Duane G. Spiker

Computerized EEG spectral analysis in elderly normal, demented and depressed subjects

Computerized spectral analysis of the EEG was performed in 35 patients with Alzheimers disease and compared to patients with major depression (23) and healthy elderly controls (61). Compared to controls, demented patients had a significant increase in the theta and alpha 1 bandwidths as well as an increased theta-beta difference. The parasagittal mean frequency, beta 1 and beta 2 activity were significantly decreased. Depressed patients differed from demented patients, particularly at the lower end of the spectrum, having significantly less delta and theta activity. Like the demented group, depressed patients also had a decreased parasagittal mean frequency, beta 1 and beta 2 when compared to controls. In demented patients, there was a high correlation between several spectral parameters (parasagittal mean frequency, delta and theta activity, and the theta-beta difference) and the Folstein score, EEG measures used for discriminant analysis were more accurate in identifying demented patients who had lower Folstein scores.

EEG sleep in elderly depressed, demented, and healthy subjects

In a prospective study of EEG sleep patterns in 25 elderly depressives, 25 elderly demented patients, and 25 healthy, elderly control subjects, the sleep of depressives was characterized by reduced REM sleep latency, increased REM percent and first REM period density, and altered temporal distribution of REM sleep, as well as by diminished sleep maintenance (correlated significantly with Hamilton ratings of depression: multiple R = -0.42, p less than 0.05). In contrast, the sleep of demented patients showed reduced REM sleep percent, but normal REM temporal distribution, increased loss of spindles and K-complexes (the latter correlating significantly with severity of cognitive impairment as measured by the Folstein score: multiple R = -0.59, p less than 0.01), and less severe sleep maintenance difficulty than for depressives. An examination of REM latency demonstrated a skewed distribution in depression (i.e., 42% of nights with sleep-onset REM periods), but a normal distribution in the controls and demented subjects. A REM latency cut-off score of 30 min correctly classified 68% of all patients (kappa = 0.36; p less than 0.005), compared with 78% correctly identified in our retrospective study (Reynolds et al. 1983).

Amitriptyline plasma levels and clinical response in primary depression.

Sixteen patients with primary depression were treated for 4 wk with amitriptyline. After clinical diagnoses were determined, patients entered a double‐blind protocol (amitriptyline or placebo) and their clinical status was determined with the Hamilton Depression Rating Scale by raters blind to the drug type, its dosage and plasma levels. Amitriptyline (AT) and nortriptyline (NT) plasma levels were assayed twice weekly by gas chromatography‐mass spectrometry. In the 16 patients, a negative correlation between the Hamilton Score and the mean total tricyclic level (p < 0.01), as well as with individual plasma levels, was found at the end of the treatment period. When the group was divided into clinical responders and nonresponders, the mean total tricyclic (AT + NT) levels discriminated the two groups by day 12 (p < 0.001) as well as at the end of the protocol (day 26, 88% of the patients were classified correctly if an arbitrary level of200 ng/ml total tricyclic plasma level was chosen). These results strongly suggest the presence of a positive correlation between plasma levels and clinical improvement in patients with primary depression.

Waking and All-Night Sleep EEG's in Anorexia Nervosa

Despite an abundance of literature on EEG findings in other psychiatric syndromes and renewed interest in the biological aspects of eating disorders, there is a surprising scarcity of published information about the EEG in anorexia nervosa. In fact, several major reviews of the EEG in psychiatric populations fail to mention this disorder entirely.(1-3) A small number of reports describe the EEGs of individual cases of the illness, but diagnostic criteria have often been poorly-defined, and the majority of these patients appear to have been suffering from concurrent neurologic illnesses.(4-8) The only systematic study of the EEG in anorexia nervosa was performed by Crisp et al.,(9) in a series of 32 patients. Of these, 59% had abnormal EEG background activity, 31% had unstable responses to hyperventilation, and 12.5% displayed epileptiform paroxysmal dysrhythmias. While a few patients presented evidence of a primary CNS etiology for these abnormalities, the majority were attributed by the investigators to reversible secondary manifestations of self-starvation: electrolyte imbalance, metabolic alkalosis, and relative hypoglycemia. All-night EEG sleep profiles have become increasingly important tools for the assessment and classification of psychiatric disorders. (10) In an earl ier controlled study of EEG sleep in a small number of patients from our laboratory, a significant reduction of both tonic and phasic components of REM sleep was found in primary anorexia nervosa.(11, 12) This type of abnormality has most frequently been observed in neurological disorders(13) and in symptomatic psychiatric syndromes accompanying primary medical illnesses.(14, 15) Unlike the clinical EEG findings of Crisp et al.,(9) this EEG sleep profile persisted even after patients had regained weight during therapy.(11) Moreover, a pedigree study revealed concordance of this sleep marker in three siblings, each of whom was in a different stage of an eating disorder or its remission.(12) The present study was designed to reexamine the clinical EEG findings of Crisp, et al.,(9) using standardized research diagnostic criteria. In addition, we compared waking EEG abnormalities to all-night EEG sleep profiles in this series of anorectics, as an extension of previous work by Foster et al. (11,12,14)

RBC and plasma choline levels in control and depressed individuals: A critical evaluation ☆

Red blood cell (RBC) and plasma choline (Ch) were measured in 78 depressed, drug-free patients and in 23 normal, drug-free control subjects. RBC Ch levels displayed a huge variability among the patients, in contrast to those measured in normal controls. Plasma Ch levels, on the other hand, were more consistent within each group, and were correlated with age among the two populations studied. RBC Ch levels would appear to be independent of plasma Ch levels, and to be highly individualized and reproducible within each subject. A segment of the depressed population exhibited significantly higher RBC Ch levels than those seen in the normal control population. A clinical correlation of RBC and plasma Ch levels within the depressed population indicated that the patients with RBC Ch levels exceeding 35 nmole/ml might represent a diagnostically distinct subpopulation with specific clinical characteristics. Results presented here, although preliminary, suggest a role for RBC Ch as a biological marker in certain categories of depressive illness.

Resting metabolic rate is reduced in patients treated with antidepressants.

Eating disturbances, most notably a decrease in appetite and weight loss, are associated with major depression (Robinson et al. 1975; Paykel 1977; Mezzich and Raab 1980). During antidepressant treatment, many symptoms of depression disappear (including appetite loss), and patients begin to gain weight. Several studies have shown that certain antidepressants, particularly tricyclic compounds, are associated with excessive weight gain (Paykel et al 1974; Kupfer et al. 1979; Berken et al. 1984). However, few

REM sleep, naps, and depression

Continued interest in rapid eye movement (REM) sleep abnormalities in depression stimulated comparative studies on daytime naps versus nighttime sleep. In a group of 15 depressed patients, REM latencies in morning and afternoon naps were similar to the shortened REM onset at night. Although REM latency did not vary across the three times, the propensity for REM sleep appeared to be greater in the morning nap than in the afternoon nap and the early portion of nocturnal sleep. Finally, the data suggest that responders to tricyclic treatment tend to be poor sleepers during daytime naps.

Prevalence of sleep apnea and nocturnal myoclonus in major affective disorders: clinical and polysomnographic findings.

We performed screening polysomnography on 86 inpatients with affective disorders and found that 13 (15.1 per cent) had sleep apnea and one had nocturnal myoclonus. The apnea tended to be extremely mild, with an average of 27.8 episodes per patient and with a mean duration of 15.0 seconds. No clinically significant cardiac arrhythmia accompanied the apnea. The apnea was predominantly obstructive or mixed, not central. Only four patients (4.7 per cent) had apnea indices greater than five, and even here the total apnea was considered mild. Much of the apnea (68.3 per cent) occurred during rapid eye movement sleep. While there was no association of apnea with gender or with type of sleep-wake complaint, a significant relationship with age emerged. On the basis of these data, we suggest that routine polysomnographic screening for sleep apnea and nocturnal myoclonus in affective disorders is not indicated. On occasion, however, both an affective disorder and a sleep-apnea syndrome co-exist in the same patient. In such cases, the sleep-wake complaint is usually very prominent and/or long-standing in relation to other psychopathology and requires appropriate polysomnographic evaluation.

EEG sleep and affective psychosis.

EEG sleep changes in delusional depression have been reported previously but no attempt has been made to examine sleep profiles among specific delusional subtypes. In 29 psychotically depressed patients, those patients with delusions of guilt or sin demonstrated both increased sleep discontinuity and decreased REM sleep, especially during the first REM period, while patients with somatic delusions showed increased REM activity, especially in the first REM period. The implications of these findings are discussed.

PLATELET MAO AND URINARY MHPG IN AFFECTIVE DISORDERS

We have determined the platelet MAO activity and urinary MHPG levels in 99 and 38 drug-free depressed patients, respectively. The unipolar and bipolar groups of patients did not differ with respect to the mean values obtained for either of these biochemical measures. However, the greater variance of platelet MAO activity in the bipolar group suggests that the group may be heterogeneous.