Schizophrenia clinical manifestations

The neurodevelopmental hypothesis of schizophrenia posits that the disorder is due to a subtle defect in prenatal brain development but is not clinically manifest until many years later (Murray and Lewis, 1987 Weinberger, 1987). This theory has two essential components a presumption of developmental neuropathology and an expectation that this developmental neuropathology results in a pattern of brain malfunction which ultimately produces the symptoms of schizophrenia. 

Schizophrenia designates a group of mental disorders rather than a uniform disease. Eugen Bleuler (1911), who coined the term schizophrenia, disputed the then current Kraepelinian concept of dementia praecox because he had recognized that the disorders in question could have very different courses and outcomes. Specifically, not all patients with schizophrenic psychoses ended up in dementia praecox, i.e. with a premature loss of their mind. Carpenter and Buchanan (1994) suggested that the clinical manifestations of schizophrenia could be grouped into three relatively separate core domains of psychopathology (the three-compartment model of schizophrenia) ... 

Owens DG, Johnstone EC, Crow TJ, Frith CD, Jagoe JR, et al. 1985. Lateral ventricular size in schizophrenia Relationship to the disease process and its clinical manifestations. Psychol Med 15(1) 27-41. 

As described in the previous sections, neuropathological studies demonstrated alterations in the levels of several synaptic proteins in the PFC, hippocampus, and cerebellum of patients with schizophrenia (13, 15, 53). These observations have lead to the hypothesis that the clinical symptoms of schizophrenia are manifestations of abnormal neural circuitry and dysfunctional communication between different brain regions (22, 51). These abnormalities affect multiple neurotransmitter systems. Although dopamine dysfunction in schizophrenia is widely accepted, a growing body of evidence suggests the involvement of glutamate, GABA, and other neurotransmitters in schizophrenia. 

In a clinical study, several patients with neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure were treated with phenothiazine, butyrophenone (haloperidol), benzamide, iminomide, benzisox-azole, antidepressants and hypnotics (benzodiazepine and barbiturate) for the treatment of schizophrenia [ 184], The clinical manifestations of neuroleptic malignant syndrome were characterized by altered consciousness, muscle rigidity and weakness, fever and excessive perspiration. All patients were successfully cured of acute renal failure by haemodialysis or haemodiafiltration. 

The differential diagnosis of depression is organized along both symptomatic and causative lines. Symptomatically, major depression is differentiated from other disorders by its clinical presentation or its long-term history. This is, of course, the primary means of distinguishing psychiatric disorders in DSM-1V. The symptomatic differential of major depression includes other mood disorders such as dysthymic disorder and bipolar disorder, other disorders that frequently manifest depressed mood including schizoaffective disorder, schizophrenia, dementia, adjustment disorder, and post-traumatic stress disorder, and, finally, other nonpsychiatric conditions that resemble depression such as bereavement and medical illnesses like cancer or AIDS. 

Manifestations of chronic intoxication Severe dermatoses, marked insomnia, irritability, hyperactivity, and personality changes have occurred. Disorganization of thoughts, poor concentration, visual hallucinations, and compulsive behavior often occur. The most severe manifestation of chronic intoxication is psychosis, often clinically indistinguishable from paranoid schizophrenia. This is rare with oral amphetamines. 

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