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Michael E. Carey, Francis C. Nance, Homer D. Kirgis, Harold F. Young, Lloyd C. Megison Jr., and David G. Kline

W e have observed six instances of pancreatitis following spinal cord injury in otherwise healthy individuals and have been unable to find any prior reports of this sequela of spinal cord trauma. The following cases are presented to alert clinicians to this complication and to emphasize the fact that spinal injury may occasionally result in mild pancreatic dysfunction manifested by fever and elevated serum amylase. Rarely, a fulminating, fatal, hemorrhagic pancreatitis may ensue. Case Reports Case 1 This infantryman was rendered quadriplegic when

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Lawrence F. Marshall, Sharen Knowlton, Steven R. Garfin, Melville R. Klauber, Howard M. Eisenberg, Dennis Kopaniky, Michael E. Miner, Kamran Tabbador, and Guy L. Clifton

I n spite of major advances in prehospital emergency medical services and in regional trauma care, the outcome from spinal cord injury appears to be little changed in recent series. Given the fact that at present we can have only a limited effect on neurological function in spinal cord-injured patients, it becomes especially important to identify factors that are responsible for further neurological deterioration in these cases. Surprisingly, this subject has been infrequently studied. Frankel, et al. , 5 reported a 2% incidence of deterioration in their

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The pathophysiological response to spinal cord injury

The current status of related research

Jewell L. Osterholm

T his is not a standard review of spinal cord management. Rather, we have tried to discuss the successes, failures, and conflicts in current research on the mechanism and treatment of spinal cord injury. The number of sound and provocative reports reflects the momentum of this rapidly expanding field of research. Historical Background of Research The contemporary chapter of acute spinal cord injury research and treatment actually begins in 1908, for it was then that Allen reported the first comprehensive clinicopathological study of human spinal cord

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George E. Locke, David Yashon, Robert A. Feldman, and William E. Hunt

S peculation in previous studies as to the effect of in vivo experimental spinal cord injury implicated ischemia as a factor contributing to the pathological process, 1, 2 and impairment of the spinal blood flow following injury has been observed using fluorescent dye techniques. 12 Spinal cord tissue lactic acid has been found to accumulate following circulatory arrest in primate studies, 6 presumably due to circulatory deprivation with resultant inadequate tissue perfusion and oxygenation. It is the purpose of this study to determine lactate levels in

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James Xie and Maxwell Boakye

the materials or methods used in this study or the findings specified in this paper. References 1 Aranyi Z , Mathis J , Hess CW , : Task-dependent facilitation of motor evoked potentials during dynamic and steady muscle contractions . Muscle Nerve 21 : 1309 – 1316 , 1998 2 Cariga P , Catley M , Mathias CJ , : Organisation of the sympathetic skin response in spinal cord injury . J Neurol Neurosurg Psychiatry 72 : 356 – 360 , 2002 3 Curt A , Dietz V : Ambulatory capacity in spinal cord injury: significance of somatosensory

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Late recovery following spinal cord injury

Case report and review of the literature

John W. McDonald, Daniel Becker, Cristina L. Sadowsky, John A. Jane Sr., Thomas E. Conturo, and Linda M. Schultz

function of up to 20% (20/100). Voluntary control of the external anal sphincter is possible (S4–5). The conversion of the patient's condition to ASIA Grade C thus occurred in July 2001. Motor recovery was first evident in the left fingers, then the right hand, and then the legs. Movement is now possible for most muscles of the upper arms but for fewer muscles in the legs. Most muscles in the legs are not yet able to oppose gravity. The following comparison puts this motor recovery into perspective. The National Acute Spinal Cord Injury Study II and III trials

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Masahiro Morita, Akira Miyauchi, Shinya Okuda, Takenori Oda, Tomio Yamamoto, and Motoki Iwasaki

CF , Spjut HJ : Neuropathic spinal arthropathy after spinal cord injury . Spine 17 : 964 – 971 , 1992 9 Harrison MJ , Sacher M , Rosenblum BR , Rothman AS : Spinal Charcot arthropathy . Neurosurgery 29 : 273 – 277 , 1991 10 Hoppenfeld S , Gross M , Giangarra C : Nonoperative treatment of neuropathic spinal arthropathy . Spine 15 : 54 – 56 , 1990 11 Kalen V , Isono SS , Cho CS , Perkash I : Charcot arthropathy of the spine in long-standing paraplegia . Spine 12 : 42 – 47 , 1987 12 Kapila A , Lines M

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James V. Gainer Jr.

A number of investigators in recent years have demonstrated that the sequential pathological changes following spinal cord injury involve alterations of vascular dynamics and progressive ischemia. 3, 8, 9 The edema and necrosis that follow have been felt to be secondary changes resulting from ischemia. Experimentally, certain modalities of therapy that provide a relative increase in available oxygen have been shown to be of benefit. Hyperbaric oxygenation was studied by Kelly, et al. , 7 and shown to be beneficial. Hypothermia by means of localized spinal

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Joseph M. Piepmeier and N. Ross Jenkins

T he majority of reports concerning neurological recovery following traumatic spinal cord injury have compared the patients' status at the time of injury to their status at discharge from the hospital, after rehabilitation, or at 1 year following injury. 1–3, 5–7, 9, 11, 12 Reports of changes in patients' neurological status after the 1st year are limited to small groups of selected patients. Since these patients require continued medical attention to monitor neurological function and to treat the complications of their spinal cord injury, a group of spinal

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James S. Harrop, Ashwini D. Sharan, and Gregory J. Przybylski

This work was supported in part by the Regional Spinal Cord Injury Center of Delaware Valley Model SCI System Grant No. H133N00027 to Thomas Jefferson University Hospital from the National Institute for Disability Research and Rehabilitation.