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Background: Earlier EEG studies reported essentially normal findings during acute manic episodes but some atypical EEG characteristics and distinctions between familial and sporadic cases were described. Recently quantitative EEG (qEEG) studies differentiating mania from schizophrenia and depression have been published., Methods: Clinical EEGs were obtained in 202 patients hospitalized for acute mania. EEGs were repeated in 75 patients rehospitalized for subsequent manic attacks. Quantitative EEGs were recorded in 37 patients who were able to cooperate after drug washout and again on completion of randomly assigned pharmacotherapy., Results: Normal EEGs were obtained in most patients. Moderately abnormal EEGs in 16% were significantly associated with absent family histories of affective disorder. Left sided abnormalities were more common than right. "Small sharp spikes" and "microsleep" were encountered in 17% and 10% respectively of patients who drowsed. EEG findings during subsequent episodes did not suggest increasing CNS vulnerability. qEEGs showed significant differences between each of the therapeutic agents compared-lithium, carbamazepine, and lithium combined with carbamazepine, haloperidol or risperidone. Nonresponders at baseline had significantly more diffuse theta activity than responders. During pharmacotherapy nonresponders had higher amplitudes in the left temporoparietal areas., Limitation: Clinical EEG findings confirmed previous reports but did not contain original observations. Applications of qEEG were limited by requirements for patient cooperation.

QEEG findings from 39 hospitalized manic patients were accomplished after a drug free period and following pharmacotherapy with lithium or carbamazepine alone or lithium combined with carbamazepine, haloperidol or risperidone. A subsample of 10 drug-free manic patients was compared with normal controls, which revealed lower qEEG amplitudes in the left anterior and midtemporal regions in the patients. Comparisons of drug therapies showed increased delta amplitudes and total power with lithium compared with carbamazepine. Increased fast frequencies were observed in the lithium and carbamazepine plus lithium groups compared with carbamazepine alone. Comparisons of the three drug combination groups revealed increased alpha and beta 1 amplitudes, most with risperidone and least with carbamazepine. Anterior delta and beta 2 amplitudes and interhemispheric coherence were increased directly proportional to plasma lithium levels. Nonresponders to treatment were identified at baseline by increased generalized theta amplitudes. After treatment, the nonresponders had higher amplitudes in the left temporal areas. Numerous qEEG associations with individual ratings of manic symptoms were found, more at baseline than after treatment. In general levels of psychopathology were negatively correlated with qEEG amplitudes. The qEEG findings appear to implicate dominant temporal lobe dysfunctions in mania.

Melatonin 3 mg and secobarbital 100 mg assigned randomly were given to 40 psychiatric patients for sleep induction during EEG recording. Nine patients who did sleep naturally comprised a comparison group. EEGs were read blind; most were interpreted as mildly abnormal or within normal limits. No statistically significant differences between the three groups were observed in response to photic stimulation, hyperventilation or in frequency of paroxysmal variants. The electroencephalographer was able to identify the melatonin patients significantly more accurately than those who received secobarbital on the basis of lack of EEG manifestations of fast frequencies typical of barbiturate effects. Self-assessments of drowsiness, anxiety and performance on a perceptual-motor task were similar in the melatonin and secobarbital patients. However, the secobarbital group showed more impairment on a locomotion test than those who received melatonin or slept spontaneously. The results suggest that melatonin is a plausible alternative for EEG sleep sedation, especially for ambulatory patients.

Clinical EEG findings from 202 hospitalized manic patients repeated during 131 recurrences of mania were described. Results were considered in the light of current issues in the literature including the incidence of EEG abnormalities and minor variations, relationships between EEG and family history, EEG lateralization and longitudinal course of illness. The majority of patients had normal EEGs or mild nonspecific deviations compatible with effects of psychoactive medications. More definitive EEG abnormalities were observed in 16-percent. Microsleep occurred in 19 percent and small sharp spikes were found in 17 percent of those who drowsed, with lower incidences of 14 and 6 positive bursts and 6 Hz spike-and-slow-waves. Significant relationships between moderate or severe EEG abnormalities and negative familial loading were identified. Lateralized EEG abnormalities appeared in 9 percent of cases, involving the left side significantly more often than the right. With one exception EEG recordings during subsequent episodes did not suggest structural brain changes. Clinical EEG studies are useful in discriminating between primary and secondary affective disorders. They are also sensitive to effects of lithium and other psychoactive medications. The significance of EEG variations including microsleep and other atypical features continues to be elusive. Issues relating to heritability, hemispheric dysfunction and longitudinal course of illness merit further investigation.

The current practice of monitoring brain electrical activity with single channel recordings during ECT induced seizures does not meet contemporary EEG standards. Multichannel recordings are essential for artifact identification, determination of seizure endpoint, and assessment of electrophysiological features in different brain regions. Careful attention to technical aspects and detailed descriptions are important for interpretation and for scientific communication. Standardized procedures for EEG monitoring during ECT should be developed for general clinical use and for research and training applications.

Forty-two patients each were randomly assigned in equal numbers to receive either zolpidem or secobarbital for sleep EEG recording. Three groups were compared; zolpidem, secobarbital and a control group of patients who drowsed spontaneously. All patients were evaluated before and immediately after the EEG and several hours later with measures of anxiety, perceptual-motor performance, locomotion, and subjective judgments of sleepiness. EEG response to standard activation procedures, signs of drowsiness and sleep and overall diagnoses were compared among the three groups. No differences emerged in demographic measures, psychiatric diagnoses, current drug treatment and experience with hypnotics. There were no statistically significant differences among the three groups or between the patients receiving the hypnotics on the anxiety performance and locomotion measures or degree of alertness. As a result of the experimental design, the unmedicated control patients showed EEG signs of drowsiness and sleep significantly sooner than patients receiving hypnotics. They also showed more slow or paroxysmal activity in response to hyperventilation, which may have been due to their greater effort. These results led us to retain secobarbital as the hypnotic for EEG sleep, mainly for economic reasons.

Rabbit Coronavirus (RbCV) infection was divided into two phases based upon day of death and pathologic findings. During the acute phase (days 2-5) heart weights (HW) and heart weight-to-body weight (HW/BW) ratios were increased with striking dilation of the right ventricle. These changes as well as increased dilation of the left ventricle were especially pronounced during the subacute phase (days 6-12). Myocytolysis, pulmonary edema, and degeneration and necrosis of myocytes, were seen during both phases. Myocarditis, pleural effusion, calcification of myocytes, and congestion in the liver and lungs were seen in the subacute phase. Electrocardiograms (ECGs) exhibited low voltage, nonspecific ST-T wave changes, sinus tachycardia, occasional ventricular and supraventricular premature complexes and 2(0) AV block consistent with myocarditis and heart failure. Forty-one percent of the survivors exhibited increased HW and HW/BW ratios, biventricular dilation, interstitial and replacement fibrosis, myocyte hypertrophy and myocarditis. ECGs exhibited nonspecific ST-T wave changes, sinus arrhythmia, occasional ventricular and supraventricular premature complexes and 2(0) AV block. These data suggest that RbCV infection may result in viral myocarditis and heart failure with a proportion of survivors progressing into DCM.

A group of 759 patients with final DSM-I and -II diagnoses of schizophrenia was identified among a cohort of 1494 adults who were hospitalized between 1965 and 1972. Admission EEG recordings were done in each patient during waking, activation procedures, drowsiness, and sleep. All cases were reclassified according to the Feighner et al. criteria, and relationships between the EEG, reassigned diagnosis, and outcome were examined. One-third of the schizophrenics were rediagnosed as having affective, organic, or other disorders. EEG abnormalities predicted diagnostic change and relatively favorable prognosis. Mean alpha frequencies were slower in schizophrenics than in patients with other DSM I-II disorders, and less in patients with Feighner et al. diagnoses of schizophrenia than in some rediagnosed categories. In 1980-82, matched samples from the original cohort with affective, schizophrenic, and mixed Feighner et al. diagnoses were followed and evaluated blindly with the SADS-L. RDC follow-up diagnoses were significantly correlated with the index EEG findings in terms of higher alpha average frequencies proportional to the amount of affective psychopathology. A subgroup of high functioning individuals within the RDC schizophrenic category was identified with affective symptomatology early in the course of illness, normal EEGs, and high alpha average frequencies. Patients with a consistent diagnosis of schizophrenia according to the three nosologic systems were shown to function better in some areas if the index EEG was abnormal. Discriminant function analysis established that DSM-I and -II categories possessed the greatest long-term predictive accuracy which was enhanced by the EEG diagnosis and alpha average to a level of more than 50%. The Feighner et al. and RDC diagnostic systems were not as relevant for prediction of long-term follow-up status.

Electroencephalographic (EEG) studies of 60 patients with bipolar manic-depressive disease disclosed an incidence of small sharp spikes plus a few other variations in 47% of the sample. In women these EEG features were significantly associated with a history of mental illness in the patient's mother or the maternal side of the family and an absence of mental disorder in the fathers. The reverse was true of women probands without these EEG characteristics. In the men small sharp spikes did not relate to parental psychopathology but half of the sisters of men with these EEG characteristics were found to be mentally ill. On the basis of these observations and previous work, we hypothesize that the small sharp spike EEG pattern might be an inherited characteristic related in some way to the familal transmission of manic-depressive disease.

In this paper we have described early applications of computerized EEG techniques in psychopharmacology. Perhaps our most remarkable finding was there were practically no differences between very chronic drug free schizophrenic patients and normals, which contradicts much of the EEG imaging literature. To us, the most likely explanation is that most of the anterior slowing observed in other studies was due to contamination from orbital artifacts, which we took exceptional pains to remove. Lingering effects of neuroleptic medications may also have contributed. Alternatively, EEG deviations in schizophrenia may recede when the illness reaches a very chronic stage, although this hypothesis is less tenable. There were significant differences between placebo and the three neuroleptics in terms of increased amplitudes in the delta and theta frequency bands in the anterior head regions, which is compatible with data from other studies. These changes were most pronounced with clozapine and least prominent with haloperidol, with chlorpromazine occupying an intermediate position. This order happens to parallel their relative antiserotonergic, antihistaminic and anticholinergic properties. The latter may have been partially obscured by the addition of benztropine. In a subgroup of patients who were recorded under each of the treatment conditions, there were more fast frequencies with clozapine than with the other neuroleptics agreeing with Roubicek and Major. This could be a function of clozapine's increased adrenergic activity as reported by Ackenheil. An unexpected finding was that patients who responded to clozapine had higher amplitudes in the alpha spectrum, most pronounced in the left anterior quadrant, than did the nonresponders. These differences between responders and nonresponders obtained whether patients were on placebo, haloperidol or clozapine. Curiously, Buchsbaum et al. found that anxious patients who responded to benzodiazepines also had higher alpha amplitudes in the same brain regions, which differentiated them from nonresponders. These findings clearly warrant future scientific investigation. In this regard, the generalizability of our data is limited by the extremely chronic, treatment-resistant population studied. However, promising directions for further research in EEG and psychopharmacology have been identified.