Schizophrenia is a Neurobiological disorder. Most people don't have the understanding that with schizophrenics it's more then just psychological.
With Schizophrenia there are psychical changes that take place in the brain once the person becomes ill. Once the illness is triggered it destroys
parts of the brain. A schizophrenics brain mass can shrink by up to 10%. They literly loose grey matter. Schizophrenia is hereditary and passed on in
our genes. Scientists have located 2 genes that are linked to schizophrenia. These genes can lay dormant a persons entire life and they may never get
the illness or they may become active and the person get schizophrenia.
There is no evidence that Schizophrenia is a neurobiological disorder.
Various genetic, organic or pathogen-based causative factors have been hypothesised for the emergence of Schizophreniform symptomology but to date,
despite over 100 years of research, medical science has yet to identify a specific biological antecedent.
Current biological research seeks to explain the aetiology of Schizophrenia via various domains; neurodevelopmental models of psychosis suggest that
cerebral damage and reduced volume of brain mass associated with the disorder may originate during gestation and that the onset of psychotic symptoms
are the end-product of abnormal brain development, inflammatory processes and immune response, rendering Schizophrenia a neurodegenerative disease
(Altamura et al, 2012). Other research has focused on non-genetic infectious factors, such as the parasite Toxoplasma Gondii, with elevated antibody
levels having been found in Schizophrenia patients by numerous studies (Fuller Torrey et al, 2012) and observable effects on human and animal
behaviour noted via the mechanism of parasitic symbiosis.
Traditional models focus on neurochemical imbalances; the efficacy of antipsychotic treatment continues to be based around the dopaminergic hypothesis
(Kapur, 2003). However, despite multi-factorial approaches, there remains no biological or genetic “test” for Schizophrenia, and no definitive
evidence to suggest that Schizophrenia is a unitary disease-entity (Tandon et al, 2008). The diagnosis has been described as being “replete with
examples of theories that have remained unproven, but still held with tenacity by their proponents,” suggesting that “Schizophrenia” is in fact
a conglomeration of similar syndromes with overlapping symptoms and phenomenologies (Keshavan et al, 2011).
In addition, the reduced volumes of brain mass typically seen in Schizophrenic patients are due to damage caused by neuroleptics rather than an innate
disease process (Moncrieff & Leo, 2010).
As Schizophrenia continues to be diagnosed via pathological criteria and first-line treatment is focused on pharmacological intervention, it is
interesting to note that 1 in 3 patients are classed as treatment-resistant (Suzuki et al, 2011), which illustrates the ineffectiveness of
disease-based interpretations and the need for greater focus on understanding and treating psychosis from a psychological perspective. Furthermore, it
gives credence to the notion that psychosis may be a manifestation of unprocessed trauma (Varese et al, 2012), with “symptoms” such as voice
hearing being a symbolic representation of this suffering; by eliminating positive symptoms via medication, an important opportunity to understand,
contextualize and recover from the experience is lost (Romme & Escher, 2011 pp 385-393).
The Continuum model of psychosis provides an integrated understanding of the psychological processes underpinning “Schizophrenia”, as well as
explaining the blurred, non-discrete boundaries between other mental disorders and the over-lapping of symptoms. Turkington & McGovern (2001)
suggested a hierarchy of psychopathology, or spectrum of disorders, ranging from stress responses to psychosis, and emphasised that factors such as an
individuals genetic predisposition, psychological make up and external environment determined where on the continuum of mental disorder psychiatric
symptoms would likely manifest.
Cognitive models of psychosis adopt a holistic, humanist approach and are based on a hypothesis of stress-vulnerability, suggesting that predisposing
social, biological and psychological factors interact with adverse life events, triggering a psychotic response. Experience of trauma, social
disadvantage and isolation are seen to influence the development of negative schemas and core beliefs, which in turn influence interpretations of the
self and others; research suggests that sufferers of psychosis tend to have negative self-perception, which directly relates to the development and
maintenance of persecutory psychotic belief systems (Jolley & Garety, 2011) as well as the social withdrawal, inertia and lack of motivation typically
characterised as “negative symptoms.”