Aside from psychogenic episodes that imitate seizures, few clinical states simulate a generalized tonic-clonic seizure, but several are worthy of mention. One is a clonic jerking of the extended limbs (usually less severe than those of a grand mal seizure) that occurs with vasodepressor syncope or a Stokes-Adams hypotensive attack. In contrast to an epileptic type of EEG, the brain waves are slow in frequency and low in amplitude during the jerking movements. A rarer phenomenon that may be indistinguishable from a generalized convulsion occurs as part of the syndrome of basilar artery occlusion. This presumably has its basis in ischemia of the corticospinal tracts in the pons (Ropper); a similar ischemic mechanism in the cortex has been invoked for “limb-shaking TIAs” (transient ischemic attacks), in which there are clonic movements of one limb or one side of the body during an episode of cerebral ischemia. Clonic limb movements occur immediately after a traumatic concussion and an observer who arrives at this moment will be unable to determine if the inciting event was a seizure causing a fall with head injury, or a collision causing a concussion and convulsive movements. In infants, a breath-holding spell may closely simulate the tonic phase of a generalized seizure. Another disorder that simulates a seizure, albeit self-induced, is the fainting lark (or in the British, the “mess trick”). By hyperventilating in a squatting position and standing rapidly combined with a Valsalva maneuver, a syncopal episode is induced that ends with generalized convulsive movements (see Lempert et al).
In contrast to major generalized seizures, absence seizures (formerly referred to as petit mal or pyknoepilepsy) are notable for their brevity, rapid onset and cessation, and frequency and the paucity of motor activity. Indeed, they may be so brief that the patients themselves are sometimes not aware of them; to an onlooker, they resemble a moment of absentmindedness or daydreaming. The attack, coming without warning, consists of a sudden interruption of consciousness, for which the French word absence (“not present,” “not in attendance”) has been retained. The patient stares and briefly stops talking or ceases to respond. Only about 10 percent of such patients are completely motionless during the attack; in the remainder, one observes a brief burst of fine clonic (myoclonic) movements of the eyelids, facial muscles, or fingers or small synchronous movements of both arms, all at a rate of 3 per second as shown many years ago by Penry and colleagues. This rate corresponds to that of the EEG abnormality, which takes the form of a generalized 3-per-second spike-and-wave pattern (see Fig. 2-7I). Absence seizures are said to be “typical” if they have a rapid onset and offset, typical three per second spike and wave, and complete loss of awareness.
Minor automatisms—in the form of lip-smacking, chewing, and fumbling movements of the fingers—are common during an attack but may be subtle. Postural tone may be slightly decreased or increased, and occasionally there is a mild vasomotor disorder. As a rule, such patients do not fall; they may even continue complex acts such as walking or riding a bicycle. After 2 to 10 s, occasionally longer, the patient reestablishes full contact with the environment and resumes his preseizure activity. Only a loss of the thread of conversation or the place in reading betrays the occurrence of the momentary “blank” period (the absence). In many such patients, voluntary hyperventilation for 2 to 3 min is an effective way of inducing absence attacks.