BIOL PSYCHIATRY 1992;31:1057-1061
1057
CASE REPORT
Syndrome of Inappropriate Secretion of Antidiuretic Hormone Associated with Schizophrenia Michio Suzuki, Osamu Takeuchi, Ichiro Mori, Kunio Takegoshi, and Masayoshi Kurachi
Introduction The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) has been occasionally described in association with psychiatric disorders. A few authors have suggested that psychosis itself is responsible for SIADH (Hobson and English 1963; Dubovsky et al 1973; Raskind et al 1975). We report a patient with schizophrenia who developed SIADH and whose hyponatremia appeared to resolve after recovery from psychosis with electroconvulsive therapy (ECT). Case Report A 48-year-old woman who had been diagnosed as schizophrenic 5 years previously was admitted to the Takaoka Municipal Hospital on July 17, 1990 because of exacerbated psychosis. She had prominent auditory hallucinations of persecutive content throughout the day mid behavioral derangements controlled by the hallucinations. On admission she was medicated with 3 mg of bromperidol (a butylophenone derivative in which the CI of haloperidol is replaced by Br), 12.5 nag of chlorpromazine, 3 mg of biperiden, and 12.5 mg of promethazine per day. Her blood pressure was 102160 mmHg and pulse rate 701r.~in. Serum sodium concentration was 131 mEq/L and other routine laboratory data were normal. On July 31, 1990 she was found to be lethargic and to have a serum sodium of 112 mEq/L. Postictal lethargy was suspected. At this time, she was treated with 3 mg of brompefidol, 6 mg of timiperone (a butylophenone derivative developed in Japan), 40 mg of levomepromazine, 12.5 mg of chlorpromazine, 3 mg of biperiden~ n_qd37.5 mg of promethazine per day. The next day, her consciousness cleared and the hyponatremia improved after the IV administration of saline. However, the serum sodium level again fell to 115 mEq/L on August 9, 1990. General physical and neurologic examinations at the: time of these episodes were otherwise unremarkable. There were no signs of edema or dehydration. Blood pressure
From the Department of NeuropsychiaUry(MS, IVlK),Toyama Medical and PlmrmaceuficalUniversity, Toyama, Japan; the Department of Nemopsychiatry(O13, and the Depamnent of Anesthesiology(lid), TalmolmMunicipal Hospital, Takaoka, Japan; Takegoshi Naika Clinic (KT), Takaolm, Japan. Address reprint requests to: Michio Suzuki, M.D., Department of NeuropsychiaUry,Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-01, Japan. Received August 23, 1991; revised January i0, 1992. ~J 1992 Society of Biological Psychiatry
0006-3223/92/$05.00
1058
BIOL PSYCHIATRY 1992;31:1057-1061
M. Suzuki et al
was 100/70 mmHg with no orthostatic drop. The patient had never smoked. Polydipsia was not observed. Laboratory data revealea the serum sodium noted above and urine sodium of 168 mEq/day. Serum osmolality was 237 mOsm/kg, and urine osmolality was 635 mOsm/kg. Simultaneously obtained plasma vasopressin was 3.1 ttg/dl (normal, 0.34.2), showing that vasopressin release was not suppressed. Renal uld hepatic function tests were normal. Further work up for causes of the hyponatremia revealed no significant abnormality, including plasma adrenocorticotropic hormone, plasma cortisol, plasma aldosterone, and thyroid function tests. Chest x.-ray and electrocardiogram were normal. Brain computed tomography (CT) scan was unremarkable, and electroencephalogram showed slower basic activities of 8 c/s with slight 0 activity contamination, which was consistent with reversible organic brain syndrome due to hyponatremia. Because the possibility of neuroleptic medication-induced SIADH was considered, all drugs were discontinued, and treatment with fluid restriction and hypertonic saline was started on August 11, 1990. After a month, however, the serum sodium level remained at less than 125 mEq/L, and the florid psychotic symptoms persisted. Informed consent for ECT was obtained from the husband of the patient. She received six ECT treatments from September 18 to 28, 1990, with her psychotic symptoms showing married improvement. Unexpectedly, the serum sodium level gradually increased after ECT and norrealized to 140 mEq/L in late October 1990. Antipsychotic medication consisting of 100 mg of pipamperone per day was restarted on October 22, 1990, with no recurrence of the hyponatremia seen subsequently. Figure 1 shows an outline of the clinical course of the patient during the hospitalization.
Discussion This report describes a patient with relatively late-onset schizophrenia whose inappropriate secretion of antidiuretic hormone appeared to resolve after ECT-ind~ced recovery from psychosis. The patient showed resolution of SIADH with remission of the psychotic illness without the use of pharmacologic agents. The clinical course provides potentially important clues about the relationship betweea psychotic exacerbation and water intoxication. SIADH is a syndrome characterized by plasma vasopressin concentrations that are inappropriately high relative to plasma osmolality. The present case fulfilled the criteria for SIADH (Barrier and Schwartz 1967), and other known causes of hyponatremia were excluded. Although patients with schizophrenia and recurrent water intoxication usually have disturbed thirst (Vieweg et al 1984), polydipsia was unremarkable in our patient. The patient received many antipsychotic drugs to treat the intractable hallucinations, excessive anxiety and insomnia, and anticholinergic drugs to prevent the extrapyramidal side effects of the antipsychotics. Several case reports have suggested an association between SIADH in psychiatric patients and neuroleptic drugs (Ajlouni et al 1974; De Rivera 1975; Vincent and Emery 1978; Peck and Shenkman 1979). In these reports, the hyponatremia improved rapidly within a week after the discontinuation of the neuroleptics. In the present case, however, moderate hyponatremia persisted for more than a month despite discontinuation of the neuroleptics and water restriction. It has been reported that ph~sma vasopressin increases when hypotension occurs in association with antipsychotic medication (Raskind et al 1987). Although the blood pressure of our patient was fairly low:, orthostatic hypotension was not present and there was no significant difference in blood pressure between the medicated and drug-free periods. Therefore, the inappropriate
BIOL PSYCHIATRY 1992;31:1057-1061
SIADH and Schizophrenia
1059
Auditory Hallucination Convu l s i o n ?
Lethargy
i flflfl
ECT BPD 3-9n~
Antipsychotic Medication
T.p
3-s~j
CPZ 12.Sing LPZ 40rag
{mg/day) Fluid Restriction
PPP IOOmg m
,
I
Serum Sodium
(n~q/1 ) IIS ,
Auool Admission
|
Septol
!
Oet.l
Nov.l
Figure 1. The course of the hospitalization with associated inte:ventions, neurologic and psychiatric symptoms, and plasma sodium levels. BPD, bromperidol; CPZ, clflo~promazine; LPZ, levomepromazine; PPP, pip&~nperone;TMP~ timiperone.
vasopressin secx~'tion in our patient cannot be attributed to the neuroleptic treatment or neuroleptic-induced hypotension. ' ~ e possible role of ECT in the pathogenesis of hyponatremia appears complex. Jos et al (1986) reported that patients with self-induced water intoxication were more likely to have receiv~ multiple courses of ECT. Narang et al (1973) reported ECT raised ADH le~,:ls in schizophrenics, and Finlayson et al (1989) descr~,ed a depressed woman with a hyponatremic seizure.,,following ECI'. In our patient, however, the ,gradual increase in the serum sodium cortcentration after ECT suggests that reversal of ~ e p,~ychosis was tbe first-order event and normalized osmoregulation the second-order event. Therefore, it is likely that the psychosis reversal induced by ECT did normalize osmoregulation, with SIADH and psychotic exacerbation appearing to be cIosely connected. Vieweg et al (!985) also reported a patient with schizophrenia, int~rn~ttent hyponatremia and polydipsia whose osmotic regulation was normalized in parallel with an improved mental state after an inadvertently induced hyperosmolar coma. A few reports have suggested that psychosis itself sometimes induces SIADH. Hobson and English (1963) were the first to note SIADH in psychiatric patient~ with poiydipsia. Dubovsky et al (1973) reported that an unmedicated 25-year-old woman with c,Monic
1060
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1992;31:1057-1061
M. Suzuki et al
schizophrenia showed recurrent episodes of SIADH during an acute psychotic state, and in whom the syndrome resolved with remission of the exacerbated psychosis. Raskind et al (1975) described three unmedicated postmenopausal women with agitated psychotic depression who developed SIADH. Raskind et al (1978, 1987) also reported that basal vasopressin levels are higher in psychotic patients than in nonpsychotic psychiatric patients or controls, and speculated that increased central nervous system dopaminergic activity may be involved in the pathophysiology of both acute psychosis and increased release of vasopressin. Other investigators, however, have failed to detect increased secretion of vasopressin in schizophrenic patients (Sorensen et al 1985). A recent study has shown that psychiatric patients with polydipsia and hyponatremia have unexplained basal defects in urinary dilution, osmoregulation of water intake, and secretion of vasopressin (Goldman et al 1988). The authors have suggested that episodes of severe hyponatremia are caused by aggravation of one or more of the basal defects that sometimes coincide with exacerbation of the psychosis, lllowsky and Kirch (1988) also provide a recent review of the pathophysiology of polydipsia and hyponatremia in psychiatric patients. This is ~ uncontrolled case report of only a single patient, and because the episodic nature of SIADH is well-known, the simultaneous resolution of SIADH and the psychosis in our patient may have been coincidental. However, this case report suggests that there is some relationship between SIADH and the pathophysiology of schizophrenia.
References Ajlouni K, Kern MW, Tures JF, Theft GB, Hagen TC (1974): Thiothixene-induced hyponatremia. Arch Intern Med 134:1103-1105. B~u~terFC, Sc;hwartzWB (I 967): The syndromeof inappropriate secretion of antidiuretic hormone. Am J Med 42:790-806. De Rivcra JLC (1975): Inappropriate secretion of antidiuretic hormone from fluphenazine therapy. Ann Intern ~ted 82:811-812. Dubovsky SL, Grabon S, Berl T, Schrier RW (1973): Syndrome of inappropriate secretion of antidiuretie ;~ormonewith exacerbated psychosis. Ann lntern Med 79:551-554. Finlayson AJR, Vieweg WVR, Wilkey WD, Cooper AJ (1989): Hypona~renficseizure following ECT. Can J Psychiatry 34:463-464. Goldman MB, |.,uchins DJ, Robertson GL (1988): Mechanisms of altered water metabolism in psychotic patients with polydipsia and hyponatremia. N Engl J Med 318:397-403. Hobson JA, Engl!sh JT (1963): Self-induced water intoxication. Ann lntern IVied 58:324.-332. lUowskyBP, Kirel~DG (1988): Polydipsiaand hyponatremiain psychiatricpatients. Am J P~chiatry 145:675-683. Jos CJ, Evenson RC, Mallya AR (1986): Self-induced water intoxication: A comparison of 34 cases with matched controls. J Clin Psychiatry 47:368-370. Narang RL, Chadhury RR, W~:gNN (1973): Effect of electroconvuisive therapy on the anfi0iuretic hormone level in the plasma of schizophrenic patients, lndian J Med Res 61:766-770. Peck V, Shenkman L (1979): Haloperidol-induced syndrome of inappropriate secretion of antidiuretic hormone. Clin Pharmacol Ther 26:442-A33.. Raskind MA, Orenstein H, Christopher TO (1975): Acute psychosis, increased water ingestion, and inappropriate antidiuretic hormone secretion. Am J Psychiatry 132:907-910. Raskind MA, Weitzman RE, Orenstein H, Fisher DA, Courtney N (1978): Is antidiuretic hormone elevated in psychosis? A pilot study. Biol Psychiatry 13:385-390. Raskind MA, Courtney N, Murburg MM, et al (1987): Antipsychoticdrugs and plasma vasopressin in normals and acute schizophrenic patients. Biol Psychiatry 22:453-462.
SIADH and Schizophrenia
BIOL PSYCHIATRY 1992;31:1o57-1o61
1061
Sorensen PS, Gjerris A, Hammer M (1985): Cerebrospinal fluid vasopressin in neurological ~nO psychiatric disorders. J Neurol Neurosurg Psychiatry 48:50-57. Vieweg WVR, Rowe WT, David JJ, Spradlin WW (1984): Hyposthenuria as a marker for selfinduced water intexication and schizophrenic disorders. Am J Psychiatry 141:1258-1260. Vieweg WVR, Rowe WT, David JJ, Buckman J, Cumow RT, Spradlin WW (1985): Possible ameliorating effect of captopril treatment and hyperosmolar coma in a patient with psychosis, intermittent hyponatremia, and polydipsia. Psychiatr Hosp 16:!83-186. Vincent EM, Emery S (1978): Antidiuretic hormone syndrome and thioridazine. Ann Intern Med 89"14"/-148.
1057
CASE REPORT
Syndrome of Inappropriate Secretion of Antidiuretic Hormone Associated with Schizophrenia Michio Suzuki, Osamu Takeuchi, Ichiro Mori, Kunio Takegoshi, and Masayoshi Kurachi
Introduction The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) has been occasionally described in association with psychiatric disorders. A few authors have suggested that psychosis itself is responsible for SIADH (Hobson and English 1963; Dubovsky et al 1973; Raskind et al 1975). We report a patient with schizophrenia who developed SIADH and whose hyponatremia appeared to resolve after recovery from psychosis with electroconvulsive therapy (ECT). Case Report A 48-year-old woman who had been diagnosed as schizophrenic 5 years previously was admitted to the Takaoka Municipal Hospital on July 17, 1990 because of exacerbated psychosis. She had prominent auditory hallucinations of persecutive content throughout the day mid behavioral derangements controlled by the hallucinations. On admission she was medicated with 3 mg of bromperidol (a butylophenone derivative in which the CI of haloperidol is replaced by Br), 12.5 nag of chlorpromazine, 3 mg of biperiden, and 12.5 mg of promethazine per day. Her blood pressure was 102160 mmHg and pulse rate 701r.~in. Serum sodium concentration was 131 mEq/L and other routine laboratory data were normal. On July 31, 1990 she was found to be lethargic and to have a serum sodium of 112 mEq/L. Postictal lethargy was suspected. At this time, she was treated with 3 mg of brompefidol, 6 mg of timiperone (a butylophenone derivative developed in Japan), 40 mg of levomepromazine, 12.5 mg of chlorpromazine, 3 mg of biperiden~ n_qd37.5 mg of promethazine per day. The next day, her consciousness cleared and the hyponatremia improved after the IV administration of saline. However, the serum sodium level again fell to 115 mEq/L on August 9, 1990. General physical and neurologic examinations at the: time of these episodes were otherwise unremarkable. There were no signs of edema or dehydration. Blood pressure
From the Department of NeuropsychiaUry(MS, IVlK),Toyama Medical and PlmrmaceuficalUniversity, Toyama, Japan; the Department of Nemopsychiatry(O13, and the Depamnent of Anesthesiology(lid), TalmolmMunicipal Hospital, Takaoka, Japan; Takegoshi Naika Clinic (KT), Takaolm, Japan. Address reprint requests to: Michio Suzuki, M.D., Department of NeuropsychiaUry,Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-01, Japan. Received August 23, 1991; revised January i0, 1992. ~J 1992 Society of Biological Psychiatry
0006-3223/92/$05.00
1058
BIOL PSYCHIATRY 1992;31:1057-1061
M. Suzuki et al
was 100/70 mmHg with no orthostatic drop. The patient had never smoked. Polydipsia was not observed. Laboratory data revealea the serum sodium noted above and urine sodium of 168 mEq/day. Serum osmolality was 237 mOsm/kg, and urine osmolality was 635 mOsm/kg. Simultaneously obtained plasma vasopressin was 3.1 ttg/dl (normal, 0.34.2), showing that vasopressin release was not suppressed. Renal uld hepatic function tests were normal. Further work up for causes of the hyponatremia revealed no significant abnormality, including plasma adrenocorticotropic hormone, plasma cortisol, plasma aldosterone, and thyroid function tests. Chest x.-ray and electrocardiogram were normal. Brain computed tomography (CT) scan was unremarkable, and electroencephalogram showed slower basic activities of 8 c/s with slight 0 activity contamination, which was consistent with reversible organic brain syndrome due to hyponatremia. Because the possibility of neuroleptic medication-induced SIADH was considered, all drugs were discontinued, and treatment with fluid restriction and hypertonic saline was started on August 11, 1990. After a month, however, the serum sodium level remained at less than 125 mEq/L, and the florid psychotic symptoms persisted. Informed consent for ECT was obtained from the husband of the patient. She received six ECT treatments from September 18 to 28, 1990, with her psychotic symptoms showing married improvement. Unexpectedly, the serum sodium level gradually increased after ECT and norrealized to 140 mEq/L in late October 1990. Antipsychotic medication consisting of 100 mg of pipamperone per day was restarted on October 22, 1990, with no recurrence of the hyponatremia seen subsequently. Figure 1 shows an outline of the clinical course of the patient during the hospitalization.
Discussion This report describes a patient with relatively late-onset schizophrenia whose inappropriate secretion of antidiuretic hormone appeared to resolve after ECT-ind~ced recovery from psychosis. The patient showed resolution of SIADH with remission of the psychotic illness without the use of pharmacologic agents. The clinical course provides potentially important clues about the relationship betweea psychotic exacerbation and water intoxication. SIADH is a syndrome characterized by plasma vasopressin concentrations that are inappropriately high relative to plasma osmolality. The present case fulfilled the criteria for SIADH (Barrier and Schwartz 1967), and other known causes of hyponatremia were excluded. Although patients with schizophrenia and recurrent water intoxication usually have disturbed thirst (Vieweg et al 1984), polydipsia was unremarkable in our patient. The patient received many antipsychotic drugs to treat the intractable hallucinations, excessive anxiety and insomnia, and anticholinergic drugs to prevent the extrapyramidal side effects of the antipsychotics. Several case reports have suggested an association between SIADH in psychiatric patients and neuroleptic drugs (Ajlouni et al 1974; De Rivera 1975; Vincent and Emery 1978; Peck and Shenkman 1979). In these reports, the hyponatremia improved rapidly within a week after the discontinuation of the neuroleptics. In the present case, however, moderate hyponatremia persisted for more than a month despite discontinuation of the neuroleptics and water restriction. It has been reported that ph~sma vasopressin increases when hypotension occurs in association with antipsychotic medication (Raskind et al 1987). Although the blood pressure of our patient was fairly low:, orthostatic hypotension was not present and there was no significant difference in blood pressure between the medicated and drug-free periods. Therefore, the inappropriate
BIOL PSYCHIATRY 1992;31:1057-1061
SIADH and Schizophrenia
1059
Auditory Hallucination Convu l s i o n ?
Lethargy
i flflfl
ECT BPD 3-9n~
Antipsychotic Medication
T.p
3-s~j
CPZ 12.Sing LPZ 40rag
{mg/day) Fluid Restriction
PPP IOOmg m
,
I
Serum Sodium
(n~q/1 ) IIS ,
Auool Admission
|
Septol
!
Oet.l
Nov.l
Figure 1. The course of the hospitalization with associated inte:ventions, neurologic and psychiatric symptoms, and plasma sodium levels. BPD, bromperidol; CPZ, clflo~promazine; LPZ, levomepromazine; PPP, pip&~nperone;TMP~ timiperone.
vasopressin secx~'tion in our patient cannot be attributed to the neuroleptic treatment or neuroleptic-induced hypotension. ' ~ e possible role of ECT in the pathogenesis of hyponatremia appears complex. Jos et al (1986) reported that patients with self-induced water intoxication were more likely to have receiv~ multiple courses of ECT. Narang et al (1973) reported ECT raised ADH le~,:ls in schizophrenics, and Finlayson et al (1989) descr~,ed a depressed woman with a hyponatremic seizure.,,following ECI'. In our patient, however, the ,gradual increase in the serum sodium cortcentration after ECT suggests that reversal of ~ e p,~ychosis was tbe first-order event and normalized osmoregulation the second-order event. Therefore, it is likely that the psychosis reversal induced by ECT did normalize osmoregulation, with SIADH and psychotic exacerbation appearing to be cIosely connected. Vieweg et al (!985) also reported a patient with schizophrenia, int~rn~ttent hyponatremia and polydipsia whose osmotic regulation was normalized in parallel with an improved mental state after an inadvertently induced hyperosmolar coma. A few reports have suggested that psychosis itself sometimes induces SIADH. Hobson and English (1963) were the first to note SIADH in psychiatric patient~ with poiydipsia. Dubovsky et al (1973) reported that an unmedicated 25-year-old woman with c,Monic
1060
BIOL PSYCHIATRY
1992;31:1057-1061
M. Suzuki et al
schizophrenia showed recurrent episodes of SIADH during an acute psychotic state, and in whom the syndrome resolved with remission of the exacerbated psychosis. Raskind et al (1975) described three unmedicated postmenopausal women with agitated psychotic depression who developed SIADH. Raskind et al (1978, 1987) also reported that basal vasopressin levels are higher in psychotic patients than in nonpsychotic psychiatric patients or controls, and speculated that increased central nervous system dopaminergic activity may be involved in the pathophysiology of both acute psychosis and increased release of vasopressin. Other investigators, however, have failed to detect increased secretion of vasopressin in schizophrenic patients (Sorensen et al 1985). A recent study has shown that psychiatric patients with polydipsia and hyponatremia have unexplained basal defects in urinary dilution, osmoregulation of water intake, and secretion of vasopressin (Goldman et al 1988). The authors have suggested that episodes of severe hyponatremia are caused by aggravation of one or more of the basal defects that sometimes coincide with exacerbation of the psychosis, lllowsky and Kirch (1988) also provide a recent review of the pathophysiology of polydipsia and hyponatremia in psychiatric patients. This is ~ uncontrolled case report of only a single patient, and because the episodic nature of SIADH is well-known, the simultaneous resolution of SIADH and the psychosis in our patient may have been coincidental. However, this case report suggests that there is some relationship between SIADH and the pathophysiology of schizophrenia.
References Ajlouni K, Kern MW, Tures JF, Theft GB, Hagen TC (1974): Thiothixene-induced hyponatremia. Arch Intern Med 134:1103-1105. B~u~terFC, Sc;hwartzWB (I 967): The syndromeof inappropriate secretion of antidiuretic hormone. Am J Med 42:790-806. De Rivcra JLC (1975): Inappropriate secretion of antidiuretic hormone from fluphenazine therapy. Ann Intern ~ted 82:811-812. Dubovsky SL, Grabon S, Berl T, Schrier RW (1973): Syndrome of inappropriate secretion of antidiuretie ;~ormonewith exacerbated psychosis. Ann lntern Med 79:551-554. Finlayson AJR, Vieweg WVR, Wilkey WD, Cooper AJ (1989): Hypona~renficseizure following ECT. Can J Psychiatry 34:463-464. Goldman MB, |.,uchins DJ, Robertson GL (1988): Mechanisms of altered water metabolism in psychotic patients with polydipsia and hyponatremia. N Engl J Med 318:397-403. Hobson JA, Engl!sh JT (1963): Self-induced water intoxication. Ann lntern IVied 58:324.-332. lUowskyBP, Kirel~DG (1988): Polydipsiaand hyponatremiain psychiatricpatients. Am J P~chiatry 145:675-683. Jos CJ, Evenson RC, Mallya AR (1986): Self-induced water intoxication: A comparison of 34 cases with matched controls. J Clin Psychiatry 47:368-370. Narang RL, Chadhury RR, W~:gNN (1973): Effect of electroconvuisive therapy on the anfi0iuretic hormone level in the plasma of schizophrenic patients, lndian J Med Res 61:766-770. Peck V, Shenkman L (1979): Haloperidol-induced syndrome of inappropriate secretion of antidiuretic hormone. Clin Pharmacol Ther 26:442-A33.. Raskind MA, Orenstein H, Christopher TO (1975): Acute psychosis, increased water ingestion, and inappropriate antidiuretic hormone secretion. Am J Psychiatry 132:907-910. Raskind MA, Weitzman RE, Orenstein H, Fisher DA, Courtney N (1978): Is antidiuretic hormone elevated in psychosis? A pilot study. Biol Psychiatry 13:385-390. Raskind MA, Courtney N, Murburg MM, et al (1987): Antipsychoticdrugs and plasma vasopressin in normals and acute schizophrenic patients. Biol Psychiatry 22:453-462.
SIADH and Schizophrenia
BIOL PSYCHIATRY 1992;31:1o57-1o61
1061
Sorensen PS, Gjerris A, Hammer M (1985): Cerebrospinal fluid vasopressin in neurological ~nO psychiatric disorders. J Neurol Neurosurg Psychiatry 48:50-57. Vieweg WVR, Rowe WT, David JJ, Spradlin WW (1984): Hyposthenuria as a marker for selfinduced water intexication and schizophrenic disorders. Am J Psychiatry 141:1258-1260. Vieweg WVR, Rowe WT, David JJ, Buckman J, Cumow RT, Spradlin WW (1985): Possible ameliorating effect of captopril treatment and hyperosmolar coma in a patient with psychosis, intermittent hyponatremia, and polydipsia. Psychiatr Hosp 16:!83-186. Vincent EM, Emery S (1978): Antidiuretic hormone syndrome and thioridazine. Ann Intern Med 89"14"/-148.
