The EEG is now little used in the differential diagnosis of stroke, except to distinguish a transient ischemic attack from a seizure. In the past, one practical value was in the ability to differentiate an acute ischemic lesion in the distribution of the middle cerebral artery, which produces a large area of slowing, from lacunar infarction deep in the cerebrum or brainstem, in which the surface EEG is usually normal despite prominent clinical abnormalities. After 3 to 6 months, in roughly 50 percent of patients with infarction in the territory of the middle cerebral artery, the focal EEG slowing becomes normal. Perhaps half of these patients will have had normal EEGs even in the week or two following the stroke. A persistent abnormality is generally associated with a poor prognosis for further recovery. Large lesions of the diencephalon or midbrain produce bilaterally synchronous slow waves, but those of the pons and medulla (i.e., below the mesencephalon) are usually associated with a normal or near-normal EEG pattern despite catastrophic clinical changes.
A brief episode of cerebral concussion in animals  produces focal EEG slowing similar to those described for cerebral infarction. Sharp waves or spikes sometimes emerge as the focal slow-wave abnormality resolves and these seizure-like changes may precede posttraumatic epilepsy; serial EEGs may be of value in this regard. During syncope, the EEG is slowed and of reduced amplitude even to the point of becoming “flat.” Upon recovery, a number of patterns have been described as discussed further in Chap. 17.
Diseases That Cause Coma and States of Impaired Consciousness
The EEG is abnormal in almost all conditions in which there is impairment of the level of consciousness. There is, for example, a fairly close correspondence between the severity of acute anoxic damage from cardiac arrest and the degree of EEG slowing. The mildest forms are associated with generalized theta activity, intermediate forms with widespread delta waves and the loss of normal background activity, and the most severe forms with “burst suppression,” in which brief isoelectric periods are followed by high-voltage sharp and irregular delta activity. The latter pattern usually progresses to the electrocerebral silence of brain death, a condition discussed earlier.
The term alpha coma refers to a unique EEG pattern in which an apparent alpha activity in the 8to 12-Hz range is distributed widely over the hemispheres rather than in its normal location posteriorly. When analyzed carefully, this background activity, unlike the normal monorhythmic alpha, is found to vary slightly in frequency. This is usually a transitional pattern after global anoxia; less often, alpha coma occurs with large acute pontine lesions. With severe hypothyroidism, the brain waves are normal in configuration but usually of decreased amplitude and frequency.
In altered states of alertness, the more profound the depression of consciousness, in general, the more abnormal and slower the EEG rhythms. In states of deep stupor or coma, the slow (delta) waves are bilateral and of high amplitude and tend to be more conspicuous over the frontal regions (Fig. 2-7L). This pertains in such differing conditions as acute meningitis or encephalitis and disorders that severely alter blood gases, glucose, electrolytes, and water balance; uremia; diabetic coma; and impairment of consciousness accompanying the large cerebral lesions discussed above. In hepatic coma, the degree of abnormality in the EEG corresponds roughly to the degree of confusion, stupor, or coma. Characteristics of hepatic coma are paroxysms of bilaterally synchronous large, sharp “triphasic waves” (Fig. 2-7L), although such waveforms may also be seen with less regularity in encephalopathies related to renal or pulmonary failure and with acute hydrocephalus (intermittent biphasic frontal slowing is more typical of hydrocephalus).