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NEUROPSYCHOPHARMACOLOGY 1993-VOL. 9, NO. 2 157 Neuroendocrine Factors Influencing Polydipsia in Psychiatric Patients: An Hypothesis Cherian Verghese, M.D., Jose De Leon, M.D., and George M. Simpson, M.D. Polydipsia and water intoxication cause considerable typical neuroleptics may increase sensitivity to morbidity and mortality in chronic psychiatric patients. angiotensin II and induce thirst. Clozapine, which has The pathophysiology of the disorder is unknown, and negligible D2 blocking action may improve polydipsia. there is no effective treatment. Angiotensin II is an Recent case reports demonstrate improvement of important dipsogen in animals; in humans, some polydipsia during clozapine therapy. Angiotensin II conditions with abnormal thirst are associated with releases vasopressin; this could explain water increased angiotensin function. Chronic D2 dopamine intoxication, which occurs later in the syndrome. This receptor blockade increases angiotensin II-induced thirst paper suggests an etiological model and a treatment in animals; in humans, increased peripheral response to modality for this disorder. [Neuropsychopharmacology angiotensin II is documented. Chronic D2 blockade with 9:157-166, 1993J KEY WORDS: Polydipsia; Hyponatremia; Angiotensins; The existing data are reviewed to put the hypothesis Vasopressin; Atrial natriuretic peptide in perspective. Polydipsia in psychiatric patients has been described Clinical Features and Natural History since the 1930s prior to the use of neuroleptics, but sys­ te matic study of the disorder has been done mostly in There are three stages of the disorder. In the frrststage, th e last two decades. There are many names for the dis­ about 5 to 15 years after the onset of the psychotic dis­ order, which include psychogenic polydipsia (Bauer order, some patients start to consume excess quanti­ 1925), compulsive water drinking (Barlow and De ties of fluids (Vieweg et al. 1984a). Polydipsia causes Wardener 1959), psychosis, intermittent hyponatremia secondary polyuria. Polydipsia is the primary and en­ and polydipsia (PIP) syndrome (Vieweg et al. 1985) and during feature, and for many patients, the only symp­ self-induced water intoxication (Hobson and English tom. It is not always recognized by care givers, and pa­ 1963). The main purpose of this paper is to propose an tients rarely complain about it. It often comes to hypothesis about the pathophysiology of the disorder attention with the onset of the second stage, water in­ andto reconceptualize some of the thinking about it. toxication, which occurs 1 to 10 years from the onset of polydipsia (Vieweg et al. 1984b). Water intoxication occurs in 50% of polydipsic patients (Jos and Perez­ Cruet 1979). The kidney is normally able to excrete large From the Medical College of Pennsylvania/EPPI, Philadelphia, Pennsylvania. amounts of fluids, but these patients become unable Address correspondence to: Cherian Verghese, M.D., Medical to excrete all the ingested fluids, resulting in hemodi­ College of Pennsylvania/EPP!, 3200 Henry Avenue, Philadelphia, lution and hyponatremia. Acute episodes of hyponatre­ Pennsylvania 19129. Received July 14,1992; revised February 17,1993 and May 25,1993; mia cause cerebral edema, the symptoms of which are accepted May 31, 1993. called water intoxication. A wide range of symptoms © 1993 American College of Neuropsychopharmacology Published by Elsevier Science Publishing Co., Inc. 655 Avenue of the Americas, New York, NY 10010 0893-133X/93/$6.00 158 C. Verghese et al. NEUROPSYCHOPHARMACOLOGY 1993-VOL.9, NO.2 is seen that include headache, blurred vision, anorexia, disorders, and personality disorders (Illowsky and nausea, vomiting and diarrhea, muscle cramps, rest­ Kirch 1988). Polydipsia has been reported to be more lessness, confusion, exacerbation of psychosis, convul­ common in females and whites Oos and Evenson 1980), sions, coma, and death. Vieweg et al. (1985b) estimated although Shah and Greenberg (1992) found an over­ that it accounts for 18% of deaths in schizophrenics un­ whelming preponderance of males in their study. Both der 53 years of age. The third stage develops 5 years studies used staff reporting as the method to identify after the onset of water intoxication, and it includes potential cases, and cases were included on the basis other physical complications (Vieweg et al. 1984a). The of differing levels of serum sodium. Staff reporting complications are bladder and bowel dilatation, renal identifIes only the more severe cases, and it varies ac­ and cardiac failure, hydronephrosis, osteopenia, and cording to the level of awareness and interest in differ­ pathological fractures (Blum et al. 1983). The latter may ent institutions. This is an episodic disorder, hence data be due to increased urinary calcium excretion in the on epidemiology and risk factors are limited by the polyuria that accompanies polydipsia (Delva et al. 1989). cross-sectional nature of most of the studies quoted. The time course is based on retrospective studies of small numbers of patients with particularly severe Diagnostic Criteria symptoms, so the time frames for the stages are approx­ imations. There are no formal, generally agreed upon criteria for The symptoms are often episodic, which was seen the syndrome. Studies have used differing criteria, in one third of the patients in a longitudinal study (Peh which varied according to whether they were study­ et al. 1990). There is also signifIcant diurnal variation ing polydipsia or water intoxication. Older studies used in severity. Patients consume large amounts of fluids staff reporting of excessive drinking or water intoxica­ over the day, resulting in diurnalweight gain. They ex­ tion to include patients, but this is an unreliable method. crete a very dilute urine and lose weight in the evening Later studies have started using more quantifIable and night, often returningto their base weight by morn­ measures. Most studies did not measure actual fluid ing (Crammer 1991). intake; obtaining measurements can be very difficult because of patient noncompliance (Lawson et al. 1992). Polyuria has been used as an index of polydipsia even Epidemiologic Data in the earlier studies (Sleeper 1935). Lawson and co­ Most of the studies on polydipsia have been done on workers (1985) used 2.5 liters as the threshold for poly­ chronically illpatients, and prevalence rates of 6.6% Oos uria. Reliable urine collection is also difficult, and hence, and Perez-Cruet 1979) to 17.5% (Blum et a1. 1983) have Vieweg and coworkers (1988a) estimated urine output been reported. Studies have used differing strategies from urine creatinine concentration. However, this for case fInding, usually chart review and staffreports, method assumes a number of factors such as muscle which results in signifIcantunderreporting. Vieweg and mass and diet and is also an approximation. These pa­ coworkers (1986) reported a rate as high as 39% using tients excrete large amounts of dilute urine, and hence, urine specifIc gravity as an estimate of polyuria. This urine specifIc gravity less than 1.008 has been used to method could cause some false positives, as other fac­ establish polyuria (Blum and Friedland 1983). Other tors like lithium can cause polyuria. causes of polyuria such as ingestion of lithium and di­ uretics can confound results. Water retention is assessed using chart reviews and Risk Factors staffreports of abnormal behavior, especially in the af­ Some studies suggest that polydipsia without water in­ ternoon(Koczapski et al. 1987). Diurnalweight changes toxication and with water intoxication may have differ­ have been used to assess drinking and water retention. ent antecedents. The former is associated with high in­ Normalized diurnal weight gain (NDWG), expressed telligence quotients (Sleeper and Jellinek 1936), good by the equation (evening weight - morning weight) premorbid functioning (Lawson et al. 1985), and posi­ x 100/morning weight, is now used in a number of tive symptoms (Kirch et al. 1985). Water intoxication studies as a measure (Vieweg et al. 1988b). Normalized is associated with tardive dyskinesia and ventricular diurnal weight gain greater than 7% is associated with dilatation (Lawson et al. 1985) and negative symptoms a signifIcantrisk of water intoxication (Delva and Cram­ (Kirch et al. 1985). Sample sizes were small, which limits mer 1988). Normalized diurnal weight gain is thus a the generalizability of these data. composite measure of both polydipsia and water reten­ Chronicity of the illness is a strong association with tion (Vieweg et al. 1988b). Studies using NDWG as the polydipsia and water intoxication in most studies. In sole criterion would miss patients with only polydip­ terms of diagnostic groups, 80% of patients have sia. Serum sodium has been used as a measure, but schizophrenia; other diagnoses include affective dis­ there is considerable interindividual variation in rest­ orders, alcohol abuse, mental retardation, organic brain ing sodium levels (Koczapski and Millson 1989), and NEUROPSYCHOPHARMACOLOGY 1993-VOL.9, NO.2 Neuroendocrine Factors in Polydipsia 159 hence, it may not be very useful for screening. Water pathophysiology of "psychogenic" polydipsia: both intoxicationis more related to acute changes in sodium conditions may be related to disturbances in angioten­ than to absolute levels. sin II function, as described later. The best approach to diagnosis is to use a combi­ Hyponatremia is seen with fluid loss (diarrhea, di­ nation of methods. We conducted a

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