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)

Woodbrige Hospital had 2,257 patients in 1975. Of these 75 percent were suffering from Schizophrenia. This pattern was similar to that of developing countries like Padistan and Malaya. A study was carried out on all new admissions in 1975. There were 1,068 patients whose age ranged from 10 to 89. Schizophrenia which constituted 62% of the cases was analysed in detail. They were mainly in the age range 10-29 (64%). The sex ratio was 3 males to 2 females. Their distribution by their type of housing was similar to that of the general populations. They were better educated. The most common presentation were reports of aggressive, violent, disturbed, abnormal or withdrawn behaviour. The 10 most common symptoms were paranoid ideas, hearing of voices, talking to oneself, insomnia, aggression, abnormal behaviour, laughing to oneself, disturbed behaviour, crying to oneself and withdrawn behaviour. The most common drugs used were trifluoperazine (47%) and chlorpromazine (45%). Electroconvulsive therapy was given to 25% of the patients. Most of the patients (63%) stayed less than 20 days.
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PMID:New admissions to Woodbridge Hospital 1975 with special reference to schizophrenia. 54 70

TRH was shown to be an extremely potent (ED50 = 0.04 mg/kg, IP) antagonist of isolation-induced aggression in male mice. The antifighting activity of TRH was selective in that it did not produce concurrent neurological impairment or significant alterations in spontaneous locomotor activity at antiaggressive doses. This activity of TRH appeared to be a direct affect on CNS structures since neither triiodothyronine nor any of the constituent amino acids of TRH antagonized aggression in isolated mice. The results are discussed in terms of the recent clinical effectiveness of TRH in some cases of mental illness (e.g., depression and schizophrenia).
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PMID:Antagonism of isolation-induced aggression in mice by thyrotropin-relasing hormone (TRH). 82 26

The classical notion of neurosis as the prototypical form of nonpsychotic personality disturbance must be rejected in favor of the categories of (a) personality pattern disturbance and disorder of life style, and most especially, (b) character disorder. Category (a) would include schizoid, paranoid, and cyclothymic personality pattern disturbances and compulsive and hysteroid personality as disorders of life style. Each of these would occupy one end of a 'psychotoid' continuum, at the other end of which would be a familiar type of psychosis such as paranoid schizophrenia or pseudoneurotic schizophrenia. The most numerous of the nonpsychotic disturbances (in the tens of millions in the USA alone) come under category (b), the character disorders, involving a special sort of failure to inhibit impulse and unsocialized self-seeking. Character disorders are seen by us as turning on an eccentric axis, alternating between the two foci of 'dependency' and 'aggression'.
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PMID:Nonpsychotic personality disturbances: a re-evaluation and reclassification. 123 19

Psychiatric illnesses can be conceived of as experiments of nature, providing a variety of pathopsychological mechanisms which may elucidate normal psychological processes. Clinically the reactive psychoses are predominantly psychogenic reaction types. They present disturbances of higher nervous activity, similar to those of the neuroses. The unconditional reflex activity is practically as in normal controls, and the most outstanding finding was the large effect of psychodynamic complex structures. This is a physiological parallel to the clinical manifestations with great concern over experienced mental trauma. In the manic-depressive psychoses the most characteristic feature is a marked disturbance of unconditional reflex activity. This factor may be an important physiological mechanism underlying the more biological than psychodynamic reaction type and partly explain the changes of mood and associated interferences with sleep, body weight, sexual activity, aggression and other instinctual and vegetative functions. Schizophrenic psychoses also present changes of unconditional reflex activity, predominantly in the direction of inhibition of response. In addition there are severe dissociations within and between the three levels of unconditional reflexes and the two signaling systems. It is suggested that schizophrenia represents a functional maladaptation, which can be explained from the principles of autokinesis and schizokinesis established by Gantt in animal experiments. Prognostic models based on experimentally established impairment of performances were shown to predict long-term risks of schizophrenic defects just as well as models based on constellations of clinical symptoms. I would predict that psychophysiology and experimental psychology will become increasingly more important for establishing diagnosis and prognosis in the functional psychoses. The data of this article point toward a basis for a prophylactic psychiatry.
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PMID:Studies of higher nervous activity in functional phychoses. 123 57

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

This article reviews current literature on the clinical efficacy of carbamazepine (CBZ) administration in schizophrenic and schizoaffective psychoses. With respect to the use of CBZ in cases of aggression, overactivity and other behavioral dyscontrol syndromes, only a few, mainly open, studies have been conducted. Attention to the efficacy of CBZ in schizophrenia and related psychoses was rather late in developing, with most of the studies done since 1981. Although the results of the different controlled and uncontrolled experiments are very difficult to compare, the results generally indicate beneficial effects--particularly if CBZ is used as an adjunct to neuroleptic medication. Suggestions for future research strategies to maximize the usefulness of CBZ in schizophrenia and related disorders are given.
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PMID:The use of carbamazepine in the treatment of schizophrenic and schizoaffective psychoses: a review. 134 23

The aggression theory of schizophrenia is a psychoanalytic theory which proposes that schizophrenia results from uncontrolled, deprivation-induced aggressive impulses. An animal model of the aggression theory is presented using predatory aggression as the source of arousal. Although neurochemical control of predatory aggression is nonspecific, anatomic control is located in the lateral hypothalamus across species. The lateral hypothalamus also controls schedule-induced polydipsia which has been implicated in schizophrenia. The aggression theory could be empirically evaluated by determining if schizophrenics respond differently than normals to scheduled feedings. Implications of the aggression theory are discussed.
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PMID:The aggression theory of schizophrenia: revisited. 155 5

Levomepromazine (LMP) unexpectedly improved 16 of 23 chronic treatment-resistant schizophrenic patients who were hospitalized in most cases for at least 2 years and who manifested positive symptoms, irritability and, in many cases, restlessness, hostility, uncooperativeness, poor concentration and aggressive behavior. Improvement led to discharge in 7 (6 to a foster home), placement on a waiting list for a foster home in 4 and improved behavior and autonomy in 5 patients. Five subjects developed seizures and 1 agranulocytosis. Whether improvement with LMP is caused by unique antischizophrenic properties or by diminished liability to induce side effects such as akathisia, a formal controlled study of LMP in treatment-resistant schizophrenia is merited.
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PMID:Is levomepromazine a useful drug in treatment-resistant schizophrenia? 156 98

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

1. PE is present in the brain in tiny quantities; it is heterogeneously distributed and present in synaptosomes. 2. It is synthesised from phenylalanine by L-AADC and oxidatively deaminated by MAO-B. Its turnover is remarkably fast. 3. Its concentration, particularly in the caudate nucleus, is affected by MAO inhibition (increased), lesion of the Substantia nigra (decreased), amine depletion (increased) and antipsychotic drugs (increased). 4. When iontophoresed (or injected) it amplifies the effects of DA and NA (and their agonists) but is without effect on other neurotransmitters. 5. It is suggested that it acts postsynaptically as a neuromodulator of catecholaminergic neurotransmission and that it is involved in the mechanism of action of Deprenyl; it is also suggested that it, or its principal metabolite PAA, may be involved in the aetiology of schizophrenia, depression and aggression as well as perhaps in other neuropsychiatric conditions.
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PMID:Phenylethylaminergic modulation of catecholaminergic neurotransmission. 165 28


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