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Pathologic reappraisal of wallenberg syndrome: a pathologic distribution study and analysis of literature.
Yonago Acta Medica 2014 March
BACKGROUND: Wallenberg syndrome was first reported by Adolf Wallenberg as arising due to the obstruction of the posterior inferior cerebellar artery (PICA), which caused an infarct in the lateral medulla oblongata (MO).
METHOD: This study was carried out on brain tissue from 2 patients with typical Wallenberg syndrome and 10 autopsy cases without central nervous system disturbances.
RESULTS: Patient 1 exhibited the 3 major neurological symptoms of right crossed sensory disturbance, right cerebellar ataxia and bulbar palsy. There was the pathological obstruction of the right vertebral artery (VA). Regarding the histopathlogical distribution, the infarct extended on the right side to the lateral spinothalamic tract, nucleus of the spinal tract of the trigeminal nerve, spinal tract of the trigeminal nerve, inferior cerebellar peduncle, spinocerebellar tract and nucleus ambiguous. Moreover, a clear infarct in the left lateral MO was pathologically identified, but pathological obstruction of the left PICA or left VA could not be found. The left cerebellar ataxia and bulbar palsy were observed among these 3 major symptoms. Patient 2 showed the 3 major symptoms of right crossed sensory disturbance, right cerebellar ataxia and bulbar palsy. A pathological luminal occlusion was identified in the right PICA. Regarding the histopathological lesion, the infarct disturbed on the right side the lateral spinothalamic tract, nucleus of the spinal tract of the trigeminal nerve, spinal tract of the trigeminal nerve, spinocerebellar tract, inferior cerebellar peduncle and nucleus ambiguus.
CONCLUSION: Based on our investigation of pathological lesions using our 2 autopsies, we suggest calling the cases that satisfy the following 3 criteria "definite pathologic Wallenberg syndrome": i) identifiable pathological obstruction of the PICA or VA; ii) infarction in the lateral MO based on PICA or VA obstruction; and iii) a 1-to-1 correspondence between clinical symptoms and neuropathological lesions.
METHOD: This study was carried out on brain tissue from 2 patients with typical Wallenberg syndrome and 10 autopsy cases without central nervous system disturbances.
RESULTS: Patient 1 exhibited the 3 major neurological symptoms of right crossed sensory disturbance, right cerebellar ataxia and bulbar palsy. There was the pathological obstruction of the right vertebral artery (VA). Regarding the histopathlogical distribution, the infarct extended on the right side to the lateral spinothalamic tract, nucleus of the spinal tract of the trigeminal nerve, spinal tract of the trigeminal nerve, inferior cerebellar peduncle, spinocerebellar tract and nucleus ambiguous. Moreover, a clear infarct in the left lateral MO was pathologically identified, but pathological obstruction of the left PICA or left VA could not be found. The left cerebellar ataxia and bulbar palsy were observed among these 3 major symptoms. Patient 2 showed the 3 major symptoms of right crossed sensory disturbance, right cerebellar ataxia and bulbar palsy. A pathological luminal occlusion was identified in the right PICA. Regarding the histopathological lesion, the infarct disturbed on the right side the lateral spinothalamic tract, nucleus of the spinal tract of the trigeminal nerve, spinal tract of the trigeminal nerve, spinocerebellar tract, inferior cerebellar peduncle and nucleus ambiguus.
CONCLUSION: Based on our investigation of pathological lesions using our 2 autopsies, we suggest calling the cases that satisfy the following 3 criteria "definite pathologic Wallenberg syndrome": i) identifiable pathological obstruction of the PICA or VA; ii) infarction in the lateral MO based on PICA or VA obstruction; and iii) a 1-to-1 correspondence between clinical symptoms and neuropathological lesions.
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