Cases reported "Paraplegia"

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1/9. Possible role of collagen in transverse myelitis and chymopapain-induced paraplegia.

    We studied the effect of nucleus pulposus (NP) on platelet aggregation. Our in vitro experiments showed that NP extract produced platelet aggregation and the addition of collagenase to the NP extract abolished this response. It was further shown that chymopapain did not affect the activity of the extract. We assume that collagen is the active platelet aggregant in the NP extract. Intravascular release of collagen may cause platelet aggregation, vascular obstruction, ischemia, and cord necrosis in a patient with acute transverse myelitis. Intradiskal chymopapain is known to cause transverse myelitis and it is possible that collagen released during the action of the enzyme initiates a similar chain of events.
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2/9. CT scan in a case of progressive generalized dystonia with amyotrophic paraplegia.

    In a case characterized by progressive generalized dystonic paraplegia with amyotrophy and mental deficiency, CT scanning shows a bilateral lenticular nucleus hypodensity. A similar picture can be found in Wilson disease. However, this patient presented no biochemical, hepatic or ocular abnormalities.
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3/9. Autosomal recessive spino-olivo-cerebellar degeneration without ataxia.

    Five adult siblings from a sibship of ten suffering from an external ophthalmoplegia with a spastic paraplegia are reported. In addition, optic nerve atrophy was present in three of the patients and dementia in two; extrapyramidal signs and cerebellar ataxia were found only in one patient. Contrary to earlier studies of patients with comparable neurological signs the pattern of inheritance was autosomal recessive. Neuropathological investigation of the index case, who had never shown ataxia, nevertheless showed demyelination of the spinocerebellar and the olivocerebellar pathways, and also a severe loss of purkinje cells, of cells in Clarke's column and in the inferior olives. The dentate nucleus was severely gliotic but showed no cell loss. Earlier neuropathological investigations of this disorder, but with an autosomal dominant heredity, were incomplete. It is concluded that the five siblings of this family have a unique autosomal recessive disorder, which should be considered a distinct entity.
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4/9. Primary lateral sclerosis: a case report.

    The syndrome of primary lateral sclerosis (PLS) has been reported clinically on many occasions. Pathologic confirmation in the modern era, however, has generally been lacking. In a recently reported case of PLS, the disorder was complicated by a pontine infarct. We describe a 65-year-old woman whose illness began with spastic dysarthria, which gradually worsened to the point that 18 months later she could barely utter a sound. Meanwhile, dysphagia, brisk reflexes, and a pseudobulbar affect had developed. Three years after onset she had a spastic contractured right-sided hemiplegia and walked with short shuffling steps. The spasticity slowly progressed, and she died of aspiration pneumonia 3.5 years after the onset of dysarthria. Neuropathologic examination showed bilateral atrophy of the precentral gyri, which microscopically showed a paucity of Betz cells. There was loss of myelin throughout the corticospinal system, yet the anterior-horn cells of the spinal cord and hypoglossal nuclei were well preserved. Intracytoplasmic eosinophilic inclusion bodies, of unknown cause and significance, were observed in occasional motor neurons, one in the hypoglossal nucleus and two in spinal cord anterior horns. Clinically and pathologically, this case meets the criteria for PLS.
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5/9. Initial results of the nucleus FES-22-implanted system for limb movement in paraplegia.

    The Nucleus 'FES-22' channel stimulation system has been developed for partial restoration of lower limb function in paraplegic individuals. One FES-22 stimulator has been implanted in a 25-year-old paraplegic subject in November 1991. Of the twenty 2.5-mm disc electrodes attached epineurally onto motor nerves, fifteen are capable of producing observable threshold and maximal muscle contractions with joint movements.
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6/9. natural history of spinal cord infarction caused by nucleus pulposus embolism.

    Nucleus pulposus embolism causing spinal cord infarction is exceptional. A 16-year-old girl was seen with sudden onset of interscapular pain and paraplegia from fatal ischemic transverse myelopathy due to arterial and venous occlusions by fibrocartilaginous embolism. In 32 cases of nucleus pulposus embolism, females predominated (69%) and age distribution was bimodal with peaks at 22 and 60 years (median, 38.5). Embolization was either arterial and venous (50%) or purely arterial (50%). Myelopathy predominated in cervical (69%) and lumbosacral (22%) segments. Schmorl's nodes, larger volume and vascularization of nucleus pulposus in the young, and spinal arteriovenous communications, trauma, and degenerative changes in older patients could be important pathogenetic factors. diagnosis requires histopathologic confirmation. Nucleus pulposus embolism may be an underlying cause in cases diagnosed as transverse myelitis and ischemic infarction of spinal cord.
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7/9. A risk/benefit analysis of spinal manipulation therapy for relief of lumbar or cervical pain.

    Approximately 12 million Americans undergo spinal manipulation therapy (SMT) every year. Renewed interest in this method requires an analysis of its reported risks and possible benefits. This review describes two patients with spinal cord injuries associated with SMT and establishes the risk/benefit ratios for patients with lumbar or cervical pain. The first case is a man who underwent SMT for recurrent sciatica 4 years after chemonucleolysis. During therapy, he developed bilateral sciatica with urinary hesitancy. After self-referral, myelography demonstrated a total block; he underwent urgent discectomy with an excellent result 3 months after surgery. The second patient with an indwelling Broviac catheter and a history of lumbar osteomyelitis underwent SMT for neck pain. Therapy continued for 3 weeks despite the development of severe quadriparesis. After self-referral, he underwent an urgent anterior cervical decompression and removal of necrotic bone and an epidural abscess with partial neurological recovery. An analysis of these cases and 138 cases reported in the literature demonstrates six risk factors associated with complications of SMT. These include misdiagnosis, failure to recognize the onset or progression of neurological signs or symptoms, improper technique, SMT performed in the presence of a coagulation disorder or herniated nucleus pulposus, and manipulation of the cervical spine. Clinical trials of SMT have been summarized in several recent articles.(ABSTRACT TRUNCATED AT 250 WORDS)
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8/9. Fibrocartilaginous embolism of the spinal cord: a clinical and pathogenetic reconsideration.

    A 16 year old girl did a handstand for fun, returned to her feet, experienced a sudden pain in her back, and became progressively paraplegic within 30 hours. MRI showed lumbar cord swelling, multiple Schmorl's nodes, a collapsed T11-T12 disc space, and intraspongious disc prolapse into the T12 vertebral body. These findings, related to the initial manoeuvre, suggested that an acute vertical disc herniation could have occurred as the first step in a process leading to spinal cord infarction due to fibrocartilaginous emboli from the nucleus pulposus of the intervertebral disc. The medical literature so far reports 32 cases of fibrocartilaginous embolism (FCE) of the spinal cord, all at necropsy, with the exception of one histologically demonstrated in a living patient. A clinical diagnosis of FCE would be desirable for many important reasons, but was never made. This causes severe limitations in the knowledge of the disease and precludes any therapeutic possibility. On the basis of the clinical features and findings in the present case, compared with data from the reported cases, a first attempt is made to identify the clinical context within which new information obtainable through MRI examination can lead to a reliable clinical diagnosis of FCE. The vexed question of the pathogenesis has been reviewed. An increased intraosseous pressure within the vertebral body, due to acute vertical disc herniation, seems to offer a consistent pathogenetic explanation and some therapeutic prospects.
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9/9. paraplegia: prolonged closed-loop standing with implanted nucleus FES-22 stimulator and Andrews' foot-ankle orthosis.

    Our object is to develop a reliable, implantable and closed-loop functional electrical stimulator (FES) hybrid system for safe prolonged standing in paraplegic individuals. Open-loop FES systems rapidly induce muscle fatigue that limits paraplegic standing to less than 20 and typically 10 min. Since December 1991, a paraplegic male (CS: 23 years old, T10 level, asia: A) has been implanted with the first Nucleus FES-22 channel stimulating system (Cochlear Ltd., Lane Cove, N.S.W., australia). Epineural platinum disc electrodes (2.5 mm) were placed on branches of the femoral, gluteal and sciatic nerves, which can be activated to produce controlled lower extremity movements for exercise and standing. No medical complications have occurred during these 5 1/2 years of implantation. The ankles are stabilized with Andrews' ankle-foot braces, the knees are free to flex. With bilateral knee goniometers fitted to sense a 10 degrees angle flexion, this hybrid closed-loop stimulation system allows the patient to achieve safe uninterrupted standing for over 60 min. The stimulator has needed to be activated 'on' for 8% (range: 3-17%) of the standing times, preventing muscle fatigue, with little or no changes found in the vital signs. The patient can manipulate and transfer objects at arm length up to 2.2 kg with good stability. New, less obstrusive sensors are currently being tested for a safer and more reliable closed-loop system.
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