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Jose De Leon - One of the best experts on this subject based on the ideXlab platform.

  • Polydipsia a study in a long term psychiatric unit
    European Archives of Psychiatry and Clinical Neuroscience, 2003
    Co-Authors: Jose De Leon
    Abstract:

    : This is a retrospective review of the author's experience with Polydipsia in a long-term unit for treatment refractory patients at a US psychiatric state hospital during a 5-year period [1996-2000]. Sixty-one patients were admitted to this long-term unit, comprising approximately 1 % of the hospital admissions. Polydipsic patients were followed with diurnal weight changes and other biological measures. This longitudinal study of 61 chronic inpatients suggests that Polydipsia is no doubt present in at least 20 % of chronic psychiatric inpatients and hyponatremia in more than 10 %. Two polydipsic patients worsened when switched from clozapine to other atypical antipsychotics. Polydipsia in severe mentally ill patients continues to be a neglected subject and a challenge for psychiatrists. Polydipsic patients should not be switched to other atypical antipsychotics, unless new prospective studies prove that they are as effective as clozapine for Polydipsia.

  • Polydipsia and schizophrenia in a psychiatric hospital a replication study
    Schizophrenia Research, 2002
    Co-Authors: Jose De Leon, Joseph I Tracy, E Mccann, A Mcgrory
    Abstract:

    A prior study in a US state hospital suggested that schizophrenia, smoking and long hospitalization were associated with Polydipsia. This study, in another US hospital, attempts to (1) replicate that schizophrenia and smoking are associated with Polydipsia, and (2) rule out that this relationship is partly explained by alcohol and drug use. Both studies have similar methodologies. The second sample included 588 inpatients. Models of variables associated with Polydipsia were developed using logistic regression. In the second study, after correcting for other factors, the association between Polydipsia and schizophrenia showed a borderline significance, while Polydipsia and smoking displayed a significant association. Neither organic brain lesions, nor alcohol or drug use, were associated with Polydipsia. An analysis combining both samples showed that: (1) schizophrenia, long hospitalization, smoking and heavy smoking were significantly associated with Polydipsia, and (2) male gender and Caucasian race (but not smoking) increased the risk of developing water intoxication in polydipsic patients. These two studies in severely mentally ill patients suggest that the association of Polydipsia with schizophrenia, smoking and chronicity is consistent and independent from the definition of Polydipsia (by staff, a biological method or the combination of both). Psychiatric medications do not appear to explain most cases of Polydipsia in these patients.

  • Polydipsia and water intoxication in a long term psychiatric hospital
    Biological Psychiatry, 1996
    Co-Authors: Jose De Leon, J K Stanilla, Mahmood Dadvand, Carla Canuso, Aruby Odomwhite
    Abstract:

    This cross-sectional survey attempts to establish the prevalence of Polydipsia and water intoxication at a state hospital ( N = 360) using staff diagnosis, specific gravity of the urine (SPGU), weight changes, and chart review. There were 150 [42%, 95% confidence interval (CI) 37 – 47%] patients diagnosed as polydipsic by the staff or by SPGU. At least 93 (26%, CI 21 – 30%) had primary Polydipsia not explained by other causes. Chart review identified 17 (5%, CI 3 – 7%) patients with a history of water intoxication. Using a case-control study design, schizophrenia, extended duration of hospitalization, and heavy smoking were associated with primary Polydipsia in a logistic regression analysis (respective odds ratios were 1.6, 1.8, and 3.6). All patients with a history of water intoxication were Caucasian (versus 83% in those without a history) and had significantly more extended hospitalizations (94 vs. 49%). Future case-control studies should combine longitudinal identification of true cases and controls and exhaustive collections of clinical information in a standardized way.

  • problems and progress in the diagnosis and treatment of Polydipsia and hyponatremia
    Schizophrenia Bulletin, 1996
    Co-Authors: Cherian Verghese, Jose De Leon, Richard C Josiassen
    Abstract:

    Fluid-electrolyte balance is regulated within a narrow range and disturbances in this system are unusual in animals and humans. Studies from the preneuroleptic era to date suggest that up to 25 percent of patients with schizophrenia have Polydipsia, suggesting that it is related to the pathophysiology of the psychoses. Polydipsia and the related phenomenon of hyponatremia cause considerable mortality and morbidity. Prevalence studies are limited by imprecise measures available at present. The treatment was limiting water intake when patients reached critical levels of water retention, which however did not improve Polydipsia. Recent case reports and open studies have shown that clozapine improves both Polydipsia and water retention. The response occurs at low doses and is not related to improvement in psychosis. This may not be applicable to all patients and better understanding of the pathophysiology of Polydipsia-hyponatremia would lead to more empirically derived treatments.

  • treatment of Polydipsia and hyponatremia in psychiatric patients can clozapine be a new option
    Neuropsychopharmacology, 1995
    Co-Authors: Jose De Leon, Cherian Verghese, J K Stanilla, Theodore Lawrence, George M Simpson
    Abstract:

    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.

J K Stanilla - One of the best experts on this subject based on the ideXlab platform.

  • Polydipsia and water intoxication in a long term psychiatric hospital
    Biological Psychiatry, 1996
    Co-Authors: Jose De Leon, J K Stanilla, Mahmood Dadvand, Carla Canuso, Aruby Odomwhite
    Abstract:

    This cross-sectional survey attempts to establish the prevalence of Polydipsia and water intoxication at a state hospital ( N = 360) using staff diagnosis, specific gravity of the urine (SPGU), weight changes, and chart review. There were 150 [42%, 95% confidence interval (CI) 37 – 47%] patients diagnosed as polydipsic by the staff or by SPGU. At least 93 (26%, CI 21 – 30%) had primary Polydipsia not explained by other causes. Chart review identified 17 (5%, CI 3 – 7%) patients with a history of water intoxication. Using a case-control study design, schizophrenia, extended duration of hospitalization, and heavy smoking were associated with primary Polydipsia in a logistic regression analysis (respective odds ratios were 1.6, 1.8, and 3.6). All patients with a history of water intoxication were Caucasian (versus 83% in those without a history) and had significantly more extended hospitalizations (94 vs. 49%). Future case-control studies should combine longitudinal identification of true cases and controls and exhaustive collections of clinical information in a standardized way.

  • treatment of Polydipsia and hyponatremia in psychiatric patients can clozapine be a new option
    Neuropsychopharmacology, 1995
    Co-Authors: Jose De Leon, Cherian Verghese, J K Stanilla, Theodore Lawrence, George M Simpson
    Abstract:

    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.

Morris B. Goldman - One of the best experts on this subject based on the ideXlab platform.

  • Diabetes insipidus
    Nature Reviews Disease Primers, 2019
    Co-Authors: Mirjam Christ-crain, Morris B. Goldman, Daniel G. Bichet, Wiebke K. Fenske, Soren Rittig, Joseph G. Verbalis, Alan S. Verkman
    Abstract:

    Diabetes insipidus (DI) is a form of polyuria–Polydipsia syndrome usually resulting from insufficient production or response to arginine vasopressin (in central, nephrogenic and gestational DI), except in primary Polydipsia. This Primer discusses the types of DI and how aetiology influences management of the disorder. Diabetes insipidus (DI) is a disorder characterized by excretion of large amounts of hypotonic urine. Central DI results from a deficiency of the hormone arginine vasopressin (AVP) in the pituitary gland or the hypothalamus, whereas nephrogenic DI results from resistance to AVP in the kidneys. Central and nephrogenic DI are usually acquired, but genetic causes must be evaluated, especially if symptoms occur in early childhood. Central or nephrogenic DI must be differentiated from primary Polydipsia, which involves excessive intake of large amounts of water despite normal AVP secretion and action. Primary Polydipsia is most common in psychiatric patients and health enthusiasts but the Polydipsia in a small subgroup of patients seems to be due to an abnormally low thirst threshold, a condition termed dipsogenic DI. Distinguishing between the different types of DI can be challenging and is done either by a water deprivation test or by hypertonic saline stimulation together with copeptin (or AVP) measurement. Furthermore, a detailed medical history, physical examination and imaging studies are needed to ensure an accurate DI diagnosis. Treatment of DI or primary Polydipsia depends on the underlying aetiology and differs in central DI, nephrogenic DI and primary Polydipsia.

  • divergent effects of two different doses of intranasal oxytocin on facial affect discrimination in schizophrenic patients with and without Polydipsia
    Psychopharmacology, 2011
    Co-Authors: Morris B. Goldman, Alexandrina M Gomes, C S Carter
    Abstract:

    Rationale Hyponatremia and dexamethasone resistance in polydipsic schizophrenic patients are attributable to changes in hippocampal-modulated antidiuretic and stress hormone activity, respectively. The relationship of the neuroendocrine findings to the psychiatric illness, however, is unknown. An impaired ability to identify facial emotions has been linked to core features of schizophrenia and to diminished levels of the closely related hormone, oxytocin, in the polydipsic subset. Intranasal oxytocin enhances facial affect discrimination in healthy subjects. Objective The aim of this study is to explore if oxytocin reverses impaired facial affect discrimination in schizophrenic patients with, relative to that in patients without, Polydipsia. Methods Intranasal oxytocin (10 or 20 IU) and placebo were administered on three occasions to five polydipsic schizophrenic patients, eight nonpolydipsic patients, and 11 healthy controls. Subsequently, subjects rated the presence and intensity of six facial emotions. Results Emotion recognition fell in both patient groups following 10 IU of oxytocin due to an increased propensity to identify all emotions regardless of whether they were displayed. By contrast, emotion recognition improved following 20 IU in polydipsic relative to nonpolydipsic patients due primarily to divergent effects on the bias to identify fear in nonfearful faces. Conclusion The effects of 20 IU oxytocin support the hypothesis that altered neuroendocrine function in polydipsic patients contributes to their psychiatric illness. Further studies are warranted to confirm these findings and assess if oxytocin treatment improves social functioning in this subset. This is the first psychopharmacologic study to compare different doses of oxytocin in the same subject, thus the significance of the opposing responses is unclear.

  • neuropsychological impairment in patients with schizophrenia and evidence of hyponatremia and Polydipsia
    Neuropsychology (journal), 2009
    Co-Authors: Ivan J Torres, Sarah K Keedy, Megan Marlowoconnor, Beth Beenken, Morris B. Goldman
    Abstract:

    : 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.

  • psychotic exacerbations and enhanced vasopressin secretion in schizophrenic patients with hyponatremia and Polydipsia
    Archives of General Psychiatry, 1997
    Co-Authors: Morris B. Goldman, Donald Hedeker, Daniel J. Luchins, Gary L Robertson, Ghanshyam N Pandey
    Abstract:

    Background: For unclear reasons, life-threatening water intoxication often coincides with acute psychosis in polydipsic schizophrenic patients with chronic hyponatremia. In contrast, most polydipsic schizophrenic patients are normonatremic and never manifest hyponatremia. To explore whether the effect of acute psychosis on water balance differs in these 2 schizophrenic subgroups, we compared their responses to drug-induced psychotic exacerbations. Methods: Matched polydipsic schizophrenic patients with (n=6) and without (n=8) hyponatremia were identified based on past and current indexes of fluid intake and hydration. A transient psychotic exacerbation was induced with an infusion of the psychotomimetic methylphenidate hydrochloride (0.5 mg/kg of body weight over a 60-second period). Antidiuretic hormone levels, subjective desire for water, and factors known to influence water balance were measured at 15-minute intervals for 2 hours. Results: Except for the expected differences in plasma osmolality and sodium, basal measures were similar in the 2 groups. Following methylphenidate administration, antidiuretic hormone levels increased more in the hyponatremic patients ( P P P P Conclusion: Psychotic exacerbations are associated with enhanced antidiuretic hormone secretion, for unknown reasons, in schizophrenic patients with hyponatremia and Polydipsia, thereby placing them at increased risk of lifethreatening water intoxication.

  • the influence of Polydipsia on water excretion in hyponatremic polydipsic schizophrenic patients
    The Journal of Clinical Endocrinology and Metabolism, 1996
    Co-Authors: Morris B. Goldman, Daniel J. Luchins, Gary L Robertson, Donald Hedeker
    Abstract:

    To determine whether Polydipsia is responsible for the altered water excretion in the subset of polydipsic schizophrenic patients who develop hyponatremia, the regulation of antidiuretic function was assessed in polydipsic schizophrenic patients with hyponatremia (n = 5), polydipsic schizophrenic patients without hyponatremia (n = 5), nonpolydipsic schizophrenic patients (n = 6), and normal controls (n = 8). The severity and duration of polyuria were similar in the two polydipsic groups. After oral water loading, maximal free water clearance was similar across all four groups. Free water clearance diminished, however, at lower plasma osmolalities in the hyponatremic polydipsics (P < 0.02) and at higher plasma osmolalities in the normonatremic polydipsics (P < 0.05) relative to that in the nonpolydipsic schizophrenics and normal subjects. The increase in plasma vasopressin after osmotic stimulation with hypertonic saline was slightly, but significantly (P < 0.02), blunted in both polydipsic groups. Hyponat...

Paolo Nencini - One of the best experts on this subject based on the ideXlab platform.

  • differences in the structure of drinking cart expression and dopamine turnover between polydipsic and non polydipsic rats in the quinpirole model of psychotic Polydipsia
    Psychopharmacology, 2014
    Co-Authors: Chiara Schepisi, Silvia Cianci, Gaurav Bedse, Jin Fu, Silvana Gaetani, Paolo Nencini
    Abstract:

    Dopaminergic D2/D3 agonist quinpirole (QNP) elicits nonregulatory drinking in rats, a model of psychotic Polydipsia. Why only a fraction of QNP-treated rats responds to the treatment becoming polydipsic is still unclear. To unveil possible factors contributing to such variability, we analyzed drinking microstructure in saline and QNP-treated rats, the hypothalamic expression of the cocaine and amphetamine regulated transcript (CART), and the monoaminergic turnover in selected brain areas. Rats were daily treated with saline or QNP 0.5 mg/kg, and their 5-h water intake was measured for five consecutive days. The number of bouts and episodes of licking, and their duration, were also measured. Brain CART expression was measured by in situ hybridization and monoamines turnover by HPLC analysis of tissue extracts. Based on the amount of water ingested during the 5-h session, QNP-treated rats were post hoc grouped in polydipsic (PD) and in nonpolydipsic (NPD) rats, and the results compared accordingly. The number of drinking bouts and episodes increased in PD rats, while NPD rats behaved as the controls. CART expression decreased in the arcuate nucleus of the hypothalamus of the PD rats. In contrast, both PD and NPD rats showed a reduction of DA turnover in both ventral tegmental area (VTA) and nucleus accumbens (NAcc). No difference was detected in the turnover of 5HT and NA. Microstructure analysis confirms that QNP acts on the appetitive component of drinking behavior, making it compulsive. CART expression reduction in response to dopaminergic hyperstimulation might sustain excessive drinking in PD rats.

  • Haloperidol both prevents and reverses quinpirole-induced nonregulatory water intake, a putative animal model of psychogenic Polydipsia
    Psychopharmacology, 2008
    Co-Authors: Davide Amato, Maria Antonietta Stasi, Franco Borsini, Paolo Nencini
    Abstract:

    Rationale Polydipsia is a severe complication of long-term schizophrenia and, despite its unknown pathogenesis, is empirically treated with typical or atypical antipsychotics. In the rat, nonregulatory water intake is induced by repeated administration of amphetamine-like compounds or by the D2/3 agonist, quinpirole. Objective This study is aimed at determining the potential activity of antipsychotic compounds with different affinities for D2 receptors in preventing and/or reversing quinpirole-induced Polydipsia. Materials and methods Male Sprague–Dawley rats were treated with five injections of quinpirole (0.5 mg/kg i.p.) to induce Polydipsia. The oral effects of haloperidol, olanzapine, clozapine, and ST2472 on QNP-induced Polydipsia were analyzed in the following two schedules. In the preventive schedule, haloperidol (0.2, 0.4, and 0.8 mg/kg), olanzapine (1.5, 3, and 6 mg/kg), ST2472 (1 and 2 mg/kg), and clomipramine (5, 10, and 20 mg/kg) were given in combination with quinpirole from day 1 to day 5. In the reversal schedule, rats showing quinpirole-induced Polydipsia on the third day received haloperidol (0.4 mg/kg), olanzapine (1.5 and 3 mg/kg), clozapine (10, 20, and 40 mg/kg), ST2472 (1, 2, 5, and 10 mg/kg), and clomipramine (5, 10, and 20 mg/kg) before quinpirole on days 4 and 5. Results Haloperidol both prevented and reversed quinpirole-induced Polydipsia, whereas olanzapine and ST2472 only reversed it. Clomipramine prevented but did not reverse quinpirole-induced Polydipsia, and clozapine did not reverse it either. Conclusions We suggest that, once developed, Polydipsia is governed by dopaminergic D2 mechanisms. In contrast, either an increase in the serotoninergic tone or an inhibition of D2 receptors can modulate the development of quinpirole-induced excessive drinking.

Ghanshyam N Pandey - One of the best experts on this subject based on the ideXlab platform.

  • psychotic exacerbations and enhanced vasopressin secretion in schizophrenic patients with hyponatremia and Polydipsia
    Archives of General Psychiatry, 1997
    Co-Authors: Morris B. Goldman, Donald Hedeker, Daniel J. Luchins, Gary L Robertson, Ghanshyam N Pandey
    Abstract:

    Background: For unclear reasons, life-threatening water intoxication often coincides with acute psychosis in polydipsic schizophrenic patients with chronic hyponatremia. In contrast, most polydipsic schizophrenic patients are normonatremic and never manifest hyponatremia. To explore whether the effect of acute psychosis on water balance differs in these 2 schizophrenic subgroups, we compared their responses to drug-induced psychotic exacerbations. Methods: Matched polydipsic schizophrenic patients with (n=6) and without (n=8) hyponatremia were identified based on past and current indexes of fluid intake and hydration. A transient psychotic exacerbation was induced with an infusion of the psychotomimetic methylphenidate hydrochloride (0.5 mg/kg of body weight over a 60-second period). Antidiuretic hormone levels, subjective desire for water, and factors known to influence water balance were measured at 15-minute intervals for 2 hours. Results: Except for the expected differences in plasma osmolality and sodium, basal measures were similar in the 2 groups. Following methylphenidate administration, antidiuretic hormone levels increased more in the hyponatremic patients ( P P P P Conclusion: Psychotic exacerbations are associated with enhanced antidiuretic hormone secretion, for unknown reasons, in schizophrenic patients with hyponatremia and Polydipsia, thereby placing them at increased risk of lifethreatening water intoxication.