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PubMed2004

Arterial stiffness in persons with paraplegia.

BACKGROUND: Arterial stiffness recently has been identified as an independent risk factor for cardiovascular disease. An accurate and noninvasive estimate of arterial stiffness can be made through close examination of the pulse wave contour, and is expressed as the augmentation index (AI). Increased stiffness is associated with increased systolic blood pressure (SBP), pulse pressure, and reduced baroreceptor sensitivity. The purpose of this study was to compare the common carotid AI in participants with paraplegia vs able-bodied controls as well as compare group differences for blood pressure while supine and in response to gravitational stress. PARTICIPANTS: Study participants were 19 healthy individuals with paraplegia (below T6) and 9 able-bodied controls matched for age, height, and weight. METHODS: An electronic tilt table was used for testing responses to gravitational stress at 4 angles (-10 degrees, 10 degrees, 35 degrees, and 75 degrees). AI was assessed at each angle of tilt using an externally applied high-fidelity strain-gauge transducer placed over the right common carotid artery. RESULTS: AI was augmented in the group with paraplegia compared with the able-bodied group (8.0 +/- 3.9 vs 6.7 +/- 2.8, respectively; P < 0.05). Supine blood pressure and the SBP response to tilt did not differ between the groups, and there were no tilt-angle effects on SBP. CONCLUSION: In normotensive persons with paraplegia, AI was increased significantly compared with matched able-bodied controls, which may suggest the premature development of arterial disease in this population.

Adult↗
PubMed1998

A new locus for autosomal recessive hereditary spastic paraplegia maps to chromosome 16q24.3.

Hereditary spastic paraplegia is a genetically and phenotypically heterogeneous disorder. Both pure and complicated forms have been described, with autosomal dominant, autosomal recessive, and X-linked inheritance. Various loci (SPG1-SPG6) associated with this disorder have been mapped. Here, we report linkage analysis of a large consanguineous family affected with autosomal recessive spastic paraplegia with age at onset of 25-42 years. Linkage analysis of this family excluded all previously described spastic paraplegia loci. A genomewide linkage analysis showed evidence of linkage to chromosome 16q24.3, with markers D16S413 (maximum LOD score 3.37 at recombination fraction [theta] of .00) and D16S303 (maximum LOD score 3.74 at straight theta=.00). Multipoint analysis localized the disease gene in the most telomeric region, with a LOD score of 4.2. These data indicate the presence of a new locus linked to pure recessive spastic paraplegia, on chromosome 16q24.3, within a candidate region of 6 cM.

Adult↗
PubMed2004

Living with paraplegia: tensions and contradictions.

Although it is well established that paraplegia results in dramatic lifestyle changes, little is understood about living in the community with paraplegia, especially from the perspective of the person with paraplegia. To develop insight into this experience, in-depth, personal interviews were conducted with seven individuals with paraplegia who had been living back in the community for less than two years. Qualitative analysis of their transcribed interviews suggests that the transitional process revolved around their struggle to reposition themselves in a holististic way that reflects the injury while moving beyond it. Four interrelated challenges textured the experience: maintaining an identity beyond the medical; contending with the stigma of difference; addressing the invisible work of day-to-day living; and balancing independence and dependence. Implications for practice are discussed.

Adaptation, Psychological↗
PubMed1991

The influence of severity of spinal cord ischemia in the etiology of delayed-onset paraplegia.

To clarify the cause of delayed-onset paraplegia, the authors evaluated the neurologic outcome after temporary (10 to 30 minutes) spinal cord ischemia in the awake rabbit. Loss of motor function occurred in less than 2 minutes in all animals. Restoration of flow within 16 minutes always resulted in full return of function, whereas with occlusion times of greater than 27 minutes all animals remained paralyzed. After temporary occlusion of 20 to 21 minutes, however, 71% of animals returned to normal neurologic function but developed delayed-onset paraplegia 14 to 48 hours later. This appears to be a reliable method for the creation of a model of delayed-onset paraplegia in the awake animal, and will facilitate more detailed studies of the pathophysiology of ischemia-induced paraplegia.

Animals↗
PubMed1995

Thoracic paraplegia after lumbar spinal surgery.

Two cases of thoracic level paraplegia after lumbar spinal surgery were retrospectively reviewed after 1 year of follow-up. Charts and perioperative records were reviewed in an effort to determine the possible etiology of this rare and devastating complication. We were unable to find any reports in the English-language literature regarding thoracic-level paraplegia in an isolated lumbar procedure (in the absence of preexisting structural instability or thoracic level lesion). We found 23 reported cases of acute spontaneous paraplegia or quadriplegia from fibrocartilaginous (disk) emboli to the spinal cord. This was a retrospective review specifically seeking possible predisposing conditions, intra- or postoperative hypotension, or technical errors that might have led to the complication of paraplegia. No preoperative thoracic level intracanal lesions were identified. There were no episodes of profound hypotension noted perioperatively. The specific pattern of paralysis found in these two patients did not correlate with the level of the surgery performed. Both patients had findings consistent with cord edema and spinal cord infarct in the thoracic region. We believe that these two cases represent acute spinal cord infarcts in the "watershed" region of the thoracic cord, the exact cause of which could not be determined. A theory of an embolic phenomenon is proposed as a possible etiology.

Adult↗
PubMed2004

Spinal cord repair with acidic fibroblast growth factor as a treatment for a patient with chronic paraplegia.

STUDY DESIGN: We present a case of a patient with chronic paraplegia with a complete spinal cord gap resulting from a stabbing injury 4 years ago recovering after an innovative surgical strategy. OBJECTIVES: To demonstrate the clinical outcome of surgical repair with sural nerve graft with fibrin glue containing acidic fibroblast growth factor in a patient with chronic spinal cord injury. SUMMARY OF BACKGROUND DATA: Spinal cord injury usually causes permanent disability, and there had been not effective surgical technique to obtain satisfactory functional motor recovery, particularly in chronic patients. Previous studies have revealed that acidic fibroblast growth factor could promote axonal regeneration and reduce neuronal death in adult rats with spinal cord injury. METHODS: The spinal cord gap at T11 level was bridged with 4 sural nerve grafts that redirected specific pathways from white to gray matter. The grafted area was stabilized with fibrin glue containing acidic fibroblast growth factor. RESULTS: Before the operation, the paraplegia was identified as ASIA-C, with a motor score for the right and left legs of 12 and 0, respectively, a pinprick score of 77, and 77 on a light touch of left side limbs. His functional status improved from being wheelchair-bound to being able to ambulate independently with a walker 2-and-a-half years after surgery. At this stage, paraplegia was ASIA-D, with motor scores for the right and left legs of 15 and 12, respectively, 86 for a pinprick, and 86 for a light touch of left side limbs. CONCLUSIONS: This case demonstrated significant motor recovery attained in a patient with chronic paraplegia following a repair surgery with nerve graft and growth factor.

Adult↗
PubMed1979

Diagnosis and management of tuberculous paraplegia with special reference to tuberculous radiculomyelitis.

Paraplegia occurred in eight of 17 patients with central nervous system tuberculosis. In six of these paraplegia was the presenting feature. Paraplegia may complicate tuberculous meningitis, or vertebral tuberculosis, but it may also occur, as in three of our cases, as a primary localised spinal tuberculous radiculomyelitis. These cases are presented in relation to the concept that paraplegia complicating these forms of tuberculosis is caused by radiculomyelitis.

Adolescent↗
PubMed2003

Pelizaeus-Merzbacher disease and spastic paraplegia type 2: two faces of myelin loss from mutations in the same gene.

Pelizaeus-Merzbacher disease and X-linked spastic paraplegia type 2 are two sides of the same coin. Both arise from mutations in the gene encoding myelin proteolipid protein. The disease spectrum for Pelizaeus-Merzbacher disease and spastic paraplegia type 2 is extraordinarily broad, ranging from a spastic gait in the pure form of spastic paraplegia type 2 to a severely disabling form of Pelizaeus-Merzbacher disease featuring hypotonia, respiratory distress, stridor, nystagmus, and profound myelin loss. The diverse disease spectrum is mirrored by the underlying pathogenesis, in which a blockade at any stage of myelin proteolipid protein synthesis and assembly into myelin spawns a unique phenotype. The continuing definition of pathogenetic mechanisms operative in Pelizaeus-Merzbacher disease and spastic paraplegia type 2, together with advances in neural cell transplant therapy, augurs well for future treatment of the severe forms of Pelizaeus-Merzbacher disease.

Alleles↗
PubMed2006

Childhood-onset spastic paraplegia with NIPAL gene mutation.

Hereditary spastic paraplegia is a heterogeneous group of inherited neurodegenerative disorders in which the predominant clinical feature is gait disturbance owing to spasticity and weakness of the lower limbs. Autosomal dominant hereditary spastic paraplegia is the predominant form of the disorder. To date, 10 autosomal dominant hereditary spastic paraplegia gene loci and genes for 6 of them have been identified. Spastic paraplegia 6, with a typical teenage onset and considered to be one of the more severe forms of the disease, is due to mutations in the gene NIPA1. We report a childhood-onset, aggressive, spastic paraparesis in a North American family with a c.316G>A mutation of the NIPA1 gene, confirming c.316 as a mutational hot spot.

Adult↗
PubMed2000

Atypical dementia and spastic paraplegia in a patient with primary lateral sclerosis and numerous necortical beta amyloid plaques: new disorder or Alzheimer's disease variant?

Primary lateral sclerosis (PLS) and hereditary spastic paraplegia (HSP) are clinically similar disorders in which progressive lower limb spasticity and corticospinal tract degeneration are characteristic. We report the occurrence of progressive spastic paraplegia and frontal systems dementia in a patient with postmortem features of PLS combined with moderate Alzheimer-like changes in neocortex and hippocampus. This combination of clinical and neuropathologic findings has not been described in PLS or HSP and varies from other cases in which spastic paraplegia, dementia, and Alzheimer neuropathology occurred concurrently. This 69-year-old woman developed spastic quadriplegia and dementia over 12 years. Left leg weakness progressed over 7 years to paraplegia, then quadriplegia by age 68. Sensory and cerebellar function were preserved and fasciculations were absent. Dementia characterized by concrete thinking, perseveration, and impaired executive function appeared in the seventh year and remained relatively stable until 6 months before death at age 69. Degeneration of the lateral corticospinal and dorsal spinocerebellar tracts confined to the spinal cord was evident at postmortem examination. Brain stem, midbrain, and cerebellum were normal. Numerous beta/A4 amyloid positive diffuse plaques (10-15/200x field) were apparent in neocortex, and neurofibrillary tangles immunopositive for paired helical filament were detected in hippocampus. This case broadens the spectrum of disorders associated with Alzheimer neuropathologic changes. The relationship between PLS, HSP, and Alzheimer's disease requires further study.

Aged↗
PubMed2003

Lack of evidence for apoptosis as a cause of delayed onset paraplegia after spinal cord ischemia in rabbits.

UNLABELLED: The mechanisms for delayed onset paraplegia after transient spinal cord ischemia are not fully understood. We investigated whether apoptotic motor neuron death is involved in its development. Spinal cord ischemia was induced for 15 min by occlusion of the abdominal aorta in rabbits. At 8, 24, or 48 h after reperfusion, hind limb motor function was assessed, and the lumbar spinal cord was examined morphologically (hematoxylin-eosin and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling staining) and biochemically (breakdown products of alpha-fodrin and patterns of DNA changes). At each time point, 14 rabbits were studied (7 for histopathology and 7 for biochemical analysis). Six rabbits served as sham controls. Delayed motor dysfunction developed in two thirds of the rabbits. The motor neurons in the rabbits with motor dysfunction (not paraplegia) showed swelling and a finely granular dispersed Nissl substance. In paraplegic rabbits, destruction of the gray matter and prominent inflammatory cell infiltration were observed. No apoptotic motor neuron was found in any rabbit. There was neither detectable increase in a caspase-3-mediated breakdown product of alpha-fodrin, nor DNA laddering in any rabbit. The results suggest that apoptosis has a negligible role in the pathophysiology of delayed paraplegia in the spinal cord ischemia model examined. IMPLICATIONS: Although the possibility of apoptotic motor neuron death cannot be completely excluded, delayed onset paraplegia after transient spinal cord ischemia is largely associated with necrotic cell death.

Anesthesia↗
PubMed1998

Work values: a comparison of non-disabled persons with persons with paraplegia.

A number of studies focus on factors that might explain the low level of employment of persons with paraplegia without questioning the social representations connected to work. Being employed is considered a priori as beneficial, constituting an important objective for rehabilitation. However sociologists have recently pointed out that work, as a means of self fulfilment, is a 'constructed' rather than a 'natural' category. The comparisons of the representations of work given by two groups: persons with paraplegia (n = 350), and non-disabled persons (n = 327) show that persons with paraplegia are more likely than non-disabled persons to consider work as a source of personal fulfilment and social recognition and less likely to positively value the fact of not-working. In addition, a demonstrated satisfaction with not working, among persons of working age, is clearly more significant among non-disabled persons than among persons with paraplegia. Among these, some of them who have generally made up their mind about not working declare that they feel satisfied being unoccupied. This satisfaction is explained, in part, by expressed representations of work. The authors suggest a reflection on the place of work in rehabilitation programmes.

Adolescent↗
PubMed1994

[Paraplegia in flexion and dementia].

The purpose of this study was to assess possible correlations between paraplegia in flexion and dementia in elderly patients in our special nursing home and geriatric hospital. At the time of our study, 10.5% of all our patients were suffering from paraplegia in flexion, with the ratio increasing with advancing age. Disorders of the nervous system, and in particular disorders caused by cerebrovascular disease were found at a high rate of frequency among the paraplegia in flexion patients, in whom the incidence of dementia was 97.8%. In most cases, the degree of dementia was severe, the types and respective percentages being as follows: vascular type 37.8%, Alzheimer's type 24.4%, mixed type 22.2% and others 15.6%. Many of these patients demonstrated pseudobulbar palsy, frontal sign, Babinski's sign, and typical reflexes of spinal automatism. We think that paraplegia in flexion is probably caused by reflexes of spinal automatism and extensive cerebral lesions.

Aged↗
PubMed1999

Non-traumatic paraplegia [correction of paraplegis] in a Zimbabwean population--a retrospective survey.

OBJECTIVES: To ascertain the aetiology of non-traumatic paraplegia in a Zimbabwean population and to compare findings with other studies from Africa. DESIGN: Retrospective survey over a six year period. SETTING: National Rehabilitation Centre, Ruwa, Zimbabwe. SUBJECTS: 159 patients referred to the National Rehabilitation Centre with non-traumatic paraplegia. RESULTS: The commonest causes of non-traumatic paraplegia were neoplasms (28% of cases) of which a third were metastatic, followed by tuberculosis (TB) (27%). Transverse myelopathy of unknown aetiology was diagnosed in 11% of cases and 6% had Guillain Barré syndrome. Miscellaneous conditions included: degenerative bone and joint conditions, degenerative cord disorders and infections. In 7% of cases no diagnosis was reached. On admission all patients were confined to wheelchairs. On discharge 49% had regained some degree of mobility. A year after discharge 48% were known to be alive and 18% had died. The fate of 34% was not known. CONCLUSIONS: The aetiology of non-traumatic paraplegia in a Zimbabwean population is similar to that reported from other African countries, with tumours and tuberculosis accounting for over half the cases. Survival appears to be related not only to the primary condition but also to the severity of the disability.

Activities of Daily Living↗
PubMed2003

Spinal epidural lipomatosis with thoracic osteoporotic compression fracture causing paraplegia.

Spinal epidural lipomatosis (SEL) frequently occurs as a result of long-term steroid administration for various disorders, and patients often present with osteoporosis. Acute paraplegia in patients with extensive thoracic SEL is rare. We report a case of acute paraplegia caused by osteoporotic compression fracture with extensive thoracic SEL in a 44-year-old man with rheumatoid arthritis who had received steroid therapy for 4 years. He presented initially with abdominal distension and weakness of lower limbs, and a sudden onset of paraplegia with complete motor and sensory loss below the T6 level ensued. Plain radiographs showed an osteoporotic compression fracture of the T6 vertebra. Magnetic resonance imaging showed osteoporotic compression fractures of the T5 and T6 vertebrae and SEL from T2 to T10 vertebrae. Decompressive laminectomy with epidural fat debulking was performed, and the pathology was confirmed as epidural lipomatosis. His neurological condition showed no improvement below the T6 level 3 months after surgery. Osteoporotic compression fracture is a risk factor for acute paraplegia in patients with thoracic SEL and decompressive surgery should be performed without delay.

Acute Disease↗
PubMed1989

[Vertebrectomy in treating fracture-dislocation of the spine with paraplegia].

From April 1980 to August 1984, 11 cases of fracture--dislocation of spine at the level of T-11 to L-2 with obvious kyphosis at the site of displacement, with paraplegia, were treated by vertebrectomy through posterior median approach. The operations were performed 2 to 28 weeks, averaging 8 weeks, after injury. 5 of the 9 patients who had complete paraplegia suffered also causalgia in both legs. The other 2 had incomplete paraplegia only. Follow-up study, 4 years and 5 months post-operation on average, revealed complete reduction of the fracture-dislocation in 10 patients and incomplete in one, getting solid bony union in all. Concerning the neurological findings of the 9 complete paraplegic patients, 5, who had suffered from causalgia got varying degree of relief, 5 regained sensation of pain in region 2 segments lower, of the 2 incomplete paraplegic patients, 1 regained sensation of pain in both legs and muscular power of degree 4 in both thighs, so that walking became possible, while the another one fell into complete paraplegia, because of compression of the cord at T-10 happened during operation and showed no signs of recovery afterward.

Adult↗
PubMed1986

Delayed paraplegia complicating sublaminar segmental spinal instrumentation.

The cases of two patients with delayed paraplegia after segmental spinal instrumentation with sublaminar wiring are reported. Both patients had complex spinal deformities and had transient neural deficits after the first-stage procedure of anterior release and spine fusion. They had uneventful spinal-cord monitoring during the second-stage procedure of posterior instrumentation and fusion, and function of the lower extremities was present immediately after that operation. Paraplegia then ensued, and was recognized thirty hours later in one patient and six days later in the other. Considering our reproducible and reliable experience (no false-negative results) with spinal cord monitoring in 307 operations, we propose that the delayed onset of paraplegia resulted from a progression of ischemic and edema-producing events that had not developed sufficiently intraoperatively to be reflected by the monitoring. The paraplegia became evident only when the subarachnoid space was obstructed because of progressive postoperative neural edema. The presence of sublaminar implants in narrow, kyphotic segments of the spinal canal probably exacerbated the neural irritation by dural impingement, which was seen myelographically.

Adolescent↗
PubMed1995

[Empirical results of adjustment to disability by adolescents with spina bifida and traumatic paraplegia].

Between June 1991 and June 1992, a total of 39 rehabilitees aged 16 to 25 years were examined, i.e., 21 patients suffering from spina bifida and 18 patients suffering from traumatic paraplegia. Diagnostic instruments used were the Freiburg questionnaire on coping with illness (FKV 102), Goldberg et al's questionnaire for the evaluation of subjective wellbeing regarding health, and a self-constructed questionnaire for evaluating satisfaction with rehabilitation. Medical interviews on the present state of health and the present situation were held with each patient. The level of paralysis was taken as an indicator of the motor handicap present. The patients examined showed distinctly less confidence in doctors than adults do. From a subjective point of view, however, the confidence in doctors was good: among the coping strategies chosen, the compliance strategies ranked first and second, respectively, in the two groups. The coping strategy of "cognitive avoidance and dissimilation" is distinctly less common among spina bifida patients than among patients with traumatic paraplegia. They are less inclined to hope for a miracle, and take their handicap much more seriously than adolescents suffering from traumatic paraplegia. The higher the level of paraplegia, the more use is made of the coping strategy of "emotional control and social withdrawal". Regressive tendencies and depressive modes of coping were equally present in both groups. When investigating satisfaction with rehabilitation and with the own person, both groups showed very high satisfaction with the physical independence achieved and the possibilities of acting independently.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Psychological↗