TL;DR: Hypodipsia should be considered as a cause of hypernatremia in elderly subjects even when they seem fully capable of requesting and obtaining water.
TL;DR: This paper found that the degree of hypodipsia was roughly proportional to the extent of the destruction of the same area, which on electrical stimulation evokes drinking in the goat, and no correlation was found between the absence of drinking and the presence of diabetes insipidus.
Abstract: Summary
Hypothalamic lesions which caused hypodipsia or adipsia lasting up to 14 days after the operation were made in dogs The animals developed marked dehydration as a consequence of the impaired water intake In contrast to the absence of “thirst”, the dogs ate and drank milk and broth readily No correlation was found between the absence of drinking and the presence of diabetes insipidus The degree of hypodipsia was roughly proportional to the extent of the destruction of the same area, which on electrical stimulation evokes drinking in the goat
TL;DR: A woman previously operated for craniopharyngioma has chronic hypernatremia without polyuria or polydipsia, and this appears to be due both to derangement of the thirst mechanism and to undiagnosis of the underlying cause.
Abstract: A woman previously operated for craniopharyngioma has chronic hypernatremia without polyuria or polydipsia. The hypernatremia appears to be due both to derangement of the thirst mechanism and to an elevation of the osmotic threshold for antidiuretic-hormone secretion. Long-term administration of hydrochlorothiazide has kept the serum sodium within normal limits, primarily by limiting renal free water clearance. Chlorpropamide and tolbutamide also proved to be strikingly effective in correcting the hypernatremia, by markedly increasing urinary osmolality. It is speculated that the sulfonylureas increase the concentration of cyclic adenosine monophosphate in the renal medulla as well as in the pancreatic beta cells, and that this accounts for their effects on urinary concentration and insulin secretion.
TL;DR: To compare the effects of the opioid antagonist, naloxone, on fluid ingestion in young and older males, in order to estimate the role of the opioids system in hypodipsia of older men.
Abstract: Objective To compare the effects of the opioid antagonist, naloxone, on fluid ingestion in young and older males, in order to estimate the role of the opioid system in hypodipsia of older men. Design Single-blinded, randomized, cross-over, placebo-controlled study. Setting Outpatient Department of Veterans Affairs. Study participants Sixteen young subjects (aged 23 to 39) and eight older subjects (aged 69 to 75). All subjects were healthy, community-dwelling, non-smoking men, on no medications. Intervention Subjects were randomized to receive either placebo or naloxone on day one. Whichever substance the subject did not receive was given on day two with days one and two separated by at least a 2-week washout period. Main outcome measures Fluid intake after overnight food and fluid deprivation, with placebo or naloxone injected in the morning. Results After overnight fluid deprivation, older individuals consumed 29% less fluid in 2 hours compared with younger individuals (ns). After overnight fluid deprivation and injection with naloxone 100 micrograms/kg, fluid intake was diminished by 42% (P less than 0.05) in young subjects compared with placebo, but only by 7% (ns) in older subjects. Subjective ratings did not differ significantly between young and old subjects. Conclusions These preliminary data suggest that the opioid system plays a role in the drinking response in young subjects while failing to alter fluid intake in older subjects. Hypodipsia in older individuals may be due to a deficit in the opioid drinking drive.
TL;DR: Most patients with cranial diabetes insipidus have normal thirst mechanisms, though clinically significant hypodipsia or hyperdipsia may co-exist with vasopressin deficiency, and one patient was shown to be Hypodipsic and compulsive water drinking was demonstrated in another.
Abstract: Patients with cranial diabetes insipidus are unable to concentrate urine, and depend on thirst and water intake to prevent hypertonic dehydration. Using a visual analogue scale (0-10 cm) we studied osmotically stimulated thirst induced by hypertonic saline infusion in 15 patients with diabetes insipidus and 15 healthy controls. Plasma osmolality in the patients rose from 292 ±1 to 316±1 mOsm/kg ( p <0.001), and 13 patients showed a progressive rise in thirst ratings (1.4 ±0.4 to 8.1 ±0.3 cm, p <0.001) with abolition of thirst by drinking, in a similar fashion to controls. Water intake following infusion was greater in patients than controls ( p <0. 001). Linear regression analysis of thirst and plasma osmolality showed no difference in the osmotic threshold for thirst onset, or the sensitivity of thirst osmoreceptors, between 13 of the patients and the control group. One patient was shown to be hypodipsic and compulsive water drinking was demonstrated in another: abnormal thirst perception caused abnormalities of salt and water balance in these two patients.
Most patients with cranial diabetes insipidus have normal thirst mechanisms, though clinically significant hypodipsia or hyperdipsia may co-exist with vasopressin deficiency.