On basis of 35 patients who have suffered from transient global amnesia the pathophysiological mechanisms of this syndrome are discussed. Our impression is that the primary cause of this syndrome is a transient ischemia of the hippocampus, an opinion common with most earlier authors. The possibility of a unilateral hippocampal disturbance resulting in transient global amnesia is discussed. We are inclined to regard the local hippocampal ischemia as arising from insufficiency of the anterior chorioidal artery and thus as a sequel of internal carotid insufficiency, which has earlier been proved to result from various rotatory, flexion, and extension movements of the neck.

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The possible role of the hypothalamo-neurohypophysial system in regulating the release of the anterior pituitary hormones was studied in the rabbit and the rat. Thyroidectomy, gonadectomy and uni- and bilateral adrenalectomy were the experimental conditions used. The neurosecretory material (N. S. M.) was demonstrated by the aldehyde-fuchsin (AF) technique. Distinct differences were not seen in the different groups of rabbits on account of the great variation between individuals. In the rats, the thyroidectomy and gonadectomy groups often had slightly more N. S. M. in the median eminence around the portal vessels than the controls. Slight depletion of N. S. M. in the infundibular process was observed in unilaterally adrenalectomized rats. N. S. M. passing into the portal vascular system showed a tendency to increase. In the bilateral adrenalectomy group, N. S. M. was reduced in the supraoptic and paraventricular nuclei, in the hypothalamo-hypophysial tract and in the infundibular process. However, considerably more numerous neurosecretory nerve fibres passing towards the portal vessels than in the controls were found in the median eminence of this group. The conclusion drawn was that N. S. M. entering the hypophysial portal vessels in the median eminence may be of significance in the regulation of corticotrophin release.

In the family described here, the grandmother, father, and 3 of his 9 children had an apparently abnormal chromosome of group 21–22. The abnormality was similar in morphology in all the affected subjects and was found in metaphases from cultures of leukocytes, and skin and bone marrow. The short arm of the abnormal chromosome seemed longer than normal; it was not possible to ascertain whether the satellite itself or the short arm, or both, were enlarged. Of the 5 subjects affected, 4 were clinically normal. The fifth, a girl, had severe abnormalities of the central nervous system. One of her brothers, who was cytogenetically normal, had a similar syndrome of unknown origin. From these data, and from those published by others, it was postulated that an apparently enlarged satellite region is compatible with normal development. Such an abnormality does not necessarily imply an association with developmental disorder in the offspring of carrier subjects.