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A 58 year old man noticed an unsteady gait when he woke up. He was unable to keep standing and fell several times to the left. On the next day, he visited our clinic. He denied vertigo, diplopia, hiccup, dysphagia, speech disturbance, numbness, and muscle weakness. On admission, ocular movements were normal in all directions. Spontaneous or gaze evoked nystagmus was undetectable with or without Frenzel’s glasses. He had no skew deviation, ocular lateropulsion, saccadic pursuit, ocular dysmetria, or Horner’s syndrome. Elevation of the soft palate was intact on phonation. There was no nasal voice, hoarseness, or dysarthria. The tongue did not deviate on protrusion. Other cranial nerve functions were intact. He had no weakness. Coordination of the extremities was intact. He was unable to keep standing without assistance due to marked lateropulsion to the left. Deep tendon reflexes were normal. He had no pathological reflexes. Facial sensation was intact, and so were light touch and pinprick sense in the trunk and upper limbs. Position sense was intact in the lower limbs.
Magnetic resonance imaging (MRI) showed an acute infarct in the left lateral medulla (fig 1A) and a flow signal abnormality in the left VA. Magnetic resonance angiography (MRA) confirmed an occlusion of the left VA (fig 1B). The patient was treated with intravenous argatroban, a thrombin inhibitor. On day 5, he started to improve. However, he noticed that he was unable to differentiate between cold and warm water with his right lower leg and foot while bathing. Re-examination demonstrated thermal and pain sensory loss in his right lower leg and foot. Posturographic data demonstrated abnormal body sway from left forward to right backward. He was discharged on day 10 with only slight unsteadiness.
A 55 year old man noticed a strong tendency to fall to the right on attempting to stand or walk. A few days after the onset, he noticed that he was unable to perceive coldness in his left buttock and thigh while sitting on a toilet. He did not have headache, vertigo, hiccup, dysphagia, hoarseness, numbness, or weakness. He visited our clinic on day 6. He had no Horner’s syndrome, skew deviation, ocular lateropulsion, ophthalmoplegia, dysarthria, bulbar palsy, muscle weakness, or limb ataxia. He did not have spontaneous or gaze evoked nystagmus with or without Frenzel’s glasses. He fell to the right on attempts to stand with his eyes closed. Deep tendon reflexes were unremarkable and pathological reflexes were negative. Sensation for light touch and position was intact. Pain and thermal sense was impaired in his left buttock and lower limb. MRI failed to show lesions in the brainstem or cerebellum. MRA demonstrated an occlusion of the right VA. He was treated with 100 mg of aspirin. Over 4 weeks, axial lateropulsion subsided, while the sensory impairment persisted.
Isolated axial lateropulsion occurs with ischemic lesions in the inferior portion of the cerebellum and tonsil1 and with a demyelinating lesion of the superior and inferior cerebellar peduncles.2 Lee et al. reported a patient with lateral medullary infarction who showed a gaze evoked horizontal nystagmus as well as axial lateropulsion.3 Thus, the critical structure for lateropulsion remains to be elucidated.
The patients described here did have pain and thermal sensory impairment in the contralateral lower limb, which is attributed to a lesion in the ventrolateral part of the spinothalamic tract. A very small lesion located superficially in the lateral medulla causes an atypical spinothalamic sensory deficit, which in some cases appears a few days after the onset of other symptoms.4 In the present cases, however, it is likely that the pain and thermal sensory deficit was present initially but was not noticed. An occlusion of the VA may have caused ischaemia in the territory of the short circumferential medullary artery directly arising from the distal VA. Structures located dorsal to the spinothalamic tract, including the spinal trigeminal tract and nucleus, and the ambiguus and vestibular nuclei were probably spared, because these patients did not have facial sensory impairment, pharyngeal or laryngeal palsy, or nystagmus. Conversely, it is highly likely that the vestibulospinal tract was involved, because it is located just ventromedial to the spinothalamic tract in the medulla. The vestibulospinal tract is considered to play an important role in the maintenance of posture by exerting strong excitatory influences on extensor muscles and inhibitory influences on flexor muscles.5 Thus, interruption of the vestibulospinal tract decreases extensor muscle tone of the trunk and lower limb on the side of the lesion, which is likely to cause ipsilateral axial lateropulsion. The anterior spinocerebellar tract was likely to be involved, because it is located just dorsolateral to the spinothalamic tract in the medulla. It is possible that axial lateropulsion is associated with a lesion of the spinocerebellar tract. In the case reported by Bertholon et al,2 axial lateropulsion may have been caused by ipsilateral lesions of the anterior and posterior spinocerebellar tracts, which are incorporated in the superior and inferior cerebellar peduncles. Given that the vestibulospinal and spinocerebellar tracts have no projections to the ocular motor system, it is natural that these two patients did not have nystagmus or oculomotor disorders. The present findings raise the possibility that axial lateropulsion in the Wallenberg syndrome is attributable to lesions of the vestibulospinal and spinocerebellar tracts as well as central vestibular pathways.