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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polydipsia, chronic or intermittent, with or without hyponatremia, frequently occurs among chronic patients with schizophrenia. The pathogenesis of polydipsia remains poorly understood. The key assumption of our hypothesis is that in some of these patients, polydipsia and hyponatremia are consequences of patients' adjustment to a prolonged intake of an insufficient diet, dominantly poor in potassium. Deficits of potassium, without significant hypokalemia, may cause impairment of the urine-concentrating ability with polyuria-polydipsia. A fall of intracellular tonicity, dominantly due to a decreased amount of K(+) and attendant anions in cells, should be accompanied with a fall of extracellular osmolality. Because of the diminished content of ions that may diffuse out of cells and because osmotic equilibrium between the ECF and ICF compartments cannot be established in a short period of time, these patients have a diminished ability to adapt to an excessive intake of fluids. These mechanisms might be related to the development of polydipsia and water intoxication in patients with different mental and somatic disorders. The experiences with the therapeutic effects of diets containing an sufficient amount of potassium in two patients with schizophrenia are described. Further investigations are needed, and we suggest a possible approach to test our hypotheses.
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PMID:A different hypothesis on hyponatremia in psychiatric patients: treatment implications and experiences. 1894 40

Primary polydipsia, excessive fluid intake without medical cause, is present in over 20% of seriously and persistently ill psychiatric inpatients. The long-term effects of primary polydipsia on longevity have not previously been examined. Inpatients in a psychiatric hospital were screened for polydipsia in 1985. Those identified to be polydipsic, the majority of whom suffered from schizophrenia, were re-evaluated in 2005 and compared with a control group of non-polydipsic patients. Chart reviews were conducted and follow-up data were obtained. Of 172 patients at the time of screening, 48 suffering from schizophrenia either had or went on to develop polydipsia; 42 non-polydipsic patients with schizophrenia from the original survey were randomly selected as controls. Primary polydipsia had a significant negative effect on longevity. The median age at death (age at which 50% of cases have died) was 59 years for polydipsic patients and 68 for non-polydipsic control patients. Adjusting for duration of schizophrenia, smoking, and diagnosis, a patient with polydipsia had a 74% greater chance of dying before a non-polydipsic patient (a hazard ratio of 2.84 [95% Confidence Interval (CI): 1.22-6.64]). Outcome was worst in patients with severe polydipsia: the median age at death was 57 years and a patient with severe polydipsia had a 75% greater chance of dying before a non-polydipsic patient (hazard ratio of 3.36 [95% CI: 1.31-8.60]). When polydipsia is associated with schizophrenia, mortality is increased in comparison to that in patients with schizophrenia who do not drink water to excess.
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PMID:Mortality over a 20-year period in patients with primary polydipsia associated with schizophrenia: a retrospective study. 1898 69

Patients with schizophrenia and water imbalance may represent a subset of patients with distinct pathophysiological abnormalities and susceptibility to cognitive impairment. Specifically, patients with polydipsia and hyponatremia have been shown to have smaller anterior hippocampal volumes, which are also associated with various impairments in neuroendocrine function. To determine whether abnormalities in patients with water imbalance extend to the cognitive realm, the present study evaluated neuropsychological functioning in three groups of patients with schizophrenia: polydipsic hyponatremic, polydipsic normonatremic, and nonpolydipsic normonatremic. Participants were administered cognitive tests assessing intelligence, attention, learning/memory (verbal, nonverbal, emotional), and facial discrimination. Hyponatremic patients showed poorer overall neuropsychological functioning relative to all other patients, and polydipsic normonatremic patients performed intermediate to the other two groups. Results indicate that patients with schizophrenia and polydipsia, and particularly those with hyponatremia, show prominent cognitive deficits relative to patients without water imbalance. The clinical, neuroendocrine, and cognitive abnormalities in these patients may arise from pathology within the anterior hippocampus and associated prefrontal/limbic brain regions.
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PMID:Neuropsychological impairment in patients with schizophrenia and evidence of hyponatremia and polydipsia. 1941 45

Several lines of studies have shown the existence of an important inhibitory mechanism for the control of water intake involving adrenergic alpha2A receptors (ADRA2A). A human study using patients with schizophrenia demonstrated an exacerbation of polydipsia by the administration of clonidine, an ADRA2A-agonist, and a relief of polydipsia by mianserin, an ADRA2A-antagonist, suggesting the involvement of the central adrenergic system in the drinking behavior of patients with schizophrenia. Based on these findings we examined a possible association between the C-1291G polymorphism in the promoter region of the ADRA2A gene and polydipsia in schizophrenia using a Japanese case-control sample. Our sample includes 348 patients with schizophrenia (DSM-IV) (84 with polydipsia and 264 without polydipsia). No significant association between the ADRA2A C-1291G polymorphism and polydipsia was found. Our result suggests that the ADRA2A C-1291G polymorphism may not confer susceptibility to polydipsia in schizophrenia in our sample. Further studies with larger samples are warranted.
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PMID:Association analysis between the C-1291G polymorphism in the promoter region of the adrenergic alpha2A receptor gene and polydipsia in schizophrenia. 1943 47

Hyponatraemia is known to occur as a rare but clinically important adverse reaction to treatment with different psychotropic drugs, including selective serotonin reuptake inhibitors and antiepileptic drugs. In past decades, reports have been published that describe the development of hyponatraemia in association with antipsychotic drug treatment. Our objective was to systematically review the available evidence on antipsychotic-induced hyponatraemia, focussing on patient characteristics, drug dosage, polydipsia and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). A search was carried out in the MEDLINE and EMBASE databases from January 1966 to 11 April 2009. Inclusion criteria were (i) hyponatraemia (serum sodium level <136 mmol/L) occurring after the start of treatment with an antipsychotic drug; and (ii) that the hyponatraemia potentially occurred as an adverse reaction to antipsychotic drug treatment in accordance with the WHO definition. Articles in languages other than English, Dutch, German, French and Spanish were excluded. Information on patient characteristics, medical and diagnostic data, pharmacological treatment, drug dechallenge and drug rechallenge were extracted from the publications whenever available. A causality assessment was performed on all case reports using Naranjo's adverse drug reaction probability scale. Correlational analysis was performed to assess correlations between antipsychotic drug dosage and both serum sodium level and time to onset of hyponatraemia. We included four studies and 91 publications containing case reports and case series; no randomized controlled studies were identified. Data from the identified case reports were further analysed. The mean age of the patients was 46 years; 57% were male. The diagnosis was schizophrenia in 70% of the cases. A history of polydipsia was diagnosed as positive in 67% of the cases and negative in 23% of the cases. Polydipsia occurred in the remaining 10% of cases, although it was reported to be drug-induced (i.e. a severe increase in water intake was observed in relation to treatment with the suspected drug). Analysis of the case reports using the adverse drug reaction probability scale indicated possible causality in most cases (80%), probable causality in a significant amount of cases (19%) and unlikely causality in one case (1%). Overall correlational analysis yielded no significant correlations between defined daily dose-equivalent dosages and serum sodium or time to onset of hyponatraemia. The incidence of hyponatraemia induced by antipsychotics may be much higher than is currently thought. Both the newer atypical antipsychotics and the older drugs have been associated with the development of hyponatraemia. Physicians, psychiatrists and other healthcare workers should be aware of the possibility of hyponatraemia associated with the use of antipsychotics. Further studies are required to establish the risks of and risk factors associated with antipsychotic-induced hyponatraemia.
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PMID:Antipsychotic-induced hyponatraemia: a systematic review of the published evidence. 2141 8

Polydipsia and episodic life-threatening water intoxication remain important clinical problems for a significant portion of persons with schizophrenia. The disorders are associated with increased morbidity and mortality from a number of causes. With a basic understanding of the pathophysiology, one can easily diagnose and assess the clinical conditions. We review here the scope and pathophysiology of disordered water imbalance, including both primary and secondary polydipsia and hyponatremia. Reversible factors and possible interventions are reviewed. Treatment options for preventing water intoxication have expanded from discontinuation of offending agents, targeted fluid restriction, and clozapine therapy to the addition of oral vasopressin antagonists. The latter, however, are extremely potent and must be carefully monitored.
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PMID:The assessment and treatment of water imbalance in patients with psychosis. 2064 34

Primary polydipsia, defined as excessive fluid intake not explained by medical causes, has been reported to occur in over 20% of chronically ill psychiatric inpatients and is especially common in schizophrenic populations. We tested the hypothesis that in an animal model of schizophrenia-like symptoms (subchronic injections of MK-801, 0.5 mg/kg twice daily for 7 days) an increase in the acquisition of schedule-induced polydipsia (SIP) will occur. Young adult, male rats acquired SIP when food-restricted and placed on a non-contingent fixed-time 1-min food schedule. In comparison with saline-treated control animals, subchronic MK-801 treatment significantly increased SIP. These findings suggest an animal model of polydipsia associated with schizophrenia in humans.
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PMID:Increased schedule-induced polydipsia in the rat following subchronic treatment with MK-801. 2071 74

Polydipsia is a less examined but prevalent condition in patients with psychiatric disorders. It is usually described in schizophrenia but is rarely reported in bipolar affective disorder (BPAD). It is important to recognize and treat this entity as it can lead to serious complications. One needs to be cautious in choosing the mood stabilizer while treating this condition. We report the successful treatment of a patient with BPAD and polydipsia on a combination of valproate and risperidone.
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PMID:Psychogenic polydipsia in bipolar affective disorder--a case report. 2135 44

Psychogenic polydipsia with associated hyponatremia is a potentially fatal condition observed in patients with chronic psychiatric illness, especially schizophrenia. Recognition and management of this condition are difficult, as patients are uncooperative and secretive about their water intake, but are important in terms of the associated complications. Different strategies, including involuntary fluid restriction and use of various pharmacological agents, such as demeclocycline, propranolol, captopril, and naloxone, have been used for the treatment of this condition with inconsistent results. Antipsychotics have also been used in the treatment of polydipsia; however, their role is not clear as there are reports of antipsychotics both improving and causing polydipsia. Typical antipsychotics have been associated with exacerbation of polydipsia, whereas clozapine has been associated with its improvement. The efficacy of risperidone in the treatment of this condition is controversial, as negative results have been reported. Herein we present a schizophrenia case with polydipsia and hyponatremia that was successfully treated with risperidone.
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PMID:Risperidone treatment for polydipsia and hyponatremia in schizophrenia: a case report. 2163 34

The polydipsia-hyponatraemia syndrome (PHS) occurs in about 5 to 10% of institutionalised, chronically psychotic patients, 80% of whom have schizophrenia. Major clinical features are polydipsia and dilutional hyponatraemia. Complications of PHS include delirium, generalised seizures, coma and death.Nonpharmacological interventions are fluid restriction, diurnal bodyweight monitoring, behavioural approaches, and supplemental oral sodium chloride administration. These interventions require an experienced and dedicated multidisciplinary staff.A number of pharmacological treatments have been assessed for PHS including the combination of lithium and phenytoin, demeclocycline, propranolol, ACE inhibitors, selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors, typical antipsychotic drugs, clozapine and risperidone. Of these agents, the most promising are the combination of lithium and phenytoin, and clozapine.Integrated treatment requires a highly informed multidisciplinary staff, meticulous monitoring of diurnal weight gain and serum sodium level, and careful record keeping. Acute interventions of observation by trained staff, fluid restriction, water-free areas and supplemental sodium chloride administration are based on diurnal weight gain employing a monthly weight chart and a base weight method. Intravenous hypertonic saline is used briefly and administered in a highly controlled manner when patients with PHS present with generalised seizures and coma. Long term strategies include behavioural interventions and the combination of lithium and phenytoin, and clozapine.
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PMID:Polydipsia-hyponatraemia syndrome : epidemiology, clinical features and treatment. 2333 31


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