Schizophrenia approaches

Rujescu D, Bender A, Keck M, Hartmann AM, Ohl F, Raeder H, Giegling I, Genius J, McCarley RW, Moller HJ, Grunze H. A pharmacological model for psychosis based on N-methyl-D-aspartate receptor hypofunction molecular, cellular, functional and behavioral abnormalities. Biol. Psychiatry 2006 59 721-729. Mouri A, Noda Y, Enomoto T, Nabeshima T. Phencyclidine animal models of schizophrenia approaches from abnormality of glutamatergic neurotransmission and neurodevelopment. Neu-rochem. Int. 2007 51 173-84. 

The validity of pharmacoeconomic data is invariably diminished by two important factors a failure to account for all direct and indirect cost outcomes, and the difficulty of assigning costs to human experiences. In schizophrenia, validity is further reduced by the near-impossibility of conducting trials over several years, or even decades, so as to approach the reality of what is usually a lifelong illness. Given these observations, it would be imprudent to act on the minutiae of data generated in even the best-conducted trials, but it may well be appropriate to draw broad conclusions. 

Byrom WD, Garratt CJ, Kilpatrick AT (1998b). Influence of antipsychotic profile on cost of treatment of schizophrenia a decision analysis approach. Inti J Psychiatry Clin Prac. 

The localisation of a particular peptide to a particular brain area and possibly associated with a particular transmitter (e.g. CCK with dopamine in mesolimbic pathways) has often prompted a prediction of function (e.g. CCK may have a role in schizophrenia). Animal studies in which the peptide has been injected into the appropriate brain area or tested on slices taken from the brain area have sometimes been taken to confirm such hypotheses. These approaches have lined up the peptides for a whole range of potential roles, some of which are listed in Table 12.4. Whether these predictions are realities will depend on the availability of chemical agents and their evaluation, not only in animals but also in humans. 

We still need much better medicines to cure cancer, heart disease, stroke, and Alzheimer s disease. We need better drugs to deal with obesity, diabetes, arthritis, and schizophrenia. The treatments of diabetes, arthritis, and mental defects such as schizophrenia or manic depression are not yet cures, just ways to keep the symptoms under control. Cures are needed. Insights from genetics may help guide us toward elegant and rational cures, but we will also make use of screens to identify natural products and libraries of randomly generated synthetic compounds (combinatorial chemistry). A semi-empirical approach may be the best hope over the next two decades to yield drugs to alleviate these diseases. 

Marcotte ER, Srivastava LK, Quirion R. 2003. cDNA microarray and proteomic approaches in the study of brain diseases focus on schizophrenia and Alzheimer s disease. Pharmacol Ther 100 63. 

When approaching the treatment of schizophrenia, it is best to view the illness in one of four distinct phases prodromal phase, acute phase, maintenance phase, and residual phase. Let us take a look at the treatment options at each of these phases of the illness. 

This is but one classihcation of symptoms and signs in schizophrenia, representing a natural progression from the positive-negative dichotomy with its proposed pathogenic correlates (Crow, 1985). Other approaches include that of... 

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