Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two hundred one non-treatment seeking women with alcoholism, anxiety disorders, alcoholism and anxiety disorders, or neither alcoholism nor anxiety disorders were interviewed to assess core psychopathology associated with eating disorders using the Eating Disorders Examination and DSM-IIIR psychiatric diagnoses using the Schedule of Affective Disorders and Schizophrenia-Lifetime version. Alcoholic women had significantly higher mean scores on each of the Eating Disorders Examination subscales of Restraint, Overeating, Eating Concern, Shape Concern, and Weight Concern compared with nonalcoholic women. Women with anxiety disorders had significantly elevated scores on subscales of Overeating, Eating Concern, and Weight Concern compared with women without anxiety disorders. Women with both alcoholism and anxiety disorders had higher rates of bulimia nervosa and/or eating disorder NOS compared with women with either disorder alone. Implications of these findings are discussed in the context of the co-morbid association between alcoholism, eating disorders, and anxiety disorders.
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PMID:Eating pathology among women with alcoholism and/or anxiety disorders. 890 68

The Kleine-Levin syndrome (KLS) is characterized by periodic, sudden-onset episodes of hypersomnia, compulsive hyperphagia, and behavioral-emotional disorders (typically indiscriminate hypersexuality, irritability, impulsive behaviors), lasting from a few days to a few weeks, with almost complete remission in the intercritical periods. Depression, confusion, and thought disorders are frequently associated with the critical symptomatology, and they may suggest other psychiatric diagnoses (schizophrenia, mood disorder, conversion disorder) or a substance abuse. A diencephalic-hypothalamic dysfunction is suspected, even if this composite symptomatology cannot easily be linked to a simple mechanism. The aim of this article is to illustrate problems in differential diagnosis, using a case approach. History, course, and therapeutic intervention in a 21-year-old patient with KLS, associated with a clear psychiatric symptomatology and a critical affective pattern, is reported. Psychiatric correlates of KLS are discussed, including the relationship with affective disorders and the possible emotional impact of the attacks. Implications regarding a combined psychological and pharmacological treatment are also discussed.
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PMID:The Kleine-Levin syndrome as a neuropsychiatric disorder: a case report. 1085 65

According to the DSM IV, pica is a trouble of alimentary behavior, which is characterized by the ingestion of non-nutriment substances during at least on the month. The main objective of this study conducted at the Clermont-de-l'Oise Interdepartmental Medical Center is to evaluate pica's prevalence for hospitalized patients. Secondary objectives are to describe clinical characteristics, complications and outcome upon the different therapeutic approaches. The patients hospitalized in the Adult and/or Pediatric Department of Psychiatry, which fulfilled the 4 criteria of the DSM IV, were considered eligible for the study. In order to better evaluate the severity of behavioral troubles evoked by item D of DSM IV definition, we elaborated specific severity and preoccupation scales. The severity scale reflects the complications due to the ingestion of the non-nutriment substances, the encountered risks in the case of persistence of these troubles as well as the patient's management. The preoccupation scale reflects the medical team's involvement towards the patient in order to prevent life-threatening complications. The two scales are graded from 0 to 5 according to the severity or to the degree of preoccupation, respectively. Only patients with scores 3 were considered as fulfilling the severity criteria. Among the 943 hospitalized patients at a selected time period, 23 adult patients have been considered eligible. According to these data, prevalence of pica was estimated at 2.44%. This value may seem an underestimation when compared to the values reported in the medical literature, which range from 9 to 25%. Additionally, among the 108 hospitalized infant patients, none fulfilled DSM IV criteria, which is surprising, as pica is relatively common in childhood. These results may be explained by the use of the more restrictive criteria of the DSM IV and also by the difficulties encountered in considering pica as an independent medical condition. Indeed, pica is often a secondary diagnosis associated with other psychiatric conditions characterized by profound mental deterioration. Two pathogenic factors were constantly searched in the medical records: iron-deficiency anemia and psychopathology. Cultural factors can be a priori eliminated, as most of these patients are in rupture with their family environment since low ages. Only two patients presented with iron-deficiency anemia and its correction did not result in pica's improvement. These findings do not support the -studies presenting pica as an iron-deficiency anemia induced trouble, which regress after a well-conducted iron replacement. Most patients were found to have precocious lack of affect in their medical history. All patients presented other associated psychiatric troubles including severe mental impairment (48%) and dysharmonic development (26%), as well as autistic troubles and schizophrenia. These data concur with other studies, which associate pica to other psychiatric disorders. Gluttony is a widely represented symptom in our study population (87%) and predisposes to food aspiration. It is the mark of frenetic orality and concerns comestible as well as non-comestible compounds. The ingestion of non-nutriment compounds could therefore be considered as an incapacity of discerning among different mouth-introduced substances. Auto- and hetero-aggressive disorders have been reported in 77% of the patients. These behaviors arise mostly in the phase of seeking of substances, especially if these are particularly attractive. The enhancement of the -anxiety, which often arises in the eventuality of hindering of the act, as well as the soothing effect of the ingestion, suggests a compulsive activity. This compulsive activity could be related to an addictive conduct. Pica could therefore be related to obsessive-compulsive disorders and benefit from its specific therapy, either behavioral or chemotherapy with serotonin-recapture inhibitors. The most common clinical forms of pica were phytophagia and geophagia, probably due to the facility of access to these substances. However, 31 distinct substances have been identified in our study. Pica's evolution often implies severe complications, which are sometimes life threatening in spite of a well-conducted treatment. Severity factors include the iteration of medical and surgical complications, as well as the type of ingested products. Our results show a high incidence of surgical complications, essentially gastro-intestinal. Due to the elevated incidence of complications and to the high rate of mortality, some authors proposed systematical search of pica for any gastro-intestinal troubles arising in patients suffering from mental disorders. For these patients for whom anamnesis is often difficult, a standard X-ray of the abdomen is an essential imaging study. Respiratory complications come in second position and infectious complications are seen mostly for the geo- and coprophagia-suffering patients, which contract intestinal parasitosis. Because of its multifactor causality, treatment of pica is complex, and results are often deceiving. Symptomatic neuroleptic therapy results in transient improvement and is indicated especially in delirious patients. Psychotherapy with behavioral approaches and different institutional approaches can be proposed. Indeed, pica could be considered as an acquired behavior, which could benefit from cognitive and behavioral therapies. Institutional management including supportive and compassionate care, restoration of self-confidence is interesting for these patients. Some authors even suggest that pica might be considered as a good indicator of the institution's care quality.
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PMID:[Pica: a descriptive study of patients in a speciality medical center]. 1461 90

Obesity is highly prevalent among patients with schizophrenia and is associated with detrimental health consequences. Although excessive consumption of fast food and pharmacotherapy with such second-generation antipsychotic agents (SGAs) as clozapine and olanzapine has been implicated in the schizophrenia/obesity comorbidity, the pathophysiology of this link remains unclear. Here, we propose a mechanism based on brain reward function, a relevant etiologic factor in both schizophrenia and overeating. A comprehensive literature search on neurobiology of schizophrenia and of eating behavior was performed. The collected articles were critically reviewed and relevant data were extracted and summarized within four key areas: (1) energy homeostasis, (2) food reward and hedonics, (3) reward function in schizophrenia, and (4) metabolic effects of the SGAs. A mesolimbic hyperdopaminergic state may render motivational/incentive reward system insensitive to low salience/palatability food. This, together with poor cognitive control from hypofunctional prefrontal cortex and enhanced hedonic impact of food, owing to exaggerated opioidergic drive (clinically manifested as pain insensitivity), may underlie unhealthy eating habits in patients with schizophrenia. Treatment with SGAs purportedly improves dopamine-mediated reward aspects, but at the cost of increased appetite and worsened or at least not improved opiodergic capacity. These effects can further deteriorate eating patterns. Pathophysiological and therapeutic implications of these insights need further validation via prospective clinical trials and neuroimaging studies.
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PMID:Food intake and reward mechanisms in patients with schizophrenia: implications for metabolic disturbances and treatment with second-generation antipsychotic agents. 1698 Sep 85

Although antipsychotics are established drugs in schizophrenia treatment, they are admittedly known to induce side effects favoring the onset of obesity and worsening its complications. Despite potential involvement of histamine receptor antagonism, or of other neurotransmitter systems, the mechanism by which antipsychotic drugs increase body weight is not elucidated. The aim of the present study was to investigate whether chronic antipsychotic treatments can directly alter the regulation of two main functions of white adipose tissue: lipolysis and glucose utilization. The influence of a classical antipsychotic (haloperidol) was compared to that of two atypical antipsychotics, one known to favor weight gain (olanzapine), the other not (ziprasidone). Cell size, lipolytic capacity and glucose transport activity were determined in white adipocytes of rats subjected to 5-week oral treatment with these antipsychotics. Gene expression of adipocyte proteins involved in glucose transport or fat storage and mobilization, such as glucose transporters (GLUT1 and GLUT4), leptin, matrix metallo-proteinase-9 (MMP9), hormone-sensitive lipase (HSL) and fatty acid synthase (FAS) was also evaluated. Adipocytes from chronic olanzapine-treated rats exhibited decreased lipolytic activity, lowered HSL expression and increased FAS expression. These changes were concomitant to enlarged fat deposition and adipocyte size. Alterations were observed in adipocytes from olanzapine-treated rats whereas the other antipsychotics did not induce any notable disorder. Our results therefore show evidence of an effect of chronic antipsychotic treatment on rat adipocyte metabolism. Thus, impairment of fat cell lipolysis should be considered as a side effect of certain antipsychotics, leading, along with the already documented hyperphagia, to the excessive weight gain observed in patients under prolonged treatment..
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PMID:Alterations of lipid metabolism and gene expression in rat adipocytes during chronic olanzapine treatment. 1721 38

Here, we report a case of Cronkhite-Canada syndrome in a patient with schizophrenia. A 64-year-old man, who had been diagnosed as having a schizophrenic disorder at the age of 30, presented with alopecia, atrophic nail changes, hyperpigmentation of the skin, and inflammatory polyposis of the stomach and colon. Endoscopic ultrasonography of the stomach and colon revealed diffuse mucosal thickening with small hypoechoic areas, corresponding to edema of the lamina propria. After treatment with parenteral hyperalimentation and tranexamic acid, his physical findings and polyposis gradually improved. This is the first report of Cronkhite-Canada syndrome in a patient with schizophrenia.
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PMID:Cronkhite-Canada syndrome associated with schizophrenia. 1730 12

Second generation antipsychotics are commonly prescribed for the treatment of schizophrenia, however some can induce metabolic dysfunction side-effects such as weight gain, obesity and diabetes. Clinical reports suggest olanzapine alters satiety signals, although findings appear conflicting. Previous animal model studies have utilised a range of olanzapine dosages, however the dosage that better mimics the human scenario of olanzapine-induced weight gain is unclear. Female Sprague-Dawley rats were treated orally, three times daily with olanzapine (0.25mg/kg, 0.5mg/kg, 1.0mg/kg, 2.0mg/kg), self-administered in a sweet cookie dough pellet at eight-hourly intervals) or vehicle (n=12/group) for 14-days. Olanzapine orally self-administered in multiple doses (eight-hourly intervals) may circumvent a drop in plasma drug concentration and ensure the maintenance of a consistently high olanzapine level in the rat. Olanzapine increased body weight (0.5mg/kg, 1.0mg/kg, 2.0mg/kg), food intake (2.0mg/kg) and feeding efficiency (0.5-2.0mg/kg), with no effect on water intake. Subcutaneous inguinal (1.0mg/kg, 2.0mg/kg) and intra-abdominal perirenal fat were increased (2.0mg/kg), but not interscapula brown adipose tissue. Olanzapine increased circulating ghrelin and cholecystokinin, but had no effect on peptide YY((3-36)). Olanzapine decreased insulin (0.25-2.0mg/kg) and locomotor activity in the open field arena (0.5-2.0mg/kg). A low dosage of 0.25mg/kg olanzapine had no effect on most parameters measured. Olanzapine-induced weight gain is associated with hyperphagia, enhanced feeding efficiency and adiposity, decreased locomotor activity and altered satiety signaling. The animal model used in the present study of self-administered oral olanzapine treatment (t.i.d.) at a dosage range of 0.5-2.0mg/kg (but not 0.25mg/kg) mimics aspects of the clinic.
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PMID:Olanzapine treatment and metabolic dysfunction: a dose response study in female Sprague Dawley rats. 2105 63

Olanzapine is known to be advantageous with respect to outcome and drug compliance in patients with schizophrenia. However, olanzapine has adverse effects, including a higher incidence of weight gain and metabolic disturbances, when compared with those of other antipsychotic agents. The mechanisms underlying these adverse events remain obscure. Female rats were orally administered olanzapine (2 mg/kg) or vehicle once a day for 2 weeks to ascertain if hypothalamic AMP-activated protein kinase (AMPK) mediates olanzapine-induced weight gain and hyperphagia. Body weight and food intake in each rat were evaluated every day and every two days, respectively. After the termination of drug treatment, we measured the protein levels of AMPK and phosphorylated AMPK in the hypothalamus using western blot analyses. Olanzapine significantly increased body weight and food intake. The phosphorylation levels of AMPK were significantly elevated by olanzapine. These results suggest that activation of hypothalamic AMPK may mediate hyperphagia and weight gain induced by chronic treatment with olanzapine.
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PMID:A role for hypothalamic AMP-activated protein kinase in the mediation of hyperphagia and weight gain induced by chronic treatment with olanzapine in female rats. 2168 59

The success of antipsychotic drug treatment in patients with schizophrenia is limited by the propensity of these drugs to induce hyperphagia, weight gain and other metabolic disturbances, particularly evident for olanzapine and clozapine. However, the molecular mechanisms involved in antipsychotic-induced hyperphagia remain unclear. Here, we investigate the effect of olanzapine administration on the regulation of hypothalamic mechanisms controlling food intake, namely neuropeptide expression and AMP-activated protein kinase (AMPK) phosphorylation in rats. Our results show that subchronic exposure to olanzapine upregulates neuropeptide Y (NPY) and agouti related protein (AgRP) and downregulates proopiomelanocortin (POMC) in the arcuate nucleus of the hypothalamus (ARC). This effect was evident both in rats fed ad libitum and in pair-fed rats. Of note, despite weight gain and increased expression of orexigenic neuropeptides, subchronic administration of olanzapine decreased AMPK phosphorylation levels. This reduction in AMPK was not observed after acute administration of either olanzapine or clozapine. Overall, our data suggest that olanzapine-induced hyperphagia is mediated through appropriate changes in hypothalamic neuropeptides, and that this effect does not require concomitant AMPK activation. Our data shed new light on the hypothalamic mechanism underlying antipsychotic-induced hyperphagia and weight gain, and provide the basis for alternative targets to control energy balance.
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PMID:Olanzapine-induced hyperphagia and weight gain associate with orexigenic hypothalamic neuropeptide signaling without concomitant AMPK phosphorylation. 2169 81

Introduction. Frontotemporal dementia is a disorder of complex etiology, with genetic components contributing to the disease. The aim of this report is to describe a young patient suffering from frontotemporal dementia, misdiagnosed as schizophrenia, related to a genetic defect on chromosome 1. Case Presentation. A 29-year-old female patient, previously diagnosed as having schizophrenia, was hospitalized with severe behavioural disturbances. She demonstrated severe sexual disinhibition, hyperphagia, lack of motivation, apathy, psychotic symptoms, suicidal thoughts, and cognitive deterioration. Focal atrophy of frontal and anterior temporal structures bilaterally was found on brain MRI, as well as bifrontal hypo perfusion of the brain on SPECT scan. The diagnosis of frontotemporal dementia was made clinically, according to Lund and Manchester groups and Neary diagnostic criteria. Chromosomal analysis was conducted and revealed decrease in length of heterochromatin on the long arm of chromosome 1 (46, XX, 1qh-). Parental karyotypes were normal. Discussion. Frontotemporal dementia, and particularly early-onset cases, can be often misdiagnosed as schizophrenia, with negative impact on case management. Genetic testing could be an aid to the correct diagnosis, which is crucial for optimal patient care.
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PMID:Frontotemporal dementia, manifested as schizophrenia, with decreased heterochromatin on chromosome 1. 2308 70


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