Guest guest Posted May 27, 2005 Report Share Posted May 27, 2005 " duramater27 " <spam-barb@c...> wrote in part: > Just took a gander at the brain SPECT and CFS literature. There are > actually a number of studies looking at this, and frankly, the data > are all over the place. Arrrggh, that sux. But at least it removes part of the paradox of the persistance of the CFS psychologization school. According to two immense reviews, the search for immunological abnormalities in CFS has similarly yielded a lot of astonishing inconsistency, except perhaps regarding natural killer cell function. Maybe gene expression assays can change that picture before too long. Dura thanks for your points, especially re SPECT abnormalities in unipolar and bipolar depression, etc. I never thought to wonder whether such existed. Have you seen Fallons chronic lyme SPECT study - I believe the one I'm thinking of is the one copied below. I dont know the first thing about the tech or the abnormalities; I only paid attention to the nice low p value Fallon derived, presumably from some sort of matrix of the SPECT signal intensities at various sites in the brain. What do depression-ologists of the CBT persuasion think of the SPECT results in that disease and other primary psych dx's? Do they have hold of anything hefty to back the hypothesis of such changes being produced in the brain by the mind, or do they rather dispute the consistency of the findings in the first place? What about the atrophy of the hippocampus in depression, is that noncontroversial? Is the question of demonstrating patient benefit from CBT as fraught as I think it is - without actually reading anything, I'll admit? I mean, doesnt it seem like CBT could change ones response to questions used to quantify depression, and even change clinical signs such as posture and eye contact, without changing ones actual experience? Do any studies purport to show brain changes by imaging as an objective index of the payoff of CBT? If brain changes after CBT cannot be demonstrated, is that percieved as slightly embarrassing by those who hold CBT to be effective? What about a disorder like PTSD which presumably is generally accepted as being caused by experience rather than, say, infection - I think it is associated with increased urinary catecholamine levels by at least some studies... any brain imaging abnormalities in that disease? While youre at it, how can an integral luminous subjectivity inhere in the electrophysical flux of the brain, and what happens to it after the brain ceases to function? Also, why is there a universe in the first place instead of nothing at all? -Captain REMERON, formerly known as " flat affect, fair eye contact, poorly groomed " ================================================== Clin Infect Dis. 1997 Jul;25 Suppl 1:S57-63. Functional brain imaging and neuropsychological testing in Lyme disease. Fallon BA, Das S, Plutchok JJ, Tager F, Liegner K, Van Heertum R. The New York State Psychiatric Institute, the Department of Psychiatry of Columbia University and Columbia-Presbyterian Medical Center, New York 10032, USA. Differentiating neuropsychiatric Lyme disease from a primary psychiatric disorder can be a daunting task. This article describes how functional brain imaging and neuropsychological testing can be particularly valuable in helping to make diagnostic distinctions. In addition to a review of the relevance of functional imaging to neuropsychiatry in general, recent findings are presented regarding the use of single photon emission computed tomographic (SPECT) imaging in Lyme disease. Publication Types: * Review * Review, Tutorial PMID: 9233666 [PubMed - indexed for MEDLINE] Quote Link to comment Share on other sites More sharing options...
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