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Evelyne Emery, Philipp Aldana, Mary Bartlett Bunge, William Puckett, Anu Srinivasan, Robert W. Keane, John Bethea, and Allan D. O. Levi

Object. Apoptosis is a form of programmed cell death seen in a variety of developmental and disease states, including traumatic injuries. The main objective of this study was to determine whether apoptosis is observed after human spinal cord injury (SCI). The spatial and temporal expression of apoptotic cells as well as the nature of the cells involved in programmed cell death were also investigated.

Methods. The authors examined the spinal cords of 15 patients who died between 3 hours and 2 months after a traumatic SCI. Apoptotic cells were found at the edges of the lesion epicenter and in the adjacent white matter, particularly in the ascending tracts, by using histological (cresyl violet, hematoxylin and eosin) and nuclear staining (Hoechst 33342). The presence of apoptotic cells was supported by staining with the terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate nick-end labeling technique and confirmed by immunostaining for the processed form of caspase-3 (CPP-32), a member of the interleukin-1β-converting enzyme/Caenorhabditis elegans D 3 (ICE/CED-3) family of proteases that plays an essential role in programmed cell death. Apoptosis in this series of human SCIs was a prominent pathological finding in 14 of the 15 spinal cords examined when compared with five uninjured control spinal cords. To determine the type of cells undergoing apoptosis, the authors immunostained specimens with a variety of antibodies, including glial fibrillary acidic protein, 2′,3′-cyclic nucleotide 3′-phosphohydrolase (CNPase), and CD45/68. Oligodendrocytes stained with CNPase and a number of apoptotic nuclei colocalized with positive staining for this antibody.

Conclusions. These results support the hypothesis that apoptosis occurs in human SCIs and is accompanied by the activation of caspase-3 of the cysteine protease family. This mechanism of cell death contributes to the secondary injury processes seen after human SCI and may have important clinical implications for the further development of protease inhibitors to prevent programmed cell death.

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Marc P. Sindou, Eric Blondet, Evelyne Emery, and Patrick Mertens

Object. Most patients with preganglionic lesions after brachial plexus injuries suffer pain that is hard to control through medication or neuromodulation. Lesioning in the dorsal root entry zone (DREZ) is undeniably effective. Fifty-five patients who had undergone the so-called microsurgical DREZotomy (MDT) procedure were studied with the two following objectives: 1) to describe the anatomical lesions observed during MDT in correlation with sensory deficits and pain features; and 2) to analyze the results in the 44 patients who were followed for more than 1 year (mean 6 years).

Methods. The observed lesions were severe: 79.6% of ventral and 78.2% of dorsal roots from C5—T1 were impaired. Damage extended to all five roots in 42% of patients. Strong arachnoiditis was present in 38.2%, pseudomeningoceles in 31%, spinal cord distortion and/or atrophy in 49%, and abundant gliotic tissue and/or microcavitations within the dorsal horn at the avulsed segments in 36.4% of cases. Sensory deficit corresponded to the entire territory of the dorsal root lesions in 52% of patients, but was larger in 30% most certainly due to the associated extrarachidian lesions. At the last evaluation after MDT, 66% of patients showed excellent (total relief without medication) or good (total relief with medication) pain relief and 71% experienced an improvement in activity level.

Conclusions. Apart from other indications not addressed in this article, MDT can be performed to treat refractory pain due to brachial plexus avulsions. The long-term efficacy of this procedure strongly indicates that pain after brachial plexus avulsion originates from the deafferented (and gliotic) dorsal horn.

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Thomas Gaberel and Evelyne Emery