With increasing CT examinations of the cerebrum, the discovery of basal ganglia calcification becomes more frequent. In order to correlate these calcifications to the symptoms believed to be accompanied with Fahr's disease 2318 cranial CT scans were examined. There was an overall incidence of basal ganglia calcification of 12.5%. The most frequent location was the globus pallidus (96.4%). In the examined population there was no correlation found between the calcifications and symptoms having been described with striopallidentate calcifications.

In severely ill patients of an intensive care unit overt peripheral thyroid hormone deficiency was noted in 22 of 33 subjects. The TRH-test was performed in 7 of these 22 patients and was negative in all. Thus, the laboratory data suggest secondary hypothyroidism. The laboratory diagnosis, however, could not be supported by clinical signs probably due to the short period of observation and to the strongly elevated body temperature of the respective patients. The pathogenetic mechanism is not clear. However, all patients developing secondary hypothyroidism were treated with dopamine and/or glucocorticoids, compounds known to inhibit pituitary TSH release and most of the patients had septic fever. A persistently "hypothyroid state" (total T4: 23 +/- 15 nmol/l, free T4: 6.1 +/- 3.2 pmol/l, total T3: 0.28 +/- 0.22 nmol/l, S.D.) is associated with a very poor prognosis. In view of the negative effects of a hypothyroid state, substitution of thyroid hormones must be considered in this situation.

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EEGs were recorded and initial CSF and blood lactate measurements (135) made in 104 patients who were in coma of differing severity from a variety of medical conditions. There were two patterns: in one, the CSF lactate alone was due to cerebral tissue hypoxia; and in the other factors, such as cerebral haemorrhage, meningitis or lactacidosis were predominantly present. In those with cerebral hypoxia there was a connection between the severity of the disease picture and the level of CSF lactate. In extreme cases with dissociated cerebral death, there was a mean CSF lactate concentration of 11.78 +/- 1.66 mmol/1. The prognosis of coma with concentrations above 9 mmol/l is, therefore, poor if not hopeless. To some extent one may draw prognostic conclusions from lower concentrations but this is not possible in individual cases. There was no definite correlation between the severity of EEG changes and the level of CSF lactate in coma, although there was some relationship to the degree of cerebral hypoxia. In case of meningitis, CSF lactate allowed differentiation between bacterial and viral cause, the average concentration in the former being four times normal.