Transient gestational diabetes insipidus: report of two cases and review of pathophysiology and treatment.

Gestational diabetes insipidus is a rare disorder characterized by polyuria and polydipsia due to the inability of the kidneys to concentrate urine. We report two cases of transient gestational diabetes insipidus in which patients responded to intranasal DDAVP (1-deamino-8-D-arginine vasopressin) with greater than 50% increase in urine osmolality and marked reduction in urine output. Intranasal DDAVP was discontinued after their discharge and both patients maintained normal urine output and appropriate urine osmolality. In determining whether diabetes insipidus is present in a patient who is polyuric and hypernatremic, a urine osmolality below that of the plasma suggests the presence of diabetes insipidus. Understanding of the pathophysiology may soon lead to improved methods of prevention, diagnosis and treatment.

Temporal resolution of gaps in noise by the rat is lost with functional decortication.

In Experiment 1 (n = 8), the rat's ability to detect brief gaps in white noise was measured by gap-produced inhibition of an acoustic startle reflex, elicited 100 ms after the gap. After bilateral application of KCl to the cortex, gaps as long as 15 ms provided no reflex inhibition; in contrast, the inhibitory threshold was between 2 and 4 ms in the saline control condition. In Experiment 2 (n = 13), noise pulses of 40, 50, or 70 dB were presented 20-500 ms before the startle stimulus, and in Experiment 3 (n = 5) noise offsets occurred so that the startle stimulus was presented at the end of a 2-30-ms gap. Noise pulses and offsets both inhibited reflex expression equally in saline- and KCl-treated animals. Differences between the normal (saline) functions of noise offsets and gaps suggest additional sensory processing with the longer lead time. The loss of gap sensitivity after KCl application indicates that gap processing, unlike pulses and offsets, depends on cortical mechanisms.