Piriformis syndrome (PS) is an uncommon neuromuscular disorder caused by the piriformis muscle (PM) compressing the sciatic nerve (SN). The main symptom of PS is sciatica, which worsens with certain triggering conditions. Because the pathophysiology is poorly understood, there are no definite diagnostic and therapeutic choices for PS. This case report presents a young woman who mainly complained of bilateral leg weakness. Electromyography revealed bilateral sciatic neuropathy and magnetic resonance imaging confirmed structural lesions causing entrapment of the bilateral SNs. After a laborious diagnosis of bilateral PS, she underwent PM releasing surgery. Few PS cases present with bilateral symptoms and leg weakness. Therefore, in such cases, a high level of suspicion is necessary for accurate and prompt diagnosis and treatment.
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To investigate the effects of asymptomatic back muscle weakness and spinal deformity on low back pain (LBP).
Sixty healthy subjects without LBP participated in this study. Radiography and an isokinetic/isometric dynamometer were used to respectively measure spinal scoliosis/lordosis and the strength of the trunk flexors/extensors. After 2 years, 48 subjects visited the hospital again and LBP episodes, its severity and the Korean version of the Oswestry Disability Index were assessed. Differences between the group with LBP and the group without LBP were evaluated and the association with LBP incidence and severity was determined.
Sex, age, and trunk strength were significantly different in both group. Sex and age were significantly positive associated with LBP incidence. The isometric trunk flexor and extensor strength, maximum isokinetic trunk flexor and extensor strength were significantly and negatively associated with the LBP severity. The maximum isokinetic trunk extensor and maximum isometric trunk extensor strength was significantly negative associated with the LBP incidence.
LBP incidence is associated with isometric and isokinetic trunk extensor weakness, whereas LBP severity is associated with age, sex, isokinetic trunk extensor and flexor weakness, isometric trunk extensor and flexor weakness.
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Myotonic dystrophy is the most common autosomal dominant myopathy in adults. Our patient, a 41 year-old female suffering from myotonic muscular dystrophy, developed upper thoracic myelopathy due to hypertrophy of the ligamentum flavum and the posterior longitudinal ligament. She had a typical hatchet face and ptosis with "head hanging forward" appearance caused by neck weakness. Motor weakness, sensory changes and severe pain below T4 level, along with urinary incontinence began 3 months ago. Genetic and electrodiagnostic studies revealed myotonic dystrophy type 1. Magnetic resonance imaging of the spine showed loss of cervical lordosis and spinal cord compression due to hypertrophied ligamentum flavum and posterior longitudinal ligament at T1 to T3 level. We concluded that her upper thoracic myelopathy was likely related to the thickness of the ligamentum flavum and posterior longitudinal ligament due to repetitive mechanical stress on her neck caused by neck muscle weakness with myotonic dystrophy.
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Objective: To observe the ipsilateral upper limb function after stroke comparing proximal with distal part and to determine how they recover after stroke.
Method: Cohort study of 72 patients with stroke in the middle cerebral arterial territory undergoing multidisciplinary stroke rehabilitation program. The main outcome was assessed by the Manual Function Test (MFT) for upper limb function, weekly.
Results: The recovery time of the ipsilateral upper limb to maximum function was 32.4 ⁑ 15.4 days. The functions of the ipsilateral shoulder and hand after stroke decreased significantly. Even at the maximum recovery, complete recovery was not seen. For ipsilateral shoulder, more severe functional deficits were seen with subcortical lesion than with cortical lesion, whereas for ipsilateral hands, no difference was seen between them.
Conclusion: Therefore, the fact that recoveries of the shoulders and hands were different according to the presence of cerebral cortical or subcortical lesions suggests that the brain structures that control these areas or the recovery mechanisms might be different.
Objective: We observed the nature of ipsilateral weakness, not hemiplegic side after stroke. And we studied correlation between ipsilateral weakness and neurologic recovery of hemiplegia.
Method: This study was prospective, follow-up clinical trial. Ipsilateral motor power was checked serially in 20 subjects using Nicholas Manual Muscle Tester (NMMT) (shoulder abduction, wrist extension, hip flexion, ankle dorsiflexion). The subjects are first attacked hemiplegic stroke patients. Other outcome measures are Mini-mental Status Examination (MMSE) and National Institutes of Health Stroke Scale (NIHSS). We studied correlations between motor power recovery in ipsilateral limbs and recovery of neurologic impairment in hemiplegic limbs of stroke patients through SPSS 7.0 program.
Results: Ipsilateral motor power in early stage stroke patients is significantly low compared with that of normal subject except ankle dorsiflexion (p＜0.05). Comparing ipsilateral proximal with distal limbs power in pre and post multidisciplinary rehabilitation program, upper proximal part recovered faster than the distal part, but which was not statistically significant. Recovery of ipsilateral upper proximal and distal limb weakness is associated with neurologic recovery in hemiplegic side.
Conclusion: After the stroke, ipsilateral upper limb motor weakness does occur and which follows similar neurologic recovery pattern to the hemiplegic side. Ipsilateral cortical and subcortical tracts take effect on the neurologic recovery of contalateral side.
In 1971 inclusion body myositis was reported by Yunis and Samaha. This disease is similar with chronic multiple myositis clinically. Pathologically, inclusion body myositis is characterized by intracytoplasmic vacuole with degenerating fibers and accompanied with inclusion body in internal nucleus and cytoplasm. Since then 240 cases of inclusion body myositis have been reported in the world including 3 cases in Korea.
A 27 years-old lady had inclusion body myositis, which show slowly progressive muscular weakness. We confirmed this with clinical symptom, muscle biopsy, and electrophysiologic study. We report the typical manifestation of inclusion body myositis in a 27 years-old lady
Glycogen Storage Disease Type II is caused by the deficiency of acid maltase resulting in lysosomal accumulation of glycogen. There are two major clinical syndromes, a severe generalized and invariable fatal disease of infancy, and a myopathy starting in juvenile or adult life.
The clinical and laboratory findings of a patient with Glycogen Storage Disease Type II are presented. The patient, a 17-year-old male, experienced slowly progressive weakness of muscle of the pelvis shoulder girdles and trunk. Muscle biopsy showed vacuolar myopathy and electromyograph showed features of myopathy with fibrillation potentials, positive sharp waves, myotonic discharges, without clinical myotonia at rest, and polyphasic potentials on volition.
Clinical features, histopathologic and electrophysiologic findings of this disease and differential diagnosis were reviewed.
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