Welcome to The International Hypnosis Research Institute Web site. Our intention is to support and promote the further worldwide integration of comprehensive evidence-based research and clinical hypnotherapy with mainstream mental health, medicine, and coaching. We do so by disseminating, supporting, and conducting research, providing professional level education, advocating increased level of practitioner competency, and supporting the viability and success of clinical practitioners. Although currently over 80% of our membership is comprised of mental health practitioners, we fully recognize the role, support, involvement, and needs of those in the medical and coaching fields. This site is not intended as a source of medical or psychological advice. Tim Brunson, PhD

Changes in mismatch negativity across pre-hypnosis, hypnosis and post-hypnosis...

Posted At : March 25, 2010 12:17 PM | Posted By : Tim Brunson, PhD
Related Categories: Research

Full Title: Changes in mismatch negativity across pre-hypnosis, hypnosis and post-hypnosis conditions distinguish high from low hypnotic susceptibility groups

The role of alterations in mismatch negativity (MMN) in hypnosis was examined by recording MMN of the auditory ERP at frontal (F3, Fz, and F4) and mastoid (M1 and M2) placements. Frontal MMN is believed to reflect activity in right anterior cortical generators, whereas MMN at mastoid leads reflects generators located bilaterally in the temporal auditory cortex. MMN recordings were obtained in 11 low and 12 high hypnotically susceptible participants in three successive blocks; pre-hypnosis, hypnosis and post-hypnosis. Frontal (but not temporal) MMN showed a significant quadratic trend across testing conditions. It increased during hypnosis and then dropped post-hypnosis for both susceptibility groups. Linear trends for frontal and temporal MMN showed directly opposite patterns of change in the interaction between hypnotic susceptibility and testing blocks. Frontal MMN built up linearly over the test blocks in high relative to low susceptibility participants. Temporal MMN showed the reverse pattern and increased linearly across test conditions in those with low relative to high hypnotic susceptibility.

Brain Res Bull. 2005 Oct 30;67(4):298-303. Jamieson GA, Dwivedi P, Gruzelier JH. Imperial College London, UK. gjamieso@pobox.une.edu.au

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Cognitive behavioral therapy versus paroxetine in the treatment of hypochondriasis

Posted At : March 25, 2010 12:15 PM | Posted By : Tim Brunson, PhD
Related Categories: Cognitive Behavioral Therapy

BACKGROUND: The present maintenance study investigated whether the reduction in hypochondriacal complaints after initial treatment with CBT or paroxetine sustained during a follow-up period and whether psychiatric severity at pretest predicted the course of hypochondriacal symptoms. METHOD: A naturalistic follow-up period of 18 months after a 16-week RCT consisting of 33 patients initially allocated to a CBT condition and 29 patients to a paroxetine condition. The main outcome measure was the Whiteley Index. RESULTS: The initial treatment effect of CBT and paroxetine sustained during the follow-up period. No significant differences between CBT and paroxetine were found. Treatment course could not be predicted by psychiatric comorbidity. CONCLUSION: CBT and paroxetine are both effective treatments for hypochondriasis in the long term.

J Behav Ther Exp Psychiatry. 2009 Sep;40(3):487-96. Epub 2009 Jun 28. Greeven A, van Balkom AJ, van der Leeden R, Merkelbach JW, van den Heuvel OA, Spinhoven P. Faculty of Social Sciences, Department of Clinical, Health and Neuropsychology, Leiden University, Leiden, The Netherlands. greeven@fsw.leidenuniv.nl

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Oxidative Metabolism and Disease

Posted At : March 25, 2010 12:06 AM | Posted By : Tim Brunson, PhD
Related Categories: General

by Derrick Lonsdale, MD

The present concept involving disease is to "make a diagnosis". The specific disease is then named in much the same way as we might use in collecting alpine flowers or stamps. It is recognized by a constellation of symptoms and signs and the "proof" is believed to come from the laboratory. If there is overlap between several diseases we go about making a "differential diagnosis", perhaps the best example being collagen diseases. The only trouble with this is that Mother Nature does not understand our classification and did not construct the model by which we diagnose. This is not the only error in our thinking. With the exception of antibiotics designed to "kill the enemy", we try to find a "cure" for each and every disease as it is described. We now have a fantastic array of potentially poisonous substances that are so numerous that they have to be catalogued in the Physicians Desk Reference, a tome that almost exceeds the dimensions of a volume of Encyclopedia Brittanica. Even with the acknowledged concept of antibiotics we have come to recognize their limitations and dangers. Louis Pasteur, on his death bed, said "I was wrong: it is the terrain that matters". He had recognized that the body could only exist in a hostile environment by initiating a defensive strategy that is an innate part of our evolution. So is an entirely new model required? Should we be content with merely treating symptoms?

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