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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the differential diagnosis of intermittent claudication some rare myopathies have to be considered. The most frequent is phosphorylase deficiency (McArdle's disease). Exercise-induced muscular pain, weakness, contractures and occasionally myoglobinuria are the most prominent clinical signs. Serum creatine phosphokinase, aldolase and lactic dehydrogenase may be elevated after exertion. In the ischemic forearm test there is no rise of serum lactic acid. The enzyme deficiency can be demonstrated by histochemical and biochemical examination of a muscle specimen. Further, but more infrequent, enzymatic disturbances of glycolysis are phosphofructokinase deficiency and phosphohexoisomerase inhibitor, which also yield an abnormal ischemic forearm test and must be demonstrated histochemically and biochemically. Apart from muscular signs, myopathy with lactic acidosis is associated with palpitation, dyspnea and exhaustion, and a disproportionate rise in serum lactic acid level after exertion. Histochemically and electronmicroscopically demonstrable fat accumulation in the muscle can be a sign of a disturbance in lipid metabolism. This type of exercise-induced myopathy has been reported only in a few cases with carnitine-pylmityltransferase deficiency, which has to be demonstrated biochemically. Muscular contractures also exercise-induced but painless and reversible within seconds may be due to deficient uptake of sarcoplasmic calcium in the tubular system. Dyskalemic paralysis causes painless paresis within minutes of hours after exertion, which disappears within hours to a few days. Myopathy with tubular aggregates can be differentiated from other exercise-induced myopathies by morphology. Myotonia combined with painful contractures characterizes myopathia myotonica.
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PMID:[Exercise-induced muscular weakness, myalgia and contractures. I. A clinical review]. 13 80

The pseudoclaudication syndrome, now a well known neurological entity, can simulate intermittent claudication of arterial origin in its clinical appearance. Walking and sometimes simply standing upright for a while can cause transitory pain, numbness or weakness in the legs. The symptoms are caused by entrapment of the cauda equina fibers. Intermittent bladder paresis with total inability of micturition despite urgency to void may sometimes be a prominent feature of the syndrome, a fact that seems to be less well known as seen from a review of the literature.
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PMID:Intermittent bladder paresis in the pseudoclaudication syndrome. 126 26

64 patients (60 to 83 years old) with intermittent claudication underwent a six months lasting supervised exercise walk training. Most of them suffered from concomitant disease impairing walking performance or just weakness by age. Walking distance was measured in the beginning and after 3 and 6 months. We found an improvement in walking distance in all groups (60-64 years: 273%; 75-83 years: 196.6%) So we recommend to apply walk training to a much more patients even with concomitant disease are of old age.
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PMID:[Walking training as basic therapy of stage II peripheral arterial occlusive disease--success despite advanced age and concomitant diseases]. 178 65

A 41-year-old man was doing well until July 1989, when he noted numbness over soles, followed 4 months later by difficulty in walking. These symptoms were progressively getting worse, and he was admitted to our department on June 12, 1990. General physical examination was unremarkable. Neurologically cranial nerves were intact except old right, traumatic strabismus. Muscle tone and deep tendon reflexes were normal throughout, but bilateral Babinski and Chaddock reflexes were present. Mild weakness of lower extremities were found on muscle testing (4/5). In sensory system, superficial sensory disturbance below T10 was seen, and markedly diminished vibration and position senses of lower extremities were noted. Cerebellar test was intact, although unsteadiness was found on heel-shin test. Romberg sign was definitely positive. His gait was wide-based and ataxic. Laboratory data showed no abnormalities in CBC, chemistry, urinalysis, serological tests and endocrinological examinations. Spinal MRI (Siemens 1.5 Tesla) showed abnormal deposition of epidural fatty tissues compressing spinal cord with flattening of cord from T4 to T8. Spinal ataxia as compressive myelopathy due to epidural lipomatosis was considered and he underwent laminectomy from T4 to T8 with improvement in walking. Epidural lipomatosis is an unusual cause of spinal cord compression, presenting compressive myelopathy, radiculopathy, cauda equina syndrome, intermittent claudication, or back pain. Most of cases were associated with long-term administration of adrenocortical steroid hormone, or underlying diseases, except only 3 cases including ours. This is the first case of spinal epidural lipomatosis presenting progressive gait disturbance due to spinal ataxia.
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PMID:[A case of epidural lipomatosis presenting spinal ataxia]. 206 Feb 46

A rare case of achondroplasia showing diffuse spinal canal stenosis is presented. A 39-year-old woman was admitted to our hospital because of numbness of lower extremities and intermittent claudication. The patient's height was 121cm and she had the typical clinical features of an achondroplastic dwarf. Neurological examination revealed spastic paraparesis, and sensory impairment below the level of T11 in the left side and L1 in the right. A plain X-ray feature of the spine showed spinal canal stenosis. The interpedicular distances were short in all vertebrae, and especially more prominent in the caudal lumbar region. The sacrum laid horizontally and the sacral angle was narrower than normal case. Myelography and computed tomographic myelography demonstrated severe stenosis of the subarachnoid space at the level of T9-11. Laminectomy was performed from the inferior half of T9 to T11. The yellow ligaments were prominently hypertrophic and these were removed as far as possible. Postoperatively, the weakness of the lower extremities was improved immediately, but numbness remained. Five months after the operation, she suffered from urinary dysfunction, so further laminectomy from T12 to L5 was performed. Also in this operation, hypertrophic yellow ligament was pathognomonic. Following this operation the patient had a good recovery course and returned to work.
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PMID:[A case of achondroplasia showing diffuse spinal canal stenosis]. 221 74

Intermittent claudication from peripheral vascular disease is sometimes difficult to distinguish from neurogenic claudication secondary to lumbar spinal stenosis. Of 172 patients with symptoms of claudication and lumbar spinal stenosis proved by myelography or computed tomography (CT), nine had peripheral vascular disease identified with ultrasonography and arteriography. All of the nine patients had a laminectomy performed to decompress the narrow spinal canal, and two had an additional posterolateral fusion. Two patients were treated with an excision of their abdominal aortic aneurysm, while one of those patients later required a bypass graft for iliac stenosis. One patient had had an aortofemoral bypass graft, one a femoropopliteal graft, and one a lumbar sympathectomy. Follow-up study ranged from three to eight years, with an average of five years after their last surgical procedure. Paresthesias generally dissipated after the spinal surgery. The cramping-type discomfort associated with walking was not easily attributed either to vascular or a neurogenic etiology. Five patients had initial weakness, which invariably improved. A secondary etiology contributing to claudication must be excluded in those patients with persistent discomfort following previous lumbar spinal or vascular surgery for arterial insufficiency.
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PMID:Concurrent lumbar spinal stenosis and peripheral vascular disease. A report of nine patients. 336 86

We describe a case of histologically proven giant cell arteritis (GCA) in a 62-year-old woman who initially presented with upper limb girdle pain and weakness, and intermittent claudication. Clinical improvement was obtained with oral prednisolone. She subsequently developed a photosensitive rash and was diagnosed as having systemic lupus erythematosus. The features of the two conditions and the possibility of an association are discussed.
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PMID:Giant cell arteritis and systemic lupus erythematosus. 340 55

Although synovial cysts are most commonly associated with rheumatoid arthritis and osteoarthritis, they may occur in many other conditions. The clinical manifestations of these cysts are numerous and may result from pressure, dissection or acute rupture. Vascular phenomena occur when popliteal cysts compress vessels, and result in venous stasis with subsequent lower extremity edema or thrombophlebitis. Rarely, popliteal cysts may cause arterial compromise with intermittent claudication. Neurological sequelae include pain, paresthesia, sensory loss, and muscle weakness or atrophy. When synovial cysts occur as mass lesions they may mimic popliteal aneurysms or hematomas, adenopathy, tumors or even inguinal hernias. Cutaneous joint fistulas, septic arthritis or osteomyelitis, and spinal cord and bladder compression are examples of other infrequent complications. Awareness of the heterogeneous manifestations of synovial cysts may enable clinicians to avoid unnecessary diagnostic studies and delay in appropriate management. Arthrography remains the definitive diagnostic procedure of choice, although ultrasound testing may be useful.
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PMID:Clinical manifestations of synovial cysts. 723

Stenosis of the vertebral canal is a form of compressive stenosis in contrast to transport stenosis of vessels or other channels. The concept, definition and pathomorphological properties are discussed. As it is a form of compressive stenosis, the diagnosis is based on measurements of diameters rather than of cross-sectional surfaces. The biomechanical action of compressive stenosis is compression of the fixed living content at two opposite sites or at all sites. The special properties of sciatica in stenosis are described and presented in tabular form. Some properties of neurogenic intermittent claudication (I. Cl.) in the presence of stenosis are discussed. There is a predominance of sciatica at rest and of motor weakness during walking. The mechanism of neurogenic I. Cl. is obscure. Stenosis of the lumbar vertebral canal is one of the conditional determinants of I. Cl. The data presented in this paper demonstrate, however, that stenosis is not an absolute determinant of I. Cl. and that its production depends on the combination with other determinants. The theory is advanced that other determinants may be related to changes in the caudal nerve roots due to either constitutional properties or to subclinical changes induced by ageing and chronic wear and tear, and compression and traction in the area of stenosis during various bodily activities. Suppression of sciatica during I. Cl. is a phenomenon which is particularly difficult to explain.
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PMID:Stenosis of the lumbar vertebral canal and sciatica. 745 68

An adult case of acrodysostosis with striking lumbar spinal canal stenosis is reported. She complained of numbness on the right arm, intermittent claudication with numbness on both legs and pain and weakness on the left leg. Although the reduced lumbar interpedicular distance has been reported, no adult case with neurologic symptoms has been reported.
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PMID:Acrodysostosis associated with spinal canal stenosis. 823 85


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