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Extra info for Electroconvulsive Therapy 4th Edition
Example text
60 capable of permanently damaging the brain? Although there are no data suggesting the possibility of such an occurrence, it remains a question of concern among many patients who receive ECT (see Chapter 12) as well as among two outspoken medical opponents of this form of therapy (Friedberg, 1977; Breggin, 1979). For obvious reasons, the question must be considered in light of the present-day practice of ECT, using barbiturate anesthesia, muscle relaxation, and oxygenation, sharply truncating the available body of data that addresses the topic, much of it obtained before modern treatment techniques became standard.
1996): frontal hypoperfusion in 15 depressives before brief-pulse ECT (electrode placement unspecified), and increased cerebral perfusion following ECT in those patients who enjoyed the best clinical response. Most discouraging is the report of Pridmore et al. (2001) who obtained HPAO SPECT scans at baseline and immediately following high-dose brief pulse unilateral, bitemporal, or bifrontal ECT in 8 patients, and were unable to detect any pre-post differences at all. To summarize: cerebral blood flow is generally reduced frontally in depressed patients at pretreatment baseline examination, increased over baseline during ECT-induced seizures, and then either increased or reduced below baseline following ECT, possibly depending on the time of reexamination and the method chosen for estimating blood flow.
2000) examined the ratio of the albumin concentration in the CSF to that in the serum in a sample of 9 depressed patients before and after a course of ECT, as a measure of blood-brain barrier dysfunction. Although several patients had signs of blood-brain barrier dysfunction at baseline, no change in the CSF/serum albumin ratioâ and therefore no blood-brain barrier dysfunctionâ was induced by ECT. To summarize, all studies confirm maintenance of the structural integ rity of the blood-brain barrier during ECT.