Hyeok Gyu Kwon

Prof. Hyeok Gyu Kwon

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Research Focus & Metrics

Academic Career Length

16Years (2011-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 June 2014 in Neuroscience Letters
Verified
Journal Article
Closed access
SJSung Ho Jang
Sung Ho Jang
KKKyoung Kim
Kyoung Kim
SKSeong Ho Kim
Seong Ho Kim
SSSu Min Son
Su Min Son
WJWoo Hyuk Jang
Woo Hyuk Jang
HKHyeok Gyu Kwon
Hyeok Gyu Kwon

1 January 2014 in Frontiers in Human Neuroscience
Verified
Journal Article
Open access
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HKHyeok Gyu Kwon
Hyeok Gyu Kwon
JHJang Sung Ho
Jang Sung Ho
Objectives: Many animal and a few human studies have reported on the neural connectivity of the substantia nigra (SN) and the ventral tegmental area (VTA). However, it has not been clearly elucidated so far. We attempted to investigate any differences in neural connectivity of the SN/VTA in the human brain, using diffusion tensor imaging (DTI).Methods: Sixty-three healthy subjects were recruited for this study. DTIs were acquired using a sensitivity-encoding head coil at 1.5T. Connectivity was defined as the incidence of connection between the SN/VTA and each brain regions in the brain.Results: The connectivity of SN was higher than that of the VTA. This included in the primary motor cortex, primary somatosensory cortex, premotor cortex, prefrontal cortex, caudate nucleus, globus pallidus, putamen, nucleus accumbens, temporal lobe, amygdala, pontine basis, occipital lobe, anterior and posterior lobe of cerebellum, corpus callosum, and external capsule (p.05).Conclusions: We found the differences in neural connectivity of the SN/VTA in the human brain. The method and results of this study can provide useful information for clinicians and researchers in neuroscience, especially who work for Parkinson’s disease and patients with brain injury.


1 June 2016 in Medicine
Verified
Journal Article
Open access
SJSung Ho Jang
Sung Ho Jang
SPSo Min Park
So Min Park
HKHyeok Gyu Kwon
Hyeok Gyu Kwon
The periaqueductal gray (PAG) plays a pivotal role in pain modulation. We attempted to examine the relation between injury of the PAG and central pain in patients with mild traumatic brain injury (TBI).Sixty-one patients with mild TBI with central pain and 31 healthy control subjects were recruited for this study. Visual analog scale (VAS) was used for evaluation of central pain. The region of interest was defined for the PAG and the fractional anisotropy (FA) and apparent diffusion coefficient (ADC) were measured.The FA value was significantly lower in the patient group than in the control group (P < 0.05). However, no significant difference in the ADC value was observed between the patient and control groups (P > 0.05). VAS score of the patient group showed significant moderate negative correlation with the FA (r = -0.38), while no significant correlation was observed between VAS score and the ADC value (P < 0.05).We demonstrated injury of the PAG in patients with central pain following mild TBI and the degree of injury of the PAG was closely related to the degree of central pain.

24 February 2014 in Brain Injury
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Journal Article
Closed access
HKHyeok Gyu Kwon
Hyeok Gyu Kwon
SJSung Ho Jang
Sung Ho Jang
Many studies have demonstrated neural injury in patients with mild traumatic brain injury, using diffusion tensor imaging (DTI). However, knowledge regarding injury of the corticoreticular pathway (CRP) is limited. This study reports on a patient with mild TBI who showed delayed gait disturbance due to injury of the CRP following head trauma, which was demonstrated by DTI. A 14-year-old female patient suffered from an in-car accident: her head was hit with the backseat during hyperextension after flexion movement when her sedan was struck by another sedan from behind. She showed mild quadriparesis after onset. At 29 days after onset, she noted gait disturbance and aggravated quadriparesis with more severe weakness of the proximal joints. No abnormality was observed on brain MRI and electromyography study performed at 10 weeks after onset. Both CRPs were discontinued at the midbrain level on 10-week DTI. It appears that the proximal weakness of this patient was attributed to injury of both CRPs following head trauma. It is assumed that the mild weakness at the onset of head trauma was caused by the primary traumatic axonal injury and the aggravated weakness that started from 29 days might be ascribed to the secondary traumatic axonal injury.