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 Table of Contents    
Year : 2018  |  Volume : 60  |  Issue : 4  |  Page : 504-506
“Mind, body, and water!” – Postherpetic polydipsia masquerading as obsessive-compulsive disorder

1 Department of Psychiatry, Medical College and Hospital, Kolkata, West Bengal, India
2 Department of Psychiatry, IPGMER, Kolkata, West Bengal, India
3 Department of Psychiatry, Orygen Youth Health, NWMH, Melbourne, Australia
4 Department of Psychiatry, NIMHANS, Bengaluru, Karnataka, India

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Date of Web Publication28-Nov-2018


Polydipsia has always been an intriguing entity in clinical psychiatry, since long. Other than being commonly associated with patients of chronic schizophrenia, as described in past, it can also mimic and present in other psychiatric disorders; and thus may be elusive for diagnosis and treatment. Here we describe a patient having polydipsia with prominent obsessive compulsive symptoms, which, after detailed investigations, was found to be secondary to herpes encephalitis. The organic nature of the illness was ascertained by distinct signal changes in right uncus, hippocampus and cingulate cortex; whereas conventional workup for polydipsia ruled out both central and nephrogenic diabetes insipidus. Treatment with fluoxetine, proper behavioural management and psychoeducation resulted in slow but sustained improvement in this patient. We then deconstruct the clinical manifestations and discuss the neurobiological explanation.

Keywords: Neurobiology, obsessive-compulsive disorder, organic psychiatry, polydipsia

How to cite this article:
Chatterjee SS, Ghosal S, Das S, Gowda GS. “Mind, body, and water!” – Postherpetic polydipsia masquerading as obsessive-compulsive disorder. Indian J Psychiatry 2018;60:504-6

How to cite this URL:
Chatterjee SS, Ghosal S, Das S, Gowda GS. “Mind, body, and water!” – Postherpetic polydipsia masquerading as obsessive-compulsive disorder. Indian J Psychiatry [serial online] 2018 [cited 2022 Nov 29];60:504-6. Available from:

   Introduction Top

Polydipsia has always been an intriguing entity in clinical psychiatry since long. Other than being commonly associated with patients of chronic schizophrenia, as described in the past, it can also mimic and present in other psychiatric disorders, and thus, may be elusive for diagnosis and treatment.[1],[2] Here, we describe a patient having polydipsia with obsessive-compulsive features which, after detailed investigations, were found to be secondary to herpes encephalitis. The case will also delineate how we can neurobiologically explain the presenting symptoms.

   Case Report Top

A 50-year-old married male presented with complaints of excessive water intake (7–8 L/day) and repetitive, intrusive ideas about the same, for the last 1 year which is further increased for the last 2 months. One year back, he had an episode of HSV encephalitis which was resolved within 1 month; however, he started having repeated thoughts of taking water and sexual obsessions (about having incestuous relationship). Although he recognized it as his own thought and tried hard to resist it, he did not succeed. For this, he additionally used to perform various compulsive rituals such as touching the head or praying, etc., however, those would only aggravate the symptoms. Over and above, for the last 8 months, he used to feel that some foul smell was coming from his mouth for which, as he reported, he started drinking excessively.

His physical examination (including examination of oral cavity) revealed no abnormality. Blood pressure was 110/70 mm of Hg, PR 76/min. Mental status examination showed that he was well kempt, tidy and was having obsessive thoughts of taking water, and an anxious affect. The obsessions were egodystonic, repetitive, intrusive, and involved minimum 6 h in a day. His routine investigation reports were within normal limits: Na: 133 mEq/L; K: 3.6 mEq/L; urea: 13 mg/dL, creatinine: 0.6 mg/dL, fasting blood sugar: 90 mmol/dL, and postprandial blood sugar: 132 mmol/dL. Urine routine examination and ultrasonography of urinary system showed no specific abnormality.

A provisional diagnosis of “Polydipsia under investigation” was made, and he was admitted to our department for observation and diagnostic clarification. On admission, his daily water intake was quantified, and it was nearly 10–12 L/day, body weight was 55 kg, and he was passing 1200 ml of urine daily. Just after the admission, the urine osmolality was documented to be 246 mOsm/kg (normal is above 300 mOsm/kg). The endocrinologist worked up for diabetes insipidus (DI) and primary polydipsia. Normal renal function tests ruled out nephrogenic causes of DI. Later, the patient was subjected to 7-hour water deprivation test and was administered vasopressin. The results ruled out pituitary DI. Further, average serum cortisol after corticotrophin stimulation test ruled out hypothalamic–pituitary–adrenal axis dysfunction.

The magnetic resonance imaging report showed nonenhancing signal intensities in the right uncus, hippocampus, and right cingulate cortex. We treated him on tablet fluoxetine, 20 mg/day, along with behavioral management and psychoeducation, and advised to add sugar and salt to his water bottle. The patient improved within 1 month and is maintaining in remission at 3 months follow-up with a Y-BOCS[3] score of 7/40.

   Discussion Top

Psychogenic polydipsia is a diagnosis of exclusion and was reported in the psychiatric literature since early 20th century, before the introduction of antipsychotic medication in chronic mental disorders particularly schizophrenia.[2] Although previously called psychogenic, nearly all polydipsia patients are hypothesized to be having some physiologic abnormities. In schizophrenia patients, ADH and vasopressin dysregulation are presumed to be responsible.[4] Moreover, primary polydipsia has an obsessive component in most of the cases, and converging evidences are being found for polydipsia being a distinct subtype of obsessive-compulsive disorder (OCD).[5],[6] Moreover, in basic research, there exists a rat model of obsessive-compulsive disorder in which rats exhibit exaggerated drinking behavior when presented with food pellets under a fixed-time schedule, schedule-induced-polydipsia, which also shows how closely those two are interlinked.[7]

Anterior cingulate cortex (ACC) is a part of the error detection system of the brain, and abnormal activity of ACC and orbitofrontal cortex has been demonstrated in OCD patients.[8] Whereas uncus is covered by part of olfactory cortex; hence, it is very intricately involved in olfaction.[9] We hypothesize that, in our case, the involvement of ACC probably caused the obsessive symptoms. Furthermore, dysfunctional uncus sequentially caused the persistent halitosis, which, afterward, was channelized to florid polydipsic behavior with further involvements of hippocampus and limbic system,[10] key components for thirst regulation [Figure 1].
Figure 1: Explanation of neurobiology of symptoms

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   Conclusion Top

Polydipsia is always an intriguing phenomenon in psychiatric patients and sometimes can be explained by sequential neurobiological phenomenon, especially when it occurs after any central nervous system infection, similar to our case. Meticulous history, brain imaging, and neurobiological correlation with psychopathology are of paramount importance not only for treatment but also for theoretical psychiatry.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

de Leon J, Verghese C, Tracy JI, Josiassen RC, Simpson GM. Polydipsia and water intoxication in psychiatric patients: A review of the epidemiological literature. Biol Psychiatry 1994;35:408-19.  Back to cited text no. 1
Sleeper FH, Jellinek EM. A comparative physiologic, psychologic and psychiatric study of polyuric and non-polyuric schizophrenic patients. J Nerv Ment Dis 1936;83:557-63.  Back to cited text no. 2
Goodman WK, Price LH, Rasmussen SA, Mazure C, Fleischmann RL, Hill CL, et al. The Yale-Brown obsessive compulsive scale. I. Development, use, and reliability. Arch Gen Psychiatry 1989;46:1006-11.  Back to cited text no. 3
Iftene F, Bowie C, Milev R, Hawken E, Talikowska-Szymczak E, Potopsingh D, et al. Identification of primary polydipsia in a severe and persistent mental illness outpatient population: A prospective observational study. Psychiatry Res 2013;210:679-83.  Back to cited text no. 4
Subramanian K, Rajan TM, Menon V, Rajkumar RP. Converging neurobiological evidence in primary polydipsia resembling obsessive-compulsive disorder. Indian J Psychol Med 2017;39:369-72.  Back to cited text no. 5
[PUBMED]  [Full text]  
Deas-Nesmith D, Brewerton TD. A case of fluoxetine-responsive psychogenic polydipsia: A variant of obsessive-compulsive disorder? J Nerv Ment Dis 1992;180:338-9.  Back to cited text no. 6
Platt B, Beyer CE, Schechter LE, Rosenzweig-Lipson S. Schedule-induced polydipsia: A rat model of obsessive-compulsive disorder. Current protocols in neuroscience 2008;43:9-27.  Back to cited text no. 7
Fitzgerald KD, Welsh RC, Gehring WJ, Abelson JL, Himle JA, Liberzon I, et al. Error-related hyperactivity of the anterior cingulate cortex in obsessive-compulsive disorder. Biol Psychiatry 2005;57:287-94.  Back to cited text no. 8
Eslinger PJ, Damasio AR, Van Hoesen GW. Olfactory dysfunction in man: Anatomical and behavioral aspects. Brain Cogn 1982;1:259-85.  Back to cited text no. 9
Sailer C, Winzeler B, Christ-Crain M. Primary polydipsia in the medical and psychiatric patient: Characteristics, complications and therapy. Swiss Med Wkly 2017;147:w14514.  Back to cited text no. 10

Correspondence Address:
Dr. Seshadri Sekhar Chatterjee
Department of Psychiatry, Medical College, Kolkata, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/psychiatry.IndianJPsychiatry_153_18

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  [Figure 1]