Kaplan + Sadock's Synopsis of Psychiatry, 11e

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1.8 Applied Electrophysiology

Table 1.8-4 Electroencephalography (EEG) Alterations Associated with Medical Disorders

Table 1.8-3 Electroencephalography (EEG) Alterations Associated with Medication and Drugs

Drug

Alterations

Seizures

Generalized, hemispheric, or focal spike, spike-wave discharge, or both Focal slowing, with possible focal spike activity

Benzodiazepines Clozapine (Clozaril) Olanzapine (Zyprexa) Risperidone (Risperdal) Quetiapine (Seroquel) Aripiprazole (Abilify)

Increased beta activity Nonspecific change Nonspecific change Nonspecific change No significant changes No significant changes

Structural lesions

Closed head injuries Focal slowing (sharply focal head trauma)

Focal delta slowing or more widespread slowing (subdural hematomas) Diffuse, often synchronous, high voltage slowing (acute phase of encephalitis) Diffuse generalized slowing of wake frequencies Triphasic waves: 1.5 to 3.0 per second high-voltage slow waves, with each slow wave initiated by a blunt or rounded spike-like transient (hepatic encephalopathy) Slowed alpha frequency and increased generalized theta slowing (diffuse atherosclerosis) Focal or regional delta activity (cerebro- vascular accidents)

Infectious disorders

Lithium Alcohol

Slowing or paroxysmal activity Decreased alpha activity; increased theta activity Decreased alpha activity; increased voltage of theta and delta waves; in overdose, slow waves Increased beta activity; in withdrawal states, generalized paroxysmal activity and spike discharges Increased alpha activity in frontal area of brain; overall slow alpha activity Diffuse slowing of delta and theta waves Increased alpha activity; in with- drawal, marked decrease in alpha activity In withdrawal, increase in amplitude or voltage of theta activity Similar to marijuana

Metabolic and endo- crine disorders

Opioids

Barbiturates

Marijuana

Vascular patho- physiology

Cocaine Inhalants

Nicotine

the analog-based electrical signals are processed digitally and converted to graphic, colored topographical displays. These images are sometimes called “brain maps.” Color Plate 1.8-5 illustrates topographic QEEG images of a patient with a closed head injury. QEEG remains primarily a research method, but it holds considerable clinical potential for psychiatry, mainly in establishing neurophysiologi- cal subtypes of specific disorders and for identifying electrophysiological predictors of response. Examples of some of the more promising results of QEEG research include the identification of subtypes of cocaine dependence and the subtype most likely to be associated with sustained abstinence; identification of subtypes of obsessive–compulsive disorder (OCD) that predict clinical responsiveness or lack of responsiveness to selective serotonin reuptake inhibitors (SSRIs); and the differentia- tion between normals, attention–deficit disorder and attention-deficit/

Caffeine

Topographic Quantitative Electroencephalography (QEEG) Unlike standard EEG interpretation, which relies on wave- form recognition, QEEG involves a computer analysis of data extracted from the EEG. Findings are compared with a large population database of subjects without any known neurologi- cal or psychiatric disorder as well as QEEG profiles that may be characteristic of some defined diagnostic group. In QEEG,

Figure 1.8-4 Diffuse slowing in a 67-year-old patient with dementia. Six- to seven cycles per second (cps) activity predominates over the parieto-occipital regions. Although reactive to eye closure, the frequency of this rhythm is abnormally slow. (Reprinted from Emerson RG, Walesak TS, Turner CA. EEG and evoked poten- tials. In: Rowland LP, ed. Merritt’s Text- book of Neurology. 9 th ed. Baltimore: Lippincott Williams & Wilkins; 1995:68, with permission.)