Current Medical Diagnosis & Treatment in Psychiatry

The Current State of Psychiatric Understanding

Current Concepts in AnxietyAug 01, 06

The state of patient-orientated research in psychiatry is affected by several problematic facts. Psychiatric diagnosis is almost entirely at a descriptive syndromal level.

Objective, specific, diagnostic tests are not available for almost all psychiatric diseases.

Therefore, our syndromal categories probably include many phenocopies comprising diverse etiologies, pathophysiologies, and moderating variables. This may account for the current wide range of treatment outcomes and our imprecise prognoses.

Both our pathophysiological and psychosocial theories have a bad historical record since few have survived pointed tests. Basic research beneficially critiqued simplistic pathophysiological notions that emphasize crucial single neurotransmitters. Although we talk about noradrenergic, serotonergic and dopaminergic systems, their functions are still obscure. Except for crude beginnings, simple rheostat models are used, positing that too much or too little neurotransmitter has some unequivocal implication concerning the direction and utility of some function. The strange fact of neuropeptide co-transmission and the multiplicity of excitatory and inhibitory preand post-synaptic receptors indicate the crudeness of such notions. Basic neurophysiological disease models are almost entirely speculative.

The hopes that molecular genetic research will sharply delineate psychiatric diseases have floundered amidst complex genetics, polygenic determinants and multiple phenocopies. Genomic linkage research requires careful, still quite obscure, distinctions among phenocopies or one is swamped by false positives.

The hope that molecular biology will provide specific remedies remains unfulfilled.

Even though a specific chromosomal defect in the classic autosomal dominant in Huntington’s Disease was isolated 15 years ago, and although the aberrant protein in question has been determined, translation into therapeutic interventions has not, as yet, occurred. This is probably due to the tremendous, still largely unknown, epigenetic, environmentally molded, cascade between gene, gene product and clinical pathophysiology. Serendipity still rules for pharmacotherapeutics, although the clinical context fostering serendipity has shrunk (Klein and Smith, 1999).

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