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

The dosage of the free tryptophan and of the total tryptophan is interesting in psychiatric diseases when a possible role of serotonin is suspected: endogenous melancolia, schizophrenia, sleep disorders. The dosage of tryptophan is made by ultracentrifugation and separation then spectrofluorimetry by increasing 15 times the native fluorescence of tryptophan. The data are given for 16 healthy volunteers and 12 schizophrenics treated and not treated. The methodology of sampling is described and must be strictly standardized to get interpretable data.
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PMID:[Blood level of tryptophan in psychiatric diseases]. 99 1

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

In the past 5 years, we have witnessed the continuation of important trends in clinical research that began earlier in the decade. With regard to the treatment of specific disorders in children and adolescents, the most significant developments have been the examination of the tricyclics for the treatment of depression and the initiation of controlled studies for the treatment of Tourette syndrome. Unfortunately, the findings from the depression studies have been uniformly negative, and the results of research on both depression and tic disorders show a relatively high rate of placebo responsivity, which raises nagging questions about the role of case reports and open trials. Another important trend in pediatric psychopharmacotherapy is the search for substitutes for the neuroleptics. Potential candidates include agents such as lithium, naltrexone, fenfluramine, clonidine, and carbamazepine. The most underresearched disorders are a combination of the least common (e.g. schizophrenia, mania) and those that are apparently perceived as less serious (e.g. sleep disorders, certain anxiety disorders). Not surprisingly, the most studied disorder and treatment is hyperactivity and stimulant medication, respectively. Considerable progress has been made in understanding the social implications of the associated symptoms and their response to stimulant drugs, aided greatly by the use of direct observation procedures. Researchers are beginning to attend to the implications of comorbidity for assessing response to medication. There has been additional confirmation of efficacy of stimulant treatment for preschoolers and adolescents. Dose-response issues remain to some extent unresolved, the primary impediments being interpretive misconceptions associated with trend analysis, an overreliance on the syndromal perspective and too little attention to target behaviors and their clinical implications, and the failure to operationalize the minimal effective dose with regard to the normalization and supranormalization of target and collateral behaviors. Disagreement over whether hyperactivity is a learning or a behavior disorder (or both) and what academic underproductivity means clinically and socially is also impeding progress. With regard to developmental disorders, controlled studies indicate that fenfluramine and naltrexone are effective for managing associated symptoms in some individuals. However, given the limited amount of research on these agents, their status as clinically useful palliatives must be considered tentative.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pediatric psychopharmacotherapy: a review of recent research. 137 Nov 22

Thirty-three years ago, Gaddum and Picarelli classified the serotonin receptors in the guinea pig ileum into D and M types based on the activity of dibenzyline and morphine to block contractions of intestinal smooth muscle caused by serotonin. The subsequent location of specific ligand binding sites for serotonin in the brain has led to the identification of at least eight serotonin receptor sub-types in rat brain. While there is some controversy over the functional importance of many of these receptor sub-types, there is evidence that they fall into two major groups according to the nature of their coupling to secondary messengers or ion channels. Thus the 5-HT1 and 5-HT2 receptors appear to occupy the G protein receptor sub-family which may be coupled either to adenylate cyclase (most 5-HT1 sub-types) or phosphatidyl inositol (5-HT2 sub-types). The central "M" receptors (now termed 5-HT3) appear to occupy a ligand gated ion channel super-family. The cloning of three of the serotonin receptor sub-types in 1989 (5-HT1A, 5-HT1C and 5-HT2) has been of importance in enabling the receptor sub-types to be classified as specific protein molecules encoded by specific genes. The problem now arises with regard to the linking of the changes in the cellular activity of the various receptor sub-types with the plethora of behavioural changes that arise as a consequence of the actions of serotonin in the brain. The present review summarizes the evidence implicating the role of specific serotonin receptor sub-types in eating disorders, sleep, sexual activity, anxiety states, aggression, schizophrenia and depression. A summary of the relationship between these receptor sub-types and their possible involvement in the aetiology of these diseases is shown in Table 2.
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PMID:Sub-types of serotonin receptors: biochemical changes and pharmacological consequences. 162 53

A review is presented of the diagnosis and drug treatment of the more common psychiatric and developmental disorders in the pediatric population. Where applicable, DSM III (Diagnostic and Statistical Manual of Psychiatric Disorders, III) criteria are utilized to describe the behavioral syndromes. The indications for usage and appropriate dosages of antipsychotics, antidepressants, anxiolytics, stimulants, and lithium are described. Those disorders discussed are attention deficit disorder, conduct disorders, anxiety disorders, sleep disorders, schizophrenia, autism, Tourette's syndrome, mental retardation, depressive illness, manic depressive illness, eating disorders, and enuresis.
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PMID:Pharmacologic treatment of psychiatric and neurodevelopmental disorders in children and adolescents (Part 1). 241 73

Diet clearly influences neurotransmission. This can be important in grossly undernourished children. It can also be important in children in whom normal homeostatic mechanisms governing food intake are bypassed. Subtle differences in behavior can occur with physiologic variation in food intake. Components of foods can also be used as drugs. Starvation can impair neuronal maturation and can have lasting effects upon behavior and intellectual performance. The extent of starvation's impact upon the brain depends upon whether undernutrition occurred during a critical phase in brain development. Short-term fasting has small, but significant, effects upon intellectual performance. Even when gross malnutrition is not present, subtle changes in diet may modulate brain function. Tryptophan, tyrosine, and choline in the diet are used as precursors for neuronal synthesis of serotonin, dopamine and norepinephrine, and acetylcholine, respectively. It is likely that the brain's sensitivity to certain components of the diet exists to permit monitoring of food intake by the central nervous system. Tryptophan, tyrosine, and choline may be useful in treatment of humans with sleep disorders, pain depression, mania, hypertension, shock, or dyskinesias. Other components of the diet that may affect behavior include food additives, sugar, and caffeine. Food additives may exacerbate hyperactive symptoms in a small proportion of children with attention deficit disorder. Given that there is little potential for harm and that there is a subpopulation that may respond, a trial of a diet that contains no food additives may be a valid diagnostic approach for children with attention deficit disorder who do not respond to stimulant therapy or for children for whom stimulant therapy is not desired. Refined sugar has been blamed for many behavioral abnormalities. Subtle effects of carbohydrate upon behavior have been reported, but the existing data do not support the hypothesis that sucrose or fructose exert special effects upon neurotransmission. Caffeine is easily detected as a stimulant by humans, but it has little effect upon cognitive function. Administration of large doses of vitamins has no beneficial effect in most humans with schizophrenia, attention deficit disorder, autism, Down's syndrome, or drug addiction. Large doses of niacinamide may even be harmful, as they may cause hepatic damage.
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PMID:Dietary influences on neurotransmission. 302 51

A comprehensive overview of the clinical aspects of lithium therapy is presented. Emphasis is placed on recent developments regarding the clinical uses of Li2CO3 in non-psychiatric conditions. The established efficacy of the drug in the treatment and prophylaxis of mania and bipolar affective disorders is noted, and the evidence supporting the use of lithium salts as a prophylactic agent in unipolar depression, aggressive behavior, schizophrenic disorders and organic brain dysfunction is discussed. The use of lithium carbonate in various disorders of movement and in certain extrapyramidal diseases is summarized, as are the results of its trials in alcoholism and drug abuse. In addition, uses of Li2CO3 in asthma, thyroid diseases, granulocytopenia, headache, bowel disease, anesthesiology, cardiology, and sleep disorders are summarized. The data suggests the potential effectiveness of Li2CO3 in a variety of clinical conditions other than those for which it is classically indicated, provided more detailed double-blind studies are performed.
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PMID:Clinical uses of lithium salts. 641 55

In patients with an anxious syndrome of the neurotic genesis, complaints of sssleep disorders correlate with the clinical pattern of asthenic disturbances and objective changes in the sleep character (a reduction in delta-leep, frequent awakenings). In cases of hysterical neuroses, there is a dissociation between the intact structure of sleep and the absence of asthenic symptomatology on the one hand and complaints of marked sleep disturbances on the other. In cases of neurosis-like schizophrenia despite a reduction in delta-sleep, asthenic symptomatology is almost absent and complaints of sleep problems are rather formal in nature. The pathogenesis of sleep disorders in neurotic patients, including the role of anxiety in objective sleep pattern alternations, is discussed. A hypothesis relating the specific characteristics of thought to a diminished need for delta-leep in schizophrenics is proposed.
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PMID:[Clinico-physiologic analysis of sleep disorders among patients with borderline states]. 662 49

Thirty-three years ago, Gaddum and Picarelli classified the serotonin (5-HT) receptors in the guinea-pig ileum into D and M types based on the activity of dibenzyline (D) and morphine (M) to block contractions of intestinal smooth muscles caused by 5-HT. The subsequent location of specific ligand binding sites for 5-HT in the brain has led to the identification of 10 5-HT receptor subtypes in rat brain. While there is some controversy over the functional importance of many of these receptor subtypes, there is evidence that they fall into two major groups according to the nature of their coupling to secondary messengers or ion channels. Thus the 5-HT1 and 5-HT2 receptors appear to occupy the G protein receptor subfamily which may be coupled either to adenylate cyclase (most 5-HT1 subtypes) or phosphatidyl inositol (5-HT2 subtypes). The central "M" receptors (now termed 5-HT3) appear to occupy a ligand-gated ion channel superfamily. The cloning of these receptor subtypes has been of importance in enabling them to be classified as specific protein molecules encoded by specific genes. A problem now arises with regard to the linking of the changes in the cellular activity of the various receptor subtypes with the plethora of behavioural changes that arise as a consequence of the actions of 5-HT in the brain. The present review summarizes the evidence implicating the role of specific 5-HT receptor subtypes in thermoregulation, modulation of cardiovascular function, eating disorders, sleep, sexual activity, anxiety states, aggression, schizophrenia and depression. A summary of the relationship between these receptor subtypes and their possible involvement in the aetiology of these diseases is also given.
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PMID:Serotonin receptors--where are they going? 802 39

Based on a review of the literature, the article deals with the major biological markers of schizophrenia. Recent developments in molecular biology have shown a possible association between schizophrenia and various HLA markers (A1, A2, A9, A10, A28, B27, BW16), and a linkage--in several families--between the disease and some polymorphisms of chromosome 5. On the other hand, chromosome X might also be involved. Neuropathological abnormalities have often been found in the brains of schizophrenics, such as cellular alterations in the basal ganglia and the limbic structures. Investigations by means of CT-scan and Magnetic Resonance Imaging have pointed out an enlargement of cerebral ventricles and/or an atrophy of frontal areas, especially amongst patients with prominent negative symptoms. The dopaminergic hypothesis of schizophrenia reposes on the major following facts: the therapeutic efficiency of neuroleptics (dopaminergic antagonists); a positive correlation between plasma homovanillic acid (metabolite of dopamine) concentration and the severity of schizophrenic illness; a higher density of dopaminergic D2-receptors (revealed by Positron Emission Tomography thanks to specific radioligands), particularly in the striatum; and an abnormal plasmatic growth-hormone response to apomorphine (dopaminergic agonist). Central noradrenergic dysfunctions might also occur in paranoid schizophrenia, as underlined by higher cerebrospinal fluid levels of norepinephrine, and a lack of decrease of plasma 3-methoxy-4-hydroxy-phenylglycol (MHPG, metabolite of norepinephrine) after clonidine (alpha-2-adrenergic agonist) dispensation. Nevertheless, in patients with predominating negative symptoms, this is a trouble in serotoninergic functions which has been suggested. In the field of immunology, some findings such as alteration in lymphocytes populations (T4/T8, CD5), anti-cerebral auto-antibodies, abnormal lymphocytes responses to mitogens, decreased production of interleukin-2, have lead to two main hypotheses: autoimmunity and immunologic incompetence. On the other hand, electrophysiological studies have shown a hypovariability of alpha-rythm on the EEG; a lower amplitude of the component P300 from visual evoked potentials; sleep disorders such as a shorter rapid eye movement sleep latency and a decreased total slow-wave sleep percent; irregular smooth pursuit eyes-movements; an electrodermal response according to either the hyper-responder either the non-responder type. At last, troubles in sensory integration, motor coordination and attention have also been demonstrated. All those many findings outline the heterogeneity of schizophrenic disorders.
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PMID:[Biological markers in schizophrenia]. 830 20


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