Localization-related seizures begin in one area of the brain and initially produce symptoms that are referable to the region of cortex involved. Simple partial seizures are focal neurologic events in which consciousness remains intact, whereas in complex partial seizures, consciousness is impaired. Simple seizures may evolve into complex partial seizures, and both of these types of focal seizures may evolve into secondarily generalized seizures. The spread of symptoms may follow the cortical representation of body parts, beginning, for example, in the fingers and spreading up the arm or down the leg.

Symptoms of complex partial seizures are numerous and include coordinated, involuntary motor activity (automatisms), such as lip smacking or chewing, olfactory or gustatory hallucinations, and behavioral automatisms. Seizure activity typically begins in the temporal lobe or its connections. Premonitory symptoms include olfactory hallucinations, epigastric discomfort, and a sense of fear or déjà vu. At times, the symptoms may resemble those of a psychosis. Episodes last 1 to 3 minutes, followed by a period of confusion with consciousness usually impaired but not lost. Localization-related seizures are the most common type of epilepsy in adults, accounting for 70% of patients presenting with epilepsy after age 18 years. More than 50% of all patients with localization-related epilepsy have both partial and secondarily generalized tonic-clonic seizures.

Generalized seizures are bilaterally symmetric and without focal onset. An episode may begin with a premonitory aura that is followed by a sudden loss of consciousness. A tonic phase of limb extension ensues, lasting 10 to 30 seconds, followed by a clonic phase of limb jerking of at least 30 seconds. The patient then becomes flaccid and comatose before regaining consciousness. Postictal confusion is characteristic and can last for hours, although 10 to 30 minutes is more typical. Tongue biting and incontinence are other characteristic features.

A number of factors have been implicated as causes of seizures, including fever, stroke, alcohol and drug use, and head trauma. Although these factors are often important, a number of misconceptions about their role are prevalent and need to be addressed.

Several conditions can mimic seizures, either by causing focal deficits or by producing episodic loss of consciousness. Among the former are transient ischemic attacks, migraine, and local pathology, such as nerve compression or movement disorders such as tics or paroxysmal chorea. Among the latter are syncopal attacks of any cause, including transient diminished cerebral
perfusion resulting from cardiac conditions, transient global amnesia, narcolepsy/cataplexy, and transient ischemic attacks (see Chapter 171). Panic attacks with or without hyperventilation and altered mental status during psychotic episodes may cause confusion with complex partial seizures. Psychogenic nonepileptic seizures may take any form and are often misdiagnosed as seizures though signs distinguishing epileptic from nonepileptic seizures have been described by several groups (eye flutter, intensification of symptoms by bystanders, variable phenomenology during different spells, and abrupt onset).

The differential diagnosis of conditions responsible for a seizure is based largely on the age of the patient at the time of the first seizure and the type of seizure as determined by the history, especially that obtained from observers. Approximately 70% of new-onset epilepsy in adults presents as partial (focal) seizures. Primary or idiopathic epilepsy is the most common cause of recurrent seizures in children, but it becomes increasingly rare in the young adult population. After age 30 years, an underlying cause (secondary epilepsy) becomes increasingly likely when a patient presents with a first seizure. Among patients with more than one documented seizure of any type, a cause becomes obvious after thorough investigation and a 10-year follow-up in only 23%. Only 15% of seizures generalized from the outset have a demonstrable cause, whereas underlying disorders can be found in more than 30% of seizures with a focal component. In the young adult population (ages 18 to 45 years), the demonstrated causes include drugs (usually alcohol withdrawal), neoplasm, and trauma. In the older adult population over age 65, underlying pathology is divided about equally among neoplasm, trauma, and cerebrovascular disease, but the cause remains unknown in 25% to 40% of older patients. A nonepileptic convulsion may occur in the context of a transient metabolic disturbance, such as cerebral hypoperfusion, hypoglycemia, a hyperosmolar state, or hyponatremia.

An effective history requires an exact description of events from both witnesses and the patient. Reports of witnesses are especially useful because the patient’s consciousness and recall of the event are likely to have been compromised. Questioning should include inquiry into the presence of an aura, focal onset, loss of consciousness, and observed injury during the convulsion. Such symptoms suggest seizure rather than syncope, although it is not possible to distinguish between them absolutely on the basis of any characteristic features.

Once it has been ascertained that a seizure has occurred, it is essential to check carefully for a history of focal onset, even in patients with a history of generalized seizure. The focal onset of a witnessed seizure that later became generalized may be an important clue to an underlying lesion of the CNS.

History is also essential for identifying precipitants and underlying disease. It should include inquiry into drugs (e.g., alcohol, cocaine, amphetamines, antidepressants, sedatives, theophylline, insulin, diuretics), cardiac arrhythmias, valvular disease, previous malignancy, stroke, HIV risk factors, and head trauma. The examiner should check for symptoms of hyperglycemia and hypoglycemia (see Chapter 102) in addition to those of meningeal irritation (headache, stiff neck). A family history of convulsions should always be sought. Travel history assumes ever greater importance as seroprevalence of neurocysticercosis, a common cause of acquired epilepsy in Central and South America, is rising in the southwestern United States.

It is not possible by clinical means to determine definitively whether a transient or persistent neurologic event is a seizure. The American Academy of Neurology Practice Parameter on evaluation of an apparent unprovoked first seizure in an adult recommends electroencephalogram (EEG), brain imaging with computed tomography or magnetic resonance imaging, and laboratory tests such as complete blood count, blood glucose, and screening for substance abuse. Liver function tests and electrolyte levels are useful before medication is started, and serum albumin levels should be measured when highly protein-bound drugs such as phenytoin or valproate are planned. Lumbar puncture and toxicology screening maybe helpful as determined by the specific clinical circumstances but need not be part of the routine.

Unless evidence of infection is found or the patient presents in status epilepticus, it is no longer common practice to perform a lumbar puncture for a patient with a first seizure. If fever is present or the history is compatible with systemic infection, lumbar puncture remains an essential part of the neurologic evaluation.