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

The psychoanalytic treatment of psychotic disorders has had a long and complicated history because of the historic preference of psychoanalysis for neurotics. Nevertheless, it has survived the prejudice of psychoanalysts and empirical psychiatrists and now enters an interdisciplinary phase in which psychotic psychopathology is understood as primarily an emotional disorder, but one that must also be considered from the point of view of neurobiology and neuropsychology as well as sociology. In this contribution, I offer the idea that perhaps the most important subtext in the psyche of the psychotic is what has been called the black hole. This massive deficit is ultimately attributable to a precocious abruption of the mother's physical and psychical presence from the infant, a phenomenon that has hereditary, congenital, perinatal, and continuing developmental reinterpretive elaborations. The psychoanalytic treatment of the psychotic consists of reversing the direction of his or her cataclysmic descent into the black hole and, at the same time, empathically loosening the control that the protective psychotic alterego has on the surviving self. Further, the psychoanalytic treatment of schizophrenia, in particular (as well as many of the other primitive mental disorders), now frequently involves both an interdisciplinary orientation and perspective and choices of interdisciplinary modalities extending across the whole biopsychosocial spectrum.
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PMID:The "black hole" as the basic psychotic experience: some newer psychoanalytic and neuroscience perspectives on psychosis. 235 72

An ability to distinguish relevance from irrelevance has been attributed to an attention-related mechanism and may be disturbed in thought-disordered schizophrenics. Stimulus choice strategies depend on such mechanisms (ia) and are anomalous in some schizophrenics. An impaired function of the ventral tegmentum (VTA) has been postulated for schizophrenia. The effects of VTA damage on the relevance/irrelevance distinction and strategy formation in rats has been studied. Over a 5 day-period food-deprived rats were given nine sessions of ten trials each on a 16-hole board. They searched for food pellets placed consistently in four holes. During testing the control group (C) reduced the number of empty holes visited more than the group with VTA damage. The proportion of repeated visits to relevant holes (had food) to irrelevant holes (never had food) increased for the C but not for the VTA group. The frequency with which a preferred sequence of food-hole visits was repeated during a session increased over sessions for the C but not the VTA group. The VTA group changed their preference between sessions more often. Animals with VTA damage were capable of simple learning, but were impaired when complexity increased. This may be due in part to a deficit in attention-related mechanisms. This encourages further study of the contribution of the VTA to putative attentional dysfunction and the use of the hole-board search task as a model for the study of cognitive function and dysfunction.
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PMID:Search strategies on a hole-board are impaired in rats with ventral tegmental damage: animal model for tests of thought disorder. 707 82

During gross anatomy dissections of the brain, a developmental abnormality of the septum pellucidum was found in a 31-year-old male cadaver. Other parts of the central nervous system in this cadaver were normal in every aspect. Histological samples were taken from the neighboring areas of this abnormality, and they were examined under light microscope and scanning electron microscope. In this abnormality of the septum pellucidum, the two laminae of the septum pellucidum were fused together and there was a hole located 1 cm anterior to its apex. The maximum diameter of the hole was 0.5 cm in the sagittal plane and 0.6 cm in the vertical plane. In the light microscopic and scanning electron microscopic examinations, the free margin of this foramen was regular, and the surrounding tissue was intact and histologically unique to the septum pellucidum. Ependymal cells were present at the free margin of the foramen. Cavum vergae, cavum septum pellucidum, and agenesis of the septum pellucidum are described in the literature. These three abnormalities are seen in cadavers usually with histories of schizophrenia and other psychiatric or neurologic disorders. In a retrospective study, the cadaver with this abnormality had a history of schizophrenia and no history or signs of any kind of brain or head operation. As far as we could ascertain, the abnormality described here has not been reported previously.
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PMID:Unreported anatomical variation of septum pellucidum. 921 41

Clinical and basic research studies have linked cannabinoid consumption to the onset of psychosis, specially schizophrenia. In the present study we have evaluated the effects of the natural psychoactive constituent of Cannabis (-)-delta9-tetrahydrocannabinol on the acute actions of the psychostimulant, D-amphetamine, on behaviour displayed by male rats on a hole-board, a proposed animal model of amphetamine-induced psychosis. Cannabinoid-amphetamine interactions were studied (1) 30 min after acute injection of (-)-delta9-tetrahydrocannabinol (0.1 or 6.4 mg/kg, i.p.); (2) 30 min after the last injection of 14-daily treatment with (-)-delta9-tetrahydrocannabinol (0.1 or 6.4 mg/kg) and 3) 24 h after the last injection of 14-daily treatment with (-)-delta9-tetrahydrocannabinol (6.4 mg/kg). Acute cannabinoid exposure antagonized the amphetamine-induced dose-dependent increase in locomotion, exploration and the decrease in inactivity. Chronic treatment with (-)-delta9-tetrahydrocannabinol resulted in tolerance to this antagonistic effect on locomotion and inactivity but not on exploration, and potentiated amphetamine-induced stereotypies. Lastly, 24 h of withdrawal after 14 days of cannabinoid treatment resulted in sensitization to the effects of D-amphetamine on locomotion, exploration and stereotypies. Since (-)-delta9-tetrahydrocannabinol is a cannabinoid CB1 receptor agonist, densely present in limbic and basal ganglia circuits, and since amphetamine enhances monoaminergic inputs (i.e., dopamine, serotonin) in these brain areas, the present data support the hypothesis of a role for the cannabinoid CB1 receptor as a regulatory mechanism of monoaminergic neuron-mediated psychomotor activation. These findings may be relevant for the understanding of both cannabinoid-monoamines interactions and Cannabis-associated psychosis.
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PMID:Chronic (-)-delta9-tetrahydrocannabinol treatment induces sensitization to the psychomotor effects of amphetamine in rats. 998 95

We developed a novel computer-assisted psychological test (the Searchlight Test) in order to explore 'cognitive fragmentation' and its relation to thought disorder in schizophrenic patients. Participants were instructed to search geometric figures through a small hole (3 cm in diameter) on a display monitor by moving a mouse device and to reconstruct an image of the whole from the temporally and spatially fragmented visual stimuli.The cognitive function measures in 24 schizophrenic patients and 14 normal controls showed that the error rates of the recall task (drawing the figure from memory) and the recognition task (selecting the correct figure from several similar figures) were significantly higher in schizophrenic patients than in normal controls. The error rates of both tasks significantly correlated with disorganization syndrome in schizophrenia, but not with reality distortion or with psychomotor poverty syndrome.The present data obtained with the Searchlight Test suggest the spatio-temporal disintegration of visual perception in schizophrenia and its correlation with disorganization. This test appears to provide a useful tool for studying the pathophysiology of disorganization syndrome, thought disorder and the related cognitive dysfunction of schizophrenia.
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PMID:Spatio-temporal disintegration of visual perception in schizophrenia as revealed by a novel cognitive task, the Searchlight Test. 1172 39

Based on clues from epidemiology, low prenatal vitamin D has been proposed as a candidate risk factor for schizophrenia. Recent animal experiments have demonstrated that transient prenatal vitamin D deficiency is associated with persistent alterations in brain morphology and neurotrophin expression. In order to explore the utility of the vitamin D animal model of schizophrenia, we examined different types of learning and memory in adult rats exposed to transient prenatal vitamin D deficiency. Compared to control animals, the prenatally deplete animals had a significant impairment of latent inhibition, a feature often associated with schizophrenia. In addition, the deplete group was (a) significantly impaired on hole board habituation and (b) significantly better at maintaining previously learnt rules of brightness discrimination in a Y-chamber. In contrast, the prenatally deplete animals showed no impairment on the spatial learning task in the radial maze, nor on two-way active avoidance learning in the shuttle-box. The results indicate that transient prenatal vitamin D depletion in the rat is associated with subtle and discrete alterations in learning and memory. The behavioural phenotype associated with this animal model may provide insights into the neurobiological correlates of the cognitive impairments of schizophrenia.
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PMID:Transient prenatal vitamin D deficiency is associated with subtle alterations in learning and memory functions in adult rats. 1592 58

Neurocognitive impairment has consistently been considered a central and stable feature of schizophrenia. There is much controversy about the effects of neuroleptics on neurocognitive deficits. Thus, further investigations are needed to clarify the pathological substrate of cognitive deficits in schizophrenia as well as to identify pharmacological tools for treatment. Transient prenatal Vitamin D deficiency is considered a developmental model in schizophrenia research. Recently, it was reported that prenatal Vitamin D-depleted rats showed a habituation deficit in the hole board. Here, we tested the effect on hole board habituation of haloperidol (Hal, 0.075 mg/kg, i.p.), risperidone (Ris, 0.2 mg/kg, i.p.) and the mGluR5 agonist CHPG (0.1 mg, i.c.v.) after subchronic treatment. Hal was found to impair habituation in control animals, Ris restored hole board habituation, whereas Hal and CHPG normalised hole board habituation in the deplete animals completely. The results of the study demonstrate that (i) the Vitamin D model might be a valuable tool in the study of neurodevelopmental aspects of schizophrenia, (ii) the model is sensitive in detecting the effect of antipsychotic drugs and (iii) the model appears to be sensitive in differentiating between typical and atypical antipsychotic drug.
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PMID:Pharmacological treatment to augment hole board habituation in prenatal Vitamin D-deficient rats. 1618 30

The contribution of the endocannabinoid system to dopamine-mediated disorganized behavior in schizophrenia is discussed. We used a model of concurrent stimulation of dopamine D1 and D2 receptors to evaluate the role of this system in dopamine-mediated stereotypies measured in a hole-board test. Pretreatment with the cannabinoid CB1 receptor antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichloro-phenyl)-4-methyl-1H-pyrazole-3-carboxamide (SR141716A; 1 mg/kg) potentiated stereotyped behavior induced by coadministration of the dopamine D1 receptor agonist SKF 38393 (0.05, 0.1 and 1 mg/kg) and the dopamine D2 receptor agonist quinpirole (0.25 mg/kg). Thus, the endocannabinoid system acts as a brake for abnormal behavior associated with dopaminergic overactivation.
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PMID:Cannabinoid CB1 receptor antagonism markedly increases dopamine receptor-mediated stereotypies. 1729 87

Neuregulin-1 (NRG1) has been identified as a candidate susceptibility gene for schizophrenia. In the present study the functional role of the NRG1 gene, as it relates to cognitive and social processes known to be disrupted in schizophrenia, was assessed in mice with heterozygous deletion of transmembrane (TM)-domain NRG1 in comparison with wildtypes (WT). Social affiliative behavior was assessed using the sociability and preference for social novelty paradigm, in terms of time spent in: (i) a chamber containing an unfamiliar conspecific vs. an empty chamber (sociability), or (ii) a chamber containing an unfamiliar conspecific vs. a chamber containing a familiar conspecific (preference for social novelty). Social dominance and aggressive behavior were examined in the resident-intruder paradigm. Spatial learning and memory were assessed using the Barnes maze paradigm, while spatial working memory was measured using the continuous variant of the spontaneous alternation task. Barnes maze data revealed intact spatial learning in NRG1 mutants, with elevated baseline latency to enter the escape hole in male NRG1 mutants reflecting an increase in activity level. Similarly, although a greater number of overall arm entries were found, spontaneous alternation was unaffected in NRG1 mice. Social affiliation data revealed NRG1 mutants to evidence a specific loss of WT preference for spending time with an unfamiliar as opposed to a familiar conspecific. This suggests that NRG1 mutants show a selective impairment in response to social novelty. While spatial learning and working memory processes appear intact, heterozygous deletion of TM-domain NRG1 was associated with disruption to social novelty behavior. These data inform at a novel phenotypic level on the functional role of this gene in the context of its association with risk for schizophrenia.
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PMID:Phenotypic characterization of spatial cognition and social behavior in mice with 'knockout' of the schizophrenia risk gene neuregulin 1. 1751 71

Developmental vitamin D (DVD) deficiency has been proposed as an environmental risk factor for a number of brain disorders. The absence of this vitamin during foetal development in the rat is known to alter behaviour in the adult, and many of these alterations are informative with respect to the clinical features of schizophrenia. Here we investigated whether DVD deficiency had a similar effect on 129/SvJ and C57BL/6J mice. Female mice were fed a diet deficient in vitamin D for 6 weeks prior to conception until birth, after which dams and their offspring were fed a normal diet (i.e. containing vitamin D). Control mice were fed a normal diet throughout the experiment. The adult offspring underwent a comprehensive behavioural test battery at 10 weeks of age. We found that DVD-deficient mice of both strains exhibited significantly higher levels of exploration, as measured by the frequency of head dipping on the hole board test. In addition, DVD-deficient 129/SvJ mice, but not C57BL/6J mice, displayed spontaneous hyperlocomotion. There was no effect of maternal diet on parameters assessed by the SHIRPA primary screen, or on tests of sensorimotor gating, social behaviour, anxiety or depression. Some of these findings resemble the rat phenotype (hyperlocomotion) but there are also novel effects of DVD deficiency on mouse behaviour (increased exploration). This study confirms that the developmental absence of this vitamin affects brain function in another species (mouse), and lends further weight to the hypothesis that DVD deficiency in humans may contribute to adverse neuropsychiatric outcomes.
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PMID:Developmental vitamin D deficiency alters adult behaviour in 129/SvJ and C57BL/6J mice. 1799 59


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