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MeSH Review

Neurobehavioral Manifestations

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Disease relevance of Neurobehavioral Manifestations


Psychiatry related information on Neurobehavioral Manifestations


High impact information on Neurobehavioral Manifestations


Chemical compound and disease context of Neurobehavioral Manifestations

  • Previous administration of D-serine to schizophrenic patients taking nonclozapine antipsychotics improved positive, negative, and cognitive symptoms, whereas the partial agonist D-cycloserine improved negative symptoms of patients taking conventional antipsychotics but worsened symptoms in clozapine-treated patients [15].
  • BACKGROUND: Phencycline (PCP, "angel dust") and other noncompetitive antagonists of N-methyl-D-aspartate (NMDA)-type glutamatergic neurotransmission induce psychotic effects in humans that closely resemble positive, negative, and cognitive symptoms of schizophrenia [16].
  • CSF 5-HIAA, serum cortisol, and age differentially predict vegetative and cognitive symptoms in depression [17].
  • The results showed that depressed patients had lower platelet serotonin (5-HT) uptake site density values than controls and that 5-HT uptake site density values were inversely correlated with the severity of cognitive symptoms of depression [18].
  • Improvements in overall, negative, and cognitive symptoms were significantly higher for risperidone compared with haloperidol (p <.001), whereas improvements across all symptoms were comparable for quetiapine and haloperidol [19].

Biological context of Neurobehavioral Manifestations

  • Dysfunction in this system in humans may give rise to affective and cognitive symptoms which may, if initiated by a postpartum fall in oestrogen and progesterone concentrations, constitute the core pathophysiology of puerperal psychosis [20].

Anatomical context of Neurobehavioral Manifestations


Gene context of Neurobehavioral Manifestations

  • Cognitive manifestations of Huntington disease in relation to genetic structure and clinical onset [22].
  • These results support the hypothesis that CNTF infusion into the striatum of HD patients not only could block the degeneration of neurons but also alleviated motor and cognitive symptoms associated with persistent neuronal dysfunction [23].
  • Platelet 5-HT2 receptor density values were higher in depressed patients than controls, and there was a trend toward a direct correlation between the cognitive symptoms of depression and 5-HT2 receptor density values [18].
  • However, in this family, an individual whose child carries the PS1 mutation died at age 67 years free from cognitive symptoms, indicating a very late age at onset or nonpenetration of the disease [24].
  • The extent to which anxiety, irritability and depression were differentiated as separate entities associated with characteristic patterns of somatic and cognitive symptoms by field dependent (FD) and field independent (FI) normal female subjects was studied with the Hidden Figures Test and Unpleasant Emotions Questionnaire [25].

Analytical, diagnostic and therapeutic context of Neurobehavioral Manifestations


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  17. CSF 5-HIAA, serum cortisol, and age differentially predict vegetative and cognitive symptoms in depression. Faustman, W.O., Faull, K.F., Whiteford, H.A., Borchert, C., Csernansky, J.G. Biol. Psychiatry (1990) [Pubmed]
  18. Platelet serotonin markers and depressive symptomatology. Sheline, Y.I., Bardgett, M.E., Jackson, J.L., Newcomer, J.W., Csernansky, J.G. Biol. Psychiatry (1995) [Pubmed]
  19. Effectiveness of antipsychotic treatments for schizophrenia: interim 6-month analysis from a prospective observational study (IC-SOHO) comparing olanzapine, quetiapine, risperidone, and haloperidol. Dossenbach, M., Erol, A., el Mahfoud Kessaci, M., Shaheen, M.O., Sunbol, M.M., Boland, J., Hodge, A., O'Halloran, R.A., Bitter, I. The Journal of clinical psychiatry. (2004) [Pubmed]
  20. Dopamine efflux in the rat nucleus accumbens evoked by dopamine receptor stimulation in the entorhinal cortex is modulated by oestradiol and progesterone. Saigusa, T., Takada, K., Baker, S.C., Kumar, R., Stephenson, J.D. Synapse (1997) [Pubmed]
  21. Decreased beta-amyloid1-42 and increased tau levels in cerebrospinal fluid of patients with Alzheimer disease. Sunderland, T., Linker, G., Mirza, N., Putnam, K.T., Friedman, D.L., Kimmel, L.H., Bergeson, J., Manetti, G.J., Zimmermann, M., Tang, B., Bartko, J.J., Cohen, R.M. JAMA (2003) [Pubmed]
  22. Cognitive manifestations of Huntington disease in relation to genetic structure and clinical onset. Jason, G.W., Suchowersky, O., Pajurkova, E.M., Graham, L., Klimek, M.L., Garber, A.T., Poirier-Heine, D. Arch. Neurol. (1997) [Pubmed]
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  24. Wide range of disease onset in a family with Alzheimer disease and a His163Tyr mutation in the presenilin-1 gene. Axelman, K., Basun, H., Lannfelt, L. Arch. Neurol. (1998) [Pubmed]
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