Mechanisms and predictors of chronic facial pain in lateral medullary infarction

The purpose of this study was to identify clinical predictors and anatomica l structures involved in patients with pain after dorsolateral medullary in farction. Eight out of 12 patients (67%) developed poststroke pain within 1 2 days to 24 months after infarction. The pain occurred in the ipsilateral face (6 patients) and/or the contralateral limbs and trunk (5 patients, 3 o f whom also had facial pain). Ipsilateral facial pain was significantly cor related with lower medullary lesions, including those of the spinal trigemi nal tract and/or nucleus, as documented by magnetic resonance imaging. The R2 blink reflex component was abnormal only in patients with facial pain. L ikewise, pain and temperature sensation in the ipsilateral face was decreas ed in all patients with facial pain but not in patients without pain. Ipsil ateral touch sensation in the face was also decreased in all patients with facial pain, but the lesions revealed on magnetic resonance imaging did not involve the principal sensory nucleus of the fifth cranial nerve, and the R1 blink reflex latencies were normal. Although facial pain was correlated with lesions of the spinal trigeminal tract and/or nucleus, none of the les ions involved the subnucleus caudalis, which contains most nociceptive neur ons. These findings suggest that facial pain after medullary infarction is due to lesions of the lower spinal trigeminal tract (axons of primary affer ent neurons), leading to deafferentation of spinal trigeminal nucleus neuro ns.