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EPILEPSY AND OTHER SEIZURE DISORDERS
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characterizes the clonic (inhibitory) phase of the focal motor or grand mal seizure By contrast, this strong element of inhibition is present diffusely throughout an absence attack, a feature that perhaps accounts for the failure of excitation to spread to lower brainstem and spinal structures (tonic-clonic movements do not occur) However, the absence seizure can also at times activate the mechanism for rhythmic myoclonus, probably at an upper brainstem level Current physiologic data indicate that the characteristic EEG patterns of both generalized forms of epilepsy (ie, tonic or tonicclonic and absence) are generated in the neocortex and are enhanced by the synchronizing in uences of subcortical structures In both instances, the generalization of the clinical and electrical manifestations depends upon activation of a deep, centrally located physiologic mechanism, which, for reasons outlined in Chap 17, includes the midbrain reticular formation and its diencephalic extension, the intralaminar and nonspeci c thalamic projection systems (originally referred to by Pen eld as the centrencephalon ) There is no evidence, however, that seizure activity originates in these deep activating structures; therefore the term centrencephalic epilepsy has been replaced by corticoreticular epilepsy Complex partial seizures are almost always of temporal lobe origin, arising in foci in the medial temporal lobe, amygdaloid nuclei, and hippocampus Only rarely do they originate in the convexity of the temporal lobe and propagate to the amygdaloid nuclei, hippocampus, and posteroinferior parts of the frontal lobe Electrical stimulation in these areas reproduces feelings of depersonalization, emotionality, and automatic behavior, the characteristic features of psychomotor epilepsy The automatic behavior appears to be a direct effect of the temporal lobe discharge in some instances and a postexcitatory or inhibitory effect in others Loss of memory for the events of the episode may be due to the paralytic effect of the discharge on neurons of the hippocampus Of theoretical importance is the observation that a seizure focus, if active for a time, may sometimes establish, via commissural connections, a persistent secondary focus in the corresponding cortical area of the opposite hemisphere (mirror focus) The nature of this phenomenon is obscure; it may be similar to the kindling phenomenon mentioned earlier in animals, where a repeated nonconvulsive electrical stimulation of normal cortex induces a permanent epileptic focus No morphologic change is visible in the mirror focus, at least by light microscopy The mirror focus may be a source of confusion in trying to identify the side of the primary lesion by EEG, but there is little evidence that it can produce chronic seizures in humans Similarly, there are no rm data supporting a role for kindling in the diagnosis and management of patients with epilepsy (Goldensohn) Severe seizures may be accompanied by a systemic lactic acidosis with a fall in arterial pH, reduction in arterial oxygen saturation, and rise in PCO2 These effects are secondary to the respiratory arrest and excessive muscular activity If prolonged, they may cause hypoxic-ischemic damage to remote areas in the cerebrum, basal ganglia, and cerebellum In paralyzed and arti cially ventilated subjects receiving electroconvulsive therapy, these changes are less marked and the oxygen tension in cerebral venous blood may actually rise Heart rate, blood pressure, and particularly CSF pressure rise briskly during the seizure According to Plum and colleagues, the rise in blood pressure evoked by the seizure usually causes a suf cient increase in cerebral blood ow to meet the increased metabolic needs of the brain
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The Electroencephalogram in Epilepsy
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(See also Chap 2) The EEG provides con rmation of Hughlings Jackson s concept of epilepsy that it represents a recurrent, sudden, excessive discharge of cortical neurons The EEG is undoubtedly the most sensitive, indeed indispensable, tool for the diagnosis of epilepsy; but like other ancillary tests, it must be used in conjunction with clinical data In patients with idiopathic generalized seizures and in a high proportion of their relatives, interictal spike-and-wave abnormalities without any clinical seizure activity are common, especially if the EEG is repeated several times Contrariwise, a proportion of epileptic patients have a perfectly normal interictal EEG; occasionally, using standard methods of scalp recording, the EEG may even be normal during a simple or complex partial seizure Furthermore, a small number of healthy persons (approximately 2 to 3 percent) show paroxysmal EEG abnormalities; some of them have a family history of epilepsy (particularly of absence seizures) and may themselves later develop seizures EEG abnormalities that characterize a spreading epileptogenic focus and generalization of seizure activity, both the grand mal and absence types, have been described in the preceding section and are illustrated in Chap 2 At rst there was thought to be a characteristic EEG picture for seizures, but further studies have not con rmed this, many patterns being possible One consistent observation, however, has been that the region of earliest spike activity corresponds best to the epileptogenic focus This rule guides epilepsy surgery The postseizure or postictal state following generalized seizures also has its EEG correlate, taking the form of random generalized slow waves Following partial or focal seizures, the EEG shows focal slowing With clinical recovery, the EEG returns to normal or to the preseizure state A single EEG tracing obtained during the interictal state is abnormal to some degree in 30 to 50 percent of epileptic patients; this gure rises to 60 to 70 percent if patients are subjected to three or more studies utilizing standard activating measures (hyperventilation, photic stimulation, and sleep; see Chap 2) With structural lesions, focal slow and sharp activity, which is not clearly epileptiform, may be the only clue to a seizure focus A higher yield of abnormalities and a more precise de nition of seizure types can be obtained by the use of several special EEG procedures Overnight EEG recording is particularly helpful because focal abnormalities, particularly in the temporal lobes, may become prominent in stage II sleep Sphenoidal leads have been used to detect inferomedial temporal seizure activity, but they are uncomfortable and probably add little more information than can be obtained by the placement of additional subtemporal scalp electrodes In our experience, nasopharyngeal electrode recordings are too contaminated by artifact to be clinically useful Activating procedures such as hyperventilation, photic stroboscopic stimulation, and sleep increase the yield of EEG recordings, as detailed in Chap 2 Beyond dependably identifying artifacts in the EEG recording, one of the main challenges for the electroencephalographer is to differentiate between normal patterns that simulate seizures and true epileptic discharges These paroxysmal but ostensibly normal patterns appear mostly during sleep, each with a highly characteristic morphology These include small sharp spikes, 14 and 6 polyspike activity, lambda and posterior occipital mu rhythm, and occipital sharp transients These are pictured in most standard textbooks on the subject of EEG
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