Brain Advance Access first published online on September 2, 2006
This version published online on September 23, 2006
Brain, doi:10.1093/brain/awl228
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1 Howard Florey Institute, University of Melbourne, Parkville, Victoria, Australia; Centre for Neuroscience, University of Melbourne, Parkville, Victoria, Australia; National Ageing Research Institute, Parkville, Victoria, Australia
* To whom correspondence should be addressed. People with Alzheimer's disease are administered fewer analgesics and report less clinical pain than cognitively intact peers with similar painful diseases or injuries, prompting speculation about the likely impact of neurodegeneration on central pain processing. The present study measured pain ratings and functional MRI (fMRI) brain responses following mechanical pressure simulation in 14 patients with Alzheimer's disease and 15 age-matched controls. Contrary to the prevailing hypothesis that this disease is likely to differentially reduce emotional responses to pain, we show that activity in both medial and lateral pain pathways is preserved. Moderate pain was evoked with similar stimuli in both groups, and was associated with a common network of pain-related activity incorporating cingulate, insula and somatosensory cortices. Between-group analyses showed no evidence of diminished pain-related activity in Alzheimer's disease patients compared with controls. In fact, compared with controls, patients showed greater amplitude and duration of pain-related activity in sensory, affective and cognitive processing regions consistent with sustained attention to the noxious stimulus. The results of this study show that pain perception and processing are not diminished in Alzheimer's disease, thereby raising concerns about the current inadequate treatment of pain in this highly dependent and vulnerable patient group.
Received March 24, 2006
Revised July 17, 2006
Accepted July 25, 2006
Article
Pain sensitivity and fMRI pain-related brain activity in Alzheimer's disease
Leonie J. Cole 1 *, Michael J. Farrell 1, Eugene P. Duff 2, J. Bruce Barber 3, Gary F. Egan 4, and Stephen J. Gibson 5
2 Howard Florey Institute, University of Melbourne, Parkville, Victoria, Australia; Department of Mathematics and Statistics, University of Melbourne, Parkville, Victoria, Australia
3 National Ageing Research Institute, Parkville, Victoria, Australia
4 Howard Florey Institute, University of Melbourne, Parkville, Victoria, Australia; Centre for Neuroscience, University of Melbourne, Parkville, Victoria, Australia
5 Department of Medicine, University of Melbourne, Parkville, Victoria, Australia; National Ageing Research Institute, Parkville, Victoria, Australia
Leonie J. Cole, E-mail: l.cole{at}hfi.unimelb.edu.au
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