Background Classically, patients with unilateral lateral medullary infarction exhibit sensory abnormalities over the ipsilateral face and contralateral hemibody. As a variant, bilateral or contralateral facial sensory changes can be seen. However, sensory changes in the ipsilateral extremities are extremely rare.
Case Descriptions We describe three patients with lateral medullary syndrome in whom impaired deep sensation in the ipsilateral limbs was found. MRI results showed that the infarcts were located superficially in the lateral (case 1) and dorsal (cases 2 and 3) areas of the lower medulla, which probably involved the ascending or crossing dorsal column sensory tracts.
Conclusions Although rare, impaired ipsilateral deep sensation is encountered in patients with lateral medullary infarction syndrome.
The classic sensory signs of lateral medullary syndrome (LMS) include the loss of spinothalamic sensation in the ipsilateral face and contralateral hemibody and extremities. The variants of sensory abnormalities include contralateral or bilateral facial sensory changes,1 2 3 partial involvement of the face,1 3 or changes in the sensory level of the trunk.4 However, sensory changes in the ipsilateral extremities have not been described even in the large series of patients with LMS.1 2 3 5 6 7 In this report we describe three patients presenting with sensory changes in the ipsilateral extremities.
A 64-year-old hypertensive, diabetic man with a previous history of myocardial infarction experienced sudden dizziness and headache while walking. On admission the only positive neurological findings were decreased temperature and pain sense below the left T4 level, more marked over the lower part of the leg, and mild gait ataxia. The neurological features were stationary until 4 days later when he experienced a sensation of weakness in the right limbs. Neurological examination at this time revealed a right Horner sign and decreased pinprick sense over the right face. Pinprick and temperature sensations were decreased over the left extremities and left half of his body. In addition, position sensation was decreased in the right fingers and toes, and vibration sense was impaired over the right extremities and the right half of his body. The patient exhibited marked ataxia and mild weakness in the right limbs and was unable to stand because of severe ataxia. Brain MRI showed an infarct involving the right lateral part of the lower medulla and the cerebellum (Fig 1⇓). MR angiography showed diffuse stenosis of the proximal portion of the left vertebral artery.
A 30-year-old woman experienced sudden left frontal headache, which was followed by dizziness, nausea, ataxia, and a tingling sensation over the left half of her body. She had a history of preeclampsia 3 years before the event. Since then she had intermittently taken antihypertensive medication. On admission her blood pressure was 180/100 mm Hg. Neurological examination revealed a left Horner sign. She was not dysarthric, and the motor strength of all limbs was normal. Her left limbs were ataxic. The patient showed mildly decreased pinprick sense over the right half of her body. However, she complained of paresthesia over the left arm, trunk, and leg, which was most marked over the left fingertips. Vibration and position sensations were decreased in the left hand and fingertips. Facial sensation was normal except for slight dysesthesia over the left perioral and periorbital areas. Brain MRI showed an infarct involving the superficial posterior part of the left lower medulla (Fig 2⇓, top panel) and middle medulla (Fig 2⇓, bottom panel). An angiogram showed nonvisualization of a portion of the left vertebral artery at the C1 level and retrograde flow of the distal vertebral artery from the right vertebrobasilar system. During hospitalization her neurological symptoms gradually improved.
A 59-year-old hypertensive male smoker experienced acute vertigo and gait ataxia. On admission his blood pressure was 180/110 mm Hg. Examination showed the presence of bilateral gaze-dependent nystagmus, left Horner sign, mild left facial paresis, and left-sided ataxia. Sensory examination showed decreased pinprick sense over the right face, more marked in the perioral area, and the distal part of the right arm. In addition, he had paresthesia over the left palm and fingertips. Pinprick and vibration sensations were diminished in the left fingers. Brain MRI showed an infarct involving the posterolateral part of the left lower medulla and the cerebellum (Fig 3⇓). An angiogram showed atherosclerotic occlusion of the left proximal vertebral artery. The results of a nerve conduction study were normal in all extremities. The sensory symptoms in the left fingertips resolved in 3 days, and those over the right lower face and arm disappeared in approximately 10 days.
These three patients with medullary lesions had symptoms consistent with LMS. The infarction was caused by atherosclerotic occlusion (cases 1 and 3) or probable dissection (case 2) of the vertebral artery.
Bilateral facial sensory symptoms caused by unilateral lateral medullary infarction have been well documented; they probably result from an involvement of the ascending as well as descending trigeminal fibers due to relatively wide lesions.1 3 Ipsilateral dysfunction of deep sensation in the extremities can be caused by medial medullary lesions located below the pyramidal decussation.8 However, sensory symptoms over the ipsilateral body and extremities were rarely reported in patients with LMS. We are aware of only one report describing a patient presenting with ipsilateral loss of deep sensation in addition to common manifestations of LMS.9 In this case, the responsible lesion was suspected to involve both the lower medulla and the upper cervical cord.
In our patients the medullary lesions involved the lateral or posterolateral part of the lower medulla near the cervicomedullary junction. Therefore, the lesions seem to have affected the ascending sensory fibers of the fasciculus gracilis and cuneatus or their crossing fibers into the medial lemniscus.10 The ipsilateral motor weakness of patient 1 suggests that the lesion involved the area at or below the pyramidal decussation, ie, the upper cervical cord. Therefore, the lesion of patient 1 and possibly those of the other two patients may have extended beyond the boundary of the lateral medulla, and one might argue against applying the term LMS to these cases. Indeed, in one pathological study of a patient presenting with LMS and ipsilateral hemiparesis, lesions extending to the decussated pyramidal fibers were found at the junction of the medulla and the spinal cord.11 Nevertheless, our patients’ clinical symptoms in general are otherwise consistent with LMS, and it has been shown that the clinical and anatomic spectra of LMS are diverse.3 12 Furthermore, the MRI-documented lesions of our patients were generally confined to the posterolateral territories supplied by either the vertebral or posterior inferior cerebellar artery.13 Therefore, we would like to regard these cases as an unusual variant of LMS, which could be attributed to a considerable degree of variation on the distribution and collateral circulation of vessels supplying the lower brain stem.13 14
Finally, the interesting early sensory sign of patient 1, ie, the sensory level at the trunk, suggests that the lesion initially involved only the superficial lateral portion of the spinothalamic tract where the fibers carrying sensation from the lower part of the body are somatotopically located.4
In summary, our three patients illustrate that sensory symptoms and signs ipsilateral to the lesion can be seen in patients with LMS. Understanding of this variant would broaden our knowledge of the clinicoanatomic spectrum of LMS.
- Received April 28, 1995.
- Revision received June 19, 1995.
- Accepted July 12, 1995.
- Copyright © 1995 by American Heart Association
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