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PubMed2006

The treatment of psychogenic polydipsia with risperidone in two children diagnosed with schizophrenia.

Polydipsia is a well-known phenomenon in adult psychiatry, but the literature regarding children is very limited. Just as the pathogenesis remains poorly understood, so does its management remain a clinical challenge. Data regarding the effect of risperidone on polydipsia are contradictory. We present case studies of remission of severe polydipsia with risperidone in two children.

Antipsychotic Agents↗

PubMed2005

Differential diagnosis of polyuria and polydipsia in a patient with spinal cord injury.

We report the case of a 35-yr-old tetraplegic man who experienced increased water intake, constant thirst, and a copious amount of urine excretion after his spinal cord injury and in whom an intermittent catheterization program was unmanageable. Laboratory evaluation revealed low serum and urine osmolality, which were suggestive of psychogenic polydipsia, and hypokalemia, which might lead to polyuria with a compensatory polydipsia. His water intake was reduced with antidepressant therapy and potassium supplementation and normalized on the third month of the treatment. Physicians should be aware of the differential diagnosis of polyuria and polydipsia, which interfere with neurogenic bladder management in patients with spinal cord injury.

Adult↗

PubMed2007

Pharmacological analysis of the effects of benzodiazepines on punished schedule-induced polydipsia in rats.

Food-deprived Wistar rats were exposed to a fixed-time 60-s food delivery schedule until they developed schedule-induced polydipsia. Every fifth lick was then followed by an electric shock during two, signalled, 5-min periods, which ran concurrently with the food delivery schedule. Shock intensities were adjusted to reduce licking to 60-70% of the unpunished licking rates. The benzodiazepine full agonists, diazepam (0.3-3.0 mg/kg), chlordiazepoxide (0.3-10.0 mg/kg), oxazepam (0.3-3.0 mg/kg) and the benzodiazepine partial agonist, RU-32698 (3.0-17.0 mg/kg), led to increases in punished responding at intermediate doses and decreases at the highest doses tested. All benzodiazepine agonists brought about dose-dependent decreases in unpunished schedule-induced polydipsia, with doses required to reduce drinking proving higher than doses required to increase punished schedule-induced polydipsia. The antipunishment effect of 0.3 mg/kg of diazepam was dose-dependently antagonized by flumazenil and the benzodiazepine inverse agonist, RU-34000. Flumazenil effects, however, could reflect actions of flumazenil as a partial inverse agonist at GABAA receptors. RU-32698 at 10.0 mg/kg further facilitated the rate-increasing effect of 0.3 mg/kg of diazepam, but at 17.0 mg/kg partially blocked such antipunishment effect. Overall, the present results extend the similarities of the effects of benzodiazepine compounds on adjunctive and operant patterns of behaviour by showing similar interactions within the benzodiazepine receptor complex.

Animals↗

PubMed1986

Neuroendocrine factors mediating polydipsia induced by dietary Na, Cl, and K depletion.

We investigated whether the increased intake of water during dietary electrolyte depletion is related to activation of the renin-angiotensin system. Young adult male rats were fed a low Na-, Cl-, K-free (low-salt) diet for 2 wk during which measurements were made of daily water intake and urine volume, plasma osmolality (Posm) and electrolytes, and plasma renin activity (PRA) and angiotensin I (ANG I) concentration. Water intake and urine output increased on day 3 of the low-salt diet, reached a maximum on day 4, and remained elevated, paralleling the time course of increases in PRA and ANG I plasma concentrations. Posm was normal after 2 days on the low-salt, although it was significantly lower by day 11. Renal concentrating ability was not different from controls after 6 days, but was significantly reduced after 11 days of treatment. Electrolytic lesions of the subfornical organ (SFO) abolished the low-salt diet-induced polydipsia, but had no effect on the diet-induced increases in PRA and plasma ANG I concentration. These data demonstrate that polydipsia induced by feeding a low-salt diet can develop in the presence of a normal or reduced Posm and precedes the development of a renal concentrating defect. The primary polydipsia is associated with elevated PRA and ANG I and appears to be mediated by angiotensin receptors in the SFO.

Animals↗

PubMed1993

Impairment of osmotically stimulated AVP release in patients with primary polydipsia.

The secretion of arginine vasopressin (AVP) from the posterior pituitary is primarily and finely regulated by the osmolality of plasma. Even though a number of factors alter osmolality-induced release of AVP, there are no published data in humans that have addressed the role of chronic overhydration on this phenomenon. To address this problem we have identified eight patients with primary polydipsia using criteria not involving measurement of AVP, and have subjected them to standardized infusions of hypertonic saline. These patients had less AVP in both plasma and urine in relation to plasma osmolality than was found in normal subjects. In addition, their rate of rise of plasma and urine AVP was less than in normal subjects. Their osmotic threshold for AVP release may have been higher than normal. These data demonstrate that chronic overhydration in humans downregulates the release of AVP in response to hypertonicity. This phenomenon may explain the impairment of urine concentration in patients with primary polydipsia and emphasizes the basis of the difficulty that may occur clinically in differentiating between patients with primary polydipsia and partial central diabetes insipidus.

Adult↗

PubMed2001

Association study of angiotensin-converting enzyme gene polymorphism with schizophrenia and polydipsia.

Angiotensin-converting enzyme (ACE) is a key enzyme in the renin-angiotensin system and can modulate dopamine turnover in the midbrain. Previous studies have revealed changes in the central ACE levels for schizophrenic patients, possibly related to the polydipsia commonly demonstrated for chronic schizophrenia. An insertion (I)/deletion (D) polymorphism of the ACE gene has been associated with ACE levels. Therefore, we elected to investigate the ACE I/D polymorphism for 124 schizophrenic patients and 117 control subjects. No significant differences for the genotype distribution or the allele frequency were revealed comparing controls and schizophrenic patients. The ACE genotypes were not associated with onset age or psychiatric symptoms for the schizophrenic cases. A modest association was revealed for this ACE polymorphism and polydipsia diagnosis for these patients. Using bearers of the D allele as baseline, the ratio for I/I homozygote was 2.31 (95% CI 0.95-5.65). This association needs further replication as it may have implications for the pathogenesis and the treatment of polydipsia for schizophrenic patients.

Adult↗

PubMed1982

Evaluation of the renin-angiotensin system in diabetes insipidus and psychogenic polydipsia.

The role of the renin-angiotensin system in polyuric patients was studied in 5 patients with pituitary diabetes insipidus, 1 patient with nephrogenic diabetes insipidus and 3 patients with psychogenic polydipsia by determining the plasma renin activity and infusing an angiotensin II analog, 1-Sar, 8-Ile angiotensin II. In all patients with diabetes insipidus, plasma renin activity was markedly increased and the blood pressure was reduced in 5 of 6 patients by the administration of the angiotensin II analog. In the other patient, the blood pressure remained unchanged. The plasma renin activity and response of blood pressure to the angiotensin II analog in a patient with nephrogenic diabetes insipidus were not significantly different from there of patients with pituitary diabetes insipidus. On the other hand, in all patients with psychogenic polydipsia, plasma renin activity was normal or low, and the blood pressure increased with the administration of the angiotensin II analog. These results suggest that evaluation of the renin-angiotensin system by determining plasma renin activity and infusing an angiotensin II analog is useful in differentiating between diabetes insipidus and psychogenic polydipsia.

1-Sarcosine-8-Isoleucine Angiotensin II↗

PubMed1995

Transient nephrogenic diabetes insipidus accompanied by possible psychogenic polydipsia.

A 50-year-old Japanese man had been suffering from polydipsia and polyuria for 2 months without any other specific symptoms. His daily urinary output reached 5 liters. On admission, no abnormalities of the kidneys, heart, thyroid, adrenals, pituitary or hypothalamus were detected by laboratory tests and MRI of the head. Pure psychogenic polydipsia was ruled out because his urine volume did not decrease sufficiently with 18 h of water deprivation and the subsequent injection of aqueous vasopressin. Plasma arginine vasopressin (AVP) levels against plasma osmolality remained within the normal range during the test. These results indicated that diabetes insipidus in this case was caused by renal insensitivity to AVP. The symptoms disappeared spontaneously, and marked improvement was observed in a second water deprivation test 1 month later, although the maximum urine concentration was still subnormal. The combination of both latent insufficiency of AVP secretion and impairment of the renal countercurrent system induced by psychogenic polydipsia was speculated as a possible mechanism for the transient nephrogenic diabetes insipidus in this case.

Arginine Vasopressin↗

PubMed1993

Association of nonsuppression of cortisol on the DST with primary polydipsia in chronic schizophrenia.

Thirteen polydipsic and 40 nonpolydipsic chronic schizophrenic patients received the dexamethasone suppression test while stabilized on psychotropic medication regimens. Thirty-eight percent (N = 5) of those with polydipsia but only 5% (N = 2) of those without polydipsia were nonsuppressors of cortisol (i.e., had an abnormal response). It is suggested that hippocampal dysfunction could cause both polydipsia and cortisol dysregulation in these patients.

Adolescent↗

PubMed1985

The medical and psychological investigation of psychogenic polydipsia: a case study.

The case of a 17 year-old female with psychogenic polydipsia is reported; 13 out of 18 members of her maternal family were known to have had polydipsia and polyuria, but only two had undergone endocrine investigations--one had diabetes insipidus and one also had psychogenic polydipsia. There are probable contributions of non-genetic family factors including imitation and identification to the development of this patient's condition. Detailed family and developmental histories may be of particular assistance in the understanding of the psychogenesis of the disorder in some patients.

Adolescent↗

PubMed1991

Intoxicated by water. Polydipsia and water intoxication in a mental handicap hospital.

A cross-sectional survey of the drinking habits of 877 mentally handicapped in-patients revealed 31 patients (prevalence 3.5%) who, in the opinion of nurses, drank five litres or more daily. Low urine specific gravity was a less useful indicator of polydipsia. Polydipsia appeared to be significantly associated with a borderline level of handicap and with a diagnosis of schizophrenia, autism or severe personality/behaviour disorder. Of five cases of water intoxication associated with polydipsia, one was fatal. In two cases excess drinking improved with increased neuroleptic medication. Lithium and demeclocycline were used in two cases to prevent hyponatraemic episodes.

Adult↗

PubMedDate not supplied

Vasopressin response to osmotic stimulation in 18 young dogs with polyuria and polydipsia.

Common disorders of water homeostasis leading to polyuria include a variety of endocrine, metabolic, and renal disturbances. After exclusion of most of these conditions, the diagnostic dilemma of differentiating between central diabetes insipidus, primary polydipsia, and nephrogenic diabetes insipidus may remain. Here, we report on 18 young dogs with polyuria that had been present in most cases since the dogs were puppies. The conditions were categorized according to the plasma vasopressin (VP) response to hypertonicity. The VP response to osmotic stimulation was tested by IV infusion of 20% NaCl for 2 hours. The VP response in all dogs was abnormal. Three categories could be distinguished: an exaggerated response (n = 3), a subnormal response (n = 4), and a nonlinear response with high plasma VP concentrations unrelated to increases in plasma osmolality (n = 11). The VP response to hypertonicity did not consistently distinguish among different clinical entities. In the 9 dogs with variations in urine osmolality compatible with primary polydipsia, exaggerated, subnormal, and nonlinear responses were observed. Examination of the present data questions the generally accepted notion that VP measurements during hypertonic saline infusion are the "gold standard" for the diagnostic interpretation of causes of polydipsia and polyuria. Studies of the peripheral reflection in plasma of the pulsatile VP release in healthy and polyuric individuals, with and without osmotic provocation, should be performed.

Animals↗

PubMed1966

The motivational properties of schedule-induced polydipsia.

Schedule-induced polydipsia occurred during initial magazine training to Noyes pellets (45 mg), disappeared when lever-pressing was acquired on a continuous reinforcement schedule (CRF), and reappeared when the food contingency was changed to a 1-min variable interval schedule (VI 1 min). Polydipsia also developed under a VI 1 min food schedule when water was concurrently available on various fixed ratios (FR), rather than being freely available. The level of the polydipsia and its motivating properties allow it to be classified as a form of adjunctive behavior.

Animals↗

PubMed1980

Polydipsia induced by intermittent delivery of salted liquid foods.

Food-deprived rats given constant access to water were exposed to fixed-time presentations of soybean milk and diluted sweetened condensed cows' milk. In some conditions these liquid foods were adulterated with varying amounts of sodium chloride. Under a fixed-time 30-sec schedule of food delivery, little water was consumed when the food was soybean milk alone, or soybean milk with sodium chloride added in concentrations of .9, 1.8, or 3.6%. However, schedule-induced polydipsia appeared when soybean milk adulterated with 7.2 or 14.4% sodium chloride was delivered under this schedule. When soybean milk containing 7.2% sodium chloride was presented under fixed-time 15-, 30-, 60-, 120-, and 240-sec schedules, schedule-induced drinking increased with the fixed-time value from 15 to 120 seconds, and decreased at 240 seconds. Like soybean milk, diluted sweetened condensed milk delivered under fixed-time schedules of 30, 60, and 120 seconds failed to evoke schedule-induced polydipsia, but did so when adulterated with 7.2% sodium chloride. Drinking induced by salted liquid foods resembled the polydipsia engendered by spaced dry-food presentations in several ways, including temporal relation to food delivery, persistence within and across sections, sensitivity to interfood interval, and magnitude relative to intake evoked by bulk-food presentation.

Animals↗

PubMed1998

Is propranolol effective in primary polydipsia?

OBJECTIVE: Psychiatric patients presenting with polydipsia are often difficult to treat with standard psychiatric interventions. Pharmacological intervention was attempted in these patients based on the hypothesis that angiotensin II, a potent dipsinogen, may be involved in the drinking behavior of patients with polydipsia. Beta-blockers inhibit renin release (and thus indirectly angiotensin II) by blocking beta receptors in the kidney. METHODS: Three patients were identified as excessive water drinkers during their hospital admissions. All three patients were eunatremic but polydipsic at the time of study. Two of the three had histories of hyponatremia and required emergency medical treatment on more than one occasion. No patients had been controlled by strict fluid restriction. Trials of propranolol were initiated to control their water drinking. RESULTS: After starting propranolol, two patients responded quickly. In one patient, fluid intake decreased from 2650 +/- 647 to 1577 +/- 361, p < .001. In the other, fluid intake decreased from over 7000 ml before starting propranolol to around 3000 ml. The mean noon body weight of the third patient, in whom it was not possible to document fluid intake or urine volume before and after administering beta-blocker, was 72.6 +/- 2.6 Kg and 66.0 +/- 1.0 Kg, respectively (p < .0001). CONCLUSIONS: These results suggest that propranolol may be useful for the treatment of polydipsia in patients with schizophrenia. Its efficacy could be related to inhibition of the renin-angiotensin system. Additional research using the controlled pharmacotherapeutic trials is required to confirm these findings.

Adrenergic beta-Antagonists↗

PubMed1984

Polydipsia's contribution to temporal discrimination of rats on a fixed interval schedule.

This experiment concerned the contribution of polydipsia on the temporal discrimination of rats during a fixed-interval 60-sec. schedule. In this study, the timing accuracy of 12 rats which had access to water during training was compared to that of 12 rats which had no water during training. The rats were trained for 25 sessions on an FI 60-sec. schedule. In early sessions before polydipsia was fully developed, no differences existed between the timing accuracy of the water group and no-water group. As the amount of water drunk by the water group increased as the number of sessions increased, a parallel increase was noted in the timing accuracy of the water group. In the final sessions, a significant difference was found between the timing accuracy of rats in the water group and that of those in the no-water group. It was concluded that polydipsia facilitated the development of the temporal discrimination which is characteristic of a fixed-interval 60-sec. schedule.

Animals↗

PubMed1999

[Effects of demeclocycline on psychiatric polydipsia in schizophrenic patients].

Excess intake of water by schizophrenic patients is referred to as psychiatric polydipsia. This symptom causes incontinence, vomiting and hyponatremia, and may sometimes lead to death. We have no effective therapeutic methods other than administrating sodium chloride solution and diuretics, or restricting the intake itself. A case was reported stating that demeclocycline, used in case where there is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), was effective for the treatment of psychiatric polydipsia. We administered demeclocycline to 8 schizophrenic patients with psychiatric polydipsia, and noticed improvement in incontinence, vomiting and hyponatremia. There was also a decrease of polydipsic behavior. Demeclocycline inhibits the antidiuretic effect of vasopressin on the distal renal tubule. Considering the function of demeclocycline and the relevance of vasopressin to the central nervous system, it has been suggested that demeclocycline has effects on the central nerve through vasopressin or cyclic AMP.

Anti-Bacterial Agents↗

PubMed2000

[Psychogenic polydipsia leading to water intoxication].

Psychogenic polydipsia and its frequent complication, water intoxication, are well-known to psychologists. There are biochemical and psychiatric theories of psychogenic polydipsia which often correlate with each other. A 48-year-old man with chronic paranoid schizophrenia developed symptoms of psychogenic polydipsia. This provoked disturbances in electrolyte balance, resulting in a rapid decrease in serum sodium concentration and eventual death. There is a paucity of information and little awareness of this problem in the professional literature.

Drinking Behavior↗