ALLODYNIA AFTER LATERAL-MEDULLARY (WALLENBERG) INFARCT - A PET STUDY

Citation
R. Peyron et al., ALLODYNIA AFTER LATERAL-MEDULLARY (WALLENBERG) INFARCT - A PET STUDY, Brain, 121, 1998, pp. 345-356
Citations number
52
Categorie Soggetti
Neurosciences,"Clinical Neurology
Journal title
BrainACNP
ISSN journal
00068950
Volume
121
Year of publication
1998
Part
2
Pages
345 - 356
Database
ISI
SICI code
0006-8950(1998)121:<345:AAL(I->2.0.ZU;2-K
Abstract
We used PET to study regional cerebral blood flow (rCBF) changes in ni ne patients with unilateral central pain after a lateral medullary inf arct (Wallenberg's syndrome). All patients presented, on the abnormal sine, a combination of hypaesthesia to noxious and thermal stimuli and allodynia to rubbing of the skin with a cold object (i.e. abnormal pa in to innocuous stimulation). The rCBF responses during allodynia were compared with those obtained during stimulation of the normal side us ing (i) a cold non-noxious stimulus identical to that applied to the p ainful side, and (ii) an electrical high-frequency stimulus at painful ranges. Statistical analysis disclosed two abnormal patterns of rCBF changes during allodynia. First, there is a quantitative change whereb y the blood flow response was out of proportion with the actual intens ity of the stimulus, i.e. the pattern of activation by innocuous rubbi ng of the skin was in our patients identical to that previously report ed in response to painful stimuli in normal subjects. This pattern con cerned primarily the contralatertal thalamus in its lateral half and t he primary and somatosensory areas, as well as inferior parietal [Brod mann area (BA) 39/40], anterior insular (BA 6) and medial prefrontal ( BA IO) cortices. Thalamic overactivity may reflect abnormal transducti on and amplification of sensory inputs after spinothalamic deafferenta tion. This might be responsible for both increased rCBF in multiple co rtical targets and the perceived shift of stimulus intensity from inno cuous to painful ranges. The second abnormality associated with allody nic sensation was qualitative. It concerned exclusively the contralate ral cingulate gyrus, which did not exhibit the usual pain-related rCBF increase reported in normal subjects. This abnormal cingulate respons e may account for the peculiar response of lateral medullary infarct p atients to allodynic pain, which is not simply perceived as an exagger ated pain sensation, but as a new strange and extremely unpleasant fee ling, not previously experienced by the patients.