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.
Ultrasonography is currently being developed as a tool for evaluating peripheral neuropathy. It is one of the painless and least-invasive methods of medical diagnostic testing that yields anatomic views of the nerves and their surrounding structures. Here I first describe the equipment settings and technique for nerve ultrasound along with typical sonographic findings for normal nerves. I then address frequently used parameters for nerve measurements that facilitate diagnoses of focal and generalized neuropathies.
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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.
Background Peripheral nerve injury rarely occurs in patients with rhabdomyolysis. Based on our experience and previous reports, we consider prolonged immobilization a risk factor for the development of peripheral neuropathy in rhabdomyolysis patients.
Methods This study analyzed 28 patients with rhabdomyolysis due to prolonged immobilization. We analyzed their demographic and laboratory data, clinical and imaging findings, and outcomes, and compared these factors between patients with and without neuropathy.
Results Seven of the 28 patients had peripheral neuropathy, including sciatic neuropathy or lumbosacral plexopathy. Compared to those without neuropathy, the patients with neuropathy were younger (p = 0.02), had higher peak creatine kinase (CK) levels (p = 0.02), had higher muscle uptake in bone scans (p = 0.03), and more frequently exhibited abnormal muscle findings in computed tomography (CT) (p = 0.004).
Conclusions Patients with prolonged immobilization-induced rhabdomyolysis and neuropathy had higher CK levels, increased uptake on bone scans, and more-frequent abnormal muscles on CT than those without neuropathy. These findings indicate that peripheral neuropathy is more likely to develop in patients with severe muscle injury.
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Evaluation of diaphragm function is challenging because no single test has a high diagnostic yield. We describe ultrasound findings in three cases with acquired unilateral diaphragmatic elevation. These cases confirm that sonographic evaluation is a valid tool for identifying diaphragm dysfunction. In addition, ultrasound measurements of diaphragm thickness and the
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Background Floppy infant syndrome has a number of different etiologies.
Methods: One hundred twenty-three consecutive patients of floppy infant syndrome were included in this study. We reviewed all the electrophysiologic tests of these patients and the medical record of patients showing abnormalities in the electrophysiologic studies.
Results Of the 123 patients, twenty-six (21.1%) showed definite abnormalities in electrophysiologic tests; 8 myopathies, 14 neuropathies and 4 unclassified. The neuropathy was further classified as 5 neuronopathies and 9 sensorimotor polyneuropathies. With muscle or sural nerve biopsy and genetic test, a final diagnosis was made of Duchenne muscular dystrophy in 4, Becker muscular dystrophy in 1, spinal muscular atrophy in 2, and metachromatic leukodystrophy in 1.
Conclusions About 21% of patients presented with floppy infant syndrome showed abnormalities in the neuromuscular system. The electrophysiologic test is valuable to guide further investigations in diagnosing the cause of floppy infant syndrome.
There have been several reports about coexistence of myasthenia and other autoimmune disease. Psoriasis is a papulosquamous disease defined by erythematous plaques with a silvery scale and a T-cell-mediated autoimmune disease. We report a case of a 49-year-old an with generalized myasthenia gravis (MG) superimposed by psoriasis. MG was diagnosed by clinical symptoms, increased acetylcholine receptor antibody titer and repetitive nerve stimulation test. Psoriasis was diagnosed by clinical manifestations and specific skin biopsy findings. MG and psoriasis are both autoimmune diseases. The coexistence of MG and psoriasis suggest a close connection of pathogenesis.
Background: Bell's palsy (BP) is a self-limited rapid onset facial palsy that is non-life-threatening and has a generally favorable prognosis. Facial paralysis can be caused by numerous conditions, all of which should be excluded before thediagnosis of BP is reached. The etiopathogenesis and clinical course of BP are uncertain. So we analyzed the epidemiology and clinical course of BP patients.
Methods: The subjects include 100 cases of BP examined during the period of 18 months. Careful clinical history, neurologic examinations, laboratory tests, electrophysiologic studies, and brain imaging were performed. Follow-up examinations were done once a week during the first month and subsequently once a month until normal function was restored or for up to 3 months. Facial nerve function was assessed by House-Brackman (HB) facial nerve grading scale and electrophysiologic studies. Results: Except 13 recurrent BP patients, we analyzed 87 BP patients. Forty-four (50.6%) were men and 43(49.4%) were women and the mean age was 51.0(
Miller Fisher syndrome (MFS) is a variant of Guillian-Barre syndrome (GBS) characterized by the triad ofophthalmoplegia, ataxia, and areflexia. Although recurrent GBS is a well known entity, the recurrence of MFS is extremely rare. Here we report an unusual case of recurrent MFS. Initially, the patient had presented with ophthalmoplegia, ataxia, areflexia, and tingling sensation of all extremities. After resolution of the first episode, the patient presented with atypical MFS characterized by ataxia, areflexia, and tingling sensation without ophthalmoplegia.
Background The medial plantar nerve (MPN) is a distal branch of the posterior tibial nerve, and various methods of nerveconduction study for MPN have been introduced so far. Hemmi et al described a new method (Hemmi's method) forrecording medial plantar sensory nerve action potentials (SNAPs), which is considered as a simple and reliable method formeasuring medial plantar SNAPs. This study was aimed to establish the normal values for the MPN conduction study amongKoreans and to compare the sensitivities of three different methods for MPN conduction study (Hemmi, Oh, and Saeed'smethod) in detecting evidence of peripheral neuropathy among diabetic patients. Methods: In 27 healthy subjects, MPN conductionstudy using Hemmi
Background Miller-Fisher syndrome (MFS) is characterized by the clinical triad of ophthalmoplegia, ataxia, and areflexia,and is considered a variant form of Guillain-Barre syndrome. Although some cases of delayed-onset facial palsy in MFShave been reported, the characteristics of this facial palsy are poorly described in the literature. Methods: Between 2007and 2010, six patients with MFS were seen at our hospital. Delayed facial palsy, defined as a facial palsy that developedwhile the other symptoms of MFS began to improve following intravenous immunoglobulin treatment, was confirmed in fourpatients. The clinical and electrophysiological characteristics of delayed facial palsy in MFS, as observed in these patients,are described here. Results: Four patients with delayed-onset facial palsy were included. Delayed facial palsy developed 8-16days after initial symptom onset (5-9 days after treatment). Unilateral facial palsy occurred in three patients and asymmetricfacial diplegia in one patient. The House-Brackmann score of facial palsy was grade III in one patient, IV in two patients,and V in one patient. None of the patients complained of posterior auricular pain. Facial nerve conduction studies revealednormal amplitude in all four patients. The blink reflex showed abnormal prolongation in two patients and the absence ofaction potential formation in two patients. Facial palsy resolved completely in all four patients within 3 months. Conclusions:Delayed facial palsy is a frequent symptom in MFS and resolves completely without additional treatment. Thus, standardtreatment and patient reassurance are sufficient in most cases.
Background Bell's palsy (BP) is a condition that causes a temporary weakness or paralysis of the muscles in the face. Some patients with BP experience rapid aggravation of facial weakness in the early stage. The objective of this study was to identify the clinical and radiologic characteristics of BP with early deterioration. Methods: This retrospective study included 603 patients of BP from July 2005 to December 2016. The clinical history, neurologic examination, electrophysiological test and brain magnetic resonance imaging (MRI) were all checked at the time of diagnosis. The severity of facial palsy was assessed using House-Blackmann facial nerve grading scale. Patients with early deterioration were identified by clinical history and neurologic examination. Comparisons of clinical characteristics, radiologic findings, and prognosis were done between the early deterioration group (group 1) and no deterioration group. Results: Of 603 patients, 576 patients were included in this study. Group 1 had 257 patients (44.6%) and group 2 had 319 patients (55.4%). Between group 1 and 2, there were no significant tatistical difference in past medical history including hypertension, diabetes mellitus, family history, recurrence history, location of BP, and prognosis. However, facial nerve enhancement on brain MRI was observed in 254 patients (98.8%) with early deterioration and in 95 patient (35.4%) without deterioration. Conclusions: Facial nerve enhancement on brain MRI is more common in patients with early deterioration, but early deterioration does not affect prognosis of BP.
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