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Toward Imaging of Pain Medication
Lawrence D. Robbins, M.D., Assistant Professor of Neurology,
Rush Medical College, Chicago
with H. S. Leith, S. Ouyang , C. C. Leith
Posted: June 2009  
To be presented at the October 2009 meeting of the American Academy of Pain Management

Background:   aDTI is a new imaging method that detects neural activity in the white matter fiber tracts in the brain. It is widely accepted that diffusion tensor imaging is a white matter structural imaging tool. With certain adaptation, we expand its capabilities in functional brain imaging and in mapping baseline neural activity in brain white matter. aDTI is fundamentally different from fMRI that relies on blood flow as an indirect measure of brain activation. In contrast, aDTI determines axonal conduction of neural impulses by capturing changes in water diffusion through channel proteins, a phenomenon that accompanies the ion flux of the action potential. We utilize aDTI scans to examine baseline impulse traffic in brain white matter fiber tracts in CM and FM.

Objective:   To understand the association of brain baseline activity and chronic pain such as chronic migraine (CM) and Fibromyalgia (FM), using adapted diffusion tensor imaging (aDTI), a new noninvasive, in vivo functional white matter imaging method.

Methods:   We applied aDTI to study chronic pain in 10 patients with CM and 10 participants with FM. A time series was acquired from every subject in analogy to fMRI data acquisition with a 1.5T MRI system. Fractional diffusion anisotropy (FA) was derived from the diffusion tensor matrix. The statistical parametric mapping method (SPM) was used to perform group analyses on FA time series, in order to capture minute changes in FA.

Results:   FM patients had loci of reduced FA of statistical significance (p < .001) in white matter of the anterior cingulate cortex, orbitofrontal cortex, and brain stem. CM patients had loci of reduced FA of statistical significance (p < .001) in the internal capsule, brainstem, and white matter components of the central pain matrix. CM patients had additional loci in the uncinate fasciculus, splenium of the corpus callosum, cerebellar peduncle, and cerebellar white matter. The FA reduction was in the magnitude manifesting neural hyperactivity. It could not be explained using the term of "nonspecific white matter damage".

Conclusions:   Baseline neural hyperactivity is a common finding in CM and FM. This common baseline abnormality has evaded detection by all hemodynamic imaging techniques. In fact, all blood-flow based imaging techniques do not reveal the baseline state. They require stimulus induced or aggravated pain in imaging studies. It is the induced pain that, unfortunately, obscures the baseline anomaly. In contrast, aDTI is capable of localizing abnormal baseline brain activity in the pathways of nociception, and in the fiber tracts involved in affective pain processing in these patients. Any new medication or treatment that aims at restoring baseline normality may be the ultimate remedy for CM and FM. aDTI may be the first imaging modality to examine medication efficacy in new drug research and development.