Allodynia after lateral-medullary (Wallenberg) infarct. A PET study

Abstract

We used PET to study regional cerebral blood flow (rCBF) changes in nine patients with unilateral central pain after a lateral medullary infarct (Wallenberg's syndrome). All patients presented, on the abnormal side, a combination of hypaesthesia to noxious and thermal stimuli and allodynia to rubbing of the skin with a cold object (i.e. abnormal pain to innocuous stimulation). The rCBF responses during allodynia were compared with those obtained during stimulation of the normal side using (i) a cold non-noxious stimulus identical to that applied to the painful side, and (ii) an electrical high-frequency stimulus at painful ranges. Statistical analysis disclosed two abnormal patterns of rCBF change during allodynia. First, there is a quantitative change whereby the blood flow response was out of proportion with the actual intensity of the stimulus, i.e. the pattern of activation by innocuous rubbing of the skin was in our patients identical to that previously reported in response to painful stimuli in normal subjects. This pattern concerned primarily the contralateral thalamus in its lateral half and the primary and somatosensory areas, as well as inferior parietal [Brodmann area (BA) 39/40], anterior insular (BA 6) and medial prefrontal (BA 10) cortices. Thalamic over-activity may reflect abnormal transduction and amplification of sensory inputs after spinothalamic deafferentation. This might be responsible for both increased rCBF in multiple cortical targets and the perceived shift of stimulus intensity from innocuous to painful ranges. The second abnormality associated with allodynic sensation was qualitative. It concerned exclusively the contralateral cingulate gyrus, which did not exhibit the usual pain-related rCBF increase reported in normal subjects. This abnormal cingulate response may account for the peculiar response of lateral medullary infarct patients to allodynic pain, which is not simply perceived as an exaggerated pain sensation, but as a new, strange and extremely unpleasant feeling, not previously experienced by the patients.

Cognitive interference is associated with neuronal marker N-acetyl aspartate in the anterior cingulate cortex: an in vivo 1H-MRS study of the Stroop Color-Word task

“…22,[63][64][65][66] Thus, it seems that the ACC does not play a specific role in cognitive interference, but rather is engaged in more general non-specific attentional states that are involved in the execution of the Stroop task (contributing to multiple cognitive functions during the Stroop performance, which become impossible without engagement of divided attention, errors detection, interference conflict, inhibition, affect). Our analysis of connectivity pattern in high vs low interference states suggests involvement of the prefrontal cortex as well, which is not surprising since this area has extensive reciprocal connections with ACC.…”

Lesions Limited to the Human Thalamic Principal Somatosensory Nucleus (Ventral Caudal) Are Associated with Loss of Cold Sensations and Central Pain

“…3, patient 3). The fourth and sixth columns lists the activations related to stimulation of the unaffected and affected side of patients with CPSP secondary to the Wallenberg syndrome (lateral medullary infarct) in response to the cold/mechanical stimulus described in Results (Peyron et al, 1998). BG, Basal ganglia; IFG, inferior frontal gyrus; insula/RI, insula/retroinsula; MFG, middle frontal gyrus; MTL, medial temporal lobe; OC, occipital cortex; PFC, prefrontal cortex; PMC, premotor cortex; SM, sensorimotor cortex; SPL, superior parietal cortex; NA, not available; lat, lateral.…”

“…The largest PET study of CPSP-induced allodynia involved patients with a lateral medullary stroke (Wallenberg syndrome) (Peyron et al, 1998). The allodynic test stimulus was a cold/ mechanical stimulus described as "a cold non-noxious stimulus (ice in a flat plastic container).…”

Pain and functional imaging

“…In patients with ongoing pain a provocation of mechanical allodynia (`pain on pain') did not provoke an ACC activation, a ¢nding that was interpreted as a di¡erent role of the ACC in chronic pain states (Peyron et al 1998). An alternative explanation, given the presence of the spontaneous pain in the group of patients studied, would be that the variability in the ACC activity would be expected to be high thereby explaining the absence of signi¢cant di¡erence between states.…”