Ipsilateral Pseudochoreoathetosis and Numbness Can Be a Sole Manifestation of Lateral Medullary Infarction

Dear Editor,The lateral medullary syndrome or Wallenberg syndrome is a well-recognized disorder to neurologists characterized by ataxia, vertigo, Horner's sign and dysphagia.However, sensory symptoms of lateral medullary lesions can vary widely 1,2 because the ascending and descending trigeminal nuclei, spinothalamic tract and dorsal column-medial lemniscus pathway are anatomically adjacent in the medulla.Pseudochoreoathetosis 3 is a choreoathetoid movement associated with proprioceptive loss and may occur anywhere from the cortex to peripheral nerves including medullary level.We report a case of dorsolateral medullary infarction (DLMI) presenting solely with pseudochoreathetosis and numbness.A 61-year-old woman with hypertension presented with numbness and "hard" sensation over her right posterior neck extending to her right upper arm over two days.The next day, the symptoms progressed to the right palm, followed by clumsiness and twisting of her fingers, which brought her to the emergency center.Neurologic examination found no bulbar symptoms such as dysarthria, dysphagia, or tongue deviation.Cranial exams and cerebellar ataxia test including finger to nose, heel to shin and gait showed no abnormality.She had no definite motor weakness.Thus, none of the typical features of lateral medullary syndrome were observed.Because the paresthesia was ipsilateral to the lesion and limited to the fingers, an additional cervical lesion was considered; however, spinal MRI was normal (Fig. 1A-D).Anti-aquaporin-4 and anti-MOG (myelin oligodendrocyte glycoprotein) antibodies were negative.Detailed sensory testing revealed impaired proprioception in all fingers except the thumb, with preserved pain and temperature sensation.She lacked graphesthesia and finger recognition and described her palm and posterior neck as feeling like rock or plaster.When attempting to extend her fingers, the index and ring fingers repeatedly hyperextended and adducted involuntarily, compatible with pseudochoreoathetosis.She struggled to perform sequential finger tapping, especially with eyes closed, and the abnormal movements intensified during finger adduction (Supplementary Video 1 in the online-only Data Supplement).Nerve conduction studies were normal, but the right median nerve somatosensory evoked potential showed cortical delay (Fig. 1E).She was treated with dual antiplatelet therapy (aspirin and clopidogrel).Two weeks later, her symptoms had largely resolved, and she regained full voluntary control of her fingers, with only minimal residual numbness in the neck and palm."Pseudochoreoathetosis, " first described by Sharp et al., 3 refers to choreoathetoid movements due to loss of position sense, likely resulting from the striatum's failure to integrate cortical sensory-motor inputs.The term "pseudo" reflects the absence of direct basal ganglia damage.In the caudal medulla, the cuneate and gracile nuclei decussate to form the medial lemniscus; before crossing, these tracts lie relatively lateral, so lateral medullary infarcts at this level can selectively disturb proprioception.