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Thanks to von Heinemann et al for reporting this brainstem stroke as a reminder of a grave complication of brainstem lesions, and that is cardiac arrest.
The writer of this case report has mentioned lateral medullary syndrome of Wallenberg after providing us with abbreviated neurological findings, and he has linked his observation with this type of brainstem stroke. The given brain imaging fi...
The writer of this case report has mentioned lateral medullary syndrome of Wallenberg after providing us with abbreviated neurological findings, and he has linked his observation with this type of brainstem stroke. The given brain imaging findings are compatible with Wallenberg’s
syndrome of a wedge-shaped infracted area in the dorso-lateral medulla; however, the patient demonstrates many symptoms and signs that strongly question the “classical” Wallenberg syndrome:
1. One of the features that strongly stand against Wallenberg is the presence of limb weakness.
The motor system (pyramids) is typically spared with lateral medullary lesions because the corresponding anatomic structure is located in the medial medulla. Therefore, hemiplegia in this patient would reflect
anterior/medial medullary damage (as part of Dejerine’s anterior bulbar syndrome). However, “ipsilateral” hemiplegia is a very rare, yet well document feature of lateral medullary lesions. This ipsilateral hemiparesis is thought to result from the involvement of the lower most
caudal end of the medulla just below the pyramidal decussation (1). This ipsilateral spastic hemiplegia that has been linked to Wallenberg syndrome is also known as the submedullary syndrome of Opalski (2). “Clumsiness” of
the ipsilateral upper limb may also result from extension of the injury into the subolivary area (3); a very rare but a well-characterized feature of Wallenberg syndrome.
2. Lateral lesions located in the “rostral” medulla are associated with more severe dysphagia, hoarseness and the presence of facial paresis. Some patients with Wallenberg syndrome display ipsilateral facial palsy presumably due to the involvement of an aberrant corticobulbar tract, or
extension of the infarct to the pons with compromise of the facial nerve nucleus or fascicles; emotional-facial paresis related to involvement of looping medullary corticofacial projections in the upper medulla (4, 5).
Therefore, the presence of “facial paresis” in this patient would be an atypical sign.
3. The classical ipsilateral facial hypalgesia and thermoanesthesia and the contralateral trunk and extremity hypalgesia and thermoanesthesia are not seen in this patient; rather, the patient displays a constellation
of sensory deficits that are not reflecting the classical Wallenberg’s syndrome. However, Matsumoto described several patients with a continuous hemisensory defect of the face, arm, and trunk (unilateral pattern), with the lower border demarcated at a sensory level. These patients were thought to have mediolateral medullary and pontine lesions contralateral to the side of the sensory defect, which affected the medial cervical and thoracic afferents of the lateral spinothalamic tract (i.e., spared the lateral sacral and lumbar afferents) and the ventral trigeminothalamic tract (accounting for contralateral facial sensory loss), but spared the spinal nucleus and tract of the trigeminal nerve (6).
It is true that “classic” or “typical” brainstem stroke syndromes are rarely encountered in clinical practice; most patients present with a constellation of signs and symptoms, which either overlap with many “adjacent” syndromes or form an incomplete syndrome, however.
This patient’s overall clinical picture points to an ischemic damage to the lower brainstem, but it does not fit the “classical” Wallenberg syndrome; this case report does mention rare features of this syndrome that are not the reason behind writing this care report (7).
Does this patient have total unilateral medullary syndrome (8, 9) on clinical basis? I would suggest linking these recurrent cardiac arrest events with “medullary” infarction, and not specifically to Wallenberg syndrome, as the damaged lower brainstem per se might result in a variety of autonomic dysfunctions (10); profound bradycardia may be seen with subsequent cardiac arrest(11).
Osama SM Amin
1. Dhamon SK, Ikbal J, Collins GH. Ipsilateral hemiplegia and the Wallenberg syndrome. Arch Neurol 1984;41:179-180.
2. Montaner J, Alvarez-Sabin J. Opalski syndrome. J Neurol Neurosurg Psychiatry 1999;67:688-689.
3. Brochier T, Ceccaldi M, Milandre L, et al. Dorsolateral infarction of the lower medulla: clinical MRI study. Neurology 1999;52:190-193.
4 . Kim JS, Lee JH, Suh DC, et al. Spectrum of lateral medullary syndrome. Correlation between clinical findings and magnetic resonance imaging in 33 subjects. Stroke 1994;25:1405-1410.
5. Cerrato P, Imperiale D, Berguy M, et al. Emotional facial paresis in a patient with a lateral medullary infarction. Neurology 2003;60:723-724.
6. Matsumoto S, Okuda B, Imai T, et al. A sensory level on the trunk in lower lateral brainstem lesions. Neurology 1988;38:1515.
7. Brazis PW, Masdeu JC, Biller J. Localization in clinical
neurology, 5th edition. Philadelphia: Lippincott Williams & Wilkins; 2007.
8. Goetz CG, Rapper EJ. Textbook of clinical neurology. Philadelphia:WB Saunders; 1999.
9. Ropper AH, Samuel M (eds.). Adams and Victor Principles of Neurology, 9th edition. New York: McGraw-Hill Professional; 2009.
10. Lassman AB, Mayer SA. Paroxysmal apnea and vasomotor instability following medullary infarction. Arch Neurol 2005;62(8):1286-1288.
11. Benarroch EE. The central autonomic network: functional
organization, dysfunction, and perspective. Myo Clin Proc 1993: 68;988-1001.