The EEG in other neurological and medical conditions and in status epilepticus

The Dementias

There are many subtypes of dementias, and EEGs are nonspecific, often showing slowing of the PDR, loss of the usual anterior beta activity, and a gradual increase in diffuse slowing. Nevertheless, certain EEG features can help with our understanding of the problem. For example, focal slowing is most prominent in the anterior regions in frontotemporal dementia. In its early stages, Alzheimer's disease may display little or no EEG abnormality. As the disease progresses, first there is slowing of the PDR, which may eventually be lost entirely. Epileptiform discharges may appear later in the process and may be focal, generalized, or even periodic ( Figure 6-1 ). Note that clinical seizures, generalized or focal, become more common as dementia progresses – particularly in its late stages.

Multi-infarct dementia (MID) is difficult to differentiate from other types of dementias on clinical grounds, as well as on EEG grounds. In MID the record is more likely to display asymmetric features. This no doubt results from multiple small strokes in the course of the illness.

Creutzfeldt–Jakob disease (CJD) has distinctive EEG and clinical characteristics. In the first place, the disease is rapidly progressive with cognitive decline and parallel EEG changes. The background rhythms become fragmented and are destroyed. Diffuse slowing appears and increases. Later, the distinctive periodic sharp wave discharges, often at 1 Hz, are recorded ( Figure 6-2 ). At first, the discharges may be more irregular and even focal, only later becoming generalized and synchronous. Background activity decreases in amplitude. Eventually the EEG is dominated by the periodic discharges with no discernible background. Before death there is a decline in, and ultimate disappearance of, the discharges, leaving an essentially featureless record. A clinical note: the appearance of periodicity is commonly associated with myoclonus. Although the periodic sharp waves are associated with myoclonus, they are not usually time-locked with the myoclonus.

Ischemic Stroke

Many patients presenting with acute ischemic stroke are relatively easy to diagnose on clinical grounds with respect to the history and physical examination. (Note to our readers: the neurological examination still retains its importance!) Others are less straightforward, and the clinician depends on an imaging study to aid in accurate diagnosis. In an acute cortical stroke, the CT of the brain may be normal while the EEG shows a focal decrease of amplitude from a reduction of cortical electrical production ( Figure 6-3 ). Note that a similar voltage attenuation can be seen when there is an increase in fluid or blood between the cortex and the electrodes (e.g., subdural hematoma). These two conditions are hard to differentiate just from an EEG. Asymmetry of beta rhythms with reduction of amplitude is the earliest and most sensitive indicator of cortical dysfunction or a local cortical lesion. Then, polymorphic focal slow waves may appear in an area of reduced amplitude, suggesting that white matter under the cortex is involved as well. In some patients with acute infarction, epileptiform potentials (sharp waves and/or spikes) may be recorded. Further, the EEG sometimes reveals a pattern of lateralized periodic discharges (LPDs).

For example, the usual EEG picture in cases of middle cerebral artery occlusion reveals reduction of fast frequencies and an irregular or polymorphic delta focus in the involved hemisphere, maximal in frontal, temporal, and parietal regions. In addition, the PDR is usually disrupted. During sleep, depression of sleep spindles and vertex sharp waves on the side of the stroke may provide additional evidence of focal cerebral dysfunction.

When edema supervenes, the slowing may be more profound. Indeed, if the patient is lethargic, possibly due to midline intracranial shift, the opposite hemisphere will also demonstrate slowing and disorganization. Associated increased intracranial pressure or infarcts in the deep white matter may be accompanied by intermittent frontally predominant generalized rhythmic delta activity (GRDA).

Occipital strokes present a different picture. Slowing over the posterior temporal and occipital regions may be evident along with the ipsilateral reduction or destruction of the PDR ( Figure 6-4 ). Note that photic stimulation may evoke an asymmetric driving response with depression over the involved side.

When the eyes open, the PDR attenuates in most normal controls. Unilateral failure of this attenuation can be caused by ipsilateral parietal and temporal lobe lesions. This can be an early and subtle sign of stroke or other lesion and is commonly known as Bancaud's phenomenon. Occlusion of the anterior cerebral artery usually results in frontal slowing, sometimes with frontal lateralized rhythmic delta activity (LRDA) or even frontally predominant GRDA. In such cases the occipital rhythms are preserved.

Many strokes are subcortical with sparing of the overlying cortex. Lacunar strokes involving the internal capsule or basal ganglia are common in patients with hypertension and are not always easy to differentiate clinically from those with cortical/subcortical involvement. Instead of demonstrating focal slowing, the record in these patients is usually normal. Alternatively, it may contain a mild diffuse abnormality without lateralizing features.

Patients with clinically suspected transient ischemic attacks are often referred for an EEG. In these cases the record is usually normal or non-focal if obtained after resolution of the neurological findings. In some cases, however, intermittent focal slowing may be evident, suggesting that residual cerebral dysfunction is indeed present despite a normal neurological examination. If the EEG is obtained while the patient is symptomatic, appropriate focal slowing may be evident.

Hemorrhagic Stroke

Hemorrhagic strokes present a highly variable EEG picture depending on the site of involvement, extent of the pathology, and the patient's state of awareness. A relatively small hemorrhage in the centrum semiovale likely results in a minor degree of lateralized slowing. On the other hand, basal ganglia hemorrhages with obtundation can demonstrate marked disruption of electrocortical activity with bilateral delta activity. Lateralization to the involved side may be seen, although in the face of depressed consciousness asymmetry may not be evident. GRDA is common in such cases.

Subdural Hematoma

The classic EEG finding in subdural hematoma (SDH) is depression of cerebral activity over the involved hemisphere. This so-called insulation defect consists of reduced amplitude as compared with the opposite hemisphere. In addition, the PDR may be disrupted or even absent. If the collection is large, associated slowing may be evident. It should be emphasized that there is considerable variability in the EEG, and the classic finding of background depression is not always seen. If the SDH is small there may be no obvious EEG findings.

We also find unilateral depression of cerebral activity in subdural hygromas and atrophic processes secondary to congenital brain damage. In addition, porencephaly leads to striking depression of the background that may present an essentially isopotential (flat) picture.