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PubMed1983

Primary polydipsia. Syndrome of inappropriate thirst.

A patient with lifelong severe polyuria and polydipsia had normal serum antidiuretic hormone (ADH) levels and responded to water deprivation with a prompt increase in urine osmolality and maintenance of normal plasma osmolality (less than 290 mOsm/kg), despite extreme thirst. When treated with desmopressin acetate and allowed free access to water, she was able to reduce plasma osmolality below 270 mOsm/kg, and her compelling thirst disappeared. The disorder is interpreted to be the result of excessive fluid intake in response to a thirst stimulus that was not inhibited by normal plasma osmolality. This study indicates that osmoreceptor control of ADH secretion is normal. Continued administration of vasopressin has relieved the symptoms and has not resulted in water intoxication.

Adult↗
PubMed1984

Empty sella turcica in intracranial sarcoidosis. Pituitary insufficiency, primary polydipsia, and changing neuroradiologic findings.

A 37-year-old man with visual loss was found to have hypopituitarism and primary polydipsia associated with sarcoidosis. Neuroradiologic studies demonstrated a dramatic evolution of CNS lesions, including a left thalamic infarct, an enhancing suprasellar mass, and ultimately an empty sella turcica. The patient has been clinically stable in spite of these changes. This case is likely to be the first reported of CNS sarcoidosis with an empty sella turcica documented by computed tomography.

Adult↗
PubMed1997

Psychotic exacerbations and enhanced vasopressin secretion in schizophrenic patients with hyponatremia and polydipsia.

BACKGROUND: For unclear reasons, life-threatening water intoxication often coincides with acute psychosis in polydipsic schizophrenic patients with chronic hyponatremia. In contrast, most polydipsic schizophrenic patients are normonatremic and never manifest hyponatremia. To explore whether the effect of acute psychosis on water balance differs in these 2 schizophrenic subgroups, we compared their responses to drug-induced psychotic exacerbations. METHODS: Matched polydipsic schizophrenic patients with (n = 6) and without (n = 8) hyponatremia were identified based on past and current indexes of fluid intake and hydration. A transient psychotic exacerbation was induced with an infusion of the psychotomimetic methylphenidate hydrochloride (0.5 mg/kg of body weight over a 60-second period). Antidiuretic hormone levels, subjective desire for water, and factors known to influence water balance were measured at 15-minute intervals for 2 hours. RESULTS: Except for the expected differences in plasma osmolality and sodium, basal measures were similar in the 2 groups. Following methylphenidate administration, antidiuretic hormone levels increased more in the hyponatremic patients (P < .02), despite their consistently lower plasma osmolality (P < .007). No known or putative antidiuretic hormone stimulus could account for this finding. Only basal positive psychotic symptoms (P < .09) and plasma sodium (P < .18) were even marginally associated with the peak antidiuretic hormone responses, but neither factor could explain the difference in the response by the 2 groups. CONCLUSION: Psychotic exacerbations are associated with enhanced antidiuretic hormone secretion, for unknown reasons, in schizophrenic patients with hyponatremia and polydipsia, thereby placing them at increased risk of life-threatening water intoxication.

Acute Disease↗
PubMed1979

[Water intoxication and brain edema in psychogenic polydipsia (author's transl)].

A case of psychogenic polydipsia is presented that showed psychic decompensation and compulsive drinking under the acute stress of an imminent operation for ovarian cyst. Without any indication of an underlying organic disease process the patient developed acute water intoxication due to the uncontrolled intake of water from the tap, this caused hyponatremia, brain edema, coma and status epilepticus. The physiology of water intoxication is reviewed in relation to this case, which is also remarkable for the acute onset and the shortness of the polydipsic state.

Adult↗
PubMed1983

Lithium-induced polydipsia: dependence on nigrostriatal dopamine pathway and relationship to changes in the renin-angiotensin system.

The dependence of lithium-induced polydipsia (LIP) on central monoamine pathways was investigated using several pharmacological manipulations. Intracisternal administration of 6-hydroxydopamine (6-OHDA) in combination with pargyline or desipramine was used to deplete dopamine (DA), norepinephrine, or both catecholamines. Significant decreases in LIP were seen after treatments that depleted brain DA, whereas depletion of norepinephrine alone did not affect LIP. Site-specific injection of 6-OHDA into the substantia nigra or caudate nucleus, but not the nucleus accumbens or noradrenergic dorsal bundle, also caused a decrease in LIP. Depletion of serotonin by intracisternal administration of 5,7-dihydroxytryptamine also had no effect on LIP. Consistent with these findings, the DA receptor blocker haloperidol attenuated LIP. Thus, LIP appears to be dependent on intact nigrostriatal DA fibers, but not on other monoaminergic systems in the brain. Lithium also increased plasma renin activity (PRA) and angiotensin I and II immunoreactivity in plasma, though the time course of LIP onset did not directly parallel these latter changes in the renin-angiotensin axis. Neither the PRA or angiotensin II immunoreactivity in lithium-treated animals was sufficiently high to account for LIP. In addition, the 6-OHDA lesions of the caudate nucleus or substantia nigra that attenuated LIP did not affect the lithium-induced increases in PRA or in angiotensin I or II concentrations. Thus, LIP probably involves mechanisms other than just being a direct response to lithium-induced increases in PRA or angiotensin II concentration and simply may not be secondary to lithium-induced polyuria. Because of the similar pharmacological characteristics of angiotensin II and lithium-induced drinking, a role for angiotensin receptors in LIP cannot be ruled out.

Angiotensin II↗
PubMedDate not supplied

Verapamil-induced "primary" polydipsia.

An 11-month-old male infant with recurrent supraventricular tachycardia (SVT) was treated with oral verapamil. Shortly thereafter he developed marked changes in behavior including lethargy, intensely increased thirst and urination, and irritability when denied fluids. "Primary" polydipsia was diagnosed following an evaluation which showed no evidence of adrenal insufficiency, diabetes insipidus, diabetes mellitus, hypercalcemia, hyperosmolality, or renal disease. The symptoms resolved 1 week after verapamil was discontinued.

Administration, Oral↗
PubMed1988

The use of demeclocycline in the treatment of patients with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome).

Eight patients (7 men and 1 woman, mean age 43.1 +/- 8.9 years) with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) underwent treatment with demeclocycline in an effort to normalize serum sodium levels and thereby protect the PIP patients against complications including hyponatremic seizures and coma. There tended to be an improvement (p = .080) in early morning serum sodium following treatment with demeclocycline (baseline 132.6 +/- SD 3.3 and treatment serum sodium 134.8 +/- SD 3.3 mEq/1). At the same time, there was an increase (p = .043) in urinary specific gravity following treatment with demeclocycline (baseline 1.0047 +/- SD .0029 and treatment urinary specific gravity 1.0063 +/- SD .0026). Clinical indications for and potential mechanisms of action of demeclocycline treatment in the PIP syndrome are discussed.

Adult↗
PubMed1993

Effect of clozapine upon schedule-induced polydipsia (SIP) resembles neither the actions of dopamine D1 nor D2 blockade.

The effects of clozapine (CLOZ) upon acquired schedule-induced polydipsia in rats were compared to the effects of the dopamine (DA) D1 antagonist SCH 23390 (SCH) and the DA D2 antagonist raclopride (RAC). All three compounds suppressed water consumption, but only SCH and RAC decreased drinking efficiency. SCH was the only compound with an effect on panel pressing (PP), causing suppression even at a dose without effect upon water intake. SCH also affected the temporal pattern of licking (TPL) at all doses, while clozapine, 10 mg/kg, only affected the pattern acutely, and raclopride was without effect. In conclusion, PP and the TPL are more sensitive to D1 than D2 blockade. While PP and the TPL are more sensitive than water intake to D1 blockade, the opposite is true for D2 blockade. It is possible to differentiate between DA D1/D2 antagonists and CLOZ in this model, focusing upon reduction in water consumption, with and without reduction in drinking efficiency. Furthermore, it is possible to differentiate between D1 and D2 blockade by analyzing water consumption, PP and the TPL.

Animals↗
PubMed1998

[Schizophreniform psychosis with polydipsia and electrolyte imbalance in multiple sclerosis].

We present the case report of a young woman who suffered from schizophrenia-like psychosis leading to polydipsia and consequent water intoxication. Because of progressive somnolence and epileptic seizures therapy on the intensive care unit became necessary. Findings of MRI and cerebrospinal fluid were consistent with the diagnosis of chronic inflammatory disease of the central nervous system. As other possible causes could be excluded, multiple sclerosis seemed to be most probable. Simultaneous incidence of schizophrenia and multiple sclerosis and the differential diagnosis of central pontine myelinolysis following hyponatremia are discussed.

Adult↗
PubMed1984

Compulsive polydipsia presenting as diabetes insipidus: a behavioral approach.

Although compulsive polydipsia or self-induced water intoxication is known to occur with a relatively high frequency in psychiatric patients, much of the literature has focused on medication treatment and interactions; little has been written describing alternative methods of intervention. This paper describes an inpatient treatment using both EMG biofeedback and response prevention. The relationship between compulsive appetitive behaviors and more classic presentations is discussed. Because the patient was treated on the endocrine service, the importance of adequately training non-psychiatric staff is emphasized. It is suggested that this may be a model for the behavioral management of psychiatric problems on medical/surgical wards.

Adult↗
PubMed1988

Behavioral treatment of psychogenic polydipsia.

This report describes the behavioral treatment of psychogenic polydipsia in an autistic, severely mentally retarded woman who had a history of self-induced water intoxication. Treatment emphasized the use of edibles and reductions in activity demands to reward water refusal. Employing this procedure, paraprofessional staff normalized the client's water consumption, and thereby prevented further episodes of potentially-fatal water intoxication.

Adult↗
PubMed1990

Successful behavioral treatment of polydipsia in a schizophrenic patient.

Behavioral treatment of a 35 year old female with chronic schizophrenia and water intoxication with seizures was conducted on an inpatient psychiatric unit. Treatment included frequent daily weights, restricted fluid intake, positive reinforcement for program compliance, and time-out from reinforcement following significant weight gain or other specified program violations. The final 6 months of the 30 month treatment program were a maintenance phase during which most contingencies were faded and all fluid restrictions were removed. There was no reported recurrence of polydipsia after 18 months of community placement.

Adult↗
PubMed1992

Behavioral intervention to reduce water intake in the syndrome of psychosis, intermittent hyponatremia, and polydipsia.

We describe a non-intensive behavioral intervention using an A-B design with extended follow-up on an open psychiatric unit to reduce water intake in a 52-year-old man with the syndrome of psychosis, intermittent hyponatremia, and polydipsia. A reinforcement schedule contingent upon weight gain secondary to water intake was employed. Mean diurnal weight gain was 7.1 pounds during a 23-week baseline which dropped to 4.1 pounds following 23 weeks of treatment and at a 1-year follow-up. Estimated fluid consumption dropped from 10 liters to 4 liters daily and incidents of hyponatremia decreased by 62%.

Behavior Therapy↗
PubMed1993

A "biofeedback" approach to the treatment of chronic polydipsia.

A novel behavioral method is described for the treatment of psychogenic polydipsia in a patient suffering from chronic schizophrenia. The patient was given feedback on serum sodium concentration, likely physical consequences, and the value of reducing fluid intake. An ABAB single-case design was used, with changes in sodium concentration (charted by the patient during the treatment phases) as the dependent variable. The patient showed substantially increased sodium concentration, which was maintained despite the withdrawal of feedback. This behavioral method appears promising in settings where restriction of fluid intake is not practical or ethical.

Adult↗
PubMed1986

Diurnal variation of urinary excretion for patients with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome).

Ten patients [8 men and 2 women, mean age (SD) 37.6 +/- 6.5 years] with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) underwent serial determinations at 6:00 AM, 12 noon, 6:00 PM, and 12 midnight of levels of urinary creatinine concentration (UCR), urinary specific gravity (SPGR), and urinary osmolality (UOSM) on 8 consecutive Thursdays. Diurnal variation (p less than 0.015) was present in the case of each parameter of urinary excretion (UCR, SPGR, and UOSM). These three parameters remained very low throughout the day (mean UCR 19.0 mg/dl, mean SPGR 1.0033, and mean UOSM 112.6 mosmol/kg), which is consistent with severe and persistent hyposthenuria, and each parameter correlated well with the other two parameters (r between 0.78 and 0.93, p less than 0.001). The 6:00 PM (UC6PM) value for UCR correlated best with the daily mean UCR (UCM), providing the simple linear regression UCM = 0.7615 X UC6PM + 6.1503 (r = 0.912, p = 0.0005) for the 10 PIP patients. Twenty-four-hour urinary volume (24UV) could then be estimated using UCM and values of 17.5 and 12.5 mg creatinine/kg body weight for male and female PIP patients, respectively, to calculate the daily urinary excretion of urinary creatinine. The group mean 24UV was 6963 ml, with a range of 4934-9884 ml. We hope that information about the diurnal variation of urinary excretion (21.6%, 20.5%, 27.4%, and 30.4% of 24UV excreted in consecutive quartiles commencing with the 12 midnight to 6:00 AM quartile), coupled with the utilization of the equation UCM = 0.7615 X UC6PM + 6.1503 (r = 0.912, p = 0.0005) to estimate UCM as an index of 24UV in the PIP syndrome, will provide tools to better elucidate the relationship between psychosis and water dysregulation.

Adult↗
PubMed1988

Treatment of psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) using lithium and phenytoin.

Six patients [5 men and 1 woman, mean age 37.3 +/- 8.2 (SD) years] with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) underwent a sequence of treatments in an effort to normalize basal serum sodium levels and thereby protect the patients against complications, including hyponatremic seizures and coma. The morning baseline group mean basal serum sodium value was 132.5 +/- 3.8 meq/liter. Over a 20-month period, the sequence of treatments was salt-added diet, lithium and phenytoin, and lithium alone. Each treatment program yielded morning group mean basal serum sodium determinations superior to baseline values, except for the program of lithium alone, which could not be tolerated. The combination of lithium and phenytoin provided a morning group mean basal serum sodium level of 140.6 +/- 3.2 meq/liter, which was superior (p less than 0.01) to all other treatment modalities. Early morning hyposthenuria persisted throughout the 20-month period of observation.

Adult↗
PubMed1984

The effects of lead administration during development on lithium-induced polydipsia and dopaminergic function.

Previous studies have demonstrated that postnatal (days 2-29 of life) administration of lead (200 mg/kg/day by gavage) to Long-Evans rats caused permanent increases in lithium-induced polydipsia (LIP). These lead-induced increases in LIP were apparently not of renal origin, did not occur in animals treated with lead after day 30, and persisted for at least 6 months. The present studies have narrowed the dose-time window for lead-induced increases in LIP. The first study showed that continuous administration of lead (200 mg/kg/day, p.o.) in the form of lead acetate during days 2-9 of life caused increases in LIP (P = 0.022). Although lead-induced increases in LIP were not statistically significant (P = 0.084) for the group administered lead from days 9 to 19, the lack of a significant difference between the 2-9- and 9-19-day groups suggested that lead treatment during either of these time periods would result in LIP increases. Lead administration between days 19 and 29 of life was not effective in increasing LIP (P = 0.8). In the second study, a single dose of lead (200 mg/kg/day) was administered either on day 5 or 15 of life. Concentrations of lead in the blood on day 30 of life averaged 23.2 micrograms/100 ml for treated rats versus 4.8 micrograms/100 ml for controls. When tested at approximately 90 days of age, both groups showed significant increases in LIP (P = 0.028). The rats from this second study were also examined for changes in nigrostriatal dopamine function, since this pathway is known to be essential for LIP.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1988

Schedule-induced polydipsia experience decreases locomotor response to amphetamine.

To investigate the influence of schedule-induced polydipsia (SIP) on central dopaminergic systems, rats trained in a SIP procedure were challenged with the psychostimulant and dopaminergic agonist, D-amphetamine. In a first experiment, rats that had access to water and developed SIP (SIP-positive) displayed a lower response to amphetamine than rats that had access to water but did not develop SIP (SIP-negative) and rats that had no access to water. There was no difference in the spontaneous activity of these different groups of animals. In a second experiment, SIP-positive rats displayed the same reduced response to amphetamine following only 10 min of SIP drinking. In addition, SIP-positive rats that were tested without access to water during the SIP test displayed an increased locomotor activity both after saline and amphetamine treatments. These results suggest that SIP has stress-reducing properties.

Animals↗