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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We assessed muscle pathology in 30 patients with ankylosing spondylitis (AS) and 22 controls to assess if skeletal muscle is affected primarily by the inflammatory process of the disease. Investigations included a questionnaire on musculoskeletal discomfort, physical exercises, dynamometric measurements, EMG, and biopsy of the quadriceps muscle. Symptoms of muscular weakness were related with enthesopathic activity index. Plasma CK was higher in patients than in controls. A myopathic EMG pattern was found in 46.4% patients. Histological changes were found in 66% and did not correlate with symptomatology. Patients with AS with clinical muscular manifestations probably have intense enthesopathic inflammatory activity. It is suggested that muscles are secondarily affected as a consequence of pain inhibition and reduced activity.
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PMID:Muscle pathology in ankylosing spondylitis: clinical, enzymatic, electromyographic and histologic correlation. 175 39

The histological appearance of percutaneous superficial paraspinal muscle biopsy specimens from eight patients with ankylosing spondylitis was compared with that of biopsy specimens from 13 control patients with similar degrees of disability and spinal immobility due to severe, chronic mechanical back pain. In both groups marked type II muscle fibre atrophy was shown. Additionally, in patients with ankylosing spondylitis there were obvious increases in perifibre connective tissue in association with central migration of cell nuclei but without evidence of inflammation. Qualitative electromyography failed to show denervation changes in either group. Paraspinal muscle fibrosis, occurring over and above atrophic changes due to disuse, seems to be a specific pathological component of ankylosing spondylitis which may be of particular importance in early disease as it may contribute towards back stiffness and weakness.
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PMID:Paraspinal muscle fibrosis: a specific pathological component in ankylosing spondylitis. 183 5

A 55-year-old man who has had ankylosing spondylitis for over 20 years developed gradually increasing pain and sensory disorders in the legs, as well as mild foot and toe elevator weakness. There was no evidence of inflammatory activity. Clinical, neurophysiological and neuroradiological examination revealed a cauda equina syndrome as a late complication of ankylosing spondylitis. There is no known causal treatment.
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PMID:[Cauda equina syndrome in ankylosing spondylitis]. 291 54

An example of a traumatic extradural hematoma of the cervical spine that occurred in a 32-year-old man who suffered from chronic ankylosing spondylitis is reported. Progressive sensory and motor deficit ensued some 3 hours after the patient fell from a standing position. The patient landed on his back, striking his head on the floor. After being helped up, he was able to walk unassisted to a nearby chair, where he sat down until his left lower extremity--and shortly afterwards, the right one--became numb and weak. On admission, the patient was found to have tetraparesis that was more pronounced in the lower extremities and associated with incomplete sensation to pinprick at level T7-T10. He also had painless distention of the urinary bladder. After a few hours, the weakness in his limbs increased and his sensory level rose to C5 bilaterally. A horizontal diastatic fracture across the vertebral body of C7 was discovered on plain x-ray films of the spine, and an extradural hematoma extending dorsally from C5 to T1 was revealed by emergency magnetic resonance imaging. After an emergency decompressive cervical laminectomy and removal of the clot, the patient rapidly regained complete neurological function, except with regard to both the urinary bladder and the rectum, which remained abnormal for almost 7 weeks after the operation.
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PMID:Traumatic extradural hematoma of the cervical spine. 292 16

A study is presented of six patients who suffered flexion (chin-on-chest) deformity of the cervical spine on a neuropathic or myopathic basis. An awareness of this possibility is recommended, differentiating these patients from those with similar deformities due to ankylosing spondylitis, trauma, or primary degenerative change. Recognition is based on a detailed history, weakness of neck extension, electrodiagnostic studies, and muscle biopsy. A mildly elevated creatine phosphokinase (CPK) was the only consistent laboratory finding. Appropriate surgical correction of severe deformity involves anterior surgical release of contracted sternomastoid muscles, halo-dependent traction, posterior vertebral inferior facet resection, and spinal fusion over an adequate length, supplemented with internal fixation. Where extension correction involves extensive vertebral body separation anteriorly, additional anterior keystone strut grafting is indicated.
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PMID:Neuro-myopathic flexion deformities of the cervical spine. 319 83

Axial traction is widely recommended for stabilization of cervical spine fractures. This procedure may be inappropriate and even dangerous in patients with long-standing ankylosing spondylitis (AS). We present the case of an 80-year-old woman with AS who fell at home and suffered an unstable large C5-C6 fracture/dislocation associated with left-sided weakness and decreased sensation. Medical treatment included placing her neck in a neutral position, despite her preference for neck flexion. This procedure increased her pain and paresthesias; the complications decreased, but did not entirely resolve, when the patient resumed a semi-flexed position. This patient's neurologic sequelae may have been exacerbated by attempts to stabilize her neck in a neutral position. Standard stabilization recommendations should be appropriately altered in some patients with cervical spine AS.
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PMID:Neurologic complications following immobilization of cervical spine fracture in a patient with ankylosing spondylitis. 661 15

Fourteen patients with cauda equina syndrome secondary to long-standing ankylosing spondylitis are described. The roughly symmetrical neurological deficits were very slowly progressive and began long after the onset of the spondylitis, usually well after the rheumatological symptoms had stopped. Eventually every patient had cutaneous sensory loss in the fifth lumbar and sacral dermatomes. All patients developed urinary sphincter disturbances of a lower motor neuron type. There was prominent loss of rectal sphincter tone, and all but 2 patients had bowel complaints, including incontinence and severe constipation. Seven patients had mild to moderate weakness in the lumbosacral myotomes. Seven patients had pain in the rectum or lower limbs. Electromyographic abnormalities were consistent with multiple lumbosacral radiculopathies. Myelography and computed tomographic scanning of the lumbosacral spine showed characteristic enlargement of the caudal sac and dorsal arachnoid diverticula that had eroded the laminae and spinous processes. Recognition of this syndrome, coupled with computed tomographic scanning of the lower spinal canal, allows one to omit myelography, a procedure that is difficult because of the associated spine abnormalities. Surgical intervention should be avoided.
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PMID:Cauda equina syndrome secondary to long-standing ankylosing spondylitis. 665 Dec 50

On the suggestion of a Chinese physician the author took up Tai Chi, a traditional Chinese exercise, in an attempt to relieve symptoms from his moderately severe ankylosing spondylitis. Conventional medical therapy, used over a 15 year period, had proven of only limited benefit. Tai Chi consists of a series of intricate exercise sequences, and after 2 1/2 years of daily practice the author now feels stronger and healthier than before. Pain, weakness and general malaise return if practice is neglected for as little as one week. It is felt that Tai Chi is of value in minimizing the flexion deformity of the spine. Improved skeletal muscle strength, limb co-ordination, balance, chest movement and ability to relax are further benefits.
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PMID:Tai Chi and ankylosing spondylitis--a personal experience. 718 8

A patient with cauda equina syndrome complicating long-standing inactive ankylosing spondylitis is described. The first neurological symptoms started 15 years after the onset of ankylosing spondylitis. Over a follow-up period of 12 years the cauda equina syndrome showed a slowly progressive but disabling course leading to sensory disturbances in the lumbar and sacral dermatomes, weakness and wasting of the muscles innervated by these nerve roots, sphincter disturbances, and impotence. Magnetic resonance imaging, computed tomography, and lumbar myelography showed enlargement of the dural sac with multiple lubar diverticula eroding the lumbosacral vertebrae. The pathophysiology of the cauda equina syndrome in ankylosing spondylitis is unclear. Surgical treatment seems justified only in patients with a short history of neurological symptoms.
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PMID:Cauda equina syndrome with multiple lumbar diverticula complicating long-standing ankylosing spondylitis. 771 15

The onset of ankylosing spondylitis is usually characterized by lower back pain and stiffness in young adults; early diagnosis is not easy, but the disease is generally identified within a few years of onset. Anterior atlantoaxial subluxation may occur in the late stage of ankylosing spondylitis, but early spontaneous subluxation is rarely seen. We present a case of ankylosing spondylitis with an initial symptom of neck pain, rather than lower back pain, due to spontaneous anterior atlantoaxial subluxation. After medical and surgical intervention, except for limited range of motion, the patient experienced neither neck pain nor weakness of his left limbs during the next 8 mo of follow-up.
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PMID:Ankylosing spondylitis manifested by spontaneous anterior atlantoaxial subluxation. 1244 95


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