Cognitive deficits of schizophrenia: the flower workshop initiative (original) (raw)
Related papers
Neurobiology of Schizophrenia: A Comprehensive Review
Cureus
Schizophrenia is a debilitating disease that presents with both positive and negative symptoms affecting cognition and emotions. Extensive studies have analyzed the different factors that contribute to the disorder. There is evidence of significant genetic etiology involving multiple genes such as dystrobrevin binding protein 1 (DTNBP1) and neuregulin 1 (NRG1). There is no clear link between neurotransmitter changes and the pathophysiology of schizophrenia; however, studies have shown that subcortical dopamine dysfunction is the key mechanism. Specific regions of gray and white matter changes are observed in patients with schizophrenia; gray matter changes being more significant after the onset of psychosis. These pathological changes may be implicated in the impairment of executive functioning, attention, and working memory. The disease can be managed with pharmacological treatments based on individual patient profile, patient compliance, and disease severity. The challenge of disease management sometimes persists due to the side effects. A better understanding of the pathological processes in schizophrenia may lead to more specific and effective therapies.
The Biological Basis of Schizophrenia
Social Work, 1987
A major obstacle which I have had to deal with both as I wrote this paper and designed my exhibit was the question, "who is this for?" Five people will have to read and approve this paper. Five people had to view and judge my exhibit. Many more may wish to read my paper and review the pieces from my exhibit in orderto decide whetherto hire me or not. There FOREWORD really understand the scientific theory, despite my best efforts. I cannot cover several years of premedical and medical education which I have not even had myself in this paper. I hope the person with minimal medical knowledge will be able to comprehend the fundamental theory behind the biological basis of schizophrenia. Non-artists may not be interested in my are many more people who saw my exhibit, as discussion of the media I chose. well.
British Medical Bulletin, 1996
The diagnosis of schizophrenia is largely based on reports of bizarre experiences such as having alien thoughts inserted into one's mind. Many patients with this diagnosis show a marked intellectual decline and particular problems with tasks involving certain kinds of memory or requiring mental flexibility. Similar patterns of performance can be seen in patients with damage in the prefrontal cortex. However, patients with schizophrenia show a very varied pattern of impairments relating to their current mental state. Chronic patients with negative features, such as poverty of speech, are most likely to show poor test performance, while the presence of severe hallucinations and delusions need not be associated with any impairment. A cognitive approach suggests that hallucinations and delusions result from the patient attributing his own actions to an external agency. This error is due to an inability to distinguish between external events and perceptual changes caused by his own actions.The basis of this failure could be a functional disconnection between frontal brain areas concerned with action and posterior areas concerned with perception.
Schizophrenia and the Dysfunctional Brain
Journal of Cognitive Science, 2010
Scientists, philosophers, and even the lay public commonly accept that schizophrenia stems from a biological or internal 'dysfunction.' However, this assessment is typically accompanied neither by well-defined criteria for determining that something is dysfunctional nor empirical evidence that schizo-phrenia satisfies those criteria. In the following, a concept of biological function is developed and applied to a neurobiological model of schizophrenia. It concludes that current evidence does not warrant the claim that schizophrenia stems from a biological dysfunction, and, in fact, that unusual neural structures associated with schizophrenia may have functional or adaptive significance. The fact that current evidence is ambivalent between these two possibilities (dysfunction versus adaptive function) implies that schizophrenia researchers should be much more cautious in using the 'dysfunction' label than they currently are. This has implications for both psychiatric treatment as well as public perception of mental disorders.
The Pathophysiology of Schizophrenia Disorders: Perspectives From the Spectrum
American Journal of Psychiatry, 2004
Objective: This overview focuses on neurobiologic abnormalities found in subjects with schizotypal personality disorder, the prototype of the schizophrenia spectrum disorders, and chronic schizophrenia in the context of common vulnerabilities shared by SPD and schizophrenia, as well as those factors that protect against the severe cognitive/social deficits and frank psychosis of chronic schizophrenia. A pathophysiologic model of the relationship between schizotypal personality disorder and schizophrenia is developed on the basis of this data.
Schizophrenia: Epidemiology, Causes, Neurobiology, Pathophysiology, and Treatment
Journal of Health and Medical Sciences, 2020
Schizophrenia is a severe mental illness that has devastating consequences for those who suffer from the disorder. The epidemiology of schizophrenia indicates that it occurs relatively often, in many different contexts, and in conjunction with other disorders, decreasing quality of life and causing premature death. There has been an enormous amount of research into the causes of schizophrenia and there is now have a much better understanding of the genetic, environmental, and psychological factors that contribute to the disease. While there are numerous ways to understand and conceptualize schizophrenia, a unified picture of the neurobiology, changes in brain structure, cognitive and social-cognitive impairments related to the disorder has yet to emerge. Convulsive therapies and psychosurgery were used unsuccessfully, indiscriminately and without scientific validation in the past to treat schizophrenia. Medical advances including advanced imaging technology have now provided the abi...
[Neurodevelopment and schizophrenia]
Vertex (Buenos Aires, Argentina)
The evidence of neuroleptics' antipsychotic action due to their antagonism of dopamine receptors led to the hyperdopaminergic theory of schizophrenia. But the functional disturbance of the dopamine neurons should explain the increase and the reduction of some symptoms at the same time through the D2 receptors blockade. The prodromical manifestations of schizophrenia include abnormal movements which precede and predict the beginning of the disease. They also suggest a dopamine deficit. An injury in the mesocortical dopamine projection during the neural development could result in a functional impairment of the prefrontal cortex which causes the cognitive deficit symptoms. It would result also in an excessive compensatory subcortical dopamine activity which would cause the psychotic symptoms. The evidence in behalf of this physiopathology is complex. The mechanism of the subcortical compensation of the prefrontal dopamine deficit remains unknown. It is necessary to find out which ...
Neuropsychology of schizophrenia
Behavioral and Brain Sciences
A model is proposed for integrating the neural and cognitive aspects of the positive symptoms of acute schizophrenia, using evidence from postmortem neuropathology and neurochemistry, clinical and preclinical studies of dopaminergic neurotransmission, anatomical connections between the limbic system and basal ganglia, attentional and other cognitive abnormalities underlying the positive symptoms of schizophrenia, specific animal models of some of these abnormalities, and previous attempts to model the cognitive functions of the septohippocampal system and the motor functions of the basal ganglia. Anatomically, the model emphasises the projections from the septohippocampal system, via the subiculum, and the amygdala to nucleus accumbens, and their interaction with the ascending dopaminergic projection to the accumbens. Psychologically, the model emphasises a failure in acute schizophrenia to integrate stored memories of past regularities of perceptual input with ongoing motor programs in the control of current perception. A number of recent experiments that offer support for the model are briefly described, including anatomical studies of limbic-striatal connections, studies in the rat of the effects of damage to these connections, and of the effects of amphetamine and neuroleptics, on the partial reinforcement extinction effect, latent inhibition and the Kamin blocking effect; and studies of the latter two phenomena in acute and chronic schizophrenics.
Schizophrenia: Unraveling the Labyrinth of Etiology and Epidemiology
International Journal of Pharmacy and Biological Sciences
Schizophrenia mental disorder is the combination of psychotic and neurotic disorder where the clinical symptoms and signs, duration and cognitive adjectives are well defined. In this, pharmacological treatments are existing successfully, even though they are likely relieving pain without dealing with the cause of the condition. The most risky constituents for schizophrenia are genetics and formational and operative abnormalities of brain. These factors are precautionable by the scientists by innovating new genetic information in the human genome and brain imaging techniques which direct inquiries the structural functionality of neurochemistry. Dopamine role does not ignore in current assumption of pathophysiology but it emphasizes the integration of neural systems in the expression of illness and symptoms generating in limbic system. Advanced observations for futuristic discovery are arising from the combination of molecular genetics and brain imaging techniques.