Over a period of 3 months a 51-year-old woman developed a depressive syndrome with loss of memory, inability to find words, impaired fine movements and phases of spacial disorientation. Biochemical tests demonstrated occasional slight rises in serum calcium (2.8-2.9 mmol/l) and parathormone (4.6-5.2 pmol/l). She had a grade II nodular goitre with normal thyroid function. Ultrasonography of the thyroid suggested a right cranial parathyroid adenoma, confirmed at a right thyroidectomy with resection of the right upper parathyroid, while the other parathyroid glands were grossly normal. Calcium and parathormone levels returned to normal after the operation, as did the neuropsychiatric symptoms (within two months). This typical case illustrates that even in seemingly isolated neuropsychiatric changes an organic disease, like primary hyperparathyroidism, needs to be thought of.

In order to investigate influences of corticotropin-releasing hormone (CRH) and corticotropin fragment (adrenocorticotropic hormone, ACTH, 4-9) on auditory perception processes, 10 subjects received either a placebo (sodium chloride 0.9%), CRH (100 micrograms) or ACTH 4-9 (Hoe 427, 300 micrograms) intravenously on different days. Late auditory evoked potentials (AEP) were computed and further analyzed using the brain electric source analysis method. As expected, CRH administration was followed by a rise in plasma cortisol and ACTH concentrations, whereas the injection of the ACTH 4-9 fragment did not alter plasma cortisol concentrations. In contrast to these different hormonal responses, both CRH and ACTH 4-9 modulated AEP in a similar manner, differing in quantity rather than in quality. The changes in AEP after the administration of ACTH 4-9 were most likely induced by a direct CNS action, whereas for the CRH effects, an indirect mechanism throughout the release of endogenous ACTH must be considered.

To investigate possible influences of growth hormone-releasing hormone (GHRH) and somatostatin (SRIF) on auditory perceptional processes, 12 subjects received either placebo (sodium chloride 0.9%), GHRH (50 μg), or SRIF (100 μg) on different days. Late auditory evoked potentials (AEP) were computed and further analyzed by using the brain electric source analysis (BESA) method. Reduced late AEP latencies were observed following GHRH administration. In contrast, SRIF had no significant effects on the AEP. The changes in late auditory processing seen after administration of GHRH were most likely induced by a direct central nervous action.

To study whether changes in late auditory evoked potentials (AF-Ps) and/or in stress-sensitive hormones of the hypothalamic—pituitary-adrenal (HPA) system take place between a first and a second placebo experiment and if so, whether these changes are possibly related to each other, we conducted two identical placebo sessions (2 ml 0.9% saline) and one cortisol session (50 mg) with 10 subjects on three different days. Plasma cortisol concentrations were significantly higher at the beginning of the first placebo experiment than the second, with a concordant decrease of plasma adrenocorticotropin hormone (ACTH) concentrations. In the AEP domain, a consistently lower P2 amplitude was observed in the first session. Since the change in late auditory processing could not be demonstrated after exogenous administration of cortisol, a direct mediation through an elevation of plasma cortisol concentrations or indirect mediation through a decrease of plasma ACTH concentrations seems unlikely. We rather propose that other stress-sensitive mechanisms, such as CCK, might account for the novelty-induced P2 amplitude lowering.

Over a period of 3 months a 51-year-old woman developed a depressive syndrome with loss of memory, inability to find words, impaired fine movements and phases of spacial disorientation. Biochemical tests demonstrated occasional slight rises in serum calcium (2.8-2.9 mmol/l) and parathormone (4.6-5.2 pmol/l). She had a grade II nodular goitre with normal thyroid function. Ultrasonography of the thyroid suggested a right cranial parathyroid adenoma, confirmed at a right thyroidectomy with resection of the right upper parathyroid, while the other parathyroid glands were grossly normal. Calcium and parathormone levels returned to normal after the operation, as did the neuropsychiatric symptoms (within two months). This typical case illustrates that even in seemingly isolated neuropsychiatric changes an organic disease, like primary hyperparathyroidism, needs to be thought of.

Over a period of 3 months a 51-year-old woman developed a depressive syndrome with loss of memory, inability to find words, impaired fine movements and phases of spacial disorientation. Biochemical tests demonstrated occasional slight rises in serum calcium (2.8-2.9 mmol/l) and parathormone (4.6-5.2 pmol/l). She had a grade II nodular goitre with normal thyroid function. Ultrasonography of the thyroid suggested a right cranial parathyroid adenoma, confirmed at a right thyroidectomy with resection of the right upper parathyroid, while the other parathyroid glands were grossly normal. Calcium and parathormone levels returned to normal after the operation, as did the neuropsychiatric symptoms (within two months). - This typical case illustrates that even in seemingly isolated neuropsychiatric changes an organic disease, like primary hyperparathyroidism, needs to be thought of.

In an acute trial, three different dosages (60, 300, and 600 micrograms) of the endocrinologically inert but behaviorally active corticotropin 4-9 (ACTH4-9) fragment ebiratide were given to three patients with clinically probable Alzheimer's disease and five patients with a major depressive episode who were psychomotorly retarded. The drug was given intravenously in a double-blind, placebo-controlled, crossover design, and cognitive as well as psychopathologic assessments were carried out predrug and postdrug treatment. In summary, no adverse effect of the ACTH fragment was detected. In this explorative study, none of the patients improved cognitively, as measured by neuropsychologic testing. However, all patients, regardless of underlying disorder, reported a decrease of the feeling of tiredness or loss of energy, respectively. They felt more vigorous and alert. This occurred after any of the three doses of ACTH4-9, but not after placebo. In concert with reports from other studies, it is concluded that the ACTH4-9 fragment ebiratide may have activating properties in humans. However, given acutely, it does not seem to have antidementia or antidepressive efficacy.

The subjects performed voluntary eyeblinks under illuminated and dark laboratory conditions. 32-channel EEG recordings were averaged in relation to the eyeblinks and a brain electric source analysis (BESA) was performed. Two dipoles located near the eyeballs and a third dipole in the occipital region of the brain were found to explain the scalp potentials. The frontally located potentials described electromechanical potentials associated with lid movements and simultaneous eye movements. The occipitally located dipole explained a visually evoked potential with a first peak at about 180 ms after the maximum of the frontal blink potential. The visually evoked potential was observed only under illumination and was probably caused by changes in luminance during the eyeblinks.