The authors undertook this study to determine the effects of age, gender, and heart rate (HR) on the results of cardiac autonomic function tests for measuring heart rate variability (HRV) in a large sample of healthy subjects (n = 309). Conventional tests (deep breathing, maximum/minimum 30:15 ratio), and a standardized 5-minute resting study, including spectral analysis of HR, were used. The main findings included (1) the indices of all tests, except for the ratio of the low- (LF) to high-frequency (HF) spectral power (LF/HF ratio) and HR itself, are inversely related to age in both sexes; (2) the 5-minute spectral bands (except for the LF/HF ratio), the variation coefficient, expiratory-inspiratory ratio during deep breathing, and the maximum/minimum 30:15 ratio are independent of HR; (3) women up to the age of 55 years have a higher resting HR compared with men; (4) young and middle-aged women show a significantly lower LF power and LF/HF ratio compared with age-matched men, whereas no significant gender differences are observed in the absolute HF power. The authors computed age- and gender-dependent normal values for each of the HRV indices studied here and discuss the clinical consequences arising from gender differences in HRV.

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Volumes of basal ganglia in postmortem brains of 8 patients with mood disorders and 8 control subjects without neuropsychiatric disorder were determined. Morphometry of serial whole-brain sections under the control of postmortem artifacts revealed reduced volumes of the left nucleus accumbens (-32%, P = 0.01), the right and left external pallidum (-20%, P = 0.04), and the right putamen (-15%, P = 0.04) in the patient group compared with the control group. These results suggest that, in particular, the limbic loop of the basal ganglia involving the nucleus accumbens and the pallidum is affected in mood disorders.

Sixty-one patients with essential thrombocythemia (ET) were followed from 1974 through 1987 at the Medizinische Poliklinik. Fifty-one patients (84%) presented with thromboembolic complications, and eight patients (13%) with hemorrhages. In seven patients (12%), a thrombocytosis was detected accidentally. Disturbances of the microcirculation (67%), mainly of the fingers and toes (53%), were the most frequent thromboembolic symptoms. The mean age of all patients was 58 years (male patients, 61 years; female patients, 56 years). The average platelet count at diagnosis was 897,000/microliter. The average maximal platelet count was 1.231 X 10(6)/microliter (range, 500,000/microliter to 4 X 10(6)/microliter). Seventy-two percent had a moderate leukocytosis (average, 12,400/microliter), 34% a splenomegaly, 29% a hepatomegaly. Signs of hypermetabolism were infrequent, lactate dehydrogenase (LDH) and uric acid elevations, if present, were moderate. Bleeding time and viscosity were normal in most patients. Spontaneous platelet aggregation was increased in 81% of patients (n = 40). Platelet aggregation studies with the aggregation inducing substances adenosine diphosphonate (ADP), platelet activating factor (PAF), thrombin, collagen, and adrenalin showed hypoaggregation in most patients. Adrenalin-induced aggregation distinguished best between ET-patients and reactive thrombocytosis showing hypoaggregation in all ET-patients tested (n = 16) and in none of 22 controls. Bone marrow studies were performed in 57 patients. The histologic studies (done in 49 patients) were consistent with a chronic myeloproliferative disorder in all cases. In 41 cases (84%) the picture of a megakaryocytic myelosis was found, in 12 of these a granulocyte-rich form of megakaryocytic myelosis. Cytologic studies only (eight patients) did not differentiate ET well from reactive thrombocytosis. Platelet aggregation studies and bone marrow histology may be of help in the diagnosis of difficult cases of thrombocytosis. The Philadelphia status was negative in all cases studied (14 patients). Fourteen patients died. The causes of death were thromboembolic complications in probably 11 and acute leukemia in two patients. The probability of 10-year survival is 64% after a mean follow-up time of approximately 5 years. It appears that considering the average age of ET patients at diagnosis, life expectancy is close to normal.

Structural changes in subcortical nuclei may underlie clinical symptoms of mood disorders. The goal was to determine whether macrostructural changes exist in brain areas assumed to be involved in regulation of mood and whether such changes differ between major depressive disorder and bipolar disorder. A case-control design was used to compare volumes of all major subcortical nuclei. Brains of patients with major depressive disorder (n = 9) or bipolar disorder (n = 11) or of individuals without a neuropsychiatric disorder (n = 22) were included. Exclusion criteria were a history of substance abuse or histological signs of neurodegenerative disorders. Volumes of the striato-pallidal nuclei, of the hypothalamus, thalamus, amygdala, hippocampus and basal limbic forebrain were determined in the right and left hemisphere by planimetry of 20 mum whole brain serial paraffin sections. Comparisons between patients with bipolar disorder, major depressive disorder and controls showed a significant (Lambda = 0.35, F(20,56) = 1.93, P = 0.028) overall difference in volumes of all investigated regions with strong effect sizes ( f > 0.40) contributed by the hypothalamus, external pallidum, putamen and thalamus. As compared to controls, a strong effect size (f > 0.40) was found in the bipolar group for smaller volumes of the hypothalamus, external pallidum, putamen and thalamus,whereas in patients with major depressive disorder a strong effect size was only found for a smaller volume of the external pallidum. In conclusion our data suggest that pathways presumably involved in mood regulation have structural pathology in affective disorders with more pronounced abnormalities in bipolar disorder.

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