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PubMedDate not supplied

[Paraplegia as a risk following catheterization of the umbilical artery. Report of a case and bibliographic review].

A case of paraplegia in a female newborn in whom an umbilical catheter was inserted for treatment of fetal maternal isoimmunization with exchange transufsion is presented. Paraplegia was diagnosed in the fifth day after the procedure was performed. A left transfemoral angiography demonstrated the absence of the segmentary artery of Adamkiewicz at the level of T-11, which is responsible of circulation of the lower segment of the spinal cord; paraplegia was considered to be secondary to spinal cord infarction due to thrombosis; other causes of spinal block were ruled out. Review of the literature shows several reports of manifestations of thrombosis after catheterization of umbilical vessels.

Catheterization↗
PubMed1994

An aetiological survey of paraplegia in Accra.

Sixty-four cases of non-traumatic paraplegia in Accra, Ghana, were investigated. The commonest cause of paraplegia was tuberculosis (29.69%). Next were transverse myelitis and the Guillain-Barré syndrome, each accounting for 10.94% of cases. Parasitic causes were not seen in this study. The other important causes are neoplastic conditions (14.07%) and degenerative conditions namely, cervical spondylosis with myelopathy (12.5%), and motor neurone disease (6.25%). It is concluded that the major causes of non-traumatic paraplegia in Accra are related to non-parasitic microbial infections (51.57%).

Adolescent↗
PubMed1994

[Burst fracture: osteoporotic vertebral compression fracture associated with paraplegia].

It is rare that vertebral compression fracture of senile osteoporosis causes paraplegia. This article reviews 164 cases reported in Japan since 1974. These fractures were characterized as follows: 1) paraplegia occurred in elderly females (average 69.3 years old) with severe osteoporosis, 2) traumatic histories were revealed in 52%, 3) 91% of the fractures were classified into burst type, 4) location was in the thoracolumber region (80.5%), 5) average onset of paraplegia was 5.7 months after fracture. One hundred and twenty nine cases were surgically treated either by anterior vertebral fusion or by posterior instrumentation and 35 cases were conservatively treated. Surgical cases showed better recovery of walking ability than conservative cases.

Aged↗
PubMed1994

Cardiac stress testing with thallium-201 imaging reveals silent ischemia in individuals with paraplegia.

The purpose of this study was to determine through noninvasive arm ergometry and radionuclide tomographic imaging the presence of latent coronary heart disease (CHD) in subjects with paraplegia. Assessment of CHD in spinal cord injury, using these methods, has not been addressed previously. Twenty asymptomatic subjects with paraplegia performed arm ergometry exercise stress testing with thallium-201 single photon emission computerized tomography (SPECT) or planar myocardial imaging studies. All subjects had normal resting electrocardiograms (ECG). Only five subjects had ECG evidence of ischemia on exercise testing, whereas 13 subjects, including the five subjects with ECG positive stress tests, had scintigraphic evidence of ischemia. Thus, eight subjects would have been undiagnosed for CHD without thallium-201 SPECT imaging. These individuals had multiple risk factors for CHD and, except for age, were without a statistically significant difference between the groups with positive or negative thallium stress imaging studies. Arm ergometry stress thallium imaging shows a high prevalence of ischemia in subjects with paraplegia.

Adult↗
PubMed1993

The relationship between total body potassium and resting energy expenditure in individuals with paraplegia.

Body composition changes occur with spinal cord injury (SCI): fat-free mass (FFM) decreases and fat mass (FM) increases. FFM has been reported to correlate with resting energy expenditure (REE) in non-SCI individuals. This report addresses the question as to whether REE correlates with measures of FFM in individuals with paraplegia. Twelve males with chronic paraplegia had measurements of total body potassium (TBK), an indicator of lean tissue, by whole body 40K counting, and FFM by dual photon x-ray absorptiometry (FFMDPX). REE was measured using a metabolic cart for exhaled gas analysis. Corrleations between REE and TBK, and REE and FFMDPX were determined. The mean TBK for the group was 2,850 +/- 190 mEq. In all subjects, TBK was below that of expected (predicted from age, height, and weight). For the group this was 34 +/- 0.04% below predicted. The mean FFMDPX was 58.3 +/- 3.3 kg. Following an overnight fast, REE was measured for each subject while in a seated position. The mean REE was 1,855 +/- 70 kcal/day. REE correlates well with both TBK (r = 0.86, p < 0.0005) and FFMDPX (r = 0.80, p < 0.005). In summary, despite losses in metabolically active tissue in individuals with chronic paraplegia, TBK and FFMDPX continue to have a strong relationship with REE. REE (kcal/d) may be used as an indicator of TBK or FFMDPX using the following linear regression equations: TBK (mEq) = 2.28.REE (kcal/d) - 1,377 (SEE = +/- 347) or FFMDPX (kg) = 0.038.REE (kcal/d) - 11.5 (SEE = +/- 7).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Exercise capacity of individuals with paraplegia.

Spinal cord injury below the first thoracic vertebra defines the condition of paraplegia, with common medical sequelae including impaired motor function, bone and muscle atrophy, poor myocardial function, and a general decline of physical fitness. Recently, there has been renewed interest in the role of exercise for improving the physical fitness, health, and rehabilitation potential of individuals rendered wheelchair dependent following spinal cord injury. This brief review examines the pathophysiology of paraplegia, outlines useful strategies for cardiorespiratory fitness assessment, discusses the current levels of cardiorespiratory fitness in individuals with paraplegia, and highlights a few unique responses to acute exercise in this population.

Cardiovascular System↗
PubMed1996

Pott's Paraplegia--67 cases.

Sixty-seven patients were treated for Pott's paraplegia: 58 were adults and 9 were children. Sixty-four patients had active disease, and 3 had healed disease. All patients had triple chemotherapy with or without decompression surgery. Thirteen patients, including 9 children, were treated conservatively, whereas 54 patients who met the selection criteria for surgery were treated surgically. Fifty-two patients had anterior radical decompression surgery, and for 14 of them, anterior surgery was preceded by posterior instrumental stabilization surgery. Two patients with healed disease had posterior decompressive corpectomy. There was functional recovery in 60 (89.6%) patients, including 13 who had active disease that was treated conservatively. In 47 of the 54 surgically treated patients there was neurologic recovery, and 2 of these recovered incompletely with some residual spasticity. In the remaining 7 patients, there was no recovery. It took 2 to 6 months for recovery for the patients with conservative treatment, whereas it took <2 months for the patients with anterior decompression. The patients who had the combined 2-stage procedure could be mobilized earlier after neurologic recovery than could the patients having the anterior radical surgery and the conservatively treated patients. It was proven that paraplegia of active disease can be treated successfully by conservative or surgical means and that paraplegia caused by healing of fibrosis in the severely deformed spine was difficult to treat successfully, even with radical surgery.

Adolescent↗
PubMed1997

Short-course chemotherapy in the treatment of Pott's paraplegia: report on five year follow-up.

OBJECTIVE: To assess the efficacy of 9-month short-course chemotherapy (SCC) and to study the pattern of neurological recovery in patients with Pott's paraplegia. DESIGN: Patients with recent onset of spastic paraplegia due to clinically and radiologically active spinal tuberculosis involving vertebral bodies of level D4-L1 were treated with streptomycin, rifampicin, isoniazid and ethambutol daily for the first 2 months, followed by rifampicin plus isoniazid twice weekly for the next 7 months. The study was conducted in 2 phases. In the first phase 10 patients were admitted to the open trial where all patients had undergone modified Hong Kong surgery in addition to chemotherapy. In the next phase 23 patients enrolled in the study were randomly allocated to receive either chemotherapy alone or surgery plus chemotherapy. All the patients were followed for 5 years from the start of treatment. A scoring system was devised to predict neurological recovery. RESULTS: In all, 33 patients were admitted and treated with SCC. Thirteen patients were allocated to the chemotherapy (CHEM) regimen; of these 3 patients had to be operated upon for clinical deterioration; the remaining 20 had surgery plus chemotherapy; 4 were excluded for various reasons, leaving 29 patients in the analysis. None relapsed requiring treatment. CONCLUSION: A combination of surgery (when indicated) and SCC of 9 months' duration is effective in the treatment of Pott's paraplegia. All patients had neurological recovery by the end of 9 months; 8 recovered with chemotherapy alone. Complete motor recovery was seen in 62% by the 3rd month and 90% by the 6th month.

Adolescent↗
PubMed1976

Injectable agent for the treatment of air emboli-induced paraplegia in rats.

Rats with air emboli-induced paraplegia were treated with dialy levodopa injections (intra-arterially or intraperitoneally). Of the control animals, 20% fully recovered from paraplegia during a period of 7 d. Of the levodopa treated animals, 85% fully recovered during the same period. It appears, therefore, that levodopa might be one of the few injectable agents enhancing recovery from air-induced paraplegia, suggesting its possible use in decompression sickness.

Animals↗
PubMed2005

Complete paraplegia following gunshot injury without direct trauma to the cord.

STUDY DESIGN: A retrospective review of all patients with neurologic deficit following gunshot wounds that did not penetrate the spinal canal. OBJECTIVES: To evaluate the possibility that neurologic deficit following gunshot wounds is possible without direct trauma to the cord. SUMMARY OF BACKGROUND DATA: Gunshot injuries to the spine account for 13% to 17% of all spinal cord injuries and are likely to result in complete paraplegia. Neurologic deficit is the result of direct trauma to the nervous tissue by the bullet, bone, or disc fragments, which compress the cord. METHODS: The medical charts, radiographs, CT scans, and myelographies or MRIs of all patients admitted to our hospital with neurologic deficit secondary to gunshot wounds between 1977 and 2003 were reviewed. Twenty-six patients were identified: 15 with complete and 11 with incomplete paraplegia. In 19 patients, the spinal canal at the level of injury was explored and decompressed. RESULTS: In 3 patients with complete paraplegia at the thoracic level, CT scan, myelography (1 patient), MRI (2 patients), and operative exploration (2 patients) did not indicate any signs of canal compromise. Two were injured by low-velocity bullets passing through the vertebra (in 1 patient) and the posterior part of the lamina (in the second). The third was injured by high-velocity bullets with no signs on MRI of any injury to the vertebral column or spinal cord. At follow-up 4.1 years later, on average, none had any neurologic recovery. CONCLUSION: Neurologic deficit following gunshot wounds is possible even without violation of the spinal canal. It is most probably the result of the kinetic energy emitted by the bullet.

Adult↗
PubMed1977

Strumpell's pure familial spastic paraplegia: case study and review of the literature.

A family with pure Strumpell's familial paraplegia is presented. There were 11 afflicted members involving three generations. The mode of inheritance was dominant, the onset in the first decade, and in this family the disease was mild. Literature data from 104 families with 536 members dating from 1880 are tabulated. This report confirms others regarding mode of inheritance, age of onset, distribution between sexes, and disease manifestations. However, contrary to other reports, we found the dominant and recessive form of pure Strumpell's familial spastic paraplegia to be similar in severity. There are now clinical and pathological data supporting the separation of pure Strumpell's familial spastic paraplegia from the other heredodegenerative diseases of the nervous system.

Adolescent↗
PubMed1976

[Involvement of the peripheral motor neuron in hereditary spastic paraplegia (author's transl)].

Two patients from families with hereditary spastic paraplegia (recessive and dominant type) were examined electromyographically. It was found that the peripheral motor neuron is involved. It is assumed that in cases of infantile recessive familial spastic paraplegia the peripheral motor neuron is rather more involved than in those of the dominant type of spastic paraplegia.

Electromyography↗
PubMed1983

Familial spastic paraplegia, mental retardation, and precocious puberty.

Two brothers had progressive spastic paraplegia and precocious puberty develop due to Leydig's cell hyperplasia when they were 2 years old. Both later had moderate mental retardation. Family members displayed brisk lower-extremity reflexes and dysarthria in a pedigree that suggested autosomal dominant inheritance with variable expression. Precocious puberty has been associated with other neurologic syndromes. Its occurrence in two brothers with spastic paraplegia has not, to our knowledge, been previously reported.

Adult↗
PubMed1997

'Complicated' autosomal dominant familial spastic paraplegia is genetically distinct from 'pure' forms.

BACKGROUND: The familial spastic paraplegias (FSPs) are hereditary neurodegenerative disorders with an unknown pathogenesis. Pure and complicated forms are currently differentiated on clinical grounds. To date, no linkage studies in complicated FSP have been reported, and candidate genes have not been suggested. Three different gene loci responsible for pure autosomal dominant FSP and 1 for pure autosomal recessive FSP recently have been found. This raises the question of whether the complicated forms may also be linked to any of these loci. OBJECTIVE: To investigate whether complicated autosomal dominant FSP is allelic to any of the pure forms with defined loci. DESIGN: Clinical characterization of a large kindred that included 4 generations and multipoint linkage analyses. SETTING: Universitätsklinikum Charité, Humboldt-Universität Berlin, Neurologische Klinik und Poliklinik, Berlin, Germany. PATIENTS: Twenty-six family members, 13 of whom were affected. RESULTS: Thirteen members of a large family of 4 generations experienced a slowly progressive syndrome of spastic paraplegia. Hypomimia, bradykinesia, axial and limb rigidity, supranuclear gaze palsy, dysarthria, bladder and sphincter disturbances, cerebellar signs, and epilepsy were noted as additional features in some of the affected individuals. The mean age at onset was 20 years (range, 5-30 years), and the pattern of transmission was compatible with an autosomal dominant mode of inheritance. The CAG-repeat expansions in the spinocerebellar ataxia type 1 and Machado-Joseph disease genes were not found. Linkage analysis with the use of a panel of (AC)n dinucleotide repeat markers from the Généthon map demonstrated exclusion of all 4 FSP loci recently mapped by linkage to pure forms of FSP on chromosomes 14q, 2p, 15q, and 8. CONCLUSIONS: Complicated FSP in this family is not linked to any of the known pure FSP loci, including the recessive one. Therefore, the clinical differentiation of both forms still is of major relevance.ACKG

Aged↗
PubMed2004

Hereditary spastic paraplegia: clinical genetic study of 15 families.

BACKGROUND: Autosomal dominant hereditary spastic paraplegia (ADHSP) is mainly caused by mutations in the SPG4 gene, which encodes a new member of the AAA (adenosine triphosphatases associated with diverse cellular activities) protein family (spastin). Accumulation of genotype-phenotype correlation is important for better understanding of SPG4-linked hereditary spastic paraplegia. OBJECTIVES: To perform a clinical and genetic study of families with ADHSP and to perform the functional analysis of the founder mutation discovered in the SPG4 gene. DESIGN: Genetic and clinical study. Patients Fifteen unrelated families with ADHSP originating from southern Scotland. MAIN OUTCOME MEASURES: Clinical assessment, linkage analysis, haplotype study, expression of mutant spastin protein in cultured cells. RESULTS: Nine families with ADHSP were linked to the SPG4 locus at 2p21-p24. Sequence analysis of SPG4showed a novel N386S mutation in all 9 of these families. Expression of mutant spastin showed aberrant distribution in cultured cells. Haplotype analysis suggested the existence of a common founder. Clinical examination of the affected members carrying the mutation showed phenotypic variations including broad range of age at onset and disease duration and additional neurologic features such as mental retardation. Magnetic resonance imaging demonstrated unique features, including thin corpus callosum and atrophy of the cerebellum in 2 patients. Linkage and sequence analyses showed no evidence of linkage to the currently known ADHSP loci in the remaining 6 families. CONCLUSIONS: A founder SPG4 mutation N386S was identified in the families with ADHSP originating from southern Scotland. Clinical investigation showed intrafamilial and interfamilial phenotypic variations. The genetic study demonstrated evidence of further genetic heterogeneity in ADHSP.

Adenosine Triphosphatases↗
PubMed2001

Silver syndrome is not linked to any of the previously established autosomal dominant hereditary spastic paraplegia loci.

The hereditary spastic paraplegias are a clinically variable and genetically heterogeneous group of disorders characterized by progressive and lower limb spasticity and weakness. Silver syndrome (SS) is a particularly disabling autosomal dominant form of the disease in which there is associated wasting of the hand muscles. In view of the fact that genes for hereditary spastic paraplegia can produce highly variable phenotypes, the eight known autosomal dominant loci were investigated for linkage to Silver syndrome. Genotyping of these loci in two large multigenerational families was incompatible with linkage to any of these regions, suggesting that an additional locus is responsible for this syndrome.

Adult↗
PubMedDate not supplied

Spastic paraplegia with iron deposits in the basal ganglia: a new X-linked mental retardation syndrome.

We report on a family with X-linked mental retardation (XLMR) and severe spastic paraplegia. Appearance is normal but there is severe involvement of the lower limbs (affected relatives never walked), with minimal involvement of the upper limbs and unusual MRI findings including macrogyria, white matter hypoplasia, lack of myelination and a markedly increased paramagnetic signal suggestive of iron deposition. Linkage studies documented possible linkage, with no recombination, between the disease locus and DXS424. A 7-point linkage analysis yielded a maximum LOD score of 1.9, (theta = 0.00) for three loci spanning Xq22-q25. The combination of the unusual clinical and MRI findings and the tentative localization to a region different than other XLMR syndromes with spastic paraplegia, provide good evidence that this is a new XLMR syndrome.

Adult↗
PubMed1993

Spastic paraplegia, epilepsy, and mental retardation in several members of a family: a novel genetic disorder.

We report on a family in which an association between spastic paraplegia and epilepsy has been observed. This disorder is an autosomal dominant trait with incomplete penetrance and variable expressivity. The onset was limited to the first four decades of life; the symptoms were typically those of progressive weakness and spasticity of lower limbs. Epilepsy was present in members of three of the four generations on whom we have information. The concomitance of spastic paraplegia and epilepsy in several members of the same family is unlikely to be fortuitous and probably represents the pleiotropic effect of a single mutant gene.

Adolescent↗