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At least 397 records · Page 22Linked to original sources
PubMed1992

Shear fracture-dislocations of the thoracic and lumbar spine associated with forceful hyperextension (lumberjack paraplegia).

Twelve patients sustained a shear fracture-dislocation of their thoracic or lumbar spines by a hyperextension mechanism of injury. Ten male and two female patients were injured; their average age was 29 years (range, 22 months to 56 years). Ten fracture-dislocations occurred in the thoracic spine, one at the thoracolumbar junction, and one in the lumbar spine. Eleven patients had complete paraplegia, and one had incomplete paraplegia at the time of injury. Dural tears were found in six of the patients. Eleven patients were treated by posterior spinal fusion with instrumentation, and one was treated with a brace. Three patients were treated with Harrington distraction rods alone, six had Harrington distraction rods supplemented with a midline Harrington compression rod or interspinous wiring, and two were treated with Cotrel-Dubousset instrumentation. No patient was lost to follow-up. The average length of follow-up was 3.5 years (range, 1-9 years). Six of the patients treated with Cotrel-Dubousset instrumentation or Harrington distraction rods supplemented with either a midline compression rod or interspinous wiring healed anatomically; two patients developed pseudarthroses. None of the patients treated with Harrington distraction rods alone healed in an anatomic position. The use of Harrington distraction rods alone was associated with overdistraction and nonanatomic alignment of the spine. The disruption of the anterior stabilizing structures of the spine associated with hyperextension injuries necessitates the use of instrumentation that can stabilize the spine and prevent overdistraction. This injury can be successfully treated with Cotrel-Dubousset or Harrington distraction rods supplemented with either a midline compression rod or interspinous wiring.

Adult↗
PubMed1997

Paraplegia due to ossification of ligamenta flava in X-linked hypophosphatemia. A case report.

STUDY DESIGN: Spinal canal decompression at the most prominent of multiple posterior calcified thoracic lesions in a case of X-linked hypophosphatemia was undertaken for treatment and diagnosis purposes, as well as to assess possible nature of the pathophysiology underlying the presenting deficits. OBJECTIVES: To discuss the clinical assessment diagnostic and treatment aspects of this rare coincidence of ossification of ligamenta flava in the patient with the skeletal deformities of X-linked hypophosphatemia. SUMMARY OF BACKGROUND DATA: The patient with the stigmata and chemical findings of an X-linked hypophosphatemia presented with paraplegia and multiple calcified posterior spinal thoracic lesions. This was studied with magnetic resonance imaging and electrophysiologic studies of the spinal sensory pathways of the legs. These data constituted the preoperative information required to assess later results of surgical intervention. METHODS: Presurgical clinical, imaging and electrophysiologic studies and laboratory and pathologic investigations of the surgical specimens. RESULTS: Resolution of the paraplegia with walking and return to work in a physically demanding job for the last 4 or 5 years of postoperative follow-up after surgical decompression of the spinal cord only at the worst and highest of the effected spinal levels. CONCLUSION: The coincidence of X-linked hypophosphatemia and ossification of ligamenta flava has been reported only in two or three cases in the literature. Removal of the offending ossifying lesion is known to result in resolution of the clinical deficits but similar lesions at other spinal levels are suspected of producing recurrences. The return of function and of the corresponding electrophysiologic correlates indicate a neurono-apractic nature of the neurologic symptoms.

Bone and Bones↗
PubMed2000

Posterior spinal shortening for paraplegia after vertebral collapse caused by osteoporosis.

STUDY DESIGN: Case report of a patient who underwent a new surgical procedure for paraplegia after vertebral collapse due to osteoporosis. OBJECTIVES: To propose a new approach to posterior spinal fusion surgery for osteoporotic patients. SUMMARY OF BACKGROUND DATA: Surgical treatment was performed on a paraplegic patient after vertebral collapse due to osteoporosis. However, the surgery was difficult because implants such as hooks and screws often dislodged during the treatment. The poor holding power of these implants to the osteoporotic spine is a challenging problem in this treatment. METHODS: When a fractured vertebra is shortened by resecting the posterior part of the spine and the application of a compression force, a short vertebra is produced. As a result, the thoracic kyphosis decreases and the force pushing the upper thoracic spine inferio-ventrally also decreases. RESULTS: A 74-year-old woman with T12 vertebral collapse was treated with this new method. Lateral Cobb angle (T10-L2) was reduced from 26 to 4 degrees after surgery. The shortened vertebral body united, and after 33 months, the implant had not dislodged and no loss of correction was seen. CONCLUSION: The posterior spinal shortening can be a choice for treating delayed paraplegia after osteoporotic vertebral fracture.

Aged↗
PubMed2002

Paraplegia as a complication of percutaneous vertebroplasty with polymethylmethacrylate: a case report.

STUDY DESIGN: A case report and review of the literature are presented. OBJECTIVE: To present the first case of paraplegia as a complication of percutaneous vertebroplasty with polymethylmethacrylate in osteoporotic compression fracture. SUMMARY OF BACKGROUND DATA: Complications of percutaneous vertebroplasty with polymethylmethacrylate (PMMA) for the treatment of osteoporotic compression fracture were found to be rare and minor, except in two cases of major neurologic complication. METHODS: The reported case is that of a 66-year-old woman with multilevel vertebral osteopenia and compression fractures. Percutaneous vertebroplasty using polymethylmethacrylate was performed at three vertebral bodies (L2, L1, and T11) using careful techniques including venography, large cannula, proper preparation and amount of polymethylmethacrylate, and continuous visualization with fluoroscopy. RESULTS: Immediately after surgery, the patient had complete motor and sensory deficits at T11. Computed tomography scan showed spinal cord compression caused by venous leakage of polymethylmethacrylate. In anticipation of recovery from paraplegia, posterior decompression was performed from L2 to T10. CONCLUSIONS: Percutaneous vertebroplasty with polymethylmethacrylate is not as simple and risk free as advocated in the literature. Careful safeguards and modifications are needed for the procedure, and new and physiologic material could be substituted for polymethylmethacrylate.

Aged↗
PubMed2001

Recent advances in hereditary spastic paraplegia.

The hereditary spastic paraplegias are a group of rare disorders that are characterized by great clinical and genetic heterogeneity. There has been an exponential increase in the number of HSP loci mapped in recent years, with nine out of the 17 loci reported during the past 2 years. Eight loci have now been identified for the autosomal-dominant form, and seven of these are associated with pure HSP. Spastic paraplegia-4 remains the most frequent locus, and is usually associated with a pure phenotype. Although the corresponding spastin gene was only recently identified, over 50 mutations have been described to date, which renders molecular diagnosis difficult. Five loci are known for autosomal-recessive HSP, and four of these are associated with complex forms, all with different phenotypes. Two genes have been identified: paraplegin and sacsin. Finally, three loci have been identified in X-linked HSP, two of which are complex forms. The genes that encode L1 and PLP were the first to be identified in HSP disorders. Surprisingly, the five genes encode proteins of different families, making understanding and diagnosis of HSP even more difficult. The discovery of new genes should hopefully help to clarify the pathophysiology of these disorders.

Chromosome Aberrations↗
PubMedDate not supplied

Hereditary spastic paraplegia.

Hereditary spastic paraplegia is a genetically transmitted disease that is usually autosomal dominant. Characterized by a slow progression of spastic paraparesis, it is frequently misdiagnosed as cerebral palsy. Our experience consists of six families with a total of 26 affected members. All initial referrals were children with a slowly progressive paraplegia. Each child was noted to have slightly delayed motor milestones, normal intellect, and no history of perinatal cerebral event. Each child was treated when necessary with appropriate tendon lengthenings. Recognition is the key to management. A careful patient and family history will reveal the hereditary nature of the disease and help develop treatment plans.

Adolescent↗
PubMed1999

Implanted functional electrical stimulation system for mobility in paraplegia: a follow-up case report.

A 16-channel functional electrical stimulation (FES) system has been implanted in a person with T10 paraplegia for over a year. The system consists of two eight-channel radio frequency controlled receiver-stimulators delivering stimuli through a network of 14 epimysial and two intramuscular electrodes. Using this system and a walker for support, the subject was able to stand up for 8 min and walk regularly for 20 m. The standing duration was limited by arm fatigue since upper extremities supported an average of 25% of body weight. This was due to suboptimal hip extension and some undesired recruitment of rectus femoris and sartorius with stimulation of quadriceps electrodes. The left quadriceps exhibited rapid fatigue that limited walking distance and duration. The metabolic energy requirements were well within the aerobic limits of the sedentary paraplegic population. At one-year follow-up evaluation all electrodes are functional except one intramuscular electrode. The implant caused no adverse physiological effects and the individual reported health benefits such as increased energy and overall fitness as a result of the FES system use. With further improvements in muscle response through innovative surgical techniques, the 16-channel implanted FES system can be a viable addition to exercise and mobility function in persons with paraplegia.

Adult↗
PubMed1978

Paraplegia and epidural analgesia.

A patient who developed paraplegia subsequent to epidural analgesia is presented. The patient was further investigated and it was proved that there was spinal canal stenosis L2-4 level and epidural analgesia had precipitated the paraplegia.

Adult↗
PubMed1994

Acute paraplegia following intrathecal phenol block in the presence of occult epidural malignancy.

A 68-year-old woman with an invading adenocarcinoma of the lung underwent intrathecal phenol block for chest wall pain. Acute paraplegia resulted immediately following the procedure. Subsequent CT scan showed dural compression from an epidural metastasis five segments above the site of the phenol injection. This was confirmed at surgical decompression of the spinal cord and by histological findings. The cause of the paraplegia, which has not recovered, was probably spinal coning.

Acute Disease↗
PubMed2004

Spinal implantation of hNT neurons and neuronal precursors: graft survival and functional effects in rats with ischemic spastic paraplegia.

Transient spinal ischemia, a complication associated with aortic cross-clamp may lead to spastic paraplegia. Once fully developed this deficit is permanent. Quantitative histopathological assessments and pharmacological studies show that the ischemic spasticity is secondary to the loss of lumbar GABA and glycinergic inhibitory interneurons. In the present study, we investigated whether human hNT neurons or committed Sprague-Dawley rat spinal neuronal precursors (SNPs) when grafted into previously ischemic spinal segments depleted of inhibitory neurons would restore local inhibitory tone and ameliorate spasticity. Rats with functionally and electrophysiologically defined spasticity that received spinal graft of hNT neurons or neuronal precursors and immunosuppressive treatment displayed a progressive recovery of motor function that correlated with the improvement of otherwise exacerbated peripheral motor response evoked by stimulation of motor cortex. In contrast, in control, medium-injected or oligodendrocyte-grafted animals no significant therapeutic effect was seen. Stereological quantification of grafted neurons revealed 1-2% survival at three months after transplantation. These surviving neurons displayed a robust axo-dendritic sprouting and expression of markers typical of mature neurons including NSE, NeuN and synaptophysin. In both treatment groups a subpopulation of grafted neurons developed GABA immunoreactivity. These data provide evidence that a region specific grafting of hNT neurons or other neuronally committed cells, which have a potential to develop inhibitory neurotransmitter phenotype, represent an effective treatment modality to modulate ischemia-induced spastic paraplegia.

Animals↗
PubMed1980

Hereditary spastic paraplegia with neurogenic bladder disturbances and syndactylia.

The present paper reports a family settled in the northern part of Norway, with a hereditary neurological disorder consisting clinically of spastic paraplegia associated with neurogenic bladder disturbances and syndactylia. Nine out of 22 members in three generations exhibit these clinical features. The bladder disturbances, being incomplete supranuclear bladder paresis (uninhibited neurogenic bladder), were the main complaint and occurred at an early stage of the disease. The family probably represents an unusual form of hereditary spastic paraplegia (HSP). The mode of inheritance is considered to be autosomal dominant.

Adolescent↗
PubMed1991

Hereditary spastic paraplegia with epileptic myoclonus.

A previously undescribed form of complicated hereditary spastic paraplegia with epileptic myoclonus in four affected offspring of consanguineous parents is reported. The disorder was inherited as an autosomal recessive trait. Age at onset varied from the prenatal period to 10 years. The main findings when examined between 26 and 42 years of age were spastic paraplegia, epileptic myoclonus, distal muscle atrophy, mental retardation or dullness, ataxia, hearing loss and a progressive course. The difference in phenotypic expression was striking. One woman had progressive epileptic myoclonus, ataxia and only slight distal wasting and could have been misdiagnosed as a case of Unverricht-Lundborg's disease. Thorough biochemical investigations revealed no cause of the disorder.

Adult↗
PubMed1976

X-linked recessive type of pure spastic paraplegia in a large pedigree: absence of detectable linkage with Xg.

A family with 24 males affected by an X-linked type of spastic paraplegia is reported. Twelve affected members were personally examined showing the pure form of the disease. Half of the affected males had many descendants, all normal. Linkage studies strongly suggest that this X-linked form of spastic paraplegia and Xg loci are not at a measurable distance on the X chromosome.

Blood Group Antigens↗
PubMed2006

Mutation in the epsilon subunit of the cytosolic chaperonin-containing t-complex peptide-1 (Cct5) gene causes autosomal recessive mutilating sensory neuropathy with spastic paraplegia.

BACKGROUND: Mutilating sensory neuropathy with spastic paraplegia is a very rare disease with both autosomal dominant and recessive modes of inheritance. We previously mapped the locus of the autosomal recessive form to a 25 cM interval between markers D5S2048 and D5S648 on chromosome 5p. In this candidate interval, the Cct5 gene encoding the epsilon subunit of the cytosolic chaperonin-containing t-complex peptide-1 (CCT) was the most obvious candidate gene since mutation in the Cct4 gene encoding the CCT delta subunit has been reported to be associated with autosomal recessive mutilating sensory neuropathy in mutilated foot (mf) rat mutant. METHODS: A consanguineous Moroccan family with four patients displaying mutilating sensory neuropathy associated with spastic paraplegia was investigated. To identify the disease causing gene, the 11 coding exons of the Cct5 gene were screened for mutations by direct sequencing in all family members including the four patients, parents, and six at risk relatives. RESULTS: Sequence analysis of the Cct5 gene revealed a missense A492G mutation in exon 4 that results in the substitution of a highly conserved histidine for arginine amino acid 147. Interestingly, R147 was absent in 384 control matched chromosomes tested. CONCLUSION: This is the first disease causing mutation that has been identified in the human CCT subunit genes; the mf rat mutant could serve as an animal model for studying these chaperonopathies.

Amino Acid Sequence↗
PubMed1998

Spastic paraplegia, optic atrophy, microcephaly with normal intelligence, and XY sex reversal: a new autosomal recessive syndrome?

Two female sibs of first cousin Iranian parents were found to have the syndrome of spastic paraplegia, optic atrophy with poor vision, microcephaly, and normal cognitive development. Karyotype analysis showed a normal female constitution in one and a male constitution (46,XY) in the other. The XY female showed normal female external genitalia, normal uterus and tubes, and streak gonads. SRY gene sequencing was normal. We conclude that the present family probably represents a new autosomal recessive trait of pleiotropic effects including XY sex reversal and adds further evidence for the heterogeneity of spastic paraplegia syndromes as well as sex reversal syndromes.

Abnormalities, Multiple↗
PubMed2003

Science in motion: common molecular pathological themes emerge in the hereditary spastic paraplegias.

The hereditary spastic paraplegias are a group of neurodegenerative conditions that all share the principal clinical feature of progressive lower limb spastic paralysis, caused by either failure of development or progressive degeneration of the corticospinal tract. The conditions are characterised by extreme genetic heterogeneity, with at least 20 genes involved. Until recently, no functional overlap was apparent in the associated molecular pathological mechanisms. However, with recent progress in hereditary spastic paraplegia gene identification, common pathological themes are now emerging.

ATPases Associated with Diverse Cellular Activitie↗
PubMed1974

Strümpell's familial spastic paraplegia: genetics and neuropathology.

Uncomplicated Strümpell's disease (Strümpell's familial spastic paraplegia) with a dominant mode of inheritance is recorded in six families. The neuropathological findings in two cases from these families are given, bringing the total of similar histologically documented reports in the literature to 11. It is concluded that, although exact classification and identification of the many different hereditary neurological degenerative diseases is not yet practicable, cases conforming to the picture described by Strümpell can be separated from larger general group of familial spastic paraplegias, show a consistent clinical picture, and have a standard pathology. It is suggested that, since the lesions are confined to the longest fibre tracts in the central nervous system, the pathological process may be different from that found in the `system' degenerations.

Adolescent↗