British Journal of Medical Practitioners. Authors. Article Citation and PDF Link. Bermudas History from 1952 to 1999 Significant news events in the final half of the 20th century. By Keith Archibald Forbes see About Us at email exclusively for. Abstract Summary. Despite progress in neurotransmitter identifications and the emergence of novel antipsychotics, the treatment of schizophrenia remains frustrating. There is now a flurry of research trying to figure out the aetiology of schizophrenia and potential etiological models other than neurotransmitter dysfunction deserve consideration. Recent years have witnessed a revival of interest in the viral and immunity based etiological models of schizophrenia. A subset of schizophrenia may have a pure biological aetiology. There are several commonalities between schizophrenia and autoimmune disorders. Coexistence of established autoimmune disorders along with schizophrenia is suggestive that the latter could also have an autoimmune component. Antipsychotics may be working on the principle of immune modulatory and neuro modulatory mechanisms. The well recognized 1 global consistency of the incidence of schizophrenia indicates that the aetiology of schizophrenia involve an evolutionary genetic vulnerability and universally present environmental factors. There may be a genetic predisposition to the hypothetical schizovirus determining the development of schizophrenia in certain individuals. Certain people are genetically vulnerable to microbial infections in the sense that they have a highly sensitive surveillance system to the microbial infection and respond to the microbial adversary in an exaggerated way. Such a vulnerability and anomalous reaction to infection could result in the schizophrenia psycho pathogenesis. Introduction. A clearer understanding of the aetio pathogenesis of schizophrenia would ultimately lead to effective treatment strategies and provide the impetus for elucidation. The autoimmune hypothesis promulgates that it is the auto antibodies that are responsible for schizophrenia and, according to the viral hypothesis, it may be the bodys abnormal response to a slow viral infection or the undefeated viral antigens causing the schizophrenia pathology. The autoimmune and viral hypotheses are interlinked, as autoimmune disorders can be triggered by microbial infection. Viral aetiology is less convincing than the autoimmune model, but from a treatment perspective, the former is more promising than the latter. To gain a detailed understanding of aetiological models of a subset of schizophrenia, herein the author has reported on a review of the literature relating to the immunity and viral based aetiological models of schizophrenia. Genetic vulnerability has been highlighted in the schizophrenia literature alongside environmental factors. The veracity and contestability of the immunity and viral based aetiological hypothesis of schizophrenia merits further investigation. Schizophrenic Syndromes. A prerequisite for incorporating autoimmune and viral aetiology into a scientific discussion would be acceptance of the heterogeneous hypothesis of schizophrenias they may be a cluster of entities with different aetiologies and the end stage of different disease processes. Autoimmune or viral aetiology may account for one subgroup. Schizophrenia has diverse signs and symptoms, and a long history of controversy. Nosologists designate it as polythetic, whereas most other mental illnesses are monothetic, seemingly affecting only one brain system. In the second half of the twentieth century, the psychosocial model gave way to evidence that it is a brain disorder. Schizophrenia has a long history of controversies and there has been much contention over the aetiology, psychopathology, nomenclature, and diagnostic criteria. Arrau Heritage Beethoven. Schizophrenia is currently seen as a neurodevelopmental encephalopathy, in which the cognitive deficits are produced due to the errors during the normal development of the brain 3 or a neuro degenerative disorder and the cognitive deficits are derived from a degenerative process that goes on unalterably. Modern neuroimaging techniques and an intensification of studies of necropsy tissue have been responsible for this shift. Researchers seem to agree that a neurodevelopmental or degenerative assault precedes the symptoms by several decades. The aetiology of the cognitive deficits is unidentified and several potential factors, genetic and epigenetic, are envisaged. Environmental factorsincluding infectious agents and disturbance in utero through malnutritionaccount for a few cases. I/51XaW6BymwL._SR600%2C315_PIWhiteStrip%2CBottomLeft%2C0%2C35_PIStarRatingFIVE%2CBottomLeft%2C360%2C-6_SR600%2C315_SCLZZZZZZZ_.jpg' alt='Grundy 2000 Pragmatic Pdf' title='Grundy 2000 Pragmatic Pdf' />Autoimmunity and viral theories would fit in with the neuro developmental and neurodegenerative hypotheses. Proponents of viral aetiology view viruses as acting alongside susceptible genes to initiate a trajectory that manifests as psychotic symptoms. Lessons from Autoimmunity. Disorders of an autoimmune nature are known to occur with increasing frequency in patients with another autoimmune disease. This is somewhat like the coexistence of multiple psychosomatic disorders in a person as per Hallidays psychosomatic formula, association of other psychosomatic afflictions justifies the diagnosis of a new psychosomatic condition. It is well recognised that the central nervous system CNS may be directly affected by autoimmune processes, as in the case of multiple sclerosis MS and autoimmune limbic encephalitis. A physical autoimmune disease, such as systemic lupus erythematosus SLE and antiphospholipid syndrome are also associated with psychiatric morbidity. Paediatric autoimmune neuropsychiatry disorder is a post infection group A Beta haemolytic streptococcal infection autoimmune disorder characterised by abrupt onset of obsessive compulsive disorder OCD and Tourettes syndrome, brought about by molecular mimicry. Nicholson et al observed that 2. OCD patients were positive for anti basal antibodies, considered to be part of a post streptococcal autoimmune reaction. Autoimmunity is a misdirected response occurring when the immune system attacks the body it is the loss of tolerance to self antigens. Immunological tolerance to ones own tissue is probably normally acquired during foetal life, helping to prevent the occurrence of the autoimmune process see Table. Some clones of cells that can produce auto antibodies forbidden clones are thought to be produced throughout life, and are suppressed by large amounts of self antigens or antigen specific T cells. Auto antibodies are produced for a wide variety of antigens some are organ specific and others are non organ specific. Some microorganisms or drugs may trigger changes in individuals who are genetically vulnerable to autoimmunity. Table 1 Mechanisms preventing and causing autoimmunity. Tolerance to self molecules a. Clonal deletion removing any lymphocytes that might react to self molecules b. Clonal anergy decreasing the responsiveness of lymphocytes that recognise self molecules. Receptor editing rearrangement of B cell receptors. Reduction or inhibition of molecules or antigens that may cause self recognition. Failure of self tolerancea. Journals/JAOA/932123/m_es18fig1.jpeg' alt='Grundy 2000 Pragmatic Pdf' title='Grundy 2000 Pragmatic Pdf' />Release of isolated auto antigens tissue trauma or infection may cause breakdown of anatomic barriers and may expose the hidden antigens for recognition of T cells that were not deleted during development. Structural alterations in self peptides Once structurally altered by a trigger such as infection, the self peptides become more antigenic and are subsequently recognised by the undetected T cells evoking immune response. The British Journal of Medical Practitioners has adopted a Continuous Publication model from the beginning of year 2010 publishing articles online as soon as. Earl Cain Japanese, Hepburn Hakushaku Kain Shirzu, also known as Count Cain, is a shjo manga series written and illustrated by.