الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 32 |  |  |
| | | from | 32 | | |
Abstract
Many patients of depression have hypercortisolemia or hypercortisoluria, suggesting a dysregulation of the limbic – hypothalamic – pituitary – adrenal axis (Reus,et al (1987).
Cognitive deficits, especially those closely related to hippocampus function, appear to be related to cortisol secretion in depressed patients (Hinkelmann et al., 2009).
Brain Synchronization therapy (BST) refers to the most effective and rapidly acting treatment that we have today for severe depression and other conditions (Lisanby, 2012).
A key risk associated with BST use is cognitive and memory dysfunction. The FDA review found that BST is likely associated with immediate general cognitive and memory dysfunction. Cognitive dysfunction is represented by disorientation. Disorientation appears to be transient and generally resolves in a matter of minutes after the procedure (Lawrence Park (2011).
Memory dysfunction in general largely resolves in the days to weeks after the completion of a course of BST. However, in certain domains, particularly in anterograde verbal memory and retrograde autobiographical memory, deficits may be more prominent and/or persistent (McClintock et al., 2010).
Although at present there is no evidence that BST, as currently administered, causes brain damage, repeated high-dose electroconvulsive shock has been found to cause neuronal death in the hippocampi of animals. Thus, Thomas Neylan (University of California) and colleagues suggest that BST-induced cognitive impairment may be related to reversible neuronal injury that is potentiated by glucocorticoids (Sapolsky, 1996).
Horne et al., 1984) found that patients administered dexamethasone while receiving BST had more memory impairment, if similar effects are seen with endogenous hypercortisolism, this would suggest that patients with elevated pre- BST cortisol levels may suffer greater post – BST memory impairment (Horne et al, 1984).