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Background@#The brain magnetic resonance imaging (MRI) findings seen in patients with Bell's palsy are abnormal contrast enhancement of affected facial nerves. Previous evaluation included mainly patients who had experienced palsy for several weeks and there are no studies to date on patients with late stage of Bell’s palsy. This study investigated the findings of MRI of Bell's palsy after 3 months of symptom onset to assess how long the enhancement last. @*Methods@#Among the patients with Bell's palsy (idiopathic unilateral facial palsy) who visited the hospital, 9 patients who underwent contrast-enhanced MRI of the internal auditory canal after 3 months of symptom onset were reviewed retrospectively. MRI examination results were investigated along with the patient's clinical symptoms and electrodiagnostic test results. Based on the MRI results, the frequency of abnormal contrast enhancement and contrast-enhanced areas were investigated. @*Results@#9 patients were included. 6 of them did MRI imaging because of incomplete recovery of facial palsy and the others did because of complication of facial palsy including synkinesis and hemifacial spasm. Time interval between symptom onset and evaluation was 17 months (3-84). Of 9 patients, 2 showed abnormal enhancement of affected nerve and they performed MRI after 5 months and 12 months of symptom onset, respectively. @*Conclusions@#Abnormal enhancement of facial nerve in Bell’s palsy could last up to one year. This awareness can be helpful in interpretation of MRI of Bell’s palsy.

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The diaphragm is the major muscle of respiration and its dysfunction is associated with problems ranging from orthopnea to prolonged recovery from surgery or ventilator management. Common causes of diaphragm dysfunction include phrenic neuropathy, motor neuron disease, neuromuscular junction disorders, and myopathy. This article reviews sonographic findings of normal diaphragm, including key quantitative ultrasound measurements that are helpful in the evaluation of diaphragm. It also discusses various clinical application of this technique in diagnosis of neuromuscular diseases.

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Background@#Unilateral peripheral facial nerve palsy may have a detectable cause (secondary facial nerve palsy) or may be idiopathic (Bell’s palsy). Facial palsy is attributable to various causes ranging from mild infection to severe neurological disorders. We investigated the prevalence and types of serious neurological disorders in patients with unilateral facial palsy. @*Methods@#We reviewed the medical records of patients with unilateral facial nerve palsy and identified patients diagnosed with facial palsy secondary to serious or life-threatening causes. We investigated the clinical characteristics, as well as electrodiagnostic and imaging findings in these patients. @*Results@#Of 924 patients with facial palsy, 11 patients (1.2%) were diagnosed with the following serious neurological disorders: acoustic schwannoma in two patients, facial nerve schwannoma, glossopharyngeal schwannoma, meningioma, epidermoid cyst, parotid gland tumor, pontine infarct, skull base osteomyelitis, brain metastasis, and pachymeningitis. @*Conclusions@#Although unilateral facial palsy is rarely associated with serious neurological disorders, early detection of the etiopathogenetic contributors is important for prompt initiation of optimal management. Therefore, clinicians should be mindful of disorders that can mimic Bell’s palsy.

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The neurotoxicity of nitrous oxide (N2O) is known to be mainly occurred by interference with action of vitamin B12. A 38-year-old male presented with progressive gait instability after recreational inhalational use of N2O for 2 months. Although spine magnetic resonance image showed typical subacute combined degeneration, nerve conduction study showed motor neuropathy that is atypical findings of vitamin B12 deficiency. This case suggests N2O-induced neuropathy can develop separately from a vitamin B12 deficiency.

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The neurotoxicity of nitrous oxide (N2O) is known to be mainly occurred by interference with action of vitamin B12. A 38-year-old male presented with progressive gait instability after recreational inhalational use of N2O for 2 months. Although spine magnetic resonance image showed typical subacute combined degeneration, nerve conduction study showed motor neuropathy that is atypical findings of vitamin B12 deficiency. This case suggests N2O-induced neuropathy can develop separately from a vitamin B12 deficiency.

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The contraceptive implant is an effective and well-established method of contraception. A 43-year-old woman presented with paresthesia and weakness of left hand. Symptoms began 3 weeks ago, immediately after removal of a contraceptive device in the left arm. A nerve conduction study showed proximal median neuropathy, and ultrasonography revealed focal swelling of the median nerve at the level of removal. Although nerve damage is a rare complication, special care should be taken to avoid nerve injury during removal procedure.

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BACKGROUND: Rhabdomyolysis is a syndrome caused by injury to skeletal muscle and characterized by myalgia and swelling of the affected muscles. Peripheral nerve injury rarely occurs in patients with rhabdomyolysis. METHODS: We reviewed the medical records of 8 consecutive patients with peripheral neuropathies associated with rhabdomyolysis. We assessed the clinical characteristics and electrodiagnostic findings of eight patients. RESULTS: In seven patients, rhabdomyolysis occurred after prolonged immobilization. In one patient, blunt trauma was a cause of rhabdomyolysis. All patients presented with weakness and paresthesia in lower extremities and electrodiagnostic tests showed peripheral nerve injury suggesting sciatic neuropathy or lumbosacral plexopathy. Although rhabdomyolysis itself recovered completely in all patients, neurologic deficits from neuropathy recovered partially and slowly. CONCLUSIONS: Sciatic nerve or lumbosacral plexus was injured in all eight patients. Among the various causes of rhabdomyolysis, prolonged immobilization is associated with development of peripheral neuropathy.

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Multifocal motor neuropathy (MMN) is an uncommon, asymmetric motor neuropathy. As MMN is a treatable disorder, its differentiation from lower motor neuron disease is important. Evidence of conduction block (CB) or positive IgM anti-GM1 is considered one of important markers for the diagnosis. However, some patients with atypical MMN have no detectable CB or anti-GM1 antibody. We experienced a case of MMN with focal nerve enlargement on ultrasound. Ultrasound can be a valuable tool in supporting the diagnosis of MMN.

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Cryolipolysis has become available for the noninvasive reduction of adipose tissue. A 33-year-old woman presented with wrist drop of the right arm that had first appeared 7 days previously. She had undergone cryolipolysis on both upper arms immediately prior to the onset of symptoms. A nerve conduction study showed radial neuropathy proximal to the elbow, and ultrasonography revealed focal swelling of the radial nerve at the spiral groove. Although cryolipolysis has been known as a safe method, nerve injury can result from compression and/or hypothermia during the procedure.

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Thymoma occurs in about 20% of patients with myasthenia gravis (MG), but the recurrence of thymoma has rarely been reported. A 68-year-old man presented with ptosis and weakness of the neck muscles. He had undergone thymectomy for ocular MG with invasive thymoma 20 years previously. Chest computed tomography revealed recurrence of the thymoma. This 20-year period is, to our knowledge, the longest reported interval for recurrence of an MG-associated thymoma. The literature on the optimal follow-up duration after thymectomy is reviewed.

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BACKGROUND: Neuromuscular ultrasound has emerged over the last decade as a useful tool for diagnosing peripheral neuropathy. Because nerve enlargement is the most important diagnostic marker of an abnormal nerve, quantification of nerve size is essential. METHODS: We included 80 healthy volunteers aged 21-60 years. The nerve cross-sectional area (CSA) was measured in all participants at the following common compressive sites: bilateral median nerve at the carpal tunnel and forearm, ulnar nerve at the wrist and medial epicondyle, radial nerve at the spiral groove, peroneal nerve at the fibular head and popliteal fossa, and tibial nerve at the popliteal fossa. Anatomical variants were also evaluated, including a bifid median nerve and persistent median artery. RESULTS: The CSAs were 9.58+/-1.55, 6.87+/-1.61, 4.72+/-0.91, 6.64+/-1.33, 6.48+/-1.68, 12.35+/-3.55, and 26.98+/-6.92 mm2 (mean+/-SD) for the median nerve at the carpal tunnel and forearm, ulnar nerve at the wrist and medial epicondyle, radial nerve at the spiral groove, peroneal nerve at the fibular head, and tibial nerve at the popliteal fossa, respectively. The nerve CSA was significantly larger in men than in women and was correlated with body mass index, weight, and height. A bifid median nerve and persistent median artery were seen in 12 (7.5%) and 4 (2.5%) of 160 hands, respectively. CONCLUSIONS: The information produced in this study can serve as reference data when evaluating these nerve sites using ultrasound.

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Guillain-Barre syndrome (GBS) is an autoimmune polyneuropathy that presents with acute onset and rapid progression of ascending quadriparesis and hyporeflexia, which can be triggered by various conditions. However, GBS following cerebral infarction is very rare. We describe herein a patient with facial diplegia, ophthalmoplegia, and areflexia that occurred during acute cerebral infarction. The symptoms were improved after intravenous immunoglobulin treatment. The details of this case suggest that GBS is triggered by immune dysregulation after acute cerebral infarction.

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BACKGROUND AND OBJECTIVES: Although disequilibrium is common type of dizziness in older people, it is sometimes difficult to identify a specific cause for this problem. The diffuse brain pathology including subcortical ischemia and atrophy can be a cause for patients with disequilibrium of unknown cause. Aim of this study is to identify the eye movements and neuroimaging features in patients with disequilibrium. MATERIALS AND METHODS: We performed a prospective investigation in patients with disequilibrium of unknown cause. We collected information on demographic characteristics and clinical features of disequilibrium. The impact of dizziness on everyday life was assessed by 25-item dizziness handicap inventory (DHI). Vestibular function test (VFT) includes smooth pursuit, saccade, optokinetic nystagmus, and rotatory chair test. Subcortical white matter lesions and brain atrophy were graded from brain magnetic resonance image (MRI). RESULTS: This study included 14 patients (12 female and 2 male), aged between 64 and 84 years, mean age 74.01+/-6.02 years. The score of DHI was 39.4+/-11.8 (20-58). Eye movements were abnormal in 13 patients and normal in only one patient. The degree of subcortical ischemia was mild in 7, moderate in 4, and severe in 3 patients. Ventricular brain ratio was 0.23+/-0.03. However, there was no significant relationship between MRI findings and the degree of oculomotor alterations (result of VFT). CONCLUSION: Patients with disequilibrium of unknown cause are usually elderly women. Alterations in oculomotor movements and diffuse brain pathology including white matter lesions and atrophy were observed in patients with disequilibrium of unknown cause.

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BACKGROUND: Clevudine (Revovir(R)) is a recently introduced antiviral drug, and clinical trials have demonstrated its potent, sustained antiviral activity without specific adverse events. However, several studies have found severe myopathy during clevudine therapy. Our study aimed to summarize the clinical and pathological features of clevudine-induced myopathy. METHODS: We analyzed the demographic data, clinical features, and pathologic findings of 18 consecutive hepatitis-B patients who developed skeletal myopathy during clevudine therapy. RESULTS: The 18 patients comprised 11 women and 7 men aged 48.2+/-14.0 years (mean+/-standard deviation; range 28-74 years). Each of the 18 patients was treated with clevudine for at least 5 months (range 5-20 months) before the development of symptoms. In all patients the main symptom was proximal muscular weakness that progressed slowly over several months. Elevated creatine kinase and myopathic patterns on electromyography were found. Muscle biopsies revealed severe myonecrosis associated with numerous ragged red fibers and cytochrome-c-oxidase-negative fibers, mitochondrial proliferation, and predominant type-II fiber atrophy. The muscle weakness gradually improved within 20 weeks after discontinuation of clevudine. CONCLUSIONS: Clevudine therapy can induce myopathy associated with mitochondrial toxicity. Careful clinical and laboratory monitoring of the skeletal muscle dysfunction is required in patients receiving clevudine therapy.

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Antineutrophil cytoplasmic antibodies (ANCA) are closely linked to primary systemic vasculitis, and ANCA detection has became an important diagnostic hallmark of ANCA-associated vasculitis (AAV). However, it has been reported that tuberculosis is associated with positivity for ANCA and it is difficult to differentiate clinically between tuberculosis and AAV. We report a patient with the concomitant appearance of AAV and pulmonary tuberculosis. Positivity for ANCA should be carefully interpreted as indicative of AAV, especially in countries with a high prevalence of tuberculosis.

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