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)

The principal finding of this manuscript is that the incidence of catalepsy observed in the rat after a single administration of low, clinically relevant doses of the dopamine receptor antagonists and antipsychotic agents, haloperidol and fluphenazine hydrochloride, grows over time such that one re-exposure to the same compound up to 8 weeks later results in a marked enhancement (i.e. sensitization) of this response. This phenomenon appears to be independent of pharmacokinetic or conditioning factors as well as alterations in dopamine or dihydroxyphenylacetic acid. It suggests that the antidopaminergic influence of acute exposure to a neuroleptic not only persists but continues to sensitize for extraordinary periods of time even after the drug is no longer detectable in the system. Our findings may hold the key to understanding the apparent paradox that although neuroleptics presumably induce their therapeutic actions in disorders such as Tourette syndrome and schizophrenia as well as their parkinsonian effects by blocking dopamine receptors, this antagonism occurs immediately while behavioral changes often require weeks for maximal development.
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PMID:Behavioral effects of a single neuroleptic treatment grow with the passage of time. 376 22

This is a case report of a 15-year-old visually impaired, mentally retarded male who presents with symptoms consistent with Tourette Syndrome, a Syndrome of approximate answers (Ganser's Syndrome) and Atypical Pervasive Developmental Disorder. The authors feel that this follow-up on the case presented earlier by Parraga and Butterfield raises the possibility of a link between a number of the symptoms of adult schizophrenia, appearing in attenuated form in these two cases, and Tourette Syndrome.
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PMID:Tourette syndrome, atypical pervasive developmental disorder and Ganser syndrome in a 15-year-old, visually impaired, mentally retarded boy. 385 81

The duration of the R-R cardiointerval (CI) in 13 patients with Tourette's syndrome (TS) aged 9 to 17 years proved to be significantly (+17%; p less than 0.001) longer than in 27 patients of the same age with other neuropsychiatric diagnoses (temporal epilepsy, schizophrenia, neurosis, residual organics) and when compared with the normal values for the respective age (+16.2%; p less than 0.001). Variability of CI as measured by standard deviations also proved to be two times higher in patients with TS (0.082 and 0.046 s respectively, p less than 0.001). "The stress index" as an indicator of the parasympathetic-sympathetic balance of the heart innervation was lower in patients with TS (23.4 and 104.2 respectively, p less than 0.001). The rate of blinking proved to be two times higher in patients with TS (28.2 and 13.6/min respectively, p less than 0.01). The significance of the elevated activity of vagus effector nuclei is discussed in the light of modern concepts of the neurochemical mechanisms of TS.
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PMID:[Various aspects of the pathophysiology of the Tourette syndrome]. 614 18

Preclinical data suggest that cholinergic precursors such as choline or lecithin, increase levels of acetylcholine in specific brain structures, and under certain conditions may enhance cholinergic neurotransmission. A variety of neuropsychiatric diseases including tardive dyskinesia. Huntington's chorea, ataxias, Tourette's syndrome, schizophrenia, affective illness, and senile dementia of the Alzheimer type, has been implicated with a general underactivity of central cholinergic mechanisms. Recent studies have investigated the possibility that cholinergic precursor loading strategies may provide viable treatments for these disorders of presumed cholinergic underactivity. Extensive data demonstrate that the symptoms of tardive dyskinesia can be reduced by choline or lecithin, whereas investigations in other disorders have met with mild success, at best, or are still in preliminary stages. Further controlled studies with choline or lecithin using broader dose ranges, longer durations of treatment, and concomitant administration of agents which may increase the release of acetylcholine are warranted.
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PMID:The use of cholinergic precursors in neuropsychiatric diseases. 621 43

This is a report of a 15 year old girl with anophthalmia who met the DSM-III criteria for Tourette's Syndrome (TS). The case presented a complex differential diagnosis with previous diagnoses of behaviour disorder and schizophrenia, complicated by the issues of blindness, pharmacological, and environmental factors. Once the diagnosis was made, and due to intricate biopsychosocial interactions, a comprehensive treatment approach was adopted with good results. The authors comment on the non-existence of studies about the incidence of TS in blind children and recommend the discrimination between the motor behaviour of the tic disorder versus mannerisms associated with blindness. Thus a reasonable degree of suspicion is warranted in the treatment of blind children with severe behavioural disturbances.
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PMID:Tourette's syndrome and anophthalmia in a girl: complex differential diagnosis. 657 37

Abnormalities of functional connection between specialized areas in the human brain may underlie the symptoms which constitute the schizophrenia syndrome. Callosal and intrahemispheric fibres may be equally involved. The clinical emergence of symptoms in the later stages of brain maturation may be dependent on myelination of these fibre groups, both of which have extended myelination cycles. Ontogenetically earlier variants of the same mechanism could theoretically result in dyslexia and the syndromes of Kanner and Gilles de la Tourette. As new and unique extensions of specialized function emerge within the evolving brain, biological trial and error of connection both within and between them may produce individuals possessing phylogenetically advanced abilities, or equally, others possessing a wide range of abnormalities including those which comprise the schizophrenia syndrome. A dormant phenotypic potential for schizophrenia may exist in individuals who never develop symptoms during the course of a lifetime though some of these may become clinically apparent under the influence of various precipitating factors. It is concluded that abnormal functional connection and its normal and "supernormal" counterparts may be natural, essential, and inevitable consequences of brain evolution, and that this may have been so throughout the history of vertebrate brain evolution.
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PMID:Schizophrenia, abnormal connection, and brain evolution. 687 13

Haloperidol is safe and effective in children for relieving psychotic symptoms associated with childhood autism, schizophrenia and mental retardation. It is the drug of choice for Tourette's syndrome, and may be useful in nonpsychotic hyperactive or aggressive children to control acute episodes, or when the stimulants normally useful in hyperactive children are ineffective. Such children taking haloperidol not only become calmer, but are often better able to respond to other modalities of therapy and to school instruction. Dosage, initially low, is increased gradually to minimize drowsiness and extrapyramidal symptoms, the most common side effects. Haloperidol in children is usually well-tolerated.
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PMID:Haloperidol -- its use in children. 693 55

This is a single case study of a 22 year old Japanese-Canadian woman who developed schizophrenia, was treated with ECT and several successive neuroleptics and subsequently, three years later, developed a tardive dyskinesia syndrome in association with a behavioral change resembling Gilles de la Tourette disease. This combined syndrome lasted seven months. After neuroleptics were withdrawn, the syndrome diminished in severity and disappeared after four months. Since both tardive dyskinesia and Tourette's disease are thought to be caused by relative overactivity or supersensitivity of the dopamine system, their reversible appearance after long term dopamine receptor blockade by neuroleptics can be expected in susceptible individuals.
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PMID:Tardive dyskinesia with Tourette-like syndrome. 694 6

For some time it has been known through the results of family, twin, and adoption studies that heredity appears to play a significant causal role in many mental disorders, including schizophrenia, bipolar disorder, and other mood disorders, Alzheimer's Disease, panic disorder, obsessive compulsive disorder, autism, dyslexia, and Tourette's Syndrome. The precise patterns of inheritance of these complex disorders have not been determined, nor have the relevant genes been localized or cloned. Because the genetics are complex and because there is also clearly an environmental contribution to behavior, we expect the analysis of the genetics of mental illness to be arduous, and not quickly resolved. There are several compelling reasons to continue to focus our attention on uncovering the genetic factors for severe mental illness. Prominent among these are the implications for better treatment of mental disorders. The National Institute of Mental Health supports a wide range of studies on psychiatric genetic research.
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PMID:Psychiatric genetic research at the National Institute of Mental Health. 772 97

Many forms of psychopathology in higher animals and humans include the production of maladaptive, repetitive behaviour. Behaviour which is both repetitive and excessive in amount can be described as stereotyped whereas behaviour which represents a restriction of behavioural possibilities without excessive production can be described as perseverative. Both types of repetition can result from pathology in the neural mechanisms which control either the production of motor output or the organisation of behaviour at a higher level. A number of forms of repetitive behaviour can be induced environmentally. Confinement in adulthood results in a functional disorder which rapidly dissipates when normal conditions are restored but confinement in infancy may have a permanent effect on the organism's ability to interact in a flexible and creative way with its environment. The permanence of these disorders suggests that the environment can affect the way in which the nervous system develops. Repetitive behaviour is also a feature of mental illness including schizophrenia, autism, OCD, addiction and some neurological disorders including frontal lobe lesions, Tourette's syndrome and PD. In experimental studies in animals, stereotyped behaviour seems to be related mainly to excess dopaminergic activity in the basal ganglia while perserverative behaviour can be produced by lesions of the frontal lobes. It is supposed that the level of dopamine activity in the basal ganglia affects the baseline level of behavioural activation such that excess activation results in the excessive execution of the most probable response to the environment to the exclusion of other possibilities (i.e. stereotypy) while deficient activation results in the production of only a few responses which can exceed the necessary activation level (i.e. perseveration). In either case behaviour is 'stimulus-bound', being driven by only the most salient feature of the environment. The symptoms of PD result from inadequate levels of dopamine in the basal ganglia while the stimulant psychoses result from excessive availability of dopamine. The frontal lobes have a modulating effect on (i) the activation of motor activity by the basal ganglia, (ii) in the generation of self-initiated behaviour, i.e. volition, and (iii) in the neural mechanisms which permit different modes of neural function (e.g. perceiving, remembering or thinking) to be identified. Failures in these three functions could result in excessive and repetitive motor activity, stimulus-bound behaviour, the paucity of volitional and creative behaviour, and the perceptual and experiential symptoms of psychosis.
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PMID:The psychology of perserverative and stereotyped behaviour. 783 78


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