Focal motor seizures may begin with forceful, sustained deviation of the head and eyes, and sometimes of the entire body, are referred to as versive or adversive. The turning movements are usually to the side opposite the electrical focus but sometimes, to the same side. The same is true for the head and eye turning that occurs at the end of the generalized tonic-clonic phase of seizures (Wylie et al). In seizures of temporal lobe origin, early in the seizure, there may be head turning ipsilaterally followed by forceful, contraversive head (and body) turning. These head and body movements, if they occur, may be preceded by quiet staring or automatisms. Nonforceful, unsustained, or seemingly random lateral head movements during the ictus do not have localizing value and suggest that the phenomena are epileptic.
Following convulsions that have a prominent focal motor signature, there is often a transient paralysis of the affected limbs. This “Todd paralysis” persists for minutes or at times for hours after the seizure, usually in proportion to the duration of the convulsion. Continued focal paralysis beyond this time usually indicates the presence of a focal brain lesion as the underlying cause of the seizure or persisting seizures in a nonconvulsive form. A similar Todd phenomenon is found in cases of focal epilepsy that involve the language, somesthetic, or visual areas; here the persistent deficit corresponds to the region of brain affected.
The high incidence of focal motor epilepsy that originates with movements in the face, hands, and toes is probably related to the disproportionately large cortical representation of these parts. Contraversive deviation of only the head and eyes can be induced most consistently by electrical stimulation of the superolateral frontal region (area 8), just anterior to area 6 (see Figs. 21-1 and 21-2). The disease process or focus of excitation is usually in or near the rolandic (motor) cortex, that is, area 4 of Brodmann (see Figs. 3-3 and 22-2); in some cases, and especially if there is a sensory accompaniment, it has been found in the postrolandic convolution.
Lesions confined to the motor cortex are reported to assume the form of clonic contractions, and those confined to the premotor cortex (area 6), tonic contractions of the contralateral arm, face, neck, or all of one side of the body. Tonic elevation and extension of the contralateral arm and flexion of the ipsilateral arm (fencing posture) and choreoathetotic and dystonic postures have been associated with high medial frontal lesions (area 8 and supplementary motor cortex), as have complex, bizarre, and flailing movements of a contralateral limb, but this always raises the suspicion of a nonepileptic phenomenon. Perspiration and piloerection occur occasionally in parts of the body involved in a focal motor seizure, suggesting that these autonomic functions have a cortical representation in or adjacent to the rolandic area. Focal motor and Jacksonian seizures have essentially the same localizing significance.
Seizure discharges arising from the cortical language areas may give rise to a brief aphasic disturbance (ictal aphasia) and ejaculation of a word or loud sound or, more frequently, a vocal arrest. Ictal aphasia is usually succeeded by other focal or generalized seizure activity but may occur in isolation, without loss of consciousness, in which case it can later be described by the patient. Postictal aphasia is more common than ictal aphasia. Verbalization at the onset of a seizure has no consistent lateralizing significance and, paradoxically, is usually associated with an origin in the nondominant hemisphere. These disturbances should be distinguished from the stereotyped repetition of words or phrases or the garbled speech that characterizes some complex partial seizures or the postictal confusional state and, of course, Wernicke aphasia.
Somatosensory, Visual, and Other Types of Sensory Seizures