Atypical antipsychotics—from bench to bedside. Edited by John G. Csernansky and John Lauriello. Published by Marcel Dekker Inc. New York, 2004. ISBN 0-8247-5412-3

✍ Scribed by B. E. Leonard

• Publisher: John Wiley and Sons
• Year: 2006
• Tongue: English
• Weight: 40 KB
• Volume: 21
• Category: Article
• ISSN: 0885-6222
• DOI: 10.1002/hup.787

✦ Synopsis

the association of depression with common neurological disorders (Parkinson's disease, Alzheimer's disease, epilepsy etc.). Aspects of the epidemiology and management of depression in the different neurological disorders are also included in this section. The first chapter of the monograph considers the phenomenology of depression, the phenomenological perspective allowing the detection and description of variants of depression that are currently grouped into a single category. It is emphasised that the classification of depression remains problematic. Classification based on purely clinical criteria may be replaced by sub-typing the disorder into precise endophenotypes. In addition, cultural and social factors affect the risk of depression.

This chapter is followed by a discussion of the neurobiology of depression and its possible impact on treatment. The chapter emphasises the neurodegenerative changes that take place and how they are reversed by chronic antidepressant treatments. The importance of neural networks, and the sub-cellular changes that occur in depression are also covered.

The changes in brain structure in depression are comprehensively discussed by Sheline in the third chapter of the monograph. I found this chapter particularly interesting as it critically reviewed evidence indication the structural changes that occur in the main limbic regions of the brain in depression. This chapter is followed by consideration of the functional imaging studies in patients with secondary depression associated with stroke, Parkinson's, Alzheimer's MS etc.

The second section of the monograph begins with an interesting chapter of the co-morbidity of neurological and psychiatric disorders in which an epilepsy prone rat is used at the model. It is apparent that defects in serotonin and noradrenaline are prominent neurological abnormalities that link epilepsy with depression. Clearly, this rodent model could be useful for studying pathological changes found in depression and how mood stabilisers and antidepressants reverse these changes.

Depression in many patients with stroke is reviewed in terms of its prevalence, clinical manifestations, possible mechanisms and the treatment. Stroke is a risk factor for depression and, vice versa, depression is a risk factor for stroke.