Cherian Verghese

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.

Neuroendocrine Factors Influencing Polydipsia in Psychiatric Patients: An Hypothesis

Polydipsia and water intoxication cause considerable morbidity and mortality in chronic psychiatric patients. The pathophysiology of the disorder is unknown, and there is no effective treatment. Angiotensin II is an important dipsogen in animals; in humans, some conditions with abnormal thirst are associated with increased angiotensin function. Chronic D2 dopamine receptor blockade increases angiotensin II-induced thirst in animals; in humans, increased peripheral response to angiotensin II is documented. Chronic D2 blockade with typical neuroleptics may increase sensitivity to angiotensin II and induce thirst. Clozapine, which has negligible D2 blocking action may improve polydipsia. Recent case reports demonstrate improvement of polydipsia during clozapine therapy. Angiotensin II releases vasopressin; this could explain water intoxication, which occurs later in the syndrome. This paper suggests an etiological model and a treatment modality for this disorder.

Treatment of polydipsia and hyponatremia in psychiatric patients can clozapine be a new option

Polydipsia occurs frequently in chronic schizophrenic patients, some of whom develop intermittent hyponatremia. Most therapeutic efforts have tried to control the hyponatremia. Four schizophrenic patients, followed for more than one year, showed improvement on clozapine. Case 1 was an outpatient without history of hyponatremia who improved from polydipsia and psychosis. The last three were inpatients with polydipsia, intermittent hyponatremia, and psychosis who showed minimal improvement of psychosis but significant decrease in polydipsia and water intoxication. Case 2 relapsed to polydipsia when clozapine was discontinued on two occasions. Case 3 demonstrated polyuria during 39% of days before clozapine and in 0% of days after two weeks of clozapine. In case 4, most baseline sodium levels were abnormal, but all became normal after clozapine. A time-series analysis for intervention effects showed a significant effect of clozapine (p =. 017). The limited information provided by these case reports suggest the need for controlled studies of the clozapine effect on polydipsic patients.

Nicotine addiction in chronic schizophrenic inpatients

27) were adult neuroleptic-medicated inpatients with a DSM-III-R diagnosis of chronic schizophrenia (n = 22) or schizoaffective disorder (n = 5). Paired t tests revealed higher B! than NAART estimates for FSIQ (NAART m =97.2, BI m z 103.8; t[23] 2.63, p < 0.05), VIQ (NAART m -93.7, BI m = 103.2; t[23] =3.5, p < 0.05), but not PIQ. NAART and BI correlations with age, illness duration, education, and mental status (MS) revealed no significant associations. A trend between NAART and MS (r 0.37, p = 0.07) emerged. The possible NAART/MS relation suggested the NAART may be sensitive to cognitive deterioration. One possibility is that the ability to read/retrieve irregular words declines in schizophrenia, consistent with models of left hemisphere dysfunction. Studies with matched controls and nonchronic patients will determine if lower NAART scores reflect lower premorbid IQ or deterioration. As four of six BI components are demographic in nature and relatively independent of schizophrenia disease processes, these results may suggest that the BI is better suited for premorbid IQ estimation in schizophrenia.