Altered experimental pain perception after cerebellar infarction.

Animal studies have suggested that the cerebellum, in addition to its motor functions, also has a role in pain processing and modulation, possibly because of its extensive connections with the prefrontal cortex and with brainstem regions involved in descending pain control. Consistently, human imaging studies have shown cerebellar activation in response to painful stimulation. However, it is presently not clear whether cerebellar lesions affect pain perception in humans. In the present study, we used experimental pain testing to compare acute pain perception and endogenous pain inhibition in 30 patients 1 to 11 years after cerebellar infarction and in 30 sex- and age-matched healthy control subjects. Compared to controls, patients exhibited a significantly increased pain perception in response to acute heat stimuli (44 °C-48 °C, average pain intensity rating for patients 3.4±2.8 and for controls 1.5±1.7 [on a numeric rating scale of 0-10], P<.01) and to repeated 256 mN pinprick stimuli (1.3±1.9 vs. 0.6±1.0 [0-10], P<.05). Heat hyperalgesia in patients was more pronounced on the body side ipsilateral to the infarction. In addition, patients showed reduced offset analgesia (change in pain intensity rating: 0.0%±15.8% vs. -16.9%±36.3%, P<.05) and reduced placebo analgesia (change in pain intensity rating: -1.0±1.1 vs. -1.8±1.3 [0-10], P<.05) compared to controls. In contrast, heat and pressure pain thresholds were not significantly different between groups. These results show that, after cerebellar infarction, patients perceive heat and repeated mechanical stimuli as more painful than do healthy control subjects and have deficient activation of endogenous pain inhibitory mechanisms (offset and placebo analgesia). This suggests that the cerebellum has a previously underestimated role in human pain perception and modulation.