• Annals of Clinical Neurophysiology
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• v.3 no.2
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• pp.164-167
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• 2001

The etiology of neuralgia amyotrophy remains unclear. Herpes zoster induced neuralgia amyotrophy has been reported in extremely rare cases. In this case report, we describe the clinical features and electrophysiologic findings in a 68-year-old patient with neuralgia amyotrophy associated with herpes zoster infection. We suggest that brachial plexus inflammation due to viral infection may be a direct cause of reversible neuralgia amyotrophy.

• The Journal of Korean Physical Therapy
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• v.14 no.4
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• pp.266-273
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• 2002

Carpal Tunnel Syndrome(CTS) is a common entrapment neuropathy of the median nerve at the wrist. An Electrophysiologic study has been widely used for the diagnosis of carpal tunnel syndrome. The subjects of this study were 48 cases (88 hands) with clinically suspected carpal tunnel syndrome who underwent electrodiagnostic examination from Jan 1, 2001 to Sep 30, 2001, The results were as follows: 1. Among 48 persons with a clinically suspected carpal tunnel syndrome, 40 patients were female 83.33$\%$ and the patients who are above 60 years old were 37.50$\%$. 2. Electrodiagnostic results were 22 cases (45.84$\%$) with bilateral carpal tunnel syndrome and 10 cases (20.83$\%$) with normal. 3. Physical findings consisted of tingling sensation in 48.86$\%$ of the involved hands, positive Phalen's Sign in 20.46$\%$ of them, thenar atrophy in 15.91$\%$ of them, and weakness in 14.77$\%$ of them. 4. Electrophysiologic studies showed a decreased sensory conduction velocity in 20 cases (22.73$\%$) of total hands, a prolonged latency in 3 cases (3.41$\%$) of them, abnormal sensory and motor fiber in 33 cases (37.50$\%$) of them, and normal in 27 cases (30.68$\%$) of them. Considering above results, we had better make a diagnosis precisely the patients with clinically suspected carpal tunnel syndrome through subjective symtoms, physical examinations, and electrophysiologic studies.

• Annals of Clinical Neurophysiology
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• v.2 no.2
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• pp.135-138
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• 2000

Both myasthenia gravis and Guillain-$Barr{\acute{e}}$ syndrome are autoimmune disorder, but it is very rare that both of them occur together. A 53-year old woman with history of myathenia gravis complained of weakness of extremities, worsening progressively for several days. Electrophysiologic study showed findings of motor axonal neuropathy without sensory involvement. She became improved in aspect of clinical symtoms and electrophysiologic findings after infusion of immunoglobulin. This is a case of Guillain-$Barr{\acute{e}}$ syndrome in a patient with myasthenia gravis.

• Annals of Clinical Neurophysiology
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• v.3 no.2
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• pp.156-159
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• 2001

Miller Fisher syndrome(MFS) has been the focus of conflicting opinions regarding the peripheral versus the central nature of the site of major neural injury. We present our electrophysiological findings in one case of MFS to help clarify the pattern of peripheral nerve injury in this syndrome. A 45-year-old man visited our hospital due to sudden diplopia. Initial examination revealed internuclear opthalmoplegia. The next day, his symptoms rapidly aggravated to complete external ophthalmoplegia, ataxia, and areflexia with hand and foot numbness. Serial electrophysiological studies were performed. The results of brainstem evoked potential(BAEP) and blink reflex were normal in the serial studies. Motor and sensory nerve conduction study(NCS) were normal findings in second hospital day, but ulnar sensory nerve shows no sensory nerve action potential(SNAP) and sural sensory conduction velocity was delayed in 7th hospital day. Our patient's clinical presentation began to improve on 15th hospital day, and his electrophysiologic study showed improvement on 29th hospital day. We believe that all the manifestations of MFS can be explained by the involvement of peripheral nerves without brainstem or cerebellar lesion with the serial electrophysiological studies.

• Annals of Clinical Neurophysiology
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• v.9 no.1
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• pp.5-10
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• 2007

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 the diagnosis 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(${\pm}16.6$) years. Three (3.4%) patients showed a familial tendency. The initial examination within 1 week after attack revealed 35.2% was below HB grade 4 and 64.8% was above grade 3. The associated symptoms are as follows; postauricular pain, increase tear flow, taste change, hyperacusis and drooling. The initial facial nerve conduction study and blink reflex within 1 week after attack showed abnormal findings in 12.6% and 100%, respectively. Brain MRI was performed in 59(67.8%) patients and showed abnormal enhancement of affected nerve in 57(96.6%). Follow-up examination showed that 78.2% of the patients partially improved within 4 weeks and completely improved within 3 months. Finally 80.5% of the total patients obtained normal function in 3 months. Conclusions: We report epidemiologic, clinical, electrophysiologic and radiologic characteristics of BP patients.

• Annals of Clinical Neurophysiology
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• v.12 no.2
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• pp.55-60
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• 2010

Background: The aim of this study is to identify the correlation between ultrasonographic findings of median nerve and clinical scale and electrophysiologic data in carpal tunnel syndrome. Methods: Forty three patients (79 hands) with electrophysiologically confirmed carpal tunnel syndrome were evaluated. Clinical symptoms were examined by Historical-Objective (Hi-Ob) scale. Electrophysiologic data and Padua scale were used for severity of electrophysiology. In ultrasonographic study, cross sectional area and flattening ratio of median nerve were measured at distal wrist crease level (DWC), 1cm proximal to distal wrist crease level, and 1cm distal to distal wrist crease level. The correlation between Hi-Ob scale, electrophysiologic data and ultrasonography was measured with Spearman rank test. Results: The mean Hi-Ob scale was 2.4. Mean Padua scale was 4.0. In ultrasnonographic study, cross sectional area and flattening ratio were $0.112\;cm^2{\pm}0.025$ and $3.0{\pm}0.6$ at 1cm proximal to DWC level, $0.118{\pm}0.026\;cm^2$ and $2.9{\pm}0.4$ at DWC level, and $0.107{\pm}0.032\;cm^2$ and $3.0{\pm}0.4$ at 1 cm distal to DWC level. Hi-Ob scale was not correlated with cross sectional area and flattening ratio of median nerve. Hi-Ob scale was correlated with Padua scale positively (r=0.44) and correlated with amplitudes of CMAP and SNAP, negatively (r=-0.33; r=-0.30). Cross sectional area of median nerve was significantly correlated with Padua scale, amplitudes and latencies of CMAP and amplitudes of SNAP. Conclusions: Ultrasonographic findings of median nerve and electrodiagnostic data had statistically significant correlation. Consequently, ultrasonography could be an adjunctive method in diagnosis of carpal tunnel syndrome.

• Annals of Clinical Neurophysiology
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• v.8 no.1
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• pp.16-22
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• 2006

Sporadic inclusion body myositis (s-IBM) is an aquired slowly progressive inflammatory myopathy with unknown etiology. Although light microscopic abnormalities and characteristic histopathology on muscle biopsy distinguishes from other inflammatory myopathies, vacuolated muscle fibers, intracellular amyloid deposits or tubulofilaments in electromicroscopic findings are not definite in some patients. This review shows the prominently involved muscles in s-IBM and specific or nonspecific electrophysiologic manifestations from reported data for helping the diagnosis of definite-or probable-IBM patients. In lower limbs, the quadriceps is predominantly involved, as is iliopsoas, and tibialis anterior is common. In the upper limbs, the greatest weakness is in forearm finger flexors. Finger extensors, biceps and triceps also are moderately to prominently involved. The majority of patients demonstrate polyphasic MUAPs that are short in duration. An additional striking feature is the concomitant documentation of long-duration, large-amplitude, polyphasic MUAPs. In spite of the frequent mixed myopathic-neurogenic electromyographic findings of IBM, just like that of chronic myositis, asymmetric, slowly progressive weakness of flexor digitorum profundus or quadriceps femoris muscles after age of 50 is very necessary condition for the diagnosis of IBM.

• Annals of Clinical Neurophysiology
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• v.4 no.2
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• pp.98-107
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• 2002

Multifocal motor neuropathy (MMN) is a chronic immune-mediated peripheral myelinopathy. The major clinical features include slowly progressive, painless, and asymmetric weakness, usually of distal limb muscle. Early in the course of the disease, weakness is not necessarily associated with muscle atrophy, owing to the initial primary involvement of peripheral myelin. Chronic progressive weakness is often associated with some degree of concurrent axonal loss and subsequent muscle atrophy. Sensory symptoms are usually mild or absent, and involvement of cranial and respiratory muscles is rare. The findings of multifocal motor conduction block, abnormal temporal dispersion, and focal conduction slowing at segments not at risk for common entrapment or compression injury, associated with normal sensory conduction studies along the same segments, are the hallmark electrophysiologic features of MMN. The slow progression and absence of upper motor neuron signs are the major clinical points that separate MMN from amyotrophic lateral sclerosis. The role of GM1 antibodies, found in high titers in 22~84% of MMN patients, remains uncertain. The contention that MMN is an autoimmune disorder is largely based on the often dramatic improvement in symptoms following the administration of intravenuos immunoglobulin or cyclophosphamide.

• Journal of Korean Neurosurgical Society
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• v.42 no.6
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• pp.484-486
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• 2007

The authors describe a case of pseudoaneurysm arising from internal iliac artery presented with radiculopathy mimicking the symptoms of lumbar disc disease or spinal cord tumor. Among the several preoperative evaluation including CT, MRI, electrophysiologic study and ultrasonography, important diagnostic clue was obtained by ultrasonographic findings of turbulence flow at the core of partially enhanced mass in the pelvic cavity. The patient was managed with endovascular coil embolization successfully. The current case makes us remind that assessment of neurological symptoms on lower extremity should include consideration of extraspinal cause in pelvis.

• Annals of Clinical Neurophysiology
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• v.9 no.1
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• pp.23-25
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• 2007

The symptomatology of suprascapular neuropathy is variable, depending principally on the etiology and location of the lesion. Among them, suprascapular nerve entrapment with isolated paralysis of the infraspinatus muscle is uncommon. We report a 27-year-old man presenting with right arm weakness. Based on the electrophysiologic and imaging findings, suprascapular neuropathy at the spinoglenoid notch due to cystic mass lesion was diagnosed.