OBJECTIVE A comparison between long-term sensory sequelae of lateral medullary infarction (LMI) and medial medullary infarction (MMI) has never been made. METHODS We studied 55 patients with medullary infarction (41 with LMI and 14 with MMI) who were followed up for >6 months. We examined and interviewed the patients with the use of a structured format regarding the most important complaints, functional disabilities, and the presence of sensory symptoms. The nature and the intensity of sensory symptoms were assessed with the modified McGill-Melzack Pain Questionnaire and the visual analog scale, respectively. RESULTS There were 43 men and 12 women, with an average age of 59 years. Mean follow-up period was 21 months. The sensory symptoms were the most important residual sequelae in LMI patients and the second most important in MMI patients. In LMI patients, the severity of residual sensory symptoms was significantly related to the initial severity of objective sensory deficits (P<0.05). Sensory symptoms were most often described by LMI patients as numbness (39%), burning (35%), and cold (22%) in the face, and cold (38%), numbness (29%), and burning (27%) in the body/limbs, whereas they were described as numbness (60%), squeezing (30%) and cold (10%), but never as burning, in their body/limbs by MMI patients. LMI patients significantly (P<0.05) more often cited a cold environment as an aggravating factor for the sensory symptoms than did the MMI patients without spinothalamic sensory impairment. The subjective sensory symptoms were frequently of a delayed onset (up to 6 months) in LMI patients, whereas they usually started immediately after the onset in MMI patients. CONCLUSIONS Our study shows that sensory symptoms are major sequelae in both LMI and MMI patients. However, the nature, the mode of onset, and aggravating factors are different between the 2 groups, which probably is related to a selective involvement of the spinothalamic tract by the former and the medial lemniscus by the latter. We suggest that the mechanisms for the central poststroke pain or paresthesia may differ according to the site of damages on the sensory tracts (spinothalamic tract versus medial lemniscal tract).