The abnormal EEG

Organization

In the awake state, in a well-organized EEG, there is a well-formed posterior dominant rhythm (PDR) occipitally, which attenuates with eye opening. Anteriorly, the frequencies are faster and lower in amplitude. This is sometimes referred to as the normal anterior-posterior (A-P) gradient. In sleep, there are distinct sleep states with sleep structures (e.g., K-complexes, vertex waves) specific to each state. If these elements are entirely lacking, the EEG is said to be poorly organized. If an individual has some elements of normal organization but not all, the organization is described as fair.

Diffuse Slowing

The presence of diffuse slowing suggests bilateral cerebral dysfunction with a broad spectrum of causes. The first major problem in making a determination of diffuse slowing is the patient's state of alertness. Many patients are quite drowsy throughout a routine EEG recording. This, of course, produces slowing of the record that would not necessarily be abnormal. The electroencephalographer must diagnose the presence of diffuse slowing during the most alert segments of recording. If this is not possible, one may have to say that the diffuse slowing may be in part, if not wholly, due to drowsiness, although a degree of cerebral pathology cannot be excluded. For patients with a depressed level of consciousness, the degree of slowing is determined after an alerting stimuli (often nailbed pressure) ( Figure 4-1 ).

When an alert segment is encountered, the PDR, if present, is determined. In adults, a PDR of 8.5 Hz or less is abnormal. If the abnormal PDR is symmetric, this is usually not secondary to a focal (i.e., posterior) problem, but a diffuse abnormality. In addition, abundant theta in the awake adult record or abundant delta in the awake child record usually indicates diffuse slowing, which correlates with either diffuse or multi-focal cerebral dysfunction.

In adults, mild slowing is used if the primary background frequency is in the high theta range (7–8 Hz), moderate slowing is used if the frequencies are mainly in the mid theta range (4–7 Hz), and severe slowing is used if the frequencies are mainly in the delta range (0–<4 Hz). Of note, diffuse slowing does not always correlate with the degree of cerebral dysfunction. The classic example of this is in alpha coma where there is no slowing but there is severe cerebral dysfunction.

A second problem relates to medication. We encounter this frequently, especially with referrals from psychiatry. Many psychotropic drugs (e.g., phenothiazines, lithium and clozapine) can cause diffuse slowing. While it is true that the record is abnormal in such cases, the patient may demonstrate no obvious neurological dysfunction. Thus, when reporting this abnormality, it is important to state that the background slowing may be due to an effect of medication(s) that the patient is taking.

Many pathologic processes lead to diffuse slowing, as well as slowing of the PDR. Alzheimer's disease, multi-infarct dementia, various toxic-metabolic disorders, post-ictal states, and congenital brain damage come to mind.

Focal Slowing

As we have seen, slow waves in and of themselves are not abnormal, but slowing that is localized or lateralized commands our attention. In fact, the EEG is highly sensitive to the presence of localized cerebral pathology, often more so than imaging studies. The most important focal abnormality is delta activity (0–<4 Hz) occurring in any cerebral location. Focal delta waves are a good indicator of structural disease. At times focal delta may not correlate with an evident structural lesion on MRI/CT studies, even though cerebral pathology of some degree underlies the EEG finding (e.g., frontotemporal slowing in non-lesional temporal lobe epilepsy).

Structural lesions producing focal delta include brain tumors, cerebral infarction, brain abscess, subdural hematoma, intracerebral hemorrhage, and other traumatic brain injuries. Focal rhythmic (monomorphic) and polymorphic delta activity can be present interictally in patients with focal seizures, with or without clear structural lesions. Delta foci are often most evident in the temporal derivations, even when the main pathology is not in the temporal lobe. We term this false localization, the slowing being projected to the temporal regions from deeper or adjacent structures.

When examining focal slowing, the prevalence of the abnormality should be noted according to ACNS guidelines ( Table 4-1 ). For example, if the slowing is present for 10–49% percent of the EEG, it is described as frequent.

Table 4-1

ACNS Standardized Critical Care EEG Terminology

Reprinted with permission from L. Hirsch, S. LaRoche, N. Gaspard, et al, American Clinical Neurophysiology Society’s Standardized Critical Care EEG Terminology: 2012 version, Journal of Clinical Neurophysiology 2013, 301p 1–27.

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Polymorphic delta is thought to be generated from lesions involving the white matter ( Figure 4-2 ). Contrast this with rhythmic delta activity that can result from lesions of gray matter – usually cortical. Polymorphic and rhythmic delta often coexist when lesions involve both cortex and subcortical white matter.

Focal Attenuation

Fast activity is believed to be generated at the level of cerebral cortex, so focal attenuation of fast activity is a useful marker of abnormal cortical function. It can happen in acute cortical injury such as ischemic stroke. It can also occur in the setting of an intervening fluid collection between the scalp and the brain, such as a subdural hematoma ( Figure 4-3 ).

Focal increased fast activity

Focal increased fast activity can be present in the setting of brain abscess, stroke, tumors, vascular malformations, and cortical dysplasia. Interestingly, these can all be associated with focal decrease in fast activity as well. It needs to be differentiated from the breach artifact, which results from an area of skull defect, usually a postsurgical finding. In the case of a breach artifact, the waveforms are often sharply contoured at higher amplitudes. The technicians are asked to note the presence of craniotomy scars in order to correctly identify this rhythm. Due to the prior surgery, breach rhythms are often associated with focal slowing ( Figure 4-4 ).

Epileptiform Discharges

In patients with epilepsy, despite the important role of the EEG, the diagnosis often rests on clinical grounds. Rarely, epileptiform discharges can be recorded in persons without epilepsy. Likewise, patients with epilepsy can have a normal EEG between seizures. Nonetheless, the EEG provides important supporting evidence for a diagnosis of epilepsy. More­over, the type of epilepsy may be confirmed, or even diagnosed. For example, the EEG differentiates between focal and generalized epilep­sies and is a principal feature in the definition of epilepsy syndromes.

The following paragraphs provide direction concerning specific findings in epilepsy.