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A 49-year-old drunken man was involved in a motorbike crash. He presented with cervical spine injury and multiple limbs fracture. Neuro-imaging demonstrated disruption of the C5-6 anterior longitudinal ligament, herniation of C3-4 and C5-6 discs, and Th1 compression fracture. The neurological deficits improved after anterior cervical decompression, fusion and fixation. One week later, he suffered from fever and severe upper back pain, and he developed paraplegia subsequently. The following image study disclosed esophageal perforation at the level of Th1 and epidural abscess spreading from levels Th1 to Th5. After proper management and rehabilitation, he achieved good recovery one year later at follow-up. We report the unique case of Th1 fracture with esophageal perforation complicated with spinal epidural abscess. The possible mechanism and the controversy concerning therapy for esophageal perforation are discussed.

Lewy bodies (LBs) are hallmark lesions of degenerating neurons in the brains of patients with Parkinson's disease (PD) and dementia with Lewy bodies (DLB). Recently, a point mutation in the gene encoding the presynaptic alpha-synuclein protein was identified in some autosomal-dominantly inherited familial PD pedigrees, and light microscopic studies demonstrated alpha-synuclein immunoreactivity in LBs of sporadic PD and DLB. To characterize alpha-synuclein in LBs, we raised monoclonal antibodies (MAbs) to LBs purified from DLB brains and obtained a MAb specific for alpha-synuclein that intensely labeled LBs. Light and electron microscopic immunocytochemical studies performed with this MAb as well as other antibodies to alpha-and beta-synuclein showed that alpha-synuclein, but not beta-synuclein, is a component of LBs in sporadic PD and DLB. Western blot analyses of highly purified LBs from DLB brains showed that full-length as well as partially truncated and insoluble aggregates of alpha-synuclein are deposited in LBs. Thus, these data strongly implicate alpha-synuclein in the formation of LBs and the selective degeneration of neurons in sporadic PD and DLB.