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)

Animal data indicate that serotonin (5-HT) is a major neurotransmitter involved in the control of numerous central nervous system functions including mood, aggression, pain, anxiety, sleep, memory, eating behavior, addictive behavior, temperature control, endocrine regulation, and motor behavior. Moreover, there is evidence that abnormalities of 5-HT functions are related to the pathophysiology of diverse neurological conditions including Parkinson's disease, tardive dyskinesia, akathisia, dystonia, Huntington's disease, familial tremor, restless legs syndrome, myoclonus, Gilles de la Tourette's syndrome, multiple sclerosis, sleep disorders, and dementia. The psychiatric disorders of schizophrenia, mania, depression, aggressive and self-injurious behavior, obsessive compulsive disorder, seasonal affective disorder, substance abuse, hypersexuality, anxiety disorders, bulimia, childhood hyperactivity, and behavioral disorders in geriatric patients have been linked to impaired central 5-HT functions. Tryptophan, the natural amino acid precursor in 5-HT biosynthesis, increases 5-HT synthesis in the brain and, therefore, may stimulate 5-HT release and function. Since it is a natural constituent of the diet, tryptophan should have low toxicity and produce few side effects. Based on these advantages, dietary tryptophan supplementation has been used in the management of neuropsychiatric disorders with variable success. This review summarizes current clinical use of tryptophan supplementation in neuropsychiatric disorders.
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PMID:L-tryptophan in neuropsychiatric disorders: a review. 130 30

1. Preclinical studies reveal that long-term treatment with antidepressant drugs induces significant changes in serotonergic (5-HT) receptor sensitivity. Similarly, clinical studies suggest that brain 5-HT function is abnormal in depression. Of the available methodologies for conducting such clinical studies, the pharmacological challenge strategy has proven particularly useful. 2. I.v. L-TRP has emerged as the most frequently used challenge agent in diagnostic and neuropsychopharmacological studies of 5-HT function. I.v. L-TRP increases serum prolactin (PRL) in humans, probably via 5-HT mechanisms. Under carefully standardized conditions, this PRL response to L-TRP appears to be a reasonably sensitive and valid measure of net 5-HT function. 3. The PRL response to L-TRP is blunted in depressed patients compared with healthy controls. Blunting has not been observed in panic disorder, obsessive compulsive disorder, or schizophrenia, although preliminary findings suggest it may occur in bulimia. 4. The PRL response to L-TRP is enhanced by certain classes of thymoleptic drugs (TCAs, MAOIs, 5-HT reuptake inhibitors, lithium) in a differentially time-dependent fashion. So-called "atypical" antidepressants (trazodone, mianserin) and benzodiazepines have no effect. Such findings are generally consistent with preclinical electrophysiological findings. 5. These clinical studies of the PRL response to L-TRP, in conjunction with emerging evidence that experimentally reduced plasma TRP can reverse the therapeutic effects of some antidepressants, suggest that antidepressant drug action may be more accurately conceptualized as 5-HT dependent rather than 5-HT enhancing. The availability of more selective 5-HT-active drugs promises to further clarify 5-HT mechanisms of neuropsychiatric disease and drug action at the clinical level.
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PMID:Clinical studies of 5-HT function using i.v. L-tryptophan. 223 80

Neurotensin (NT) concentrations in cerebrospinal fluid (CSF) were measured by a sensitive and specific radioimmunoassay in psychiatric patients and age- and sex-matched normal controls. No increase in CSF NT concentrations was observed after antipsychotic drug treatment. CSF NT concentrations were significantly lower in one group of schizophrenic subjects. NT concentrations were unaltered in patients with depression, anorexia/bulimia, or premenstrual syndrome, and no rostral-caudal gradient for NT in CSF was evident. NT concentrations were not related to age or sex, and probenecid treatment did not alter CSF NT concentrations. Finally CSF NT concentrations were unaltered in paranoid schizophrenic subjects. These findings confirm and extend previous studies of CSF NT that showed certain patients with schizophrenia, nonparanoid type, have reduced CSF concentrations of this tridecapeptide.
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PMID:Neurotensin-like immunoreactivity in cerebrospinal fluid of patients with schizophrenia, depression, anorexia nervosa-bulimia, and premenstrual syndrome. 257 18

Detailed clinical and psychological experimental study of 103 schizophrenia patients with anorexia nervosa revealed its most characteristic correlations with a specific variant of the pathology of drive--bulimia bouts and induced vomiting. This variant of the pathology of drive appeared to be similar to narcomania.
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PMID:[A peculiar variant of drive pathology in schizophrenia with the anorexia nervosa syndrome]. 381 36

Thirty-three bulimic and 14 restrictive anorexics were compared on DSM-III diagnoses of affective and anxiety disorders, observer-rated and self-rated measures of depression and anxiety, and family history. A subgroup of 18 eating disorder subjects was administered the dexamethasone suppression test. The same 18 subjects were compared to 13 subjects with affective disorder on the Schedule for Affective Disorders and Schizophrenia. It was found that a large group with bulimia and restrictive anorexia nervosa was subject to a depressive disorder. Thirty-eight percent of the sample fulfilled criteria for a major depressive episode. The dysphoric experience seemed as intense in the bulimic and restricter group. There was a high incidence of dexamethasone nonsuppression (55%), which was found to be related to various measures of depression. Bulimics and restricters differed in their family history of affective disorder. While 61% of bulimics had a positive history of depression, this was found in only 23% of restricters (p less than .03).
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PMID:Affective disturbance in eating disorders. 385 81

In recent years several lines of evidence have emerged suggesting that eating disorders in general, and bulimia in particular, are in some way linked to affective illness. However, there are few data on the frequency of affective syndromes among patients who have anorexia nervosa or bulimia. This report describes the results of semistructured interviews using the Schedule for Affective Disorders and Schizophrenia (SADS) to evaluate the frequency of the current and lifetime diagnoses of affective illness among 50 female patients meeting DSM-III criteria for bulimia. Seventy percent of the patients had, at some time during their lives, met Research Diagnostic Criteria (RDC) for an episode of major depression and 88% had met RDC at some time during their lives for some affective disturbance. The implications of this high frequency of affective disturbance among patients with bulimia are discussed.
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PMID:Bulimia and depression. 386 57

In a sample of 130 consecutive patients with a lifetime diagnosis of anorexia nervosa and/or bulimia, 17 displayed psychotic symptoms. In 16 patients, these symptoms appeared attributable to major affective disorder or schizo-affective disorder, while in one, they appeared to represent factitious psychosis. No cases of schizophrenia or organic psychosis were identified.
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PMID:Psychosis in anorexia nervosa and bulimia. 643 12

The 420 first-degree relatives of 14 patients with anorexia nervosa, 55 patients with bulimia, and 20 patients with both disorders were evaluated for the presence of psychiatric illness, using DSM-III criteria, by the family history method. The morbid risk for affective disorder in the families of the eating disorder probands was similar to that found in the families of patients with bipolar disorder; but was significantly greater than that found in the families of patients with schizophrenia or borderline personality disorder. These results add to the growing evidence that anorexia nervosa and bulimia are closely related to affective disorder.
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PMID:Family history study of anorexia nervosa and bulimia. 657 24

We administered the National Institute of Mental Health Diagnostic Interview Schedule to 41 patients with a lifetime history of anorexia nervosa (25 with and 16 without bulimia) and to 49 patients with bulimia alone. Results showed that 77% of the patients with eating disorders had a lifetime diagnosis of DSM-III major affective disorder, a rate significantly higher than that found in comparison groups composed of the first-degree relatives of probands with schizophrenia and bipolar disorder. High lifetime rates of anxiety disorders, substance use disorders, and kleptomania were also observed. By contrast, few cases of personality disorders and no cases of schizophrenia were found. These findings combine with the results of studies of family history, long-term outcome, response to biological tests, and treatment response to suggest that anorexia nervosa and bulimia may be closely related to major affective disorder.
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PMID:Phenomenologic relationship of eating disorders to major affective disorder. 658 Jun 63

Anorexia nervosa is a disease of increasing frequency with serious medical and psychological consequences. The presentation is one of significant weight loss. The initial assessment of such a patient must differentiate between an underlying systemic medical illness and an eating disorder. This paper will review the more common medical conditions causing weight loss and their distinguishing characteristics, including malignancy, inflammatory bowel disease, infections and metabolic disorders. Once an organic disease is ruled out, anorexia nervosa must then be differentiated from other eating disorders such as bulimia or other psychological diseases such as depression, schizophrenia, drug abuse, conduct disorders, and anxiety reactions. The pathogenesis of anorexia nervosa includes complex societal, family, and individual factors which require evaluation in the treatment process.
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PMID:Differential diagnosis and pathogenesis of anorexia nervosa. 659 95


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