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At least 19 recordsLinked to original sources
PubMed2000

Development of stereotypies and polydipsia in wild caught bank voles (Clethrionomys glareolus) and their laboratory-bred offspring. Is polydipsia a symptom of diabetes mellitus?

The development of stereotypies and polydipsia was studied in wild caught bank voles (P: n=92) and their laboratory-bred offspring (F1: n=248). All animals were kept isolated in barren cages in the laboratory. In the P generation, no individuals developed stereotypies, but 22% developed polydipsia (>21 ml/day water intake against normally 10 ml/day). Polydipsia was more frequent among males (34%) than females (13%). In F1, 30% developed locomotor stereotypies alone, 21% showed polydipsia alone, and, additionally, 7% developed both stereotypies and polydipsia. Fewer males than females developed stereotypies (23% vs. 38%), whereas polydipsia was more frequent in males than in females (30% vs. 11%). The occurrence and distribution of polydipsia among sexes were the same in F1 and P. The distribution of different types of stereotypies in stereotyping voles were backward somersaulting (BS, 80%), high-speed jumping (JUMP, 29%), pacing following a fixed route (PF, 12%) and windscreen wiper movement (WIN, 5%). Some individuals (10%) showed two or more different types of stereotypies. The average age for developing stereotypies was 96 days while polydipsia was registered at the age of 63 days in both sexes. Voles showing both polydipsia and stereotypies developed polydipsia later (79 days) than polydipsic voles not showing stereotypies. This difference was especially pronounced in stereotyping females in which the occurrence of polydipsia was postponed to the age of 114 days. Polydipsic voles were tested positive for glucosuria indicating that polydipsia could be a symptom of diabetes mellitus. It is suggested that the development of stereotypies and polydipsia among bank voles in the laboratory are the results of frustration and prolonged stress. Stereotypies seem to depend on frustrative experiences early in life, while polydipsia may be related to diabetes mellitus caused by the experience of prolonged stress. Moreover, circumstances related to the development of stereotypies may be adaptive by reducing the risks of prolonged stress, including the development of fatal polydipsia.

Journal Article↗
PubMed2001

Behavioral treatment of chronic psychogenic polydipsia with hyponatremia: a unique case of polydipsia in a primary care patient with intractable hiccups.

Psychogenic polydipsia is recognized as a dangerous and potentially life threatening disorder. Few studies have focused on the treatment of polydipsia presenting in the outpatient setting. A review of the behavioral treatment literature pertaining to psychogenic polydipsia is presented. This review is followed by a case illustration of an outpatient behavioral approach to the treatment of psychogenic polydipsia in a non-psychiatric, primary car, adult, male patient suffering from intractable hiccup. An ABA single-case design was used, with sodium concentration as the dependent variable. This behavioral method appears promising in settings where restriction of fluid intake is not practical.

Adult↗
PubMed1992

Septal polydipsia in rats is a primary polydipsia not mediated by dopamine.

Bilateral lesions of nucleus septal lateralis resulted in a sustained and significant increase in water intake, without any change in food intake. Intracerebral injection of dopamine (DA) or of spiperone (a central D2-receptor antagonist) did not elicit any change in water or food intake. The polydipsia resulting from septal lesions is thus a primary polydipsia, which is independent of food intake, and is not mediated by neurotransmitter dopamine.

Animals↗
PubMed2005

Association between three functional polymorphisms of the dopamine D2 receptor gene and polydipsia in schizophrenia.

The underlying pathophysiology of polydipsia in schizophrenia is poorly understood. However, several studies suggest there may be a genetic predisposition to polydipsia, including our previous study demonstrating familial concordance of polydipsia among first-degree relatives with schizophrenia. Antipsychotic medications may contribute to the development of polydipsia and studies show that dopamine D2 receptors are involved in drinking behaviour pathophysiology. Our hypothesis is that polymorphisms in the dopamine D2 receptor gene (DRD2) may confer susceptibility to polydipsia in schizophrenia. We tested for an association between polydipsia in schizophrenia and three functional polymorphisms of DRD2. The three polymorphisms, -141C Ins/Del, Ser311Cys, and TaqIA, were genotyped in patients with polydipsia (n = 64) and in those without polydipsia (n = 91). Of the three polymorphisms, TaqIA was significantly associated with polydipsia [genotype: chi2 = 6.59, df = 2, p = 0.037; allele: chi2 = 6.52, df = 1, p = 0.011, OR 1.81, 95% CI 1.15-2.86]. Haplotype analysis of the three markers found increased significance of the association (global, p = 0.00091). Although based on a relatively small portion of the sample, individual comparison of the common haplotypes showed that haplotype Ins-Cys-A1 was significantly less frequent in patients with polydipsia (p = 0.00082). The present data suggests polymorphisms in DRD2 may confer susceptibility to polydipsia in schizophrenia. To confirm our findings, further studies are warranted on larger samples using more extensive biological measures for diagnosing the polydipsia phenotype.

Adult↗
PubMed2002

Polydipsia and schizophrenia in a psychiatric hospital: a replication study.

A prior study in a US state hospital suggested that schizophrenia, smoking and long hospitalization were associated with polydipsia. This study, in another US hospital, attempts to (1) replicate that schizophrenia and smoking are associated with polydipsia, and (2) rule out that this relationship is partly explained by alcohol and drug use. Both studies have similar methodologies. The second sample included 588 inpatients. Models of variables associated with polydipsia were developed using logistic regression. In the second study, after correcting for other factors, the association between polydipsia and schizophrenia showed a borderline significance, while polydipsia and smoking displayed a significant association. Neither organic brain lesions, nor alcohol or drug use, were associated with polydipsia. An analysis combining both samples showed that: (1) schizophrenia, long hospitalization, smoking and heavy smoking were significantly associated with polydipsia, and (2) male gender and Caucasian race (but not smoking) increased the risk of developing water intoxication in polydipsic patients. These two studies in severely mentally ill patients suggest that the association of polydipsia with schizophrenia, smoking and chronicity is consistent and independent from the definition of polydipsia (by staff, a biological method or the combination of both). Psychiatric medications do not appear to explain most cases of polydipsia in these patients.

Analysis of Variance↗
PubMed2003

A potential causal association between gastrointestinal disease and primary polydipsia in three dogs.

Polydipsia, defined as a water intake of over 100 ml/kg/day, is a common presenting medical complaint in dogs. Polydipsia can be secondary (eg, to central or nephrogenic diabetes insipidus) or primary in origin, where increased water intake cannot be explained as a response to obligatory water loss. Primary polydipsia is confirmed by ruling out other known causes of polydipsia and demonstrating that renal concentrating ability is intact. The causes and associations of primary polydipsia in dogs are poorly defined. This report describes three dogs presented with signs of gastrointestinal disease with concurrent polydipsia. Investigations (including water deprivation testing) showed normal renal urinary concentrating ability and indicated primary polydipsia. Treatment of the gastrointestinal signs resulted in resolution of the polydipsia in each case. This is the first description of a possible association between gastrointestinal disease and primary polydipsia in the dog, the pathophysiology of which remains obscure.

Animals↗
PubMed1994

The consulting psychiatrist and the polydipsia-hyponatremia syndrome in schizophrenia.

OBJECTIVE: The authors seek to extend understanding and treatment of hospitalized schizophrenics presenting with complications of polydipsia and dilutional hyponatremia. Attending physicians may ask the consultation/liaison psychiatrist to see schizophrenics with hyponatremically-induced delirium or other psychiatric syndromes. The referring physician may or may not have identified polydipsia and dilutional hyponatremia and their complications. This article will help the consultation/liaison psychiatrist recognize early evidence of water imbalance, describe evaluation, and provide somatic and behavioral treatment approaches to this life-threatening syndrome. METHOD: Over the past ten years, the authors have treated more than 100 patients with the polydipsia-hyponatremia syndrome. The authors discuss their and others' experience with drugs that help and hinder patients suffering from dilutional hyponatremia. They review current key articles from the polydipsia-hyponatremia syndrome literature including articles identified via Medline search 1985-94. RESULTS: Schizophrenics with the polydipsia-hyponatremia syndrome most commonly present with polydipsia, polyuria, urinary incontinence, cognitive, affective, and behavioral changes, seizures, or coma. Quantitating polydipsia, hyponatremia, and diurnal changes in body weight facilitate therapeutic interventions. Treatment include patient and caregiver education, drug therapies to better treat psychosis and better treat osmotic dysregulation, behavioral interventions to interdict polydipsia, and diurnal weight monitoring. CONCLUSIONS: Once recognized, acute, subacute, and chronic complications of the polydipsia-hyponatremia syndrome are readily treatable. Besides treating the patient, consultation/liaison psychiatrists can teach their medical colleagues about this syndrome. In so doing, they will enhance the quality of their patients' lives and help the internist and surgeon feel more comfortable when working with schizophrenics.

Angiotensin II↗
PubMed2001

Polydipsia, psychosis, and familial psychopathology.

OBJECTIVE: To compare the demographic and clinical factors and familial psychopathology of chronic psychiatric inpatients with, and without, polydipsia. METHOD: We undertook a case-control study of chronic psychiatric inpatients both with, and without, polydipsia. Clinical and demographic data were gathered using a predesigned questionnaire, the Positive and Negative Syndrome Scale (PANSS), the Abnormal Involuntary Movement Scale (AIMS), the Mini-Mental State Examination Scale (MMSE), and the Family History-Research Diagnostic Criteria (FH-RDC). RESULTS: The prevalence rate of polydipsia was 20.2%. The group with polydipsia was significantly younger, both at the time of their first-ever psychiatric and current psychiatric admissions, compared with the group without polydipsia. The 2 groups were similar in terms of their illness characteristics and psychiatric diagnoses. In the group with polydipsia, alcohol abuse predated the psychotic illness by a mean of 10.5 (SD 4.4) years, compared with 4.8 (SD 1.6) years for the same period in the unaffected group. The 2 groups did not differ significantly regarding the antipsychotic medication dosage, the proportion on concomitant anticholinergic medication, the documented previous response to antipsychotic medication, or past treatment with electroconvulsive therapy (ECT). First-degree relatives of patients with polydipsia were found to have significantly higher rates of alcohol dependence. CONCLUSION: This study provides further evidence for the higher rate of polydipsia among chronic psychiatric patient populations and for high rates of alcohol-related problems among their first-degree relatives.

Adult↗
PubMed2002

Pharmacological treatments for psychosis-related polydipsia.

BACKGROUND: Polydipsia is the intake of more than three litres of fluids per day. Primary polydipsia occurs when excessive drinking cannot be explained by an identified medical condition, and is not secondary to polyuria. The prevalence of this problem in psychiatric inpatients has been estimated at between 6 and 17%. It can hinder standard care and be a highly disabling, even life-threatening condition. OBJECTIVES: To review the effect of pharmacological interventions for the treatment of psychosis-related polydipsia. SEARCH STRATEGY: The reviewers searched the Cochrane Schizophrenia Group's Register (January 2002) which is compiled by up-to-date methodical searches of BIOSIS, The Cochrane Library, CINAHL, Dissertation abstracts, EMBASE, LILACS, MEDLINE, PSYNDEX, PsycINFO, RUSSMED and Sociofile and is supplemented with hand searching of relevant journals and numerous conference proceedings. References of all identified studies were also searched for further trials. SELECTION CRITERIA: All randomised controlled trials involving people with a psychotic illness and secondary polydipsia, which evaluated drug treatments, and measured clinically meaningful outcomes. DATA COLLECTION AND ANALYSIS: Reviewers, working independently, inspected citations, ordered papers, and then re-inspected and quality assessed the studies. They also worked independently to extract data. For homogeneous dichotomous data, the relative risk (RR), 95% confidence interval (CI), and, where appropriate, the number needed to treat (NNT) and the number needed to harm (NNH), were calculated on an intention-to-treat basis. Reviewers assumed that people who left the study early or were lost to follow-up had no improvement. Weighted mean differences (WMD) were calculated for continuous data. Data was excluded if loss to follow-up was greater than 50%. MAIN RESULTS: The reviewers identified two trials which fulfilled the inclusion criteria, (total n=17, duration 3-6 weeks). Few data were reported and, because of inappropriate use of crossover methodology, it could not all be used in this review. For the few chronically ill people in these trials, neither the 'active' tetracycline bacteriostatic agent, oral demeclocycline, nor the opiate antagonist naloxone, nor placebo, gave any suggestion of serious adverse effects for a period of up to six weeks. The two small studies did not report any useful data on measures of polydipsia, physical symptoms secondary to increased fluid intake, mental state, general functioning or economic outcomes. REVIEWER'S CONCLUSIONS: The trials offer little to the clinician hoping to treat psychosis-related polydipsia with drugs, except that further evaluative studies need to be conducted in this area. Treatment of any sort for psychosis related polydipsia might only be informative within a well designed, conducted and reported randomised study. The two pioneering studies suggest that larger trials, though difficult, would not be impossible with adequate support and co-ordination.

Drinking↗
PubMed2006

Pharmacological treatments for psychosis-related polydipsia.

BACKGROUND: Polydipsia is the intake of more than three litres of fluids per day. Primary polydipsia occurs when excessive drinking cannot be explained by an identified medical condition, and is not secondary to polyuria. The prevalence of this problem in psychiatric inpatients has been estimated at between 6 and 17%. It can hinder standard care and be a highly disabling, even life-threatening condition. OBJECTIVES: To review the effect of pharmacological interventions for the treatment of psychosis-related polydipsia. SEARCH STRATEGY: We searched the Cochrane Schizophrenia Group's Register (January 2002 and February 2005) which is compiled by up-to-date methodical searches of BIOSIS, The Cochrane Library, CINAHL, Dissertation abstracts, EMBASE, LILACS, MEDLINE, PSYNDEX, PsycINFO, RUSSMED and Sociofile and is supplemented with hand searching of relevant journals and numerous conference proceedings. References of all identified studies were also searched for further trials. SELECTION CRITERIA: We included all randomised controlled trials involving people with a psychotic illness and secondary polydipsia, which evaluated drug treatments, and measured clinically meaningful outcomes. DATA COLLECTION AND ANALYSIS: Working independently, we inspected citations, ordered papers, and then re-inspected and quality assessed the studies and extracted data. For homogeneous dichotomous data, we calculated the relative risk (RR), 95% confidence interval (CI), and, where appropriate, the number needed to treat (NNT) and the number needed to harm (NNH), on an intention-to-treat basis. We assumed that people who left the study early or who were lost to follow-up had no improvement. We calculated weighted mean differences (WMD) for continuous data. We excluded data if loss to follow-up was greater than 50%. MAIN RESULTS: We identified two small trials (Alexander 1991 and Nishikawa 1996) which fulfilled the inclusion criteria, (total n=17, duration 3-6 weeks). Few data were reported and, because of inappropriate use of crossover methodology, we could not include all of the data in this review. For the few chronically ill people in these trials, neither the 'active' tetracycline bacteriostatic agent, oral demeclocycline, nor the opiate antagonist naloxone, nor placebo, gave any suggestion of serious adverse effects for a period of up to six weeks. The studies did not report any useful data on measures of polydipsia, physical symptoms secondary to increased fluid intake, mental state, general functioning or economic outcomes. AUTHORS' CONCLUSIONS: The trials offer little useful data to the clinician hoping to treat psychosis-related polydipsia with drugs, except that further evaluative studies need to be conducted in this area. Treatment of any sort for psychosis related polydipsia might only be informative within a well designed, conducted and reported randomised study. The two pioneering studies suggest that larger trials, though difficult, would not be impossible with adequate support and co-ordination.

Drinking↗
PubMed1994

Polydipsia and water intoxication in psychiatric patients: a review of the epidemiological literature.

Polydipsia among chronic psychiatric patients is poorly understood and underdiagnosed. It may have three stages: simple polydipsia, polydipsia with water intoxication, and physical complications. Epidemiological surveys have used staff reports and polyuria measures to identify polydipsic patients. Water intoxication has been screened by chart review, weight, or serum sodium data. According to these surveys, polydipsia, not explained by medically induced polyuria, may be present in more than 20% of chronic inpatients. Up to 5% of chronic inpatients had episodes of water intoxication although mild cases may have been missed. Single time point surveys show that 29% of polydipsic patients had presented water intoxication. Methodologically limited clinical studies suggest that polydipsia with water intoxication rather than simple polydipsia may be associated with poor prognosis in schizophrenia. Epidemiological surveys found polydipsia with water intoxication to be associated with chronicity, schizophrenia, smoking, some medications, male gender, and white race. New pathophysiological models need to elucidate these findings.

Chronic Disease↗
PubMed1997

Hypouricemia in chronic schizophrenic patients with polydipsia and hyponatremia.

BACKGROUND: Polydipsia is a common disorder among chronic psychiatric patients. Impaired water excretion due to enhanced action and secretion of antidiuretic hormone has been reported in hyponatremic patients with polydipsia. Hypouricemia coexisting with hyponatremia is a hallmark of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The transitory coexistence of hyponatremia and hypouricemia in patients with polydipsia-hyponatremia syndrome is presented. METHOD: We examined the course of hypouricemia and hyponatremia in three schizophrenic patients with a long-standing history of polydipsia resulting in the presence of these conditions. In addition, we investigated the renal clearance of uric acid in five polydipsic patients without a previous history of water intoxication or hyponatremia (simple polydipsia). RESULTS: Both hyponatremia and hypouricemia were demonstrated in the presence of SIADH in one patient, during an episode of acute water intoxication in another, and in association with chronic hyponatremia in a patient who was following the target weight procedure. Elevated fractional excretion of uric acid percentage (FEUA%) was detected in two patients. These states appeared to be episodic or transitory. In the five patients with simple polydipsia, serum uric acid concentrations and FEUA% were maintained within the normal range. CONCLUSION: Altered uric acid regulation that resembles SIADH is present in patients with polydipsia-hyponatremia syndrome. Monitoring the uric acid concentration and FEUA% in polydipsic patients may be useful in identifying those patients with transiently impaired water excretion.

Adult↗
PubMed2003

Genetic approaches to polydipsia in schizophrenia: a preliminary report of a family study and an association study of an angiotensin-converting enzyme gene polymorphism.

The pathophysiology of polydipsia in patients with schizophrenia is inadequately understood. This study aims to investigate the genetic influence on polydipsia in schizophrenia, and is comprised of a family study and an association study. First, we screened in-patients in 14 psychiatric hospitals and found a total of 36 pairs of a proband and his/her first-degree relative, both of whom were diagnosed with schizophrenia. Among these pairs, a significant familial concordance of polydipsia was found (Fisher's exact test, two-sided, P = 0.0014; odds ratio, 88.20; 95% confidence interval, 7.31-1064.34). These results indicate that genetic factors may underlie the pathophysiology of polydipsia in patients with schizophrenia. Subsequently, we examined the genetic association between polydipsia/water intoxication and the angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism in patients with chronic schizophrenia (polydipsics: n = 65; non-polydipsics: n = 97) because several lines of evidence suggested that ACE might be involved in the development of polydipsia in schizophrenia. The D allele of ACE was found to be associated with a non-significant trend toward an increased risk of polydipsia (P = 0.086). Furthermore, a significant allelic association was found between the D allele of ACE and water intoxication (P = 0.0392). This significance remained after the data were adjusted for confounding variables by regression analysis. These results suggest that the ACE D allele may be a risk factor for polydipsia/water intoxication in patients with schizophrenia.

Adult↗
PubMed2003

Solute loss plays a major role in polydipsia-related hyponatraemia of both water drinkers and beer drinkers.

BACKGROUND: Polydipsia-related hyponatraemia is generally considered an acute dilutional state. AIM: To determine whether solute loss plays a role in the pathogenesis of polydipsia-related hyponatraemia. DESIGN: Prospective uncontrolled study. METHODS: We studied routine biochemical volume-related parameters before and after 2 l isotonic saline infusion over 24 h, in 10 consecutive hyponatraemic polydipsia patients (mean age 55 +/- 11 years; 6 beer drinkers and 4 compulsive water drinkers) with initial urinary osmolality <220 mosm/kg H(2)O. In five of these patients, we measured balance data over 24 h. RESULTS: Mean initial plasma protein concentration in the 10 studied polydipsia patients was 7 +/- 0.7 g/dl, unexpectedly high for an acute dilutional state. Mean plasma sodium concentration increased from 126 +/- 5 mmol/l before saline, to 135 +/- 5 mmol/l after infusion of 2 l isotonic saline (p < 0.01). Balance data in five polydipsia patients showed a mean decrease of 1.6 kg of their initial body weight and a mean salt retention of 406 mosm. DISCUSSION: Polydipsia-related hyponatraemia is a mixed disorder, in which about half of sodium decrease is due to solute loss. This explains the apparent paradox of a normal plasma protein concentration, despite the increase in body weight due to water intoxication.

Adult↗
PubMedDate not supplied

Psychogenic polydipsia after traumatic brain injury. A case report.

Electrolyte abnormalities are common medical complications of traumatic brain injury (TBI). Hyponatremia is the most common of these disorders. The syndrome of inappropriate antidiuretic hormone and cerebral salt-wasting are the most well known causes of hyponatremia following TBI. In the presence of polydipsia and polyuria, psychogenic polydipsia should be included in the differential diagnosis. It is important to distinguish among these entities because treatment differs to such an extent that improper diagnosis may lead to a worsening of the patient's condition. We present a patient who presented with a new onset of polyuria and polydipsia after sustaining a TBI. Evaluation, including monitoring of fluid intake and output, serum and urine sodium and osmolarity, as well as a fluid deprivation test revealed the cause to be psychogenic polydipsia. The patient's symptoms improved after institution of a behavioral program and fluid restriction. Various models of drinking behavior have been used to identify the site of dysregulation. Dopaminergic, cholinergic, and hippocampal etiologies have been implicated in this abnormality of fluid homeostasis. If disorders of these systems can lead to psychogenic polydipsia, it is reasonable to believe that a person who has sustained a TBI would be at higher risk of developing psychogenic polydipsia.

Adult↗
PubMed1996

A demographic study of polydipsia in an institution for the intellectually disabled.

OBJECTIVE: To measure the prevalence of primary polydipsia in an Ontario institution for residents with developmental disabilities and to explore the associations of polydipsia with age, sex and level of mental retardation. METHOD: All 798 residents were screened for polydipsia using a behavioural questionnaire completed by caregivers. RESULTS: Thirty-three cases were detected: the prevalence among the mobile resident population (n = 660) was 5%. We found no association of polydipsia with age, sex, or level of mental retardation. CONCLUSIONS: Physicians should be aware of polydipsia because it is common among residents with moderate, severe, and profound mental disability. Unless screened for specifically, polydipsia may go unrecognized and may place the residents with mental handicap at risk for serious acute and chronic complications.

Adult↗
PubMed2006

Association study between functional polymorphisms in the cytochrome P450 1A2 and 2D6 genes and polydipsia in schizophrenia.

The underlying pathophysiology of polydipsia in schizophrenia is poorly understood. Several studies, however, have suggested that there might be a genetic predisposition to polydipsia. In the present study, using a case-control sample that is independent from the previous family sample, we examined a possible association between polydipsia and functional polymorphisms in the genes of cytochrome P450 (CYP) 1A2 and 2D6, primarily important enzymes to the pharmacokinetics of antipsychotic drugs. Japanese patients with schizophrenia (63 polydipsics and 78 nonpolydipsics) were genotyped for two functional polymorphisms, the 734C/A polymorphism in the CYP1A2 gene and the 2D6*10 allele of the CYP2D6 gene. Neither of the polymorphisms was found to be associated with polydipsia nor was any evidence found that the two polymorphisms have an additive effect on the liability to polydipsia. Our results suggest that the CYP1A2 and CYP2D6 polymorphisms are not likely to play a major role in the development of polydipsia in schizophrenia, although further studies testing other alleles of CYP1A2 and CYP2D6 using different ethnic populations are warranted.

Aged↗