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and CFS Pain
have attempted to
identify abnormalities in brain structures that might contribute to the painful
symptoms of CFS. Their studies have focused on magnetic resonance imaging (MRI)
of brain structure and neuroimaging of regional cerebral blood flow (rCBF) in
brain structures that process or modulate pain.
The results of these studies are difficult to interpret
because they are characterized by great variation in research methods that can
influence the validity of research findings.31 Nevertheless, three of
four relatively well-designed studies have reported CFS patients, compared to
healthy controls, display a significantly greater number of white matter lesions
in the cortex of the brain.32-34 The relationship between these
lesions and pain in persons with CFS remains unclear.
of functional brain
Single photon emission computed tomography (SPECT), positron
emission tomography (PET) and functional MRI (fMRI) allow investigators to
measure activity in brain structures either during rest or during exposure to
stimuli that evoke acute pain.
All of the peer-reviewed neuroimaging studies performed to date with CFS
patients have examined brain activity during rest.35-38 Six
investigations have reported that CFS patients are characterized by low levels
of rCBF in numerous brain structures.
There is little
the specific brain structures that show low rCBF. Nevertheless, two
investigations found that CFS patients, relative to controls, show significantly
lower levels of rCBF in the brainstem.36,37 Low brainstem rCBF levels
may contribute to abnormal function of the locus
ceruleus-norepinephrine/autonomic nervous system in CFS patients. This
abnormality, in turn, may contribute to pain since the locus ceruleus is
involved in controlling descending pathways from the brain to the spinal cord
that inhibit pain.14
It should be noted, however, that Lewis
colleagues38 recently used SPECT imaging to compare brain rCBF in 22
identical twin pairs in which only one twin met criteria for CFS. There was no
difference in the number of brain rCBF abnormalities between twins with CFS and
those without the disorder. At present, then, it is not possible to state with
confidence whether a relatively large number of resting state abnormalities in
brain function are found in persons with CFS, or whether any abnormalities that
are found may contribute to persistent pain in persons with CFS.
Despite the inconsistent findings described
above, it may be possible to better understand the causes of painful symptoms in
CFS by measuring changes in brain rCBF that are produced by noxious stimulation
(e.g., pressure, heat, or cold) in persons with CFS and healthy individuals. We
recently completed brain SPECT imaging on nine patients with CFS who did not
meet criteria for FM and 25 healthy controls.39 Preliminary analyses
indicate that, despite the fact that all of the CFS patients reported
experiencing musculoskeletal pain, their pain thresholds for pressure
stimulation did not differ from those of the healthy controls.
However, the CFS patients tended to
different pattern of brain activation than the healthy controls when they were
exposed to a five-minute period of repetitive, painful, pressure stimulation.
That is, the controls showed the expected pattern of increased activity in brain
structures involved in processing the sensory and emotional dimensions of pain
located in the cerebral hemisphere opposite to the stimulation site (e.g.,
right-side stimulation evoked left brain activation). Interestingly, the CFS
patients tended to show activation in the same structures in both cerebral
hemispheres, despite the fact that there was no difference in the intensity of
pressure stimulation delivered to patients and controls. This suggests that the
pressure stimulation produced greater transmission of sensory input to the
brains of the patients with CFS.