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

There are many conflicting theories regarding the mechanism and prognosis of acute foot drop during labor. We report seven women who had arrested labor and foot drop. Six had short stature and one had a large newborn. All had weakness of ankle dorsiflexion, eversion, and inversion, and sensory loss in the L-5 dermatome. Superficial peroneal sensory nerve action potentials (SNAPs) were small or absent in six patients, and the sural SNAP was attenuated in one. Peroneal compound muscle action potential (CMAP) amplitude (recording from extensor digitorum brevis) was low in five, whereas the tibial CMAP was normal in all patients. Peroneal CMAP amplitude (recording from the tibialis anterior) was normal in three and small in three. Needle electromyography revealed decreased recruitment and fibrillation potentials in L-5-innervated muscles, mostly below the knee. We conclude that intrapartum foot drop occurs mostly in short women and is caused by lumbosacral trunk compression by the fetal head at the pelvic brim. The primary pathology is predominantly demyelination and recovery is complete in up to 5 months.
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PMID:Intrapartum maternal lumbosacral plexopathy. 1221 Mar 62

Foot drop is a common and debilitating finding in patients with lumbar spinal disorders. Recovery of function after surgical treatment of the underlying disorder is not well documented in the literature. The purpose of this retrospective study was to analyze the prognosis of preoperative foot drop after lumbar surgery in 55 patients with foot drop and herniated nucleus pulposus and/or lumbar spinal stenosis. Preoperative dorsiflexion motor strength improved measurably in 98%, and 71% had full recovery of strength. All patients had associated neurologic findings and 71% experienced complete resolution. No statistically significant relationship was found between the extent of recovery and age, diagnosis (herniated nucleus pulposus lumbar spinal stenosis), duration of symptoms, or severity of preoperative weakness. In our series, the prognosis of preoperative foot drop and associated neurologic deficits treated by lumbar spine surgery was excellent.
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PMID:Improvement of preoperative foot drop after lumbar surgery. 1246 76

Foot drop resulting from weakness of the anterior tibial muscle is commonly encountered in clinical practice. We analyzed the incidence of needle electromyographic (EMG) abnormalities in the anterior tibial and gastrocnemius muscles from traumatic injuries to the sciatic nerve and also from different non-traumatic lower motor neuron conditions. In both traumatic and non-traumatic cases, the anterior tibial muscle showed relatively more EMG abnormalities compared to the gastrocnemius. It appears that the anterior tibial muscle is more susceptible to injury from a variety of pathologic conditions, as opposed to the gastrocnemius muscle.
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PMID:Relative incidence of needle EMG abnormalities in the anterior tibial and gastrocnemius muscles. 1248 49

This review briefly describes current concepts concerning the nosological status, pathogenesis and management of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). CIDP is an uncommon variable disorder of unknown but probably autoimmune aetiology. The commonest form of CIDP causes more or less symmetrical progressive or relapsing weakness affecting proximal and distal muscles. Against this background the review describes the short-term responses to corticosteroids, intravenous immunoglobulin (IVIg) and plasma exchange that have been confirmed in randomised trials. In the absence of better evidence about long-term efficacy, corticosteroids or IVIg are usually favoured because of convenience. Benefit following introduction of azathioprine, cyclophosphamide, cyclosporin, other immunosuppressive agents, and interferon-beta and -alpha has been reported but randomised trials are needed to confirm these benefits. In patients with pure motor CIDP and multifocal motor neuropathy, corticosteroids may cause worsening and IVIg is more likely to be effective. General measures to rehabilitate patients and manage symptoms, including foot drop, weak hands, fatigue and pain, are important.
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PMID:Management of chronic inflammatory demyelinating polyradiculoneuropathy. 1253 32

Bilateral acute foot drop is reported in a 30-year-old healthy male. He presented with a 7-day history of sudden severe backache, radiating to both the lower limbs and 1-day history of sudden bilateral ankle weakness that progressed to bilateral foot drop within 6 hours. He also developed retention of urine. Investigations revealed a large central disc prolapse at L3-4 with significant canal stenosis at that level. Following surgery the patient had progressive improvement.
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PMID:Sudden bilateral foot drop: an unusual presentation of lumbar disc prolapse. 1286 23

A neoplasm of the peripheral nerves can be obscured, especially during the early phase. The authors report a patient with sciatic nerve leiomyosarcoma. The patient's presentation and initial management are unique. A 51-year-old man with clinical manifestations of von Recklinghausen's disease reported numbness and weakness of the left leg for one and a half years. The symptoms gradually progressed. The symptoms were consistent with peripheral neuritis. The patient developed foot drop one month before coming to our service. Two episodes of biopsy confirmed leiomyosarcoma. A long, large sciatic nerve leiomyosarcoma was found intra-operatively, positioned from the upper thigh to the point where the tibial nerve passes beneath the upper margin of the soleus muscle. Surgical resection was done and confirmed the diagnosis. Decreased sensation was still intact after resection.
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PMID:Leiomyosarcoma in peripheral nerve: the first case report. 1469 91

A 58-year-old man with a 15-year history of idiopathic pulmonary fibrosis was hospitalized for rapid progression of muscle weakness to bilateral foot drop. Although laboratory data revealed high titers of myeloperoxidase anti-neutrophil cytoplasmic antibody (489 EU), the patient was diagnosed as polyarteritis nodosa limited to the lower portions of the legs. Despite of the treatment with large doses of corticosteroids and cyclosporin A, his symptoms barely improved during the following two months.
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PMID:A case of polyarteritis nodosa limited to lower legs with a high titer of MPO-ANCA under precedence of idiopathic pulmonary fibrosis. 1506 40

5-fluorouracil (5-FU)-associated peripheral neuropathy is an uncommon event. Capecitabine (CAP) is a pro-drug of 5-FU and peripheral neuropathy associated with CAP has not been reported. During analysis of 28 patients receiving CAP with concomitant radiation (XRT) for pancreatic cancer (resected or locally advanced), two patients developed signs and symptoms consistent with peripheral neuropathy. Patients received CAP 1200-1600 mg/m2 in two divided doses with XRT (total 5040-5400 Gy) x 6 weeks, followed by 4 weeks rest, then 6 cycles of CAP 2000-2500 mg/m2 in two divided doses x 14 days every (q) 3 weeks. Patients were assessed weekly during CAP-XRT and q 3 weeks during CAP alone. Patient A reported right leg weakness (foot drop) during week 4 of CAP-XRT (1600 mg/m2). Patient B developed perioral and upper extremity paresthesias during the fourth cycle of CAP alone (2500 mg/m2). Dihydropyrimidine dehydrogenase (DPD) activity was measured by radioisotopic assay using lysates of peripheral blood mononuclear cells. Neurologic examination revealed right foot drop in Patient A and was unremarkable in Patient B. Central nervous system imaging was negative. Electromyogram and nerve conduction studies showed sensorimotor peripheral neuropathy in both patients. DPD activity was normal in both patients. There was no evidence of disease progression. Neurologic symptoms resolved after stopping CAP for 4 weeks in Patient A, with no recurrence after reinitiating CAP alone at 2000 mg/m2. Patient B continued at 80% of standard dose (2000 mg/m2) and symptoms resolved without further intervention. We conclude peripheral neuropathy with 5-FU is rare. Neurotoxicity occurs most often with intermittent high dose 5-FU as bolus injection or 24- to 48-h infusions. The etiology of neurotoxicity in our two patients remains unclear; however, as CAP is rapidly metabolized to 5-FU in patients with normal liver function, it is likely that 5-FU or its active metabolites (fluoro-beta-alanine) were contributing factors. Knowledge regarding potential adverse effects of CAP is paramount and dose modification is indicated with development of neurotoxicity.
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PMID:Peripheral neuropathy associated with capecitabine. 1549 38

A 75-year-old man, previously diagnosed as having chronic hepatitis C virus (HCV) infection, suddenly developed left foot drop, followed by progressive motor weakness and sensory disturbance in all of the extremities. Because of an elevated level of the rheumatoid factor (RF), he had been treated with antirheumatic drugs three years before the onset of his neurological symptoms. Within two months, he became unable to walk any more, and was transferred to our hospital. Neurologic examination showed asymmetrical severe muscular weakness and atrophy of all the limbs, and a sensory deficit under the level of the wrists and knees. Livedo reticularis was also noted in bilateral legs. Nerve conduction study revealed severe sensorimotor axonal neuropathy, and muscle biopsy specimens showed necrotizing vasculitis of small arteries in the perimysium. Serological tests indicated type II cryoglobulinemia (monoclonal IgAkappa + polyclonal IgG). A diagnosis of vasculitic neuropathy associated with HCV-related mixed cryoglobulinemia was made. A high-dose intravenous immunoglobulin therapy (IVIg) and a high-dose steroid therapy were not effective, and he died of alveolar hemorrhage probably due to pulmonary vasculitis. Postmortem pathological examination revealed severe vasculitis, accompanied by fibrinoid degeneration and the infiltration of predominant mononuclear cells into the small and medium-sized vascular walls of multiple organs such as the liver, kidney, pancreas and intestine as well as the peripheral nerves and skeletal muscles. A severe loss of myelinated fibers were also observed in the multiple peripheral nerves examined. We emphasize that patients with HCV infection and mixed cryoglobulinemia may develop severe systemic vasculitis resembling polyarteritis nodosa leading to often life-threatening polyvisceral failure, particularly in patients showing progressive mononeuropathy multiplex.
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PMID:[An autopsy case of systemic vasculitis associated with hepatitis C virus-related mixed cryoglobulinemia presenting severe peripheral neuropathy]. 1556 85

Organophosphate-induced delayed polyneuropathy (OPIDP) is a rare toxicity resulting from exposure to certain organophosphorus (OP) esters. It is characterised by distal degeneration of some axons of both the peripheral and central nervous systems occurring 1-4 weeks after single or short-term exposures. Cramping muscle pain in the lower limbs, distal numbness and paraesthesiae occur, followed by progressive weakness, depression of deep tendon reflexes in the lower limbs and, in severe cases, in the upper limbs. Signs include high-stepping gait associated with bilateral foot drop and, in severe cases, quadriplegia with foot and wrist drop as well as pyramidal signs. In time, there might be significant recovery of the peripheral nerve function but, depending on the degree of pyramidal involvement, spastic ataxia may be a permanent outcome of severe OPIDP. Human and experimental data indicate that recovery is usually complete in the young. At onset, the electrophysiological changes include reduced amplitude of the compound muscle potential, increased distal latencies and normal or slightly reduced nerve conduction velocities. The progression of the disease, usually over a few days, may lead to non-excitability of the nerve with electromyographical signs of denervation. Nerve biopsies have been performed in a few cases and showed axonal degeneration with secondary demyelination. Neuropathy target esterase (NTE) is thought to be the target of OPIDP initiation. The ratio of inhibitory powers for acetylcholinesterase and NTE represents the crucial guideline for the aetiological attribution of OP-induced peripheral neuropathy. In fact, pre-marketing toxicity testing in animals selects OP insecticides with cholinergic toxicity potential much higher than that to result in OPIDP. Therefore, OPIDP may develop only after very large exposures to insecticides, causing severe cholinergic toxicity. However, this was not the case with certain triaryl phosphates that were not used as insecticides but as hydraulic fluids, lubricants and plasticisers and do not result in cholinergic toxicity. Several thousand cases of OPIDP as a result of exposure to tri-ortho-cresyl phosphate have been reported, whereas the number of cases of OPIDP as a result of OP insecticide poisoning is much lower. In this article, we mainly discuss OP pesticide poisoning, particularly when caused by chlorpyrifos, dichlorvos, isofenphos, methamidophos, mipafox, trichlorfon, trichlornat, phosphamidon/mevinphos and by certain carbamates. We also discuss case reports where neuropathies were not convincingly attributed to fenthion, malathion, omethoate/dimethoate, parathion and merphos. Finally, several observational studies on long-term, low-level exposures to OPs that sometimes reported mild, inconsistent and unexplained changes of unclear significance in peripheral nerves are briefly discussed.
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PMID:Organophosphate-induced delayed polyneuropathy. 1604 3


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