The disturbance of circulation in traumatic paraplegia in acute and late stages: A pathological study

Wolman, Lionel

doi:10.1038/sc.1964.39

Cited by 68 publications

(29 citation statements)

References 16 publications

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“…5,6 This describes in essential detail the neuropathology of human SCI. Those who wish to read further are referred to Hughes (1978) 1 and Wolman (1965), 10 who have produced excellent monographs on the neuropathology of human SCI in earlier times. More information can be derived from Tator 11,12 who provides a more recent account of the neuropathology of SCI and also draws attention to secondary or continuing damage after the event of injury.…”

Section: Clinicopathological Correlationmentioning

confidence: 99%

Neuropathology: the foundation for new treatments in spinal cord injury

2004

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The first step essential in the search for a cure of human spinal cord injury (SCI) is to appreciate the complexity of the disorder. In this regard, it is not only the loss of ambulation but the sensory and autonomic changes that are equally important in recovery. In addition, there are the serious social emotional psychological and lifestyle effects of SCI which should also be taken into account. It is also true that no two SCI lesions are alike as each is the result of a SCI unique to that individual. Clinically of utmost importance is the segmental level of injury and whether it is complete, incomplete or discomplete (loss of all neurological functions below the injury but with physiological or anatomical continuity of Central nervous system tracts across the lesion). We are not concerned here with primary and secondary prevention or methods designed to limit the severity of the lesion after the event, important as they are, but with the requirements for a cure. Clearly, the greater the number of nerve fibers that can be preserved in the acute stage, the better will be the end result. Our focus at present is on the end-stage lesion with the aim of showing that a cure for SCI will depend upon establishing functionally useful central axonal regeneration and reestablishing physiological reconnections. Existing experimental methods are based on stimulating axonal regeneration by neutralizing inhibitory factors, adding positive trophisms and creating a permissive environment. Better results are obtained by bridging the gap with grafts of peripheral nerves or transplants of Schwann cells and genetically engineered fibroblasts. Recently, the potential for stem cells to enhance this process has created great interest. This is because of the ability of pluripotential cells to differentiate into neural tissue. A cure based on the physiopathology of SCI requires pyramidal, extrapyramidal, sensory, cerebellar and autonomic pathways to be regenerated with their appropriate neurotransmitters restored and reflexes integrated physiologically and in synchrony. In human SCI, there is a very long distance anatomically for axonal regrowth to occur in order to reach their relevant nuclei. This is because of continuing Wallerian degeneration. It also presumes that the target neurons are intact and that there has been no transneuronal degeneration above or below the lesion. Alternatively, in place of regenerated long axons, a multisynaptic pathway may be constructed from stem cells that have developed into neurons. Whether such a pathway would restore useful neurological functions is unknown. At present, the transplant and grafting research teams are exploring these possibilities in experimental animals. Moderate success in gaining axonal regeneration has been reported; however, it must be appreciated that the human lesion differs considerably from that of the experimental animal. In order to be successful, the neuropathology and neurophysiology of human SCI must be taken into account. The purpose of this review is to place the req...

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Section: Clinicopathological Correlationmentioning

confidence: 99%

Neuropathology: the foundation for new treatments in spinal cord injury

2004

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“…The remaining 16 are listed in Table 1. 1,2,5,[11][12][13][14][15][16][17][18][19][20][21][22][23] The table shows the absence of PE in autopsy surveys, a very low prevalence of PE as a cause of death or even in survivors of SCI registered for continuing care, but a relatively high prevalence of PE in the records screened by electrocardiogram (ECG). Reasons for these discrepancies are discussed below.…”

Section: Pe Prevalence In Chronic Scimentioning

confidence: 99%

“…1,2 Since these autopsy surveys of nearly 50 years ago, a concept that the chronic SCI subject has developed some protection from PE has prevailed. However, two recent deaths from late PE in chronic SCI subjects at our hospital have led us to reexamine the question.…”

Section: Introductionmentioning

confidence: 99%

The prevalence of pulmonary embolism in chronically paralyzed subjects: a review of available evidence

Frisbie¹,

Sharma

2011

Spinal Cord

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Study design: Qualitative systematic review. Objectives: To examine the validity of the prevailing notion that pulmonary embolism (PE) is rare in the chronic spinal cord injury (SCI) population. Setting: USA. Methods: Review surveys of adult SCI subjects 42 months after injury in which PE has been looked for and its prevalence estimated. Results: A total of 16 surveys of chronic SCI subjects published between 1956 and 2009 offered data on PE prevalence. Two autopsy surveys, 178 subjects paralyzed 42 months, revealed no PE. Eleven surveys of the cause of death, 3193 subjects paralyzed 1-25 years, revealed PE in 2.1%. Two surveys of survivors of SCI, 5761 subjects paralyzed 1-25 years, revealed PE in 0.4%. Our survey of 112 subjects paralyzed 1-50 years before death, revealed PE in 21 (18.7%), based on autopsy, imaging, clinical and electrocardiographic evidence. In 7 (33%) of the 21 subjects with PE, pulmonary hypertension by transthoracic echocardiography was detected, indicating recurrent and/or unresolved PE. Conclusion: PE is not infrequent in the chronic SCI subject; but its presentation may be subclinical; and its apparent recurrence may lead to pulmonary hypertension.

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“…In spite of the relatively high prevalence of fatal pulmonary embolism in acute spinal cord injury (SCI), [1][2][3] fatal PE in the chronic SCI patient is seldom reported. [4][5][6] Recurrent PE in the chronic SCI patient, resulting in chronic and eventually fatal pulmonary hypertension, is rarer still.…”

Section: Introductionmentioning

confidence: 99%

Recurrent pulmonary embolism and pulmonary hypertension in chronic tetraplegia

Frisbie

Sharma

Brahma³

et al. 2005

Spinal Cord

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Study design: Case report. Objective: To describe an unusual case of progressive pulmonary hypertension due to recurrent pulmonary embolism in a chronically paralyzed spinal cord injury patient. Setting: Veterans Administration Hospital, West Roxbury, MA, USA. Subject: A 57-year-old man, tetraplegic, sensory incomplete and motor complete for 30 years due to a diving accident, complained of lightheadedness and shortness of breath intermittently for 7 years. Examination during the latest episode revealed anxiety, confusion, respirations 28 per min, blood pressure 80/60 mmHg, and arterial pH 7.41, P CO 2 28 mmHg, P O 2 95 mmHg on 2 l of oxygen. A chest film 2 weeks earlier had revealed a right-sided cutoff of pulmonary vasculature; the current film showed right-sided pleural effusion. Review of EKGs showed a trend of increasing right axis deviation with recovery and recurrences during the previous 9 years and a current incomplete right bundle branch block with clockwise rotation and inverted T waves in V1-4. Computerized tomography with contrast material revealed small pulmonary emboli, but only in retrospect. The patient died shortly after scanning. Autopsy: The pulmonary arteries were free of thromboemboli on gross examination but medium and small-sized arteries were constricted or obliterated with thrombotic material microscopically. The estimated ages of the thromboemboli ranged from days to years. The right ventricle was hypertrophied; the coronary arteries were patent. Conclusion: Recurrent pulmonary emboli resulted in chronic pulmonary hypertension and eventual death in a patient with chronic tetraplegia.Spinal Cord (2005) 43, 625-630.

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The disturbance of circulation in traumatic paraplegia in acute and late stages: A pathological study

Cited by 68 publications

References 16 publications

Neuropathology: the foundation for new treatments in spinal cord injury

Neuropathology: the foundation for new treatments in spinal cord injury

The prevalence of pulmonary embolism in chronically paralyzed subjects: a review of available evidence

Recurrent pulmonary embolism and pulmonary hypertension in chronic tetraplegia

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