (2) a primary subcortical abnormal trigger, and (3) an abnormal cortical innervation from subcortical structures.

TP

A generalized seizure may be preceded by a prodrome, which consists of nonspecific premonitory symptoms for minutes to hours before the seizure, or an aura, which consists of the focal onset and helps localize the causative lesion within the cortex. A generalized seizure is characterized by a sudden loss of consciousness, with a tonic phase (bilateral stiffening, eyes open and rolled upward, loud vocalization, and incontinence) followed by a clonic phase (synchronous muscle jerking, tongue biting). The seizure is typically followed by a postictal state, at which time the patient is drowsy and confused.

Dx

The EEG reveals generalized epileptiform discharges. The frequency and type (polyspike or spike-and-wave) of epileptiform discharges vary depending on the epilepsy type. Focal onset of discharges with spread to the bilateral hemispheres can be seen in secondarily generalized seizures. During the postictal phase, the EEG is generally slow and disorganized.

Pφ

Focal abnormal neuronal discharges without alteration of consciousness constitute this diagnosis.

TP

Symptoms depend on the brain area where the abnormal neuronal discharge originates. Focal motor seizures originate from the frontal lobe. Typically head and eyes turn to the side opposite the seizure focus, which shows tonic contractions, possibly followed by clonic movements. A typical, albeit less common, presentation is the classic “Jacksonian march,” characterized by the progressive involvement of muscle groups that follows the distribution of the homunculus along the motor cortex. When the epileptic focus is in the occipital lobe there may be unformed visual phenomena. Autonomic symptoms such as rising epigastric sensation, pallor, flushing, or pupillary changes may occur when the focus is in the temporal lobe, as well as automatisms, formed visual phenomena, and unpleasant odors or taste. Finally, abnormal sensory events can arise from a parietal lobe focus.

Dx

Focal EEG abnormalities confirm the involvement of only one cerebral region or hemisphere.

Pφ

Focal onset of neuronal discharges with alteration of consciousness is diagnostic. Complex partial seizures typically originate from the temporal lobe and less frequently from the frontal lobe. They are usually associated with an acquired structural lesion such as a tumor or mesial temporal (hippocampal) sclerosis.

TP

Complex partial seizures are typically preceded by an aura (e.g., a rising gastric sensation, emotional content, déjà vu, or visual disturbances). The aura is followed by automatisms, characterized by stereotyped, repetitive actions such as lip smacking, swallowing, or chewing. Patients can be confused and disoriented during the postictal phase for several minutes.

Dx

EEG reveals focal epileptiform discharges.

Pφ

SE can be either convulsive or nonconvulsive. Convulsive SE is life-threatening and can originate as a focal seizure with secondary generalization or be primary generalized. The most frequent cause of SE is noncompliance with seizure medications in a patient with known epilepsy. Other common causes include metabolic derangements, consumption of alcohol or other drugs, anoxia, infection, underlying cerebral lesion (such as stroke or tumor), and trauma.

TP

Convulsive SE is a medical emergency that requires prompt recognition and treatment. Traditionally, SE is defined as either continuous seizure activity that lasts at least 30 minutes or two or more seizures occurring without recovery of consciousness between the seizures. However, a more practical definition suggests that any seizure activity lasting >5 minutes should be considered SE. Nonconvulsive SE can present as a confusional state or a failure to return to baseline mental status after convulsive seizures are treated.

Dx

It is important to promptly formulate a diagnosis of convulsive SE, since early treatment increases the likelihood of effective seizure control and prevention of irreversible neuronal injury or death. Diagnosis of nonconvulsive SE can be challenging on purely clinical grounds. It usually requires the demonstration of ictal EEG patterns in a confused or comatose patient in the absence of active convulsions.

Pφ

In PNES, an underlying psychological problem is translated into a physical symptom, which clinically mimics a convulsion. PNESs have a wide range of associated psychiatric morbidities, including depression, anxiety, psychosis, or post-traumatic stress disorder (PTSD). PNESs and epileptic seizures can frequently coexist in the same patient.

TP

Patients have atypical or variable attacks with triggers that may include an emotional or psychological etiology. Certain seizure phenomena point toward PNES, including flailing or thrashing of arms and/or legs, side-to-side head movements, pelvic thrusting, starting and stopping of symptoms, and eyes closed. Incontinence and physical injuries during the seizure are unlikely with non-epileptic seizures.

Dx

Long-term video and/or EEG monitoring is often necessary to make a diagnosis. PNES clinical spells are not associated with typical EEG epileptic activity. Diagnosis may also be suggested by a history of physical or sexual abuse, or psychiatric disease.