We report a patient with medial medullary
infarction who showed deep sensory impairment as his prominent
neurological manifestation. A 54-year-old man with a history of
hypertension was admitted to our hospital with
numbness of the bilateral upper and lower extremities, followed by
dysarthria and right
hemiparesis. Physical examination revealed no abnormalities except for
high blood pressure. He hiccuped continuously. On neurological examination, he exhibited
dysarthria, mild
dysphagia and right
hemiparesis without facial or lingual
paresis. Sensitivity to light touch and pinprick was normal, but sensitivity to vibration and joint position was severely decreased in the bilateral upper and lower extremities, predominantly in the lower extremities and on the right side in the upper extremities. He had been treated with antiedema agents and
thromboxane synthetase inhibitor. His
hiccups stopped within two weeks, and his right
hemiparesis gradually improved within one month. However, his deep sensory impairments remained prominent. Blood examinations disclosed positive
lupus anticoagulant. MRI showed bilateral
infarction at the medial portion of the upper medulla oblongata, extending to both pyramids, especially on the left. Somatosensory evoked potentials (SEP) after median nerve stimulation showed P14 and the later components with prolonged latency. No SEP were recorded after posterior tibial nerve stimulation. The latency of P14 was well correlated with the severity of deep sensory impairments in the upper extremities.
Neurological manifestations of our patient are not typical of medial medullary
infarction, and are informative about the functional anatomy of the deep sensory tract in the medulla oblongata. We discuss the relation of the intractable
hiccups to the bilateral medial medullary lesions, and emphasize the importance of
lupus anticoagulant as one of the risk factors in
brainstem infarction.