Schizophrenia definition

Andreasen, N.C. and Olsen, S. (1982) Negative and positive schizophrenia definition and validation. Arch Gen Psychiatry 39 789-794. 

Andreason NC. 1982. Negative symptoms in schizophrenia Definition and reliability. Arch Gen Psychiatry 39 784-788. 

Andreason NC, Smith MR, Jacoby CG, Dennert JW, Olsen SA. 1982a. Ventricular enlargement in schizophrenia Definition and prevalence. Am J Psychiatry 139(3) 292-296. 

For approximately 20% to 30% of people with schizophrenia, drug treatment is ineffective. A standard definition of treatment resistance includes patients who have persistent positive symptoms despite treatment with at least two different antipsychotics given at adequate doses (at least 600 chlorpro-mazine equivalents) for an adequate duration (4 to 6 weeks). In addition, patients must have a moderately severe illness as defined by rating instruments, and have a persistence of illness for at least 5 years.40 These patients are often highly symptomatic and require extensive periods of hospital care. 

Again, the character of the patient s prior episodes, premorbid functioning, and family history all are helpful. By definition, schizophrenia is marked by a 6-month decline in social and occupational functioning that is seldom seen in bipolar illness. In addition, the delusions and hallucinations of schizophrenia are present during periods of normal mood, whereas bipolar patients only experience psychotic symptoms in the context of severe mood disturbance (i.e., mania or depression). 

Although this is an area in which research is burgeoning, definite evidence of the effectiveness of EFAs in the treatment of mental disorders is lacking. There are some controlled trials of varying methodological quality in adult patients with schizophrenia, and unipolar and bipolar depression, with conflicting results (Fenton et ah, 2000 Maidment, 2000). The most encouraging trial is a preliminary study of 30 patients with bipolar disorder. It found that EFAs concurrent with mood stabilizers reduced the rate of recurrence of episodes (Stoll et al., 1999). 

Remschmidt, H. (2001) Definition and classification. In Remschmidt, H., ed. Schizophrenia in Children and Adolescents. Cambridge UK Cambridge University Press, pp. 24 2. 

To attempt to obtain a claim for a nonspecific symptom in a single disease model would, by definition, be pseudospecific, since such a claim would give the impression that the symptom is specific to that disease. For example, if there were agreement that psychomotor agitation could be considered a nonspecific psychiatric symptom, it would be important to study a drug treatment proposed for this symptom in several different disease models, such as schizophrenia, autism, and mental retardation. 

Schizophrenia-related disorders, such as schizophreniform disorder, can closely mimic an acute exacerbation of mania. Attention to premorbid personal and family history may help differentiate them from mood disorders. A definitive diagnosis may not be possible, however, until the course of the illness is followed for a period of time. Clinical clues include the propensity of bipolar manics (in contrast to schizophrenics) to demonstrate pressured speech, flight of ideas, grandiosity, and overinclusive thinking. Hallucinations are less common than delusions in both mania and depression, with delusions normally taking on the qualities of expansivity, hyperreligiosity, or grandiosity. Delusions are also relatively less fixed than in schizophrenia. 

The first generation antipsychotics, now known as typical drugs, were all D2 receptor blockers and, as such, very likely to produce Parkinsonian side effects. Because antipsychotic potency was associated with D2 receptor affinity, it was assumed that dopamine overactivity was the essential defect in schizophrenia and that a direct dopamine blockade was the definitive route to treatment. But these drugs affected both the target dopamine pathways of the mesolimbic projection and the uninvolved nigrostriatal projection. Unfortunately, that meant that movement disorders were the price that had to be paid for antipsychosis. 

Sleep disorders are definitively part of the clinical picture in schizophrenia. Due to the lack of space, EEG studies, dream studies and correlative studies have not been reviewed. The evidence is clear that clinical status [20] and daytime cognitive performance [21] covary with sleep in schizophrenia. Future studies should include these issues in their protocol strategies. 

In addition to acute and chronic schizophrenia, the neuroleptics are sometimes used in the management of mania, delirium, and severe agitation, whatever the cause of these symptom complexes. It must be noted that unlike parkinsonism, where a definite dysfunction in the DA system has been established, for schizophrenia and other psychiatric diseases, no unequivocal evidence has yet been presented to prove that there is a disturbance of the DA system (e.g., dopaminergic overactivity or receptor hypersensitivity). In untreated schizophrenics the production of DA metabolites is normal. Conflicting results have been obtained in studies of the DA receptors in schizophrenics (11,12,13), but in the case of patients who have not received neuroleptics, the receptor density and affinity appear to be normal (13). The "dopamine hypothesis" in these disorders derives from the beneficial effects of drugs that block DA receptors. 

One PET study involving unmedicated patients found no frontal hy-poactivity (Sheppard et al., 1983). Another with unmedicated patients showed increased frontal metabolism (Cleghorn et al., 1989). The failure to demonstrate hypoactivity in the frontal lobes of unmedicated patients confirms that the effect, when found, is probably caused by the antipsychotic medications. As an exception to this, Buchsbaum et al. (1992) found hypofrontality in never-medicated patients diagnosed with schizophrenia. However, the results were not definitive The hypofrontality effect was modestly sensitive and not strongly specific. ... 

There is a very cogent reason to believe that the atrophy found on CT scans cannot be the product of schizophrenia. Brain atrophy is far more accurately and definitively evaluated by a direct postmortem pathological examination than on a CT or MRI brain scan. The actual pathology, if it exists, can more easily be identified and accurately measured by direct observation and microscopic analyses. 

Meisenzahl EM, Zetzsche T, Preuss U, Frodl T, Leinsinger G, et al. 2002. Does the definition of borders of the planum temporale influence the results in schizophrenia . Am J Psychiatry 159(7) 1198-1200. 

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