Nonepileptic EEG Abnormalities

The most common focal EEG abnormality consists of slow wave activity. Increased “slow activity” (i.e., theta and delta activity in a waking record) is virtually always abnormal. Almost all conditions that diffusely affect the brain increase slow activity.

In particular, focal delta activity is usually irregular in configuration and is termed polymorphic delta activity (PDA) (Figure 75-2). PDA is usually indicative of a focal brain lesion (such as tumor, stroke, hemorrhage, or abscess).¹³ Before the advent of modern neuroimaging, focal delta abnormalities were used to localize cerebral lesions. Focal cerebral lesions may also cause asymmetric slowing of the background alpha waves or asymmetric beta activity.

Figure 75-2 Polymorphic delta activity in the left hemisphere in a patient with a brain tumor.

The EEG may also show generalized abnormalities, particularly in encephalopathies. As a general rule, the EEG is a sensitive, though nonspecific, test for encephalopathies. The most common pattern with metabolic encephalopathies is generalized moderate- to high-amplitude theta and delta activity without an alpha resting background.¹⁴ Another common pattern observed with hepatic and renal encephalopathies is the presence of triphasic delta waves.¹⁵ These are high-voltage, diffuse periodic discharges, and are at times difficult to differentiate from epileptiform generalized spike/sharp-slow wave discharges.¹⁶ In infectious encephalopathies, particularly in encephalitides, an admixture of slow activity and epileptogenic activity is often seen.

Intermittent rhythmic delta activity may be seen focally or diffusely. Such activity is frequently confined to the frontal region in adults, and is called frontal intermittent rhythmic delta activity (FIRDA); in children, this pattern is most often located posteriorly. Although initially believed to have been a sign of increased intracranial pressure in young people, these monomorphic high-amplitude waves are most often seen in diffuse encephalopathies.¹⁷

In hypoxic encephalopathies, low-amplitude slow waves are typically observed.¹⁸ In more severe cases, one may observe a burst-suppression pattern, in which a voltage-suppressed background is interrupted by generalized high-amplitude sharp activity. In most severe cases of coma, generalized suppression of amplitude (i.e., electrocerebral silence) on the EEG in the absence of possible modifying factors (e.g., medications and hypothermia) is an ancillary test to confirm brain death.¹⁹

EEG Abnormalities in Seizure Disorders

The EEG has been particularly useful in the analysis of patients with seizure disorders. Paroxysmal abnormalities are common between overt seizures (i.e., interictally), as well as during seizures (ictally). Paroxysmal abnormalities include the spike and the sharp wave. A spike is a single wave that stands out from the background activity and has a duration of less than 70 ms. A sharp wave is similar with a duration between 70 and 200 ms. A spike or sharp wave has an asymmetric up-phase and down-phase and is often followed by a slow wave. The existence of a spike or sharp wave is highly specific; a single sharp wave in the proper clinical context may be sufficient to confirm a seizure disorder. However, such findings are insensitive; the EEG is frequently normal and devoid of such discharges even in patients known to have epilepsy. Multiple recordings may be required to capture an abnormality and to make a diagnosis.²⁰

Epileptic paroxysmal abnormalities can be either generalized or focal. The classic generalized abnormality is the 3-Hz spike and wave pattern that underlies the petit mal absence attack (Figure 75-3). A typical focal abnormality is a focal single spike followed by a slow wave. This abnormality can be seen interictally in focal epilepsy, such as temporal lobe epilepsy (TLE). EEG recorded during a seizure may show a variety of patterns, including repetitive spikes/sharp waves, spike–slow wave complexes, rhythmic theta activity, and others. After a seizure (postictally), the EEG most frequently shows pronounced slow waves. Scalp EEGs are notoriously unreliable for the detection of simple partial seizures.

Figure 75-3 Generalized spike-wave discharges in absence seizures.

The relationship of any of these abnormalities to the particular patient is complex. For example, paroxysmal activity on an EEG may (or may not) mean that the patient’s problem is related to epilepsy; the final determination typically rests on the overall clinical picture and on the results of a therapeutic trial. One should resist the temptation to consider the EEG independently. In particular, a normal EEG does not exclude epilepsy, since the EEG may be normal during a focal seizure that is observed clinically.

Medication Effects

Benzodiazepines are well known to increase the beta frequency and mild background slowing in EEG recordings.²¹ Barbituates, in small doses, increase the beta activity, predominantly in the frontal leads. With increasing doses, there is increased slow activity and attenuation of alpha activity, indicative of increasing drowsiness. With sufficiently high doses, a burst suppression pattern and eventually electrocerebral silence ensues.²² Withdrawal will result in generalized sharp activity and may be accompanied by withdrawal seizures. General anesthetics will induce fast frontal activity and attenuation of alpha, and, with deeper coma, a burst suppression pattern.²³ Conventional antiepileptic medications have not been associated with definite EEG changes at therapeutic levels.²²

Few definite electrographic changes have been reported with most typical antipsychotic drugs at therapeutic doses; background slowing and even epileptic activity may be seen at higher doses. Clozapine induces abnormalities (such as slowing and spikes) in more than half of patients.²⁴ Lithium may produce diffuse slowing and enhance preexisting epileptiform activity on the EEG.²² No specific EEG changes are seen with use of antidepressants.

Alcohol and Other Recreational Drugs

Patients with alcoholism are vulnerable to falls and to other head trauma. In these patients, focal EEG abnormalities and partial seizures may be seen. During acute intoxication, slowing is seen on the EEG, but it diminishes with tolerance. Alcohol withdrawal seizures are generalized, even in patients with focal injuries. The EEG in chronic alcoholism is associated with a greater incidence of low-voltage (less than 25 μV) recordings with little slowing in more than half the patients (56%) as compared to control subjects without a history of alcoholism (13.9%).²⁵ This can be helpful in distinguishing delirium tremens (DTs) from other toxic metabolic encephalopathies that are associated with diffuse theta and delta slow waves. An increase in beta activity is seen on the EEG with use of cocaine and other central nervous system (CNS) stimulants.^22,26 No clinically useful changes on the EEG are seen with other recreational drugs.

Dementia and Pseudodementia

Obtaining an EEG may be helpful in the process of differentiating dementia with secondary depression from depressive pseudodementia. In patients with either depression or depressive pseudodementia, the EEG has been shown to be either normal or mildly slowed. In contrast, in patients with dementia with secondary depression, the majority have abnormal EEGs; in up to one-third of patients, there may be moderate or severe abnormalities.²⁷

Schizophrenia

Studies have demonstrated that patients who demonstrate normal EEG findings with decreased reactivity to stimuli, deemed to be “hypernormal,” had an unfavorable prognosis.²⁸ Increased delta and beta activity, as well as decreased alpha frequencies, have been reported in patients with schizophrenia.²⁹ Electroencephalography has been used to evaluate the theory that schizophrenia is the result of functional disconnections in cerebral networks. Decreased intrahemispheric coherence in the EEG has been demonstrated in patients with schizophrenia.³⁰ In general, EEG studies in schizophrenic patients have produced inconsistent results, and it has been debated whether EEG abnormalities in these patients are due to the state of the patient or due to the trait of the disease.³¹

Peripheral Nerve Conduction Studies

Late Responses

Studying the most proximal segments of nerves is difficult, because they are deep and not easily accessible as they leave the spinal column. However, it is useful to study the proximal segments of nerves since processes such as radiculopathies from disc protrusion and certain neuropathies (e.g., Guillain-Barré) predominantly affect this segment. The so-called late responses (the H-reflex and the F-response) provide a relatively easy technique for study of the proximal segments of nerves. These responses are produced in certain circumstances after an electrical stimulus to a peripheral nerve, and are late with respect to the muscle response (the M-response) produced by the orthodromic volley of action potentials traveling to the muscle directly from the electrical stimulus.

The H-reflex is a monosynaptic reflex response similar in its pathway to that of the tendon jerk. The electrical stimulus activates the I-a afferents (coming from the muscle spindles) and action potentials travel orthodromically to the spinal cord. In the cord, the I-a afferents make excitatory monosynaptic connections to the alpha motor neurons; a volley of action potentials is set up in the motor nerve, which runs orthodromically the entire length of the nerve from the cell bodies to the muscle. Hence, action potentials travel through the proximal segment of the nerve twice during the production of the H-reflex (once in the sensory portion of the nerve and once in the motor portion). Obtaining an H-reflex depends on the ability to stimulate the I-a afferents. If a motor axon is electrically stimulated, an action potential will travel along the axon antidromically toward the spinal cord, as well as orthodromically toward the muscle. The antidromic action potential will collide either in the proximal motor axon or in the cell body with the developing H-reflex in that axon and nullify it. In routine clinical practice, it is possible to get this differential stimulation and to produce E-reflexes only in the posterior tibia1 division of the sciatic nerve while recording from the triceps surae.

The F-response or F-wave has an advantage over the H-reflex in that it can be found in most muscles. It is a manifestation of recurrent firing of an anterior horn cell after it has been invaded by an antidromic action potential. After a motor nerve is stimulated, an action potential runs antidromically as well as orthodromically; a small percentage of anterior horn cells that have been invaded antidromically will produce an orthodromic action potential that is responsible for the F-response. Thus, to produce an F-response, action potentials must travel twice through the proximal segment of the motor nerve.⁴¹

The Physiology Underlying Electromyography

Understanding the concept of the motor unit is central to the understanding of the physiology of electromyography (EMG). A motor unit is composed of all the muscle fibers innervated by a single anterior horn cell. In most proximal limb muscles, there are hundreds of fibers in each motor unit. In the normal situation, the muscle fibers from the same unit are not clumped together, but are intermingled with fibers from other motor units. When a motor axon fires, each muscle fiber in its motor unit is activated in a constant time relationship to the other fibers in the unit.

EMG activity is ordinarily recorded with a needle placed into the muscle. Because the muscle fibers of a single motor unit are not packed closely together, the EMG needle records from only about 10 fibers from each motor unit. The amplitude, duration, and configuration of the electrical activity recorded from a motor unit vary as the needle changes its orientation to the muscle fibers. Despite its variability it is possible to specify a normal range for the amplitude, duration, and configuration of motor unit action potentials (MUAPs) for each muscle and each age.

When an EMG needle is placed in a normal muscle at rest, there is no electrical activity. With weak effort, first one and then several motor units are activated. At this low level of activation, it is possible to see the individual MUAPs and evaluate their parameters. With maximal effort so many units are brought into action that individual MUAPs cannot be discerned; all that can be seen is a dense electrical pattern, called an interference pattern, which can be characterized by its density and peak-to-peak amplitude. The normal density would be either “full,” if there are no gaps, or “highly mixed,” if there are a few, short gaps. Some people are not willing or able to exert a maximal effort and the pattern will be less dense as a result. Hence, the degree of effort has to be taken into account when assessing the interference pattern.

Findings on the Electromyogram