• Journal of the Korean Academy of Clinical Electrophysiology
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• v.8 no.1
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• pp.23-29
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• 2010

Purpose : This study is to offer clinical primary data that examines the change of imaging structure and the quantitative evaluation of muscle activity on myofascial trigger points. This study examines neuromuscular physiological characteristic by comparing the differences in physical findings, pressure pain threshold, imaging, and electrophysiological characteristics in latent and active myofascial trigger points muscle and normal muscle through the following experimental procedures. Methods : The participants for the study were thirty-three adults in their twenties. We divided three groups into normal, latent and active myofascial trigger points groups by physical findings. We analyzed the results of measured pressure pain, threshold for pain, ultrasound imaging perform for structure characteristic of muscle, surface EMG according to type of muscle contraction for function of muscle contraction. Results : Significant differences were indicated in pressure pain threshold (p<0.05). Significant differences were discovered in the ultrasound imaging analysis. There were increases in muscle Echogenicity white area index (p<0.001). There were significant differences that decrease in %MVIC (p<0.05), increase in MDF (p<0.05). Conclusion : From these results, active rnyotascial trigger points muscle showed quality deterioration on ultrasound imaging and decreased function of muscle contraction, increased motor unit action potential of II type fiber, and electrophysiologically. Imaging structure and neuromuscular physiological characteristic can be diagnostic and quantitative analytical techniques for myofascial pain syndrome and a primary factor that reflected in physical therapy intervention.

• Journal of Korean Neurosurgical Society
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• v.60 no.2
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• pp.165-173
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• 2017

Objective : To explore and analyze the influencing factors of facial nerve function retainment after microsurgery resection of acoustic neurinoma. Methods : Retrospective analysis of our hospital 105 acoustic neuroma cases from October, 2006 to January 2012, in the group all patients were treated with suboccipital sigmoid sinus approach to acoustic neuroma microsurgery resection. We adopted researching individual patient data, outpatient review and telephone followed up and the House-Brackmann grading system to evaluate and analyze the facial nerve function. Results : Among 105 patients in this study group, complete surgical resection rate was 80.9% (85/105), subtotal resection rate was 14.3% (15/105), and partial resection rate 4.8% (5/105). The rate of facial nerve retainment on neuroanatomy was 95.3% (100/105) and the mortality rate was 2.1% (2/105). Facial nerve function when the patient is discharged from the hospital, also known as immediate facial nerve function which was graded in House-Brackmann : excellent facial nerve function (House-Brackmann I-II level) cases accounted for 75.2% (79/105), facial nerve function III-IV level cases accounted for 22.9% (24/105), and V-VI cases accounted for 1.9% (2/105). Patients were followed up for more than one year, with excellent facial nerve function retention rate (H-B I-II level) was 74.4% (58/78). Conclusion : Acoustic neuroma patients after surgery, the long-term (${\geq}1year$) facial nerve function excellent retaining rate was closely related with surgical proficiency, post-operative immediate facial nerve function, diameter of tumor and whether to use electrophysiological monitoring techniques; while there was no significant correlation with the patient's age, surgical approach, whether to stripping the internal auditory canal, whether there was cystic degeneration, tumor recurrence, whether to merge with obstructive hydrocephalus and the length of the duration of symptoms.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.3
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• pp.233-240
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• 1997

Neurons in the nucleus raphe magnus are involved in descending modulation of nociceptive transmission. In this study, we attempted to investigate electrophysiological properties of the NRM neurons dissociated from the postnatal rat medulla. The NRM neurons in the coronal slices of and the dissociated neurons from the postnatal rat medullae were immunohistochemically identified using antibody against serotonin. Relatively small number of neurons were positively stained in both preparations. The positively stained neurons displayed large cell body with double or multiple neurites. Using whole-cell patch clamp configuration ionic currents were recorded from the dissociated NRM-like neurons selected by criteria such as size and shape of cell body and cell population. Two types, high- and low-threshold, of voltage-dependent calcium currents were recorded from the dissociated NRM-like neurons. Some neurons displayed both types of calcium currents, whereas others displayed only high-threshold calcium current. Voltage-dependent potassium currents were also recorded from the dissociated NRM neurons. Some neurons displayed both transient outward and delayed rectifier currents but others showed only delayed rectifier current. These results suggest that there are at least two types of calcium currents and two types of potassium currents in the dissociated NRM neurons.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.119-127
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• 2016

Dihydropyridine (DHP) calcium channel blockers (CCBs) have been widely used to treat of several cardiovascular diseases. An excessive shortening of action potential duration (APD) due to the reduction of $Ca^{2+}$ channel current ($I_{Ca}$) might increase the risk of arrhythmia. In this study we investigated the electrophysiological effects of nicardipine (NIC), isradipine (ISR), and amlodipine (AML) on the cardiac APD in rabbit Purkinje fibers, voltage-gated $K^+$ channel currents ($I_{Kr}$, $I_{Ks}$) and voltage-gated $Na^+$ channel current ($I_{Na}$). The concentration-dependent inhibition of $Ca^{2+}$ channel currents ($I_{Ca}$) was examined in rat cardiomyocytes; these CCBs have similar potency on $I_{Ca}$ channel blocking with $IC_{50}$ (the half-maximum inhibiting concentration) values of 0.142, 0.229, and 0.227 nM on NIC, ISR, and AML, respectively. However, ISR shortened both $APD_{50}$ and $APD_{90}$ already at $1{\mu}M$ whereas NIC and AML shortened $APD_{50}$ but not $APD_{90}$ up to $30{\mu}M$. According to ion channel studies, NIC and AML concentration-dependently inhibited $I_{Kr}$ and $I_{Ks}$ while ISR had only partial inhibitory effects (<50% at $30{\mu}M$). Inhibition of $I_{Na}$ was similarly observed in the three CCBs. Since the $I_{Kr}$ and $I_{Ks}$ mainly contribute to cardiac repolarization, their inhibition by NIC and AML could compensate for the AP shortening effects due to the block of $I_{Ca}$.

• Korean Journal of Veterinary Research
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• v.33 no.2
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• pp.199-209
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• 1993

The effects of ${\alpha}_1$-adrenergic stimulation on membrane potential, intracellular sodium activity $(a_N{^i{_a}})$, and contractility were investigated in the isolated papillary muscle of euthyroid, hyperthyroid, and hypothyroid guinea pigs. Cardiac alterations in the thyroid state have been shown to induce marked changes in action potential characteristics, the most pronounced shortening of action potential duration by hyperthyroidism and an increase in duration by hypothyroidism. $10^{-5}M$ Phenylephrine produced a decrease in $(a_N{^i{_a}})$ in euthyroid and hypothyroid preparations, but an increase in $(a_N{^i{_a}})$ in hyperthyroid ones. The major findings were that phenylephrine produced a stronger positive inotropic effect(PIE) without initial negative inotropic effect(NIE) in hyperthyroid preparations, while phenylephrine produced markedly NIE in hypothyroid ones. The alterations in membrane potential, $(a_N{^i{_a}})$, and contractility were abolished by $3{\times}10^{-5}M$ prazosin in hypothyroidism. In hypothyroid ventricular muscle, the decrease in $(a_N{^i{_a}})$ caused by phenylephrine were not abolished or reduced by $10^{-5}M$ strophanthidin, $10^{-5}M$ TTX, $3{\times}10^{-4}M$ lidocaine, or $100^{-5}M$ verapamil. These results indicate that the ${\alpha}_1$-adrenoceptor-mediated decrease in $(a_N{^i{_a}})$ is not associated with a stimulation of the $Na^+$-$K^+$ pump, inhibition of the $Na^+$ or $Ca^+$ channel in hypothyroid ventricular muscle. $10^{-5}M$ Phenylephrine decreased $(a_N{^i{_a}})$ but increased $(a_N{^i{_a}})$ in the presence of a PKC activator phorbol dibutyrate$(PDB_u)$. In conclusion, it is suggested that the following sequence of events in response to phenyleplhane occur in guinea pig ventricular muscle. First, changes in thyroid state may contribute to the ventacular electrophysiological propeties or ion transport system. Second, the adrenoceptor-mediated initial transient NIE may be associated with the decrease in $(a_N{^i{_a}})$ by PKC activation.

• The Journal of Korean Medicine
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• v.24 no.3
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• pp.108-117
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• 2003

Objective : The central opioid mechanism of acupuncture analgesia has been fairly well documented in acute behavioral experiments, but little electrophysiological study has been performed on the peripheral mechanism and subtypes of opioid receptors responsible for acupuncture-induced antinociception in chronic animal models. In the present electrophysiological experiment, we studied the peripheral mechanism and opioid receptor subtypes which Were implicated in electroacupuncture-induced antinociception in the rat with chronic inflammatory and neurogenic pain. Methods : In the rat with complete Freund's adjuvant-induced inflammation and spinal nerve injury, dorsal horn cell responses to afferent C fiber stimulation were recorded before and after electroacupuncture (EA) stimulation applied to the contralateral Zusanli point for 30 minutes. Also studied Were the effects of specific opioid receptor antagonists and naloxone methiodide, which can not cross the blood-brain barrier, on EA-induced inhibitory action. Results : EA-induced inhibitory action was significantly attenuated by naloxone methiodide, suggesting that EA-induced inhibition was mediated through peripheral mechanism. Pretreatment, but not posttreatment of naltrexone and spinal application significantly blocked EA-induced inhibitory actions. In inflammatory and neurogenic pain models, ${\mu}-$ and ${\delta}-opioid$ receptor antagonists (${\beta}-funaltrexamine$ & naltrindole) significantly reduced EA-induced inhibitory action, but ${\kappa}-opioid$ receptor antagonist had weak inhibitory effect on EA-induced antinociception. Conclusion : These results suggest that 2Hz EA-stimulation induced antinoeiceptive action is mediated through peripheral as well as central mechanism, and mainly through ${\mu}-$ and ${\delta}-opioid$ receptors.

• Annals of Clinical Neurophysiology
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• v.15 no.2
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• pp.48-52
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• 2013

Background: Meralgia paresthetica (MP) is a mononeuropathy affecting the lateral femoral cutaneous nerve. The disease is often diagnosed clinically, but electrophysiological tests play an important role. The aim of this study is to clarify clinical characteristics of MP as well as the role of sensory nerve conduction study (NCS) in the diagnosis of MP. Methods: Sixty-five consecutive patients with clinical diagnosis of MP between March 2001 and June 2012 were retrospectively reviewed at a single tertiary center. General demographics, clinical characteristics and sensory NCS findings were investigated. Measurements of sensory NCS included the baseline-to-peak amplitude, side-to-side amplitude ratio and the conduction velocity. To compare between the normal and abnormal NCS groups, independent t-tests and chisquare test were performed. Results: Sixty-five patients had male predominance (56.9%) with mean age of $48.4{\pm}13.4$ years (range: 16-75). Seven patients (13.5%) had undergone operation or procedure before the symptom onset. The sensory nerve action potentials were obtainable in 52 (80%) of 65 clinically diagnosed MP patients. Sensory NCS revealed abnormalities in 38 patients (73.1%), and others (n=14, 26.9%) showed normal findings. Between the normal and abnormal NCS groups, there is no statistically significant difference on demographics or clinical features. Conclusions: We clarify the clinical features and sensory NCS findings of MP patients. Due to several limitations of sensory NCS, the diagnosis of MP could be accomplished both clinically and electrophysiologically.

• Molecules and Cells
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• v.37 no.3
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• pp.202-212
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• 2014

ClC-1 is a member of a large family of voltage-gated chloride channels, abundantly expressed in human skeletal muscle. Mutations in ClC-1 are associated with myotonia congenita (MC) and result in loss of regulation of membrane excitability in skeletal muscle. We studied the electrophysiological characteristics of six mutants found among Korean MC patients, using patch clamp methods in HEK293 cells. Here, we found that the autosomal dominant mutants S189C and P480S displayed reduced chloride conductances compared to WT. Autosomal recessive mutant M128I did not show a typical rapid deactivation of Cl- currents. While sporadic mutant G523D displayed sustained activation of $Cl^-$ currents in the whole cell traces, the other sporadic mutants, M373L and M609K, demonstrated rapid deactivations. $V_{1/2}$ of these mutants was shifted to more depolarizing potentials. In order to identify potential effects on gating processes, slow and fast gating was analyzed for each mutant. We show that slow gating of the mutants tends to be shifted toward more positive potentials in comparison to WT. Collectively, these six mutants found among Korean patients demonstrated modifications of channel gating behaviors and reduced chloride conductances that likely contribute to the physiologic changes of MC.

• Annals of Clinical Neurophysiology
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• v.3 no.2
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• pp.143-146
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• 2001

Background : Backpack palsy was described in military personnel with shoulder girdle and proximal upper extremity symptoms, predominantly motor in nature related to the use of heavy backpack. Currently, backpack were used for sports, transporting school books and child carriers. We evaluated clinical and electrophysiological feature of backpack palsy. Methods : We included 11 patients with brachial plexopathy as a result of wearing a heavy backpack on long distance marches. All patients were done routine blood sampling, chest X-ray, C-spine X-ray and electrophysiological studies. Results : All patients were right handed person and were not as having a thoracic outlet syndrome. Sensory changes were main initial symptoms and major persistent symptoms were motor weakness. 9 patients(81.8%) were damaged the brachial plexus on non-dominant side, 1 patient was dominant and 1 patient was bilateral involvement. 10 patients(90.9%) were damaged to upper trunk of the brachial plexus by EMG findings. The prognosis was good, 10 patients(90.9%) were complete recovery during 8 weeks, 1 patient was developed reflex sympathetic dystrophy confirmed by 3-phase bone scan. Conclusions : Depression of the clavicle and costoclavicular space probably plays a certain role in pathogenic mechanism. The non-dominant side is more frequently affected, probably due to underdevelopment of the musculature in that side.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.6
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• pp.483-491
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• 2019

Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer's disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. ${\beta}$-Amyloid ($A{\beta}$) and ibotenic acid (IBO)-induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed $A{\beta}$ + IBO-induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in $A{\beta}$ + IBO-induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against $A{\beta}$ + IBO-induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine $A_1$ receptor-specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the $A{\beta}$ + IBO-induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of $A_1R$ is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.