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A sensory level on the trunk and sparing the face from vertebral artery dissection: how much more subtle can we get?
  1. THANH G PHAN,
  2. EELCO F M WIJDICKS
  1. Department of Neurology, Mayo Medical Center and Foundation, Rochester, MN, USA
  1. Dr E F M Wijdicks, Mayo Clinic, Department of Neurology (W8A), Correspondence to: E F M Wijdicks, MD, 200 First Street SW, Rochester, MN 55905, USA. Telephone 001 507 284 5443; fax 001 507 284 4795; email wijde{at}mayo.edu

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We read with interest the short report on sensory loss in lateral medullary infarction by Vuadens and Bogousslavsky.1 Unusual sensory variants include contralateral leg and lower trunk with ipsilateral lower face hypalgesia; or contralateral upper trunk, arm, and face hypalgesia; or contralateral hypalgesia with facial sparing; or hemibody sensory loss.1-3 We recently encountered a patient with sensory loss of the spinothalamic type involving only the contralateral leg and lower trunk from vertebral artery dissection. The sensory level in our patient with facial sparing differs from those in the literature; it suggests a thoracic hemicord lesion and is false localising.

A 44 year old, right handed man with no relevant history presented with sudden onset of vertigo and left eye pain. There was no history of trauma or neck manipulation. However, the patient had had a dental abscess involving the lower incisors requiring drainage 4 weeks previously. He has a 30 pack-year history of smoking. Vertigo developed while he was changing his car tyre. He noted that the vertigo was worse when he sat down and put his head between his knees. The vertigo lasted 15 minutes and was associated with profuse sweating in the upper half of his body. There was no nausea or vomiting. This recurred twice that day each time lasting 15 minutes.

Examination disclosed normal visual acuity and fundoscopy. There was scleral injection in the left eye. The left pupil was 4 mm compared with 5 mm on the right. Both reacted briskly to light. There was counterclockwise rotatory nystagmus in the primary position. The eye movements were normal. Corneal reflex was intact, as was sensation to the upper and lower face. The other cranial nerves were normal. The gag reflex was brisk. There was no cranial bruit. Tone, power, and reflexes were normal. The sensory examination was normal to all modalities. There was no upper limb ataxia. He tilted to the left on sitting and on standing he fell to the left. The next day he noted loss of pinprick and appreciation of temperature on the right leg and trunk with a sensory level at T9 with preservation of touch, vibration, and joint position sense in all limbs (figure).

(A) Drawing of sensory deficit; (B) MRI showing clot in the left vertebral artery and infarcts in the lateral medulla and cerebellum (arrows), (C) arrowhead pointing at the occlusion of the left vertebral artery.

Brain MRI showed a small infarct in the lateral medulla and left cerebellum in the distribution of the lateral branches of the left posterior inferior cerebellar artery.4 There was a crescent sign involving the left vertebral artery from the skull base to the basilar artery suggesting vertebral artery dissection (figure).

Four types of lateral medullary infarct are recognised: small midlateral infarct, inferolateral infarct, and a large inferodorsolateral and dorsolateral infarct. The topography of the lesion in our patient corresponds to inferolateral medullary infarct.3 The patients with inferolateral infarcts and midlateral infarcts in the literature were not recognised to have cerebellar infarct and magnetic resonance angiography in those patients was normal by contrast with our patient.3 The partial lesion of the lateral spinothalamic tract in our patient involved only the far lateral fibres containing sacral afferents leading to sparing of the arm and face. The spinal trigeminal nucleus and tract, which contain afferents for the face ipsilateral to the lesion, reside dorsolaterally and the crossed ventral trigeminothalamic tract, which contains afferents for the contralateral face, resides medial to the lateral spinothalamic tract. Lesion of the spinocerebellar tract involving only the sacral fibres explains the presence of severe gait ataxia but no upper limb ataxia.3 The counterclockwise rotatory nystagmus is likely due to imbalance of projections from the anterior and posterior semicircular canals and the otolith receptor.5

A sensory level to the trunk may point to a lateral brainstem lesion in the presence of other features suggesting brainstem disease. In our patient these signs were transient and sensory loss predominated. This new pattern of sensory loss should be recognised as symptomatic of lateral medullary infarction in addition to other sensory variants.1-3

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