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

Dropfoot is a catchall term for ankle equinus, equinovarus, and equinovalgus. The deformity can be flexible or rigid and may be associated with other pathology. In the adult, dropfoot may be congenital or acquired. Acquired dropfoot results from weakness of the ankle dorsiflexors, overpull of the plantarflexors, contracture of the soft tissues, bony deformity, or any combination of these factors. Appropriate treatment includes observation, orthotic devices, bracing, tendon transfers, arthrodesis, and neurolysis. The purpose of this paper is to review the pathophysiology and treatment of acquired dropfoot.
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PMID:Management of acquired adult dropfoot. 134 93

A retrospective study of 9 patients with infantile facioscapulohumeral muscular dystrophy defines orthopedic deformities and progression. Patients presented in the early months of life with facial diplegia. Sensorineural hearing loss occurred in 8 out of 9 with a mean onset at 5 (2-9) years. Walking began at the normal time, but worsened progressively, which was due mainly to gluteus maximus muscle weakness. Scapular winging, extreme lumbar lordosis, and foot drop were characteristic. The majority of patients (in this and other series) lose walking ability in the second decade. Efforts to control lumbar lordosis by bracing while the patients were still walking were ineffective. Control of lumbar lordosis after the patients are wheelchair-dependent is important.
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PMID:Locomotor problems in infantile facioscapulohumeral muscular dystrophy. Retrospective study of 9 patients. 188 79

A 52-year-old human immunodeficiency virus type 1-seropositive bisexual black man was evaluated at UCLA because of the recent onset of progressive lower-extremity weakness. Initial neurologic examination showed that the patient's distal weakness was greater than his proximal weakness, with bilateral foot drop and electrophysiologic evidence of denervation in the distal lower extremities. Magnetic resonance imaging of the brain and spinal cord disclosed no abnormalities. Subsequent neurologic evaluation 8 months later showed a myelopathy, with progression of lower-extremity weakness, spasticity, and flexor spasms, and urinary incontinence, as well as the peripheral neuropathy noted previously. A second magnetic resonance imaging scan of the brain showed patchy foci of increased signal intensity in white matter and cortex, with mild generalized cerebral and cerebellar atrophy and no lesions in the spinal cord. Specimens of the patient's serum and cerebrospinal fluid contained antibodies to human immunodeficiency virus type 1. Additionally, specimens of his serum and cerebrospinal fluid were tested for antibody to human T-cell leukemia virus type I by Western blotting and radioimmunoprecipitation, and found to be positive for human T-cell leukemia virus type I gag, env, and tax antibodies. The primary cause of severe myelopathy in this patient may be infection with human T-cell leukemia virus type I rather than with human immunodeficiency virus type 1. Treatment with prednisolone resulted in improvement of the lower-extremity weakness, reduction in flexor spasms, and slower but significant improvement in urinary symptoms. Patients who are infected with human immunodeficiency virus type 1 and have unusual motor findings should be tested for concomitant human T-cell leukemia virus type I infection.
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PMID:A patient with progressive myelopathy and antibodies to human T-cell leukemia virus type I and human immunodeficiency virus type 1 in serum and cerebrospinal fluid. 232 40

A 17-year-old retarded male developed unilateral leg weakness with foot drop, pain, and incontinence. Workup disclosed a cauda equina tumor which, on surgical exploration, was demonstrated to merge with the conus medullaris. Pathological examination of the subtotally resected tumor led to a diagnosis of malignant ganglioglioma. Further evaluation of the patient documented marginal macro-orchidism, and chromosome studies showed fragile X. Since some neoplasms are known to be associated with chromosomal deletions and other abnormalities, we suggest that the occurrence of this tumor in this patient indicates a more than coincidental relationship between the two diagnoses.
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PMID:Central nervous system neoplasm in a young man with Martin-Bell syndrome--fra(X)-XLMR. 381 81

Rehabilitation of the multiple sclerosis patient must be individualized because of the varied manifestations and fluctuating course of the disease. The activity schedule must be modified to compensate for muscle weakness and fatigability. Spasticity and the preventable complication of joint contractures may be treated with joint ranging, medications, motor-point blocks and surgical intervention. Mobility problems, such as foot drop, may be improved with an ankle-foot orthosis, but ultimately a patient may require a wheelchair. Measures to prevent pressure sores include position change, pressure release, incontinence management and special equipment.
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PMID:Multiple sclerosis: Part I. Common physical disabilities and rehabilitation. 405 Jun 40

A 64-year-old Black woman presented with high titer serum rheumatoid factor (RF), pelvic girdle weakness, sensory mononeuropathy, pulmonary fibrosis, and muscle histologic evidence of small artery necrotizing vasculitis. High dose corticosteroid therapy was followed by clinical improvement and reduction in serum RF titer. Four years later, and 9 months after discontinuance of corticosteroids, she developed an inflammatory polyarthritis, recurrent muscle weakness, and left foot drop, concomitantly with circulating immune complexes and extremely high titer serum RF. Necrotizing vasculitis is a distinctly rare presenting manifestation of rheumatoid disease.
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PMID:Necrotizing vasculitis as the initial manifestation of rheumatoid arthritis. 686 90

Forty-six separate gait studies were analysed for 21 ambulatory patients with Duchenne muscular dystrophy. Three groups were defined on the basis of significant gait variables: early, transitional and late. Disease progression can be predicted with 91 per cent accuracy by three gait variables: cadence, dorsiflexion in swing, and anterior pelvic tilt. The patients in the early group manifested a positive Gower's sign but gait changes were subtle, being principally slightly increased hip flexion in swing, decreased dorsiflexion in swing and reduction in cadence. The force line moved in front of the knee center early in single-limb support. In the transitional stage, anterior pelvic tilt was exaggerated, cadence was further reduced, and foot drop in swing phase was increased. Shoulder sway was noted as a compensation for gluteus medius weakness. The base of support widened. The force line remained behind the hip joint and in front of the knee joint throughout single-limb support. In the late stage, work output increased, cadence continued to drop, shoulder sway increased further, and there was a wider base of support. The force line remained very close to the center of the hip and in front of the knee at all times during single-limb support. The authors' conclusions are: (1) the earliest postural change in gait is increased lumbar lordosis secondary to gluteus maximus weakness, and at this time the quadriceps are relatively competent; (2) quadriceps insufficiency was the key factor in gait deterioration. It appeared in the transitional stage and was characterized by exaggerated anterior pelvic tilt, restricted hip extension in stance phase, equinus posturing, and maintenance of the force line in front of the knee throughout single-limb support. Long-leg bracing is indicated when these signs of quadriceps insufficiency are noted.
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PMID:The pathomechanics of gait in Duchenne muscular dystrophy. 720 68

The demyelinating type of hereditary motor and sensory neuropathy (HMSN I) is characterized by progressive weakness and atrophy of leg muscles. Six patients (age, 25-79 yr) belonging to three generations had calf hypertrophy (6 of 6), foot drop or difficulty with heel walking (4 of 6), pes cavus (3 of 6), absent or depressed tendon jerks in the lower limbs (4 of 6), and mild distal sensory loss (3 of 6). No other family member had leg atrophy. Motor conduction velocities ranged from 20 to 40 m/sec. Sural nerve biopsy showed loss of large myelinated fibers, numerous onion bulbs, and segmental demyelination and remyelination. Computed tomographic scans of leg muscles and histological and morphometric findings in gastrocnemius revealed true muscular hypertrophy. Southern blot and fluorescence in situ hybridization documented the duplication of the entire 17p11.2 segment associated with classical HMSN IA. The pathogenesis of muscle hypertrophy in our cases is unclear. Chronic leg muscle weakness and long-standing partial denervation might cause calf enlargement by a combination of compensatory "work-induced" and "stretch-induced" fiber hypertrophy. Alternatively, that all the affected family members presented calf hypertrophy might suggest the action of a genetic factor associated with the duplication at 17p11.2.
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PMID:Hereditary motor and sensory neuropathy with calf hypertrophy is associated with 17p11.2 duplication. 817 1

Twenty-one patients with spinal stenosis who developed foot drop after total hip arthroplasty were reviewed. Patients with other risk factors for nerve injury, such as dislocation, hematoma, intraoperative limb lengthening, revision surgery, and direct operative trauma, were excluded. Also excluded were patients without symptoms of spinal stenosis. Patients in this series had back and leg pain without weakness before their hip arthroplasty. When foot drop developed and persisted four months after hip arthroplasty, patients were examined with magnetic resonance imaging or myelography and computed tomography. High-grade spinal stenosis was found in each patient. Sixteen patients were treated by lumbar decompression. Twelve patients improved; six had complete recovery of foot drop. None of the five patients who did not have surgery significantly recovered. One patient developed a foot drop in the other leg after undergoing lumbar decompression. Coexisting spinal stenosis may be a risk factor for symptomatic nerve injury during hip arthroplasty. Selected patients may benefit from lumbar decompression surgery.
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PMID:Lumbar decompression to treat foot drop after hip arthroplasty. 819 29

Peripheral nerve lesions are uncommon but serious injuries which may delay or preclude an athlete's safe return to sports. Early, accurate anatomical diagnosis is essential. Nerve lesions may be due to acute injury (e.g. from a direct blow) or chronic injury secondary to repetitive microtrauma (entrapment). Accurate diagnosis is based upon physical examination and a knowledge of the relative anatomy. Palpation, neurological testing and provocative manoeuvres are mainstays of physical diagnosis. Diagnostic suspicion can be confirmed by electrophysiological testing, including electromyography and nerve conduction studies. Proper equipment, technique and conditioning are the keys to prevention. Rest, anti-inflammatories, physical therapy and appropriate splinting are the mainstays of treatment. In the shoulder, spinal accessory nerve injury is caused by a blow to the neck and results in trapezius paralysis with sparing of the sternocleidomastoid muscle. Scapular winging results from paralysis of the serratus anterior because of long thoracic nerve palsy. A lesion of the suprascapular nerve may mimic a rotator cuff tear with pain a weakness of the rotator cuff. Axillary nerve injury often follows anterior shoulder dislocation. In the elbow region, musculocutaneous nerve palsy is seen in weightlifters with weakness of the elbow flexors and dysesthesias of the lateral forearm. Pronator syndrome is a median nerve lesion occurring in the proximal forearm which is diagnosed by several provocative manoeuvres. Posterior interosseous nerve entrapment is common among tennis players and occurs at the Arcade of Froshe--it results in weakness of the wrist and metacarpophalangeal extensors. Ulnar neuritis at the elbow is common amongst baseball pitchers. Carpal tunnel syndrome is a common neuropathy seen in sport and is caused by median nerve compression in the carpal tunnel. Paralysis of the ulnar nerve at the wrist is seen among bicyclists resulting in weakness of grip and numbness of the ulnar 1.5 digits. Thigh injuries include lateral femoral cutaneous nerve palsy resulting in loss of sensation over the anterior thigh without power deficit. Femoral nerve injury occurs secondary to an iliopsoas haematoma from high energy sports. A lesion of the sciatic nerve may indicate a concomitant dislocated hip. Common peroneal nerve injury may be due to a direct blow or a traction injury and results in a foot drop and numbness of the dorsum of the foot. Deep and superficial peroneal nerve palsies could be secondary to an exertional compartment syndrome. Tarsal tunnel syndrome is a compressive lesion of the posterior tibial nerve caused by repetitive dorsiflexion of the ankle--it is common among runners and mountain climbers.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Peripheral nerve injuries in athletes. Treatment and prevention. 837 68


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