• Annals of Clinical Neurophysiology
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• v.21 no.1
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• pp.7-15
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• 2019

Clinical evaluations, nerve conduction studies, and electromyography play major complementary roles in electrophysiologic diagnoses. Electromyography can be used to assess pathologic changes and localize lesions occurring in locations ranging from motor units to anterior-horn cells. Successfully performing electromyography requires knowledge of the anatomy, physiology, and pathology of the peripheral nervous system as well as sufficient skill and interpretation ability. Electromyography techniques include acquiring data from visual/auditory signals and performing needle positioning, semiquantitation, and interpretation. Here we introduce the basic concepts of electromyography to guide clinicians in performing electromyography appropriately.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.2
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• pp.69-76
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• 2004

A variety of G protein coupled receptors (GPCRs) are expressed in the presynaptic terminals of central and peripheral synapses and play regulatory roles in transmitter release. The patch-clamp whole-cell recording technique, applied to the calyx of Held presynaptic terminal in brainstem slices of rodents, has made it possible to directly examine intracellular mechanisms underlying the GPCR-mediated presynaptic inhibition. At the calyx of Held, bath-application of agonists for GPCRs such as $GABA_B$ receptors, group III metabotropic glutamate receptors (mGluRs), adenosine $A_1$ receptors, or adrenaline ${\alpha}2$ receptors, attenuate evoked transmitter release via inhibiting voltage-activated $Ca^{2+}$ currents without affecting voltage-activated $K^+$ currents or inwardly rectifying $K^+$ currents. Furthermore, inhibition of voltage-activated $Ca^{2+}$ currents fully explains the magnitude of GPCR-mediated presynaptic inhibition, indicating no essential involvement of exocytotic mechanisms in the downstream of $Ca^{2+}$ influx. Direct loadings of G protein ${\beta}{\gamma}$ subunit $(G{\beta}{\gamma})$ into the calyceal terminal mimic and occlude the inhibitory effect of a GPCR agonist on presynaptic $Ca^{2+}$ currents $(Ip_{Ca})$, suggesting that $G{\beta}{\gamma}$ mediates presynaptic inhibition by GPCRs. Among presynaptic GPCRs glutamate and adenosine autoreceptors play regulatory roles in transmitter release during early postnatal period when the release probability (p) is high, but these functions are lost concomitantly with a decrease in p during postnatal development.

• Annals of Clinical Neurophysiology
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• v.12 no.2
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• pp.79-81
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• 2010

• Annals of Clinical Neurophysiology
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• v.13 no.1
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• pp.68-70
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• 2011

• Annals of Clinical Neurophysiology
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• v.14 no.1
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• pp.7-11
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• 2012

Polysomnography is used to diagnose many types of sleep disorders including sleep apnea, periodic limb movement disorder, REM sleep behavior disorder, parasomnias, and narcolepsy. It is a comprehensive recording of the biophysiological changes that occur during sleep. The polysomnography monitors many body functions parameters including EEG, EOG, EMG, ECG, respiratory airflow, respiratory effort, and pulse oximetry during sleep. Multiple Sleep Latency Test (MSLT) is performed for diagnosing narcolepsy and excessive daytime sleepiness. It is usually to be done after an overnight polysomnography. The test consists of four or five 20-minute nap opportunities that are scheduled two hours apart.

• Annals of Clinical Neurophysiology
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• v.6 no.2
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• pp.103-105
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• 2004

Horner's syndrome may rarely accompany herpes zoster ophthalmicus (HZO). A 78-year-old woman suffered from HZO accompanied ipsilateral ptosis and miosis. Before skin eruption, she was diagnosed as a paratrigeminal syndrome of Raeder. She was treated with intravenous acyclovir and prednisone for 7 days. Ptosis and miosis was not completely improved after 5 months of follow-up.

• Annals of Clinical Neurophysiology
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• v.4 no.2
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• pp.91-97
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• 2002

The field of critical care medicine has flourished, but an unfortunate result of improved patient survival in the intensive care unit is the occurrence of certain acquired neuromuscular disorders. During the last two decades, various neuromuscular disorders were recognized as common causes of weakness occurring in critically ill patients. The two most common disorders are an acute quadriplegic myopathy predominantly associated with the use of intravenous corticosteroids and neuromuscular junction blocking agents and severe systemic illness termed critical illness myopathy(CIM), and an axonal sensorimotor polyneuropathy termed critical illness polyneuropathy. I will review briefly about general components of the CIM.

• Annals of Clinical Neurophysiology
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• v.2 no.2
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• pp.125-129
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• 2000

Benign monomelic amyotrophy(BMA) is an uncommon cause of progressive mildly disabling atrophy and weakness of a limb. It predominantly affects the distal upper limb of young men. I present two men with BMA of the lower extremities. Although the disorder seemed clinically confined to a arm or leg, I confirmed by electromyography evidence of denervation in the other extremities. I reviewed the literatures and discuss the differential diagnosis. BMA is a diagnosis of exclusion that requires consideration in men with unilateral arm or leg atrophy and weakness.

• Annals of Clinical Neurophysiology
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• v.15 no.1
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• pp.27-29
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• 2013

• Annals of Clinical Neurophysiology
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• v.17 no.1
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• pp.35-37
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• 2015