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PubMed1986

The value of more aggressive management in traumatic paraplegia.

In the last decade, operative decompression of cord and cauda, internal fixation with rods, bony fusion and early ambulation, have become more popular in the management of thoracolumbar injuries with neurological deficit. Computer-tomography, CT myelography and peroperative ultrasonography provided direct evidence, that, without surgical decompression, reduction of displaced bone and disc fragments, propelled into the spinal canal, is often incomplete, not only after postural reduction, but also after rod instrumentation. The percentage of patients with incomplete paraplegia who show improvement of neurological deficit after surgical reduction and stabilization, is probably greater than that noted with postural management. There are, however, shortcomings in the classification of neurological deficit, which hamper adequate comparison. Further research in this field is necessary. The value of the surgical approaches is mainly in immediate stabilization, which diminishes pain, facilitates nursing care and allows more rapid mobilization. This results in a shorter stay in hospital and earlier active rehabilitation. That decompression of the neural elements provides improved neurological recovery seems likely, but has so far not been proven. Management of these patients, preferably admitted to specialized units, should be carried out by an orthopedic surgeon and a neurosurgeon in cooperation. The orthopedic surgeon is mainly concerned with management of the spine; the neurosurgeon with management of the paraplegia, operations being carried out by both.

Fractures, Bone↗
PubMed2000

Anesthesia for Cesarean section in a patient with paraplegia resulting from tumour metastases to spinal cord.

PURPOSE: Spinal cord injured patients present multiple unique challenges to the anesthesiologist. These include choice of muscle relaxant and management of autonomic hyperreflexia. We report the anesthetic management for Cesarean delivery in a patient who was paraplegic due to spinal canal metastases. Preeclampsia and fever complicated this case. CLINICAL FEATURES: The patient presented at 29 wk gestation with progressive paraplegia at the T10 level due to metastatic osteosarcoma. She had a decompressive laminectomy without improvement in her paralysis. She subsequently developed preeclampsia at 31 wk gestation, and underwent Cesarean delivery for breech presentation under general anesthesia. Anatomical concerns left us unsure of the efficacy or safety of neuraxial anesthesia. CONCLUSIONS: Preeclampsia and autonomic hyperreflexia are generally indications for regional anesthesia for Cesarean section. Tumour in her spinal canal and laboratory abnormalities including thrombocytopenia and a potential urosepsis dissuaded us from this option. Additionally, rapid sequence induction and intubation were not preferred due to paraplegia, leading us to secure the airway fibreoptically.

Adult↗
PubMed2005

[Thoracic injuries associated with acute traumatic paraplegia of the upper and middle thoracic spine].

AIM: The aim of this study was to analyse the number of thoracic injuries associated with acute traumatic paraplegia of the upper and middle thoracic spine and review the early management in respect to treatment standards. METHODS: Using a prospective study protocol, data were sampled and analyzed from 12 December 2000 to 31 March 2002 at a level 1 trauma center. RESULTS: Twenty-two consecutive patients were included in the study. Sixteen suffered severe chest traumata. Lung contusion was diagnosed in 81%, followed by haemopneumothorax (75%) and fracture of the bony chest (75%). Intubation was performed 12 times in all. Chest drainage was performed in 14 patients. The mean duration of artificial ventilation was 20 days (range 2-93) and of intensive care treatment 25 days (range 2-93). Five patients died. CONCLUSIONS: Acute traumatic paraplegia of the upper and middle thoracic spine caused by high energy trauma is highly associated with severe chest trauma. Therefore, respiratory impairment must be kept in mind during the early treatment. If respiratory failure becomes more evident, emergency procedures such as intubation and chest drainage have to be performed. Secondary transfer should be avoided.

Accidental Falls↗
PubMed2003

[Hereditary spastic paraplegias].

Hereditary spastic paraplegias (HSP) are characterised by symmetric spastic paraplegia, pallhypaesthesia, and urinary dysfunction (uncomplicated HSP). Complicated HSP is present if uncomplicated HSP additionally presents with epilepsy, dementia, cataract, extrapyramidal dysfunction, amyotrophy, polyneuropathy, or ichthyosis. Clinically, HSP are similar but genetically even more heterogeneous. The disease course is slowly progressive and, the earlier the disease onset, the slower the course. Causes of HSP are mutations in 20 different genes, of which eight have been identified so far. A single mutation can cause complicated and uncomplicated HSP. Onset and severity can be quite variable between both groups and within families. Despite molecular genetic advances, diagnosis of HSP still relies on clinical features and the exclusion of various differential diagnoses. Neuropathologically, there is degeneration of corticospinal, posterior column, and spinocerebellar axons. Most likely, degeneration of the longest CNS axons is due to an impaired energy supply of the anterograde and retrograde axonal transport.

Axons↗
PubMed2005

Spinal cord magnetic resonance imaging in autosomal dominant hereditary spastic paraplegia.

Hereditary spastic paraplegia (HSP) is a genetically heterogeneous group of neurodegenerative disorders characterized by progressive lower extremity weakness and spasticity. HSP pathology involves axonal degeneration that is most pronounced in the terminal segments of the longest descending (pyramidal) and ascending (dorsal columns) tracts. In this study, we compared spinal cord magnetic resonance imaging (MRI) in 13 HSP patients with four different types of autosomal dominant hereditary spastic paraplegia (SPG3A, SPG4, SPG6, and SPG8) with age-matched control subjects. The cross-section area of HSP subjects at cervical level C2 was 59.42 +/- 12.57 mm2 and at thoracic level T9 was 28.58 +/- 5.25 mm2. Both of these values were less than in the healthy controls (p < 0.001). The degree of cord atrophy was more prominent in patients with SPG6 and SPG8 who had signs of severe cord atrophy (47.60 +/- 6.58 mm2 at C2, 21.40 +/- 2.4 mm2 at T9) than in subjects with SPG3 and SPG4 (66.0 +/- 8.94 mm2 at C2, p < 0.02; 31.75 +/- 2.76 mm2 at T9, p < 0.001). These observations indicate that spinal cord atrophy is a common finding in the four genetic types of HSP. Spinal cord atrophy was more severe in SPG6 and SPG8 HSP subjects than in other types of HSP we studied. This may suggest a different disease mechanism with more prominent axonal degeneration in these two types of HSP when compared with HSP due to spastin and atlastin mutations.

Adult↗
PubMed2006

Cerebral metabolic and structural alterations in hereditary spastic paraplegia with thin corpus callosum assessed by MRS and DTI.

INTRODUCTION: Hereditary spastic paraplegia with thin corpus callosum (HSP-TCC) is a complicated form of autosomal-recessive hereditary spastic paraplegia. Characteristic clinical features comprise progressive spastic gait, cognitive impairment, and ataxia. Diagnostic MRI findings include thinning of the corpus callosum and non-progressive white matter (WM) alterations. METHODS: To study the extent of axonal involvement, we performed localized proton magnetic resonance spectroscopy (MRS) of the cerebral WM and cortical grey matter (GM) in a patient with HSP-TCC at 20 and 25 years of age. The second investigation included diffusion tensor imaging (DTI). RESULTS: While MRS of the GM was normal, affected WM was characterized by major metabolic alterations such as reduced concentrations of N-acetylaspartate and N-acetylaspartyl-glutamate, creatine and phosphocreatine, and choline-containing compounds as well as elevated levels of myo-inositol. These abnormalities showed progression over a period of 5 years. DTI revealed increased mean diffusivity as well as reduced fractional anisotropy in periventricular WM. The metabolic and structural findings are consistent with progressive neuroaxonal loss in the WM accompanied by astrocytic proliferation-histopathological changes known to occur in HSP-TCC. CONCLUSION: Our results are in agreement with the hypothesis that the primary pathological process in HSP-TCC affects the axon, possibly due to impaired axonal trafficking.

Adult↗
PubMed2001

Acute paraplegia revealing an intraspinal neurenteric cyst in a child.

The authors report a case of intraspinal neurenteric cyst in a 22-month-old child, who presented with acute paraplegia following a vesicourethrogram. Despite 8 days' delay in surgical decompression, he made a complete neurological recovery. Neurenteric cysts are rare congenital lesions of the spinal canal lined with an epithelium of endodermal origin. They are usually located at the cervicothoracic junction and present with progressive mild to moderate signs of myelopathy. This is a unique case in regard both to its clinical presentation and to the excellent outcome after 8 days of complete paraplegia.

Acute Disease↗
PubMed2005

The R495W mutation in SPG3A causes spastic paraplegia associated with axonal neuropathy.

Mutations in the SPG3A gene cause a form of pure, early-onset autosomal dominant hereditary spastic paraplegia linked to chromosome 14q. The encoded protein, atlastin, is a putative member of the dynamin superfamily of large GTPases involved in cellular trafficking patterns. We report a new atlastin mutation causing spastic paraplegia in association with axonal neuropathy in an Italian family.

Adolescent↗
PubMed1999

The hereditary spastic paraplegias.

The hereditary spastic paraplegias are a complex group of neurodegenerative conditions which are characterised by slowly progressive lower limb spasticity. This article describes the main clinical features of pure and complicated hereditary spastic paraplegias and summarises recent advances in our understanding of the molecular genetics of these conditions.

Diagnosis, Differential↗
PubMed1998

The effect of lower body positive pressure on the cardiovascular response to exercise in sedentary and endurance-trained persons with paraplegia.

Exercise intolerance in persons with paraplegia (PARAS) is thought to be secondary to insufficient venous return and a subnormal cardiac output at a given oxygen uptake. However, these issues have not been resolved fully. This study utilized lower-body positive pressure (LBPP) as an intervention during arm crank exercise in PARAS in order to examine this issue. Endurance-trained (TP, n = 7) and untrained PARAS (UP, n = 10) with complete lesions between T6 and T12, and a control group consisting of sedentary able-bodied subjects (SAB, n = 10) were tested. UP and TP subjects demonstrated a diminished cardiac output (via CO2 rebreathing) during exercise compared to SAB subjects. Peak oxygen uptake (O2peak) remained unchanged for all groups following LBPP. LBPP resulted in a significant decrease in heart rate (HR) in UP and TP (P < 0.05), but not SAB subjects. LBPP produced an insignificant increase in cardiac output (Q) and stroke volume (SV). The significant decrease in HR in both PARA groups may indicate a modest hemodynamic benefit of LBPP at higher work rates where circulatory sufficiency may be most compromised. We conclude that PARAS possess a diminished cardiac output during exercise compared to the able-bodied, and LBPP fails to ameliorate significantly their exercise response irrespective of the conditioning level. These results support previous observations of a lower cardiac output during exercise in PARAS, but indicate that lower-limb blood pooling may not be a primary limitation to arm exercise in paraplegia.

Adult↗
PubMed2003

Narrowing of the critical region in autosomal recessive spastic paraplegia linked to the SPG5 locus.

Hereditary spastic paraplegias are neurodegenerative disorders characterized clinically by progressive spasticity of the lower limbs. They are inherited as autosomal dominant, autosomal recessive, and X-linked traits. Four Italian families with autosomal recessive pure spastic paraplegia are reported. We show evidence of linkage to the SPG5 locus on chromosome 8p and our data reduce the candidate interval for SPG5 to the11-cM interval spanned by D8S285 and D8S544. We also report the search for mutations in five genes located in the region and their exclusion as candidates for SPG5.

Adult↗
PubMed2005

A novel NIPA1 mutation associated with a pure form of autosomal dominant hereditary spastic paraplegia.

The hereditary spastic paraplegias (HSPs) are a clinically and genetically heterogeneous group of neurodegenerative disorders characterised by lower limb spasticity and weakness. Mutations in NIPA1 (Nonimprinted in Prader-Willi/Angelman syndrome 1) have recently been identified as a cause of autosomal dominant pure HSP, with one mutation described in two unrelated families. NIPA1 has no known function but is predicted to possess nine transmembrane domains and may function as a receptor or transporter. Here we present a large British pedigree in which linkage analysis conclusively demonstrates linkage to the NIPA1 locus (maximum multipoint LOD score 4.6). Subsequent mutation analysis identified a novel missense substitution in a highly conserved NIPA1 residue (G106R) which further confirms a causative link between NIPA1 mutation and autosomal dominant hereditary spastic paraplegia.

Adolescent↗
PubMed2005

Collecting duct carcinoma of the renal medulla presenting with paraplegia.

We report an interesting case of a patient with collecting duct carcinoma arising from the left kidney who presented with paraplegia secondary to metastases. The diagnosis was based on CT and histology. To our knowledge this is the first case of collecting duct carcinoma to present with paraplegia. The literature review also highlights the rarity of this disease with less than a hundred cases reported to date and the aggressive nature and poor prognosis despite prompt interventions.

Adult↗
PubMed1986

Brown tumor in secondary hyperparathyroidism causing acute paraplegia.

The first known case of a "brown tumor" associated with secondary hyperparathyroidism causing paraplegia is described. A 69-year-old white woman with chronic renal failure due to hypertension was admitted for back pain, and while she was under observation, paraplegia developed. A complete block was demonstrated by myelography. Computed tomography confirmed a mass at the level of obstruction, and results of biopsy were consistent with "brown tumor." Neurologic symptoms were markedly improved with high-dose corticosteroids and a debulking procedure. This entity is important to recognize because prompt treatment of the hyperparathyroidism or decompression of the tumor mass by surgical means or corticosteroid administration can provide marked improvement in symptoms.

Aged↗
PubMed1991

Reducing postischemic paraplegia using conjugated superoxide dismutase.

Paraplegia after thoracic aortic aneurysm repair has an incidence of 2.2% to 24%. Oxygen-derived free radicals after reperfusion of an ischemic spinal cord may be partly responsible for neuronal destruction. We studied the effects of polyethylene glycol-conjugated superoxide dismutase (PEG-SOD), a free radical scavenger, as a way of increasing spinal cord tolerance to ischemia. Thirty rabbits underwent 40 minutes of aortic occlusion (a known model of paraplegia). Ten of these animals received 25,000 U/kg of PEG-SOD 24 hours before aortic occlusion and two additional doses of 10,000 U/kg, one before and one subsequent to spinal ischemia. Ten animals received superoxide dismutase in the same dosages as those receiving PEG-SOD. Ten control animals received placebo. All animals were studied for 96 hours, at which time a final neurological examination was performed and the results were recorded. Of the 10 animals treated with PEG-SOD, 2 were completely paralyzed whereas 8 had less (7) or no (1) neurological impairment. Eight of the 10 control animals and 9 of the 10 animals receiving superoxide dismutase were completely paralyzed. None of the control animals or animals receiving superoxide dismutase had a normal neurological examination (p less than or equal to 0.05). Treatment with PEG-SOD before and during occlusion increased the rabbit spinal cord tolerance to a 40-minute ischemic insult. Scavenging free radicals may lessen experimental spinal cord injury.

Animals↗
PubMed1986

Standing performance of persons with paraplegia.

This study measures standing stability of four individuals with paraplegia using knee-ankle-foot orthoses (KAFOs) with a center-of-force monitoring platform as compared with similar data from 10 neurologically healthy subjects. Both groups were compared under conditions of quiet standing with eyes open and closed and with hands on and off parallel bars. Individuals with paraplegia were also tested under similar conditions with the ankles of their KAFOs mechanically unlocked and with bilateral functional neuromuscular stimulation of the quadriceps muscles. Sway path, mean amplitude, and mean frequency were measured for each subject. We found that postural stability in paraplegic individuals using KAFOs compared favorably with the control group under conditions of eyes open and closed with hands on parallel bars; however, visual information was much more important for paraplegic individuals during quiet stance. Unlocking the ankles of the KAFOs resulted in an increase in swap path and mean frequency. Functional muscular stimulation of the quadriceps muscles resulted in standing stability slightly less than with KAFOs. Although KAFOs may not be the ideal assistive device for various reasons, postural stability appears reasonable, and other proposed orthoses must be comparable in order to be considered as an alternative.

Adult↗
PubMed1980

Visual evoked potentials in two forms of hereditary spastic paraplegia.

Visual evoked potentials (VEPs) were used to study two forms of hereditary spastic paraplegia. We recorded the VEP in 6 homozygotes and 5 obligate heterozygotes in one family with recessively transmitted disease and in 5 persons with dominantly transmitted hereditary spastic paraplegia. The VEPs in the affected persons from both families were similar; both had delayed conduction times and changes in the wave form. The VEPs of the obligate heterozygotes were indistinguishable from those of the unaffected control subjects. Comparison of our findings with those of other disease processes that affect the VEPs suggest that the conduction delays in our patients' VEPs may be associated with changes in myelin.

Adult↗
PubMed1981

Visual, auditory and somatosensory pathway involvement in hereditary cerebellar ataxia, Friedreich's ataxia and familial spastic paraplegia.

Pattern-reversal visual, auditory and somatosensory evoked potentials were recorded from 11 patients with hereditary cerebellar ataxia, 13 with familial spastic paraplegia and 7 with Friedreich's ataxia. In all the 31 patients the conduction velocity along the median and tibial nerves to the level of the spinal cord was normal. Five of the 7 patients with Friedreich's ataxia had reduced sural nerve sensory potentials. There was electrophysiological evidence of malfunction along one or several pathways within the CNS in 8 of the 11 patients with cerebellar ataxia, 4 of the 13 with familial spastic paraplegia, and in all 7 cases of Friedreich's ataxia. The increase in latency of visual, auditory and somatosensory evoked cortical potentials is attributed to nerve fibre loss in the central pathways with associated slowing of conduction.

Adolescent↗