Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Differentiation between peroneal palsy and L5 radiculopathy poses a diagnostic challenge. However, clinical weakness of the tibialis posterior muscle indicates that the involvement must lie outside the peroneal territory, potentially at a radicular level. Electromyographically this muscle should provide similar information but it has been relatively ignored, possibly for reasons of presumed inaccessibility. A retrospective study was undertaken to delineate the potential electrical discriminatory value of this muscle. Patients selected were those with clinical evidence of lower extremity neurogenic dysfunction in whom needle electrode examination had been performed on the tibialis posterior as well as other posterior and anterior compartment musculature. The parameters measured were the presence of abnormal spontaneous activity suggestive of denervation plus neurogenic motor unit alterations. Abnormalities were detected in the tibialis posterior which were reflected equally in the anterior but not posterior compartment muscles, indicating a shared L5 radicular innervation. Thus this muscle represents a useful source of electrical information assisting in the differentiation between peroneal and radicular dysfunction.
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PMID:Electromyographic value of the tibialis posterior muscle. 22 37

Chordoma at the T-9 level, originally manifested by lumbosacral radiculopathy, developed in a 50-year-old man. The patient underwent three operations and radiation therapy for this condition, but ten years later, thoracic myelopathy developed, followed by left facial weakness. On autopsy, extensive dissemination of chordoma was found along the base of the brain and in the leptomeninges of the spinal cord.
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PMID:Subarachnoid dissemination of thoracic chordoma. 48 98

Three cases of musculocutaneous nerve injury distal to its innervation of the coracobrachialis muscle are reported. The syndrome typically features painless weakness of the biceps brachii and brachialis muscles, sensory loss in the distal volar forearm, a history of recent vigorous upper extremity resistive exercise, and resolution of the problem on resting the affected extremity. In all three reported cases the dominant arm was involved. The condition should not be confused with C-5 or C-6 radiculopathy, brachial plexopathy, or rupture of the biceps brachii muscle belly or tendon.
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PMID:Musculocutaneous nerve injury after heavy exercise. 66 61

In diabetes mellitus, pain and weakness in a lower extremity can result from lumbosacral radiculopathy. However, abdominal pain caused by a similar type of thoracic nerve root disease is not generally recognized. Four diabetic patients with abdominal pain were studied. In none of the patients was the actual cause--radiculopathy--suspected until after extensive negative diagnostic investigation, which frequently included invasive procedures. Their clinical features were suggestive of malignant disease. Electromyographic examination revealed the correct diagnosis, and all four of the patients had a spontaneous and complete recovery.
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PMID:Abdominal pain caused by diabetic radiculopathy. 83 36

The natural history of cervical spondylotic myelopathy in a series of 55 patients resulted in a moderate to severe disability during a mean period of 45 months. Results of operation for myelopathy indicated improvement in one group that was maintained for a mean of 85 months. In another group, progressive worsening occurred after operation, or late worsening occurred, in some instances as long as 8 to 12 years after improvement and plateau. Patients with cervical spondylotic radiculopathy tended to be separated from those with myelopathy with respect to presentation, symptom complex, and operative result. Results of operation for radiculopathy were consistently good. A worsened disability postoperatively for patients with cervical spondylotic myelopathy was associated with the preoperative symptom of sphincter disturbance and the sign of lower extremity weakness. Change in hand movement after operation for myelopathy and change in distance walking ability were not correlated with numerous preoperative factors. A trend of improvement in disability following anterior interbody fusion and a tendency to worsen in disability following all varities of laminectomy were significant.
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PMID:Cervical spondylotic radiculopathy and myelopathy. A long-term follow-up study. 96 44

We performed lower extremity somatosensory evoked potential (SEP) studies in 59 patients with signs or symptoms suggestive of lumbosacral radiculopathy and compared them with results of myelography with post-myelogram CT (myelogram/CT), MRI, and other electrodiagnostic studies. Of 38 patients with abnormal myelogram/CTs, 32 had abnormal SEPs, while 11 demonstrated EMG abnormalities. All 21 patients with normal myelogram/CTs had normal SEPs. SEP improved electrodiagnostic sensitivity in patients with weakness or reflex changes as well as in those with sensory deficits only. SEP was less sensitive in patients in whom spinal stenosis was the only radiographic finding. MRI generally corresponded well with the results of myelogram/CT and SEP but overestimated the significance of disk bulges in some patients. SEP is useful in the electrodiagnostic evaluation of lumbosacral radiculopathy, particularly when EMG is nondiagnostic.
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PMID:Somatosensory evoked potentials in the evaluation of lumbosacral radiculopathy. 131 22

A 55-year-old man had felt numbness of the bilateral peroneal sides of legs for 6 months. Then hepatosplenomegaly, anemia, body weight loss and fever developed, and a diagnosis of malignant histiocytosis (MH) was made by revealing the presence of innumerable atypical histiocytes with hemophagocytosis in the bone marrow. Soon later, sensory disturbance of bilateral peroneal sides of legs (right side dominant) developed and aggravated with painful dysesthesia and weakness of the legs for the last 2 weeks before death. Electrophysiologically, sensory conduction velocity of the sural nerve was normal and somatosensory evoked potentials from tibial nerve were normal before P15 but were not evoked at all after the lumbar potential, suggesting lumbosacral radiculopathy. Autopsy showed multifocal ischemic lesions and secondary degeneration of the lumbosacral nerve roots associated with necrosis and fibrosis of the radicular vessels and intravascular infiltration of atypical mononuclear cells which were positive for B cell markers. The neurological manifestations and the distribution of ischemic lesions, which were similar to those of vasculopathic mononeuropathy multiplex, would deserve the name of "monoradiculopathy multiplex".
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PMID:[Mono-radiculopathy multiplex--multiple infarction of the cauda equina caused by intravascular lymphomatosis]. 181 93

We reported a patient with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), presenting localized radiculopathy as an initial symptom. The patient, a 38-year-old man, developed muscle atrophy of right shin and calf. In April 1988, neurological examination revealed decreased superficial sensation and muscle atrophy in right L-4 distribution. MRI of the lumbar spinal cord and myelography were negative. In April 1989, he was admitted to Chiba University Hospital. There were slight weakness of right ankle extension and flexion, muscle atrophy of bilateral shin and calf (that of the right leg was more marked), decreased sensation of polyneuropathy type in all modalities and generalized hypo- or a-reflexia. Nerve conduction study revealed marked prolongation of F response and focal conduction block in various site. The CSF was acellular and total protein was 177 mg/dl. Sural nerve biopsy disclosed decreased number of large myelinated fibers and scattered thin myelinated fibers. This case indicates that CIDP may present localized radiculopathy in early phase and is important to point out various mode of onset among CIDP.
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PMID:[Chronic inflammatory demyelinating polyradiculoneuropathy presenting localized radiculopathy as an initial symptom]. 189 72

A 47-year-old woman developed radiating right lower extremity pain with weakness in the L5 myotomes. A CT scan, subsequent myelogram, and postmyelogram CT scan were reported as negative. Two months of bed rest diminished the radiating symptoms, but the weakness persisted. Three months post onset a severe burning dysesthesia developed in the right foot, and the patient became unable to bear weight on that extremity. Physical examination revealed 4-/5 weakness of the ankle dorsiflexors, foot evertors, toe extensors, and hip abductors. The entire right foot was swollen and had a red, mottled discoloration. An EMG was equivocal, and a three-phase bone scan was positive in the right foot in all three phases, which is characteristic of reflex sympathetic dystrophy. A repeat CT scan and review of the earlier scans revealed a high lateral disc fragment at the exit foramina of the L5 nerve root. Upon laminectomy, a free disc fragment at the exit foramina was removed, and the patient's symptoms resolved completely. Reflex sympathetic dystrophy syndrome is very rarely reported in association with lumbar radiculopathy. This case emphasizes the need to carefully evaluate the far lateral exit foramina on CT scan in patients with symptoms of radiculopathy. Myelogram is characteristically normal in these cases.
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PMID:Reflex sympathetic dystrophy syndrome secondary to L5 radiculopathy. 205 41

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


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