• Proceedings of the Korean Society for Emotion and Sensibility Conference
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• 2003.05a
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• pp.78-83
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• 2003

We investigated the physiological patterns of cybersickness in a Virtual Reality(VR). Subject were exposed to the VR for 9.5 min, and required to detect specific virtual objects. Sixteen electrophysiological signals were recorded before, during, and after the virtual navigation. five questionnaires on the VR experience were acquired form 61 healthy subjects. During the virtual navigation, subjects with the high cybersickness susceptibility showed significant physiological changes, which included increased gastric tachyarrhythmia, eyeblink frequency, and EEG delta wave and decreased EEG beta wave. These results suggest that cybersickness may induce or accompany the changes in central nervous system and autonomic nervous system. Also, these results suggest that there may be increased sympathetic activation in autonomic drive for cybersickness.

• Journal of Genetic Medicine
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• v.11 no.1
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• pp.11-15
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• 2014

Congenital central hypoventilation syndrome (CCHS) is a disorder of the autonomic nervous system characterized by a decreased response to hypercarbia. CCHS is frequently associated with congenital megacolon; the combination is called Haddad syndrome. CCHS is associated with dysfunction in respiratory features of the autonomic nervous system and with other disorders, including facial deformities, cardiovascular symptoms, and tumors. Patients with CCHS frequently have a mutation in the homeobox protein 2b (PHOX2B) gene. Most mutations involve heterozygous expansion of alanine repeats (GCN). Interestingly, a higher polyalanine repeat number is associated with a more severe clinical phenotype. To clarify the role of PHOX2B in disease pathogenesis, we introduce and review the clinical and molecular features of CCHS and Haddad syndrome.

• The Korean Journal of Pain
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• v.35 no.3
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• pp.327-335
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• 2022

Background: The pathophysiology of fibromyalgia (FM) involves many mechanisms including central nervous system sensitization theory, autonomic nervous system (ANS) dysfunction, and recently small fiber neuropathy. While the small fiber neuropathy itself can cause ANS dysfunction and neuropathic pain (NP), it is still unknown whether ANS problems have an association with severity of disease and NP in patients with FM. The aim of this study was to evaluate ANS dysfunction in FM patients and to explore possible associations of ANS dysfunction with disease severity and NP. Methods: Twenty-nine FM patients and 20 healthy controls were included in this cross-sectional study. Participants were tested using sympathetic skin responses (SSR) and R-R interval variation analyses for sympathetic and parasympathetic ANS dysfunction, respectively. Disease severity and somatic symptoms of patients with FM were evaluated using the ACR-2010 scales and Fibromyalgia Impact Questionnaire, and NP symptoms were evaluated using the Pain Detect Questionnaire and Douleur Neuropathique questionnaire. Results: FM patients were found to have ANS dysfunction characterized by increased sympathetic response and decreased parasympathetic response. SSR amplitudes were found to be correlated with a more severe disease. Although nonsignificant, NP severity tended to be associated with a decrease in sympathetic and parasympathetic activities. Conclusions: ANS dysfunction may play a role in the pathophysiology of FM. The trend of decreased ANS functions in FM patients exhibiting NP contradicts the notion that FM is a sympathetically maintained NP and may be explained with small fiber involvement.

• Tuberculosis and Respiratory Diseases
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• v.41 no.2
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• pp.73-86
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• 1994

In addition to classic cholinergic and adrenergic pathways, the existence of a third division of autonomic control in the human airways has been proved. It is called a nonadrenergic noncholinergic(NANC) nervous system, and difficult to study in the absence of specific blockers. Neuropeptides are certainly suggested to be transmitters of this NANC nervous system. It is very frustrating to understand the pathophysiologic role of these peptides in the absence of any specific antagonists. However, further studies of neuropeptides might eventually lead to novel forms of treatment for bronchial asthma. Another study of the interaction between different components of the autonomic nervous system, either in ganglionic neurotransmission or by presynaptic modulation of neurotransmitters at the end-organ will elute neural control in airway disease, particularly in asthma. Studies of how autonomic control may be disordered in airway disease should lead to improvements in clinical management. Epithelial damage due to airway inflammation in asthma may induce bronchial hyperresponsiveness. Axon reflex mechanism is one of possible mechanisms in bronchial hyperresponsiveness. Epithelial damage may expose sensory nerve terminals and C-fiber nrve endings are stimulated by inflammatory mediators. Bi-directional communication between the nerves and mast cells may have important roles in allergic process. The psychological factors and conditioning of allergic reactions is suggested that mast cell activation might be partly regulated by the central nervous system via the peripheral nerves. Studies in animal models, in huamn airways in vitro and in patients with airway disease will uncover the interaction between allergic disease processes and psychologic factors or neural mechainsms.

• Biomolecules & Therapeutics
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• v.5 no.4
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• pp.412-418
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• 1997

General pharmacological properties of AG 60 (mixture of acriflavine and guanosine (1:1, w/w)), which has anticancer effect, following intramuscular administration were examined in terms of effects on central nervous system, gastrointestinal system, cardiovascular system, respiratory system and autonomic nervous system in mice, rats, guinea-pigs and rabbits. AG 60 at the dose of 15 mgtg had no influences on pentobarbital sleeping time, spontaneous motor activity, chemoshock produced by pentylenetetrazole solution, writhing syndromes induced by 0.8% acetic acid solution, and motor coordination of mice. However, AG 60 at the dose of 7.5 and 15 mg/kg caused significant decrease of normal body temperature 1 and/or 2 h after the administration. No influence on body temperature was observed at 3.75 mg/kg in mice. Gastric secretion of rat and intestinal motility of mice were not influenced by the dose of 15 mg/kg. In terms of autonomic nervous system, AG 60 did not show direct effect and inhibitory or augmentative action of histamine- or acetylcholine-induced contractions at the concentration of 5 mg/L in the isolated ileum of guinea-pig. The administration of 15 mg/kg of AG 60 did not affect mean arterial blood pressure and heart rate in rat. AG 60 (15 mg/kg) given to anesthetized rabbits showed no effect on respiratory rate.

• Biomolecules & Therapeutics
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• v.5 no.4
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• pp.369-375
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• 1997

General pharmacological effects of SB-31$^{R}$, the extracts of Pulsatilla koreana, were investigated in mice, rats and guinea-pigs. Intravenous injection of SB-31 (3 and 6 ml/kg) produced almost no effect on central nervous system no effects on the general symptom and behaviors of mice, spontaneous locomotor activity, pentobarbital- induced sleeping time , rotared performance , electroshock and pentylenetertrazole -induced seizures, acetic acid-induced writhing and normal body temperature in mice. SB-31 showed little effects on the spontaneous movement of the isolated ileum and contraction induced by agonists in isolated ileum, suggesting no influence on autonomic nervous system. Administration of SB-31 also did not show any effect on blood pressure in conscious rats. However, a slight decrease in heart rate was observed at high doses (6 and 10 ml/kg) of SB-31 in conscious rats. Similarly, a slight increase in respiratory rate was observed at 6 m1/kg of SB-31 in anesthetized rats. SB-31 did not produce any effect at the dose of 3 ml/kg, but showed a tendency to increase the urinary volume at 6 ml/kg, and produced a decrease in urinary excretions of N $a_{+}$and $K_{+}$at 6 ml/kg. However, transport capacity within the gastrointestinal tract and the secretion of the gastric juice were not influenced by 6 ml/kg of SB-31. In conclusion, these results suggest that SB-31 did not pro-duce any acute effects on the central nervous system, autonomic nervous system, respiratory and circulatory systems, digestive system and kidney function at the dose of below 3 ml/kg.ml/kg.

• Proceedings of the Korean Society for Emotion and Sensibility Conference
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• 1999.03a
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• pp.7-10
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• 1999

• Journal of Chest Surgery
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• v.27 no.1
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• pp.9-14
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• 1994

Substance P[SP] has been known to be a peptide which may be plays a role as a neurotransmitter in central nervous system as well as peripheral autonomic nervous system. It has been reported that SP was widely distributed in the nerve of the tracheal smooth muscle and induced the muscle contraction. However, definite action mechanism of SP in the tracheal smooth muscle was not clear, yet. Thus, present experiment was performed to elucidate an effect of substance P and an action mechanism on contraction of the smooth muscle in rabbits. In order to find a neural mechanism to the effect of SP on the tracheal smooth muscle contraction, atropine sulfate, tetrodotoxin, propranol and phentolamine were administered at 10 min before the addition of SP. Otherwise,to find effect of SP antagonists on the action of SP, [D-Pro2, D-Try7,9]SP, [D-Arg1, D-Pro2, D-Trp7,9, Leu11]SP and [D-Pro4, D-Trp7,9]SP were administered as a same fashion. These following results were obtained. 1] SP induced contraction of the tracheal smooth muscle under resting condition and the contraction was increased dose-dependently. 2] Cholinergic blocker[atropine], neural blocker[tetrodotoxin] and adrenergic blocker[propranol and phentolamine] didn`t have an effect on the contractile response. 3] Three SP antagonists inhibited the contractile response. 4] Isoproterenol relaxed the contraction induced by SP. The above results suggested that SP induced contraction of the tracheal smooth muscle directly act to the smooth muscle in rabbits. The autonomic nervous system did not seem to participate in the SP action.

• Tuberculosis and Respiratory Diseases
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• v.46 no.3
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• pp.317-326
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• 1999

Background: Neural control of airway function is through parasympathetic, sympathetic and non-adrenergic, non-cholinergic mechanisms. The autonomic nervous system controls the airway smooth muscle tone, mucociliary system, permeability and blood flow in the bronchial circulation and release of mediators from the mast cells and other inflammatory cells. The cardiovascular and respiratory autonomic efferent fibers have a common central origin, so altered cardiovascular autonomic reflexes could reflect the altered respiratory autonomic status. Therefore, we performed this study to assess the autonomic abnormality and determine the correlating factors of severity of autonomic neuropathy in patients with chronic obstructive pulmonary disease(COPD) using easily reproducible cardiovascular autonomic reflex function test. Method: The study included 20 patients with COPD and 20 healthy persons obtained on Health Promotion Center in Yeungnam university hospital. All the patients had history and clinical features of COPD as defined by the American Thoracic Society. Any patients with myocardial ischemia, cardiac arrythmia, hypertension, central or peripheral nervous system disease, diabetes mellitus, or any other diseases known to produce autonomic neuropathy, has excluded. The autonomic nervous system function tests included three tests evaluating the parasympathetic system and two tests evaluating the sympathetic system. And also all subjects were subjected to pulmonary function test and arterial blood gas analysis. Results: Autonomic dysfunction was more commonly associated with patients with COPD than healthy person The parasympathetic dysfunction was frequent in patient with COPD, but sympathetic dysfunction seemed preserved. The severity of parasympathetic dysfunction in patients with COPD was correlated with the degree of duration of disease, smoking, reductions in the value of $FEV_1$ and FVC, and arterial hypoxemia but no such correlation existed for age, type of COPD, $FEV_1$/FVC, or $PaCO_s$. Conclusion: There is high frequency of parasympathetic dysfunction associated with COPD and the parasympathetic abnormality in COPD is increased in proportion to severity of airway disease. In COPD, parasympathetic dysfunction probably does not the cause of disease, but it may be an effect of disease progression.

• Journal of Korean Neurosurgical Society
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• v.55 no.5
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• pp.277-279
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• 2014

Autonomic dysreflexia is a clinical emergency syndrome of uncontrolled sympathetic output that can occur in patients who have a history of spinal cord injury. Despite its frequency in spinal cord injury patients, central nervous system complications are very rare. We report a man with traumatic high level incomplete spinal cord injury who suffered hypertensive right thalamic hemorrhage secondary to an episode of autonomic dysreflexia. Prompt recognition and removal of the triggering factor, the suprapubic catheter obstruction which led to hypertensive attack, the patient had a favorable functional outcome after the resorption of the hematoma and effective rehabilitation programme.