• Annals of Clinical Neurophysiology
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• v.10 no.2
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• pp.109-111
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• 2008

Ossification of the ligamentum flavum (OLF) usually occurs in the lower thoracic spine, and is rare in the cervical region. We report the case of a 67-year-old woman who presented a seven month's history of progressive weakness and paresthesia in her right upper extremity. MRI and CT scans of the spine revealed the presence of ossified ligamentum flavum from C3-C4. A cervical laminectomy resulted in a good post-operative improvement of muscle strength.

• Annals of Clinical Neurophysiology
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• v.12 no.1
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• pp.1-2
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• 2010

Chronic non-specific low back pain (CLBP) is one of the major health problems casting substantial amount of economic expenses and negative impact on quality of life onto an individual as well as society. On contrary to public familiarity, the ways of management of CLBP are diverse and there is yet no general consensus about which approach is better than others or to whom the specific management should be applied. Some hold the negative point of view on the efficacy of the invasive maneuver such as epidural injection because there is no controlled clinical trial (RCT) yielding better long term outcome of those invasive managements over conservative ones. But the experts of interventional or surgical treatment stress the methodological difficulty in performing RCT and assert that those invasive treatments can bring the prompt and complete resolution of low back pain and restoration of function in appropriately selected cases. These seemingly opposite views on the invasive management on CLBP are rather complimentary each other than to be contradictory.

• Annals of Clinical Neurophysiology
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• v.12 no.1
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• pp.7-10
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• 2010

Chronic low back pain (CLBP) is a distinct disease entity in that its clinical course and response to the treatment are quite different from acute low back pain (ALBP). CLBP is also closely related with systemic or preexisting psychosocial factors rather than focal or localized factors. Since there has been little consensus in practice regarding the proper management of CLBP, clinicians tend to approach and manage patients with CLBP in an empirical manner rather than an evidence-based one. In this article, I will review the difficulties of therapeutic choice in CLBP and provide superior aspects of medical treatment over invasive interventional treatments.

• Annals of Clinical Neurophysiology
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• v.12 no.1
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• pp.27-31
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• 2010

Ullrich disease is a rare congenital muscular dystrophy, which is clinically characterized by generalized muscular weakness, distal joint hyperextensibility, proximal joint contractures, protuberant calcanei and high-arched palate. The disease is caused by collagen VI deficiency in interstitum and/or sarcolemma of skeletal muscles, for which mutations either in COL6A1, COL6A2 or COL6A3 are responsible. We report a girl who presented with symptoms typical of Ullrich disease, in whom the diagnosis was confirmed by immunohistochemistry and molecular genetic study.

• Annals of Clinical Neurophysiology
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• v.12 no.2
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• pp.70-72
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• 2010

We report a 53-year-old male having Kennedy disease who complained of severe bilateral tinnitus and autophony. He was diagnosed as patulous Eustachian tube based on the observation of fluttering motion of the tympanic membrane associated with respiration, which is presumed to occur secondary to bulbar weakness. The patulous Eustachian tube affected the management of his respiratory problem by impairing his ability to tolerate BiPAP. We report this rare condition with a literature review.

• Annals of Clinical Neurophysiology
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• v.12 no.2
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• pp.66-69
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• 2010

A 73-year-old man with progressive quadriparesis was diagnosed as Guillain-Barr$\acute{e}$ syndrome. On the 6th hospital day, the patient complained of sudden chest discomfort. The blood test and echocardiography suggested myocardial injury, and acute myocardial infarction was considered. However, coronary angiography displayed no vascular lesion, and the electrocardiography and echocardiogram showed marked improvement 14 days later. We concluded the patient had a reversible cardiomyopathy which is a rare complication of Guillain-Barr$\acute{e}$ syndrome.

• Annals of Clinical Neurophysiology
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• v.13 no.1
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• pp.26-30
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• 2011

Although the pathophysiologic mechanism is unknown, there has been long-running debate on whether periodic discharges such as periodic lateralized epileptiform discharges (PLEDs) and generalized periodic epileptiform discharges are an ictal or interictal EEG pattern. The goal of this review is to give evidence that such periodic discharges on EEG are not ictal phenomenon and just represent underlying acute brain damage. This review includes coma with epileptiform EEG pattern and its prognostic and therapeutic implications. Based on previous reports, rather than taking the view PLEDs represent either an underlying ictal process or an electrographic correlate of neuronal injury, it would be more reasonable that PLEDs are considered as a dynamic pathophysiological state in which unstable neurobiological processes create an ictal-interictal continuum.

• Annals of Clinical Neurophysiology
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• v.13 no.1
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• pp.21-25
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• 2011

Periodic lateralized epileptiform discharges (PLEDs) had been debated whether it is ictal or non-ictal phenomenon. As most of PLEDs occur in patients with acute structural lesions, some epileptologists prefer PLEDS as a non-ictal phenomenon, rather an obscure epiphenomenon of etiological diseases. But, almost half of the patients with PLEDs do not have acute structural lesions in the brain and metabolic disorders or old CNS lesions may cause PLEDs and even more, no brain lesion was identified in some patients. There are many data supporting PLEDs as ictal phenomena. Occurrence of PLEDs usually accompanied by decreased mentality and is improved as PLEDs disappeared. Current SPECT study showed marked hyperperfusion in the lesion side of PLEDs, that is striking evidence of PLEDs as ictal phenomena. Also careful review of EEG with PLEDs revealed it is a dynamic process rather than a static state. Despite of these evidences, as PLEDs are an end-stage of animal status epilepticus models, it may be a transition of ictal to interictal state.

• Annals of Clinical Neurophysiology
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• v.13 no.1
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• pp.38-43
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• 2011

Background: In the brain, the dominant primary motor cortex (M1) has a greater hand representation area, shows more profuse horizontal connections, and shows a greater reduction in intracortical inhibition after hand exercise than does the non-dominant M1, suggesting a hemispheric asymmetry in M1 plasticity. Methods: We performed a transcranial magnetic stimulation (TMS) study to investigate the hemispheric asymmetry of paired associative stimulation (PAS)-induced M1 plasticity in 9 right-handed volunteers. Motor evoked potentials (MEPs) were measured in the abductor pollicis brevis (APB) muscles of both hands, and MEP recruitment curves were measured at different stimulation intensities, before and after PAS. Results: MEP recruitment curves were significantly enhanced in the dominant, but not the non-dominant M1. Conclusions: These results demonstrate that the dominant M1 has greater PAS-induced plasticity than does the non-dominant M1. This provides neurophysiological evidence for the asymmetrical performance of motor tasks related to handedness.

• Annals of Clinical Neurophysiology
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• v.13 no.1
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• pp.48-50
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• 2011

Myotonic dystrophy type 1 (DM1) is an autosomal dominant multisystem disorder caused by the expansion of cytosine-thymine-guanine (CTG) repeats in the myotonic dystrophy protein kinase (DMPK) gene. Some literatures indicated that DM1 had incidental CNS lesions such as white matter lesions and diffuse gray matter atrophy. We report a patient with DM1 whose brain magnetic resonance image (MRI) showed multifocal hyperintense lesions and cystic lesion on both frontotemporoparietal lobes.