• Molecules and Cells
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• v.45 no.11
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• pp.781-788
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• 2022

Proline plays a multifaceted role in protein synthesis, redox balance, cell fate regulation, brain development, and other cellular and physiological processes. Here, we focus our review on proline metabolism in neurons, highlighting the role of dysregulated proline metabolism in neuronal dysfunction and consequently neurological and psychiatric disorders. We will discuss the association between genetic and protein function of enzymes in the proline pathway and the development of neurological and psychiatric disorders. We will conclude with a potential mechanism of proline metabolism in neuronal function and mental health.

• Therapeutic Science for Rehabilitation
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• v.2 no.1
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• pp.24-35
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• 2013

The Purpose of this study was to determine the clinical effectiveness of mirror therapy for stroke. Moreover, this paper was designed to summarize clarified information of neurological plasticity by mirror therapy to finally define the neurological mechanism. Mirror therapy improves the stroke patients' hand and arm motor function. It also has a positive influence on recovering performance of activities of daily living and relieving pain. However, it is not evident that mirror therapy restores visual neglect. There are various ways of recovering stroke. Fundamentally, all the theories are on a bases of restoration of premotor area. Premotor area which is associated with motor control increases the activation of primary motor area and finally improves patients' motor function. If primary motor area is completely damaged, premotor area and supplementary motor substitute for primary motor area. In summary of literature survey, there are not enough evidence to verify the effectiveness and neurological mechanism of mirror therapy. In future, more researches should be conducted to verify the neurological recovery through mirror therapy. Then, mirror therapy will be acknowledged as a clinically effective treatment.

• Journal of Korean Neurosurgical Society
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• v.30 no.2
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• pp.231-238
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• 2001

Vertebral artery injury is a rare complication of anterior cervical approach. We report two patients who suffered injury to vertebral artery during anterior cervical spine surgery. The mechanism of injury, their operative management, and the subsequent outcome were assessed and relevant literatures reviewed. The awareness of the possibility of vertebral artery injury is most important to prevent and it's occurrence is best avoided by a thorough understanding of the anatomical relationships of the artery, the spinal canal, and the vertebral body and careful use of surgical instruments.

• Journal of Korean Neurosurgical Society
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• v.56 no.2
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• pp.108-113
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• 2014

Objective : Ankylosing spondylitis is an inflammatory rheumatic disease mainly affecting the axial skeleton. The rigid spine may secondarily develop osteoporosis, further increasing the risk of spinal fracture. In this study, we reviewed fractures in patients with ankylosing spondylitis that had been clinically diagnosed to better define the mechanism of injury, associated neurological deficit, predisposing factors, and management strategies. Methods : Between January 2003 and December 2013, 12 patients with 13 fractures with neurological complications were treated. Neuroimaging evaluation was obtained in all patients by using plain radiography, CT scan, and MR imaging. The ASIA Impairment Scale was used in order to evaluate the neurologic status of the patients. Management was based on the presence or absence of spinal instability. Results : A total of 9 cervical and 4 thoracolumbar fractures were identified in a review of patients in whom ankylosing spondylitis had been diagnosed. Of these, 7 fractures were associated with a hyperextension mechanism. 10 cases resulted in a fracture by minor trauma. Posttraumatic neurological deficits were demonstrated in 11 cases and neurological improvement after surgery was observed in 5 of these cases. Conclusions : Patients with ankylosing spondylitis are highly susceptible to spinal fracture and spinal cord injury even after only mild trauma. Initial CT or MR imaging of the whole spine is recommended even if the patient's symptoms are mild. The patient should also have early surgical stabilization to correct spinal deformity and avoid worsening of the patient's neurological status.

• The Journal of Korean Academy of Sensory Integration
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• v.14 no.1
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• pp.50-59
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• 2016

Objective : The goal of this study was to investigate neurological mechanism of emotional regulation and to examine the relationship between the regulation and sensory processing. Subjective : Emotional regulations are mainly processed in limbic system, particularly the basal-lateral group of amygdala takes on a major role in the regulations. The basal-lateral group of amygdala links to thalamus directly and/or indirectly which processes sensory information together. This sensory information connects to orbital and medial prefrontal cortex. Inadequate sensory processing may cause difficulties in emotional regulations and behaviors because of a circuit linking the amygdala, the thalamus, and the orbital and medial prefrontal cortex. These difficulties and impairments has been reported in neurological studies for children with ASD and ADHD. Conclusion : Neurological states are different between the normal children and children with ASD and ADHD and these represent various aspects in sensory processing, emotional regulations and behaviors. Thus, therapists working with children with ASD and ADHD need to understand mechanisms of sensory processing and emotional regulations in order to provide adequate treatments.

• Annals of Clinical Neurophysiology
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• v.16 no.1
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• pp.1-7
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• 2014

Iron is an important element for brain oxygen transport, myelination, DNA synthesis and neurotransmission. However, excessive iron can generate reactive oxygen species and contribute neurotoxicity. Although brain iron deposition is the natural process with normal aging, excessive iron accumulation is also observed in various neurological disorders such as neurodegeneration with brain iron accumulation, Parkinson's disease, Alzheimer's disease, multiple sclerosis, Friedreich ataxia, and others. Magnetic resonance image (MRI) is a useful method for detecting iron deposits in the brain. It can be a powerful tool for diagnosis and monitoring, while furthering our understanding of the role of iron in the pathophysiology of a disease. In this review, we will introduce the mechanism of iron toxicity and the basics of several iron-related MRI techniques. Also, we will summarize the previous results concerning the clinical application of such MR imagings in various neurological disorders.

• Reproductive and Developmental Biology
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• v.35 no.2
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• pp.167-174
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• 2011

Acute ischemic stroke results from sudden decrease or loss of blood supply to an area of the brain, resulting in a coinciding loss of neurological function. The antioxidant action of melatonin is an important mechanism among its known effects to protective activity during ischemic/reperfusion injury. The focus of this research, therapeutic efficacy of melatonin on recovery of neurological function following long term treatment in ischemic brain injured rats. Male Sprague-Dawley rats (n=40; 8 weeks old) were divided into the control group, and MCAo groups (Vehicle, MT7 : MCAo+ melatonin injection at 7:00, MT19 : MCAo+melatonin injection at 19:00, and MT7,19 : MCAo+melatonin injection at 7:00 and 19:00). Rat body weight and neurological function were measured every week for 8 weeks. After 8 weeks, the rats were anesthetized with a mixture of zoletil (40 mg/kg) and xylazine (10 mg/kg) and sacrificed for further analysis. Tissues were then collected for RNA isolation from brain tissue. Also, brain tissues were analyzed by histological procedures. We elucidated that melatonin was not toxic in vital organs. MT7,19 was the most rapidly got back to mild symptom on test of neurological parameter. Also, exogenous melatonin induces both the down-regulation of detrimental genes, such as NOSs and the up-regulation of beneficial gene, including BDNF during long term administration after focal cerebral ischemia. Melatonin treatment reduced the loss of primary motor cortex. Therefore, we suggest that melatonin could be act as prophylactic as well as therapeutic agent for neurorehabilitative intervention.

• The Journal of the Society of Stroke on Korean Medicine
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• v.8 no.1
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• pp.48-57
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• 2007

Stroke is a disease which results in impairment of body functions and affects everyday life. The ability of cerebral neurons to become reorganized and restore function after damage is called plasticity. Motor impairment typically appears contralateral to the affected cerebral hemisphere in patients with cerebral lesions. The authors report a case of a patient with hemiplegia ipsilateral to affected cerebral hemisphere, along with its conjectured mechanism.

• Clinical and Experimental Pediatrics
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• v.48 no.9
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• pp.920-923
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• 2005

Epilepsy is a neurological disorder from many molecular and biochemical responses. In the underlying mechanism, free radicals play an important role in seizure initiation and seizure-induced brain damage. Excessive production of oxygen free radicals and other radical species have been implicated in the development of seizures under pathological conditions and linked to seizure-induced neurodegeneration.

• Molecules and Cells
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• v.45 no.4
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• pp.216-230
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• 2022

SERTA domain-containing protein 1 (Sertad1) is upregulated in the models of DNA damage and Alzheimer's disease, contributing to neuronal death. However, the role and mechanism of Sertad1 in ischemic/hypoxic neurological injury remain unclear. In the present study, our results showed that the expression of Sertad1 was upregulated in a mouse middle cerebral artery occlusion and reperfusion model and in HT22 cells after oxygen-glucose deprivation/reoxygenation (OGD/R). Sertad1 knockdown significantly ameliorated ischemia-induced brain infarct volume, neurological deficits and neuronal apoptosis. In addition, it significantly ameliorated the OGD/R-induced inhibition of cell viability and apoptotic cell death in HT22 cells. Sertad1 knockdown significantly inhibited the ischemic/hypoxic-induced expression of p-Rb, B-Myb, and Bim in vivo and in vitro. However, Sertad1 overexpression significantly exacerbated the OGD/R-induced inhibition of cell viability and apoptotic cell death and p-Rb, B-Myb, and Bim expression in HT22 cells. In further studies, we demonstrated that Sertad1 directly binds to CDK4 and the CDK4 inhibitor ON123300 restores the effects of Sertad1 overexpression on OGD/R-induced apoptotic cell death and p-Rb, B-Myb, and Bim expression in HT22 cells. These results suggested that Sertad1 contributed to ischemic/hypoxic neurological injury by activating the CDK4/p-Rb pathway.