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Hans L. Frankel

Researcher at Stoke Mandeville Hospital

Publications -  68
Citations -  6079

Hans L. Frankel is an academic researcher from Stoke Mandeville Hospital. The author has contributed to research in topics: Spinal cord injury & Paraplegia. The author has an hindex of 31, co-authored 68 publications receiving 5832 citations. Previous affiliations of Hans L. Frankel include Churchill Hospital.

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The value of postural reduction in the initial management of closed injuries of the spine with paraplegia and tetraplegia

TL;DR: The incidence of various types of fracture and fracture-dislocation and the degree of reduction achieved by postural reduction is analysed in relation to the initial and late neurological lesions.
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Mortality, morbidity, and psychosocial outcomes of persons spinal cord injured more than 20 years ago.

TL;DR: Declines with age were found in measures of handicap and life satisfaction, but three quarters of those interviewed reported generally good health and rated their current quality of life as either good or excellent.
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Long-term survival in spinal cord injury: a fifty year investigation

TL;DR: Examination of long-term survival in a population-based sample of spinal cord injury survivors in Great Britain showed that higher mortality risk was associated with higher neurologic level and completeness of spinal Cord injury, older age at injury and earlier year of injury.
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The value of intermittent catheterisation in the early management of traumatic paraplegia and tetraplegia.

TL;DR: The non-touch technique of intermittentCatheterisation has proved superior to any other form of early management of the paralysed bladder hitherto described and has disproved the prejudice held against intermittent catheterisation for so many years by urologists and other workers in the field of spinal paraplegia.
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Plasma catecholamines, plasma renin activity and plasma aldosterone in tetraplegic man, horizontal and tilted.

TL;DR: Findings indicate a failure of sympathetic activity in response to head-up tilt in the tetraplegic patients, probably caused by interruption of pathways by which the brain normally controls sympathetic outflow.