• Physical Therapy Korea
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• v.3 no.1
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• pp.57-64
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• 1996

Spinal cord injury in child often occurs without evidence of fracture or dislocation. The mechanisms of neural damage in this syndrome of spinal cord injury without radiographic abnormality(SCIWORA) include flexion, hyperextension, longitudinal distraction, and ischemia. Inherent elasticity of the vertebral column in infants and young children, among other age-related anatomical peculiarities, render the pediatric spine exceedingly vulnerable to deforming forces. The neurological lesions encountered in this syndrome include a high incidence of complete and severe partial cord lesions. Children younger than 8years old sustain more serious neurological damage and suffer a larger number of upper cervical cord lesions than children aged over 8 years. Of the children with SCIWORA. 52% have delayed onset of paralysis up to 4 days after injury, and most of these children recall transient paresthesia, numbness, or subjective paralysis. The long-term prognosis in cases of SCIWORA is grim. Most children with complete and severe lesions do not recover; only those with initially mild neural injuries make satisfactory neurological recovery.

• The Journal of Korea Assosiation for Disability and Oral Health
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• v.7 no.1
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• pp.15-20
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• 2011

A person with neurological disorder is defined as a person with limitation of ambulation or basic life activity due to the cerebral palsy or traumatic brain damage, stroke. Recently, the DMFT of the children with neurological disorders is similar or lower than the DMFT of the children with no disability. But, this article is about the severe-early childhood caries in children with grade 1 neurological disorder. It is supposed that the primary motor impairment and secondary physical weakness, frequent hospitalization, sugar- rich food and drugs, lack of oral care, delayed dental visit made high caries susceptibility. In case of treatment of the children with severe neurological disorders, dentists should make a thorough caries preventive plan based on individualized caries risk assessment. Also parents and medical doctors should recognize the importance of oral care and do the early dental visit and home care.

• Journal of Ginseng Research
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• v.47 no.1
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• pp.23-32
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• 2023

Coronavirus disease 2019 (COVID-19) is a highly infectious respiratory disease caused by a severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). SARS-CoV-2 infection may cause clinical manifestations of multiple organ damage, including various neurological syndromes. There are currently two oral antiviral drugs-Paxlovid and molnupiravir-that are recognized to treat COVID-19, but there are still no drugs that can specifically fight the challenges of SARS-CoV-2 variants. Nucleotide-binding oligomerization domain-like receptor pyrin domain-containing-3 (NLRP3) inflammasome is a multimolecular complex that can sense heterogeneous pathogen-associated molecular patterns associated with neurological disorders. The NLRP3 activation stimulates the production of caspase-1-mediated interleukin (IL)-1β, IL-18, and other cytokines in immune cells. Panax (P.) ginseng is a medicinal plant that has traditionally been widely used to boost immunity and treat various pathological conditions in the nervous system due to its safety and anti-inflammatory/oxidant/viral activities. Several recent reports have indicated that P. ginseng and its active ingredients may regulate NLRP3 inflammasome activation in the nervous system. Therefore, this review article discusses the current knowledge regarding the pathogenesis of neurological disorders related to COVID-19 and NLRP3 inflammasome activation and the possibility of using P. ginseng in a strategy targeting this pathway to treat neurological disorders.

• Clinical and Experimental Pediatrics
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• v.46 no.2
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• pp.137-142
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• 2003

Purpose : This study was performed to determine the sensitivity of neonatal electroencephalography (EEG) in detecting underlying brain disease, to compare the sensitivity and specificity of EEG with those of brain ultrasonography and to determine the prognostic value of EEG for neonatal neurologic diseases. Methods : Eighty-seven newborn babies were subjected to a electroencephalographic examination for the evaluation of underlying neurological diseases and EEGs were recorded at least before three days of life. The findings of early ultrasonography performed within three days after birth were compared with those of magnetic resonance imaging(MRI) or ultrasonography after seven days of life. Results : The EEG results were more sensitive and specific than ultrasonography for the detection of neonatal brain damage. The EEG results showed 91.7% sensitivity for mild grade neurological sequelae and 100.0% sensitivity for moderate and severe-grade neurological sequelae in predicting the neurological outcome. However, early ultrasonography results showed 20.8% and 18.8% of sensitivity and specificity, respectively. Conclusion : EEG is a highly sensitive diagnostic tool for detecting neonatal brain disease and is valuable for predicting the long-term outcome of neurologic sequelae.

• Clinical and Experimental Pediatrics
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• v.57 no.6
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• pp.251-256
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• 2014

Severe intraventricular hemorrhaging (IVH) in premature infants and subsequent posthemorrhagic hydrocephalus (PHH) causes significant mortality and life-long neurological complications, including seizures, cerebral palsy, and developmental retardation. However, there are currently no effective therapies for neonatal IVH. The pathogenesis of PHH has been mainly explained by inflammation within the subarachnoid spaces due to the hemolysis of extravasated blood after IVH. Obliterative arachnoiditis, induced by inflammatory responses, impairs cerebrospinal fluid (CSF) resorption and subsequently leads to the development of PHH with ensuing brain damage. Increasing evidence has demonstrated potent immunomodulating abilities of mesenchymal stem cells (MSCs) in various brain injury models. Recent reports of MSC transplantation in an IVH model of newborn rats demonstrated that intraventricular transplantation of MSCs downregulated the inflammatory cytokines in CSF and attenuated progressive PHH. In addition, MSC transplantation mitigated the brain damages that ensue after IVH and PHH, including reactive gliosis, cell death, delayed myelination, and impaired behavioral functions. These findings suggest that MSCs are promising therapeutic agents for neuroprotection in preterm infants with severe IVH.

• Laboraroty Animal Research
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• v.33 no.3
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• pp.244-250
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• 2017

${\alpha}$-Synuclein is abundantly expressed in neuronal tissue, plays an essential role in the pathogenesis of neurodegenerative disorders, and exerts a neuroprotective effect against oxidative stress. Cerebral ischemia causes severe neurological disorders and neuronal dysfunction. In this study, we examined ${\alpha}$-synuclein expression in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic injury and neuronal cells damaged by glutamate treatment. MCAO surgical operation was performed on male Sprague-Dawley rats, and brain samples were isolated 24 hours after MCAO. We confirmed neurological behavior deficit, infarction area, and histopathological changes following MCAO injury. A proteomic approach and Western blot analysis demonstrated a decrease in ${\alpha}$-synuclein in the cerebral cortices after MCAO injury. Moreover, glutamate treatment induced neuronal cell death and decreased ${\alpha}$-synuclein expression in a hippocampal-derived cell line in a dose-dependent manner. It is known that ${\alpha}$-synuclein regulates neuronal survival, and low levels of ${\alpha}$-synuclein expression result in cytotoxicity. Thus, these results suggest that cerebral ischemic injury leads to a reduction in ${\alpha}$-synuclein and consequently causes serious brain damage.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.1
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• pp.125-131
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• 2017

Status epilepticus is the most common serious neurological condition triggered by abnormal electrical activity, leading to severe and widespread cell loss in the brain. Lithium has been one of the main drugs used for the treatment of bipolar disorder for decades, and its anticonvulsant and neuroprotective properties have been described in several neurological disease models. However, the therapeutic mechanisms underlying lithium's actions remain poorly understood. The muscarinic receptor agonist pilocarpine is used to induce status epilepticus, which is followed by hippocampal damage. The present study was designed to investigate the effects of lithium post-treatment on seizure susceptibility and hippocampal neuropathological changes following pilocarpine-induced status epilepticus. Status epilepticus was induced by administration of pilocarpine hydrochloride (320 mg/kg, i.p.) in C57BL/6 mice at 8 weeks of age. Lithium (80 mg/kg, i.p.) was administered 15 minutes after the pilocarpine injection. After the lithium injection, status epilepticus onset time and mortality were recorded. Lithium significantly delayed the onset time of status epilepticus and reduced mortality compared to the vehicle-treated group. Moreover, lithium effectively blocked pilocarpine-induced neuronal death in the hippocampus as estimated by cresyl violet and Fluoro-Jade B staining. However, lithium did not reduce glial activation following pilocarpine-induced status epilepticus. These results suggest that lithium has a neuroprotective effect and would be useful in the treatment of neurological disorders, in particular status epilepticus.

• Journal of Veterinary Science
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• v.23 no.6
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• pp.84.1-84.15
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• 2022

Background: Stroke is caused by disruption of blood supply and results in permanent disabilities as well as death. Chlorogenic acid is a phenolic compound found in various fruits and coffee and exerts antioxidant, anti-inflammatory, and anti-apoptotic effects. Objectives: The purpose of this study was to investigate whether chlorogenic acid regulates the PI3K-Akt-Bad signaling pathway in middle cerebral artery occlusion (MCAO)-induced damage. Methods: Chlorogenic acid (30 mg/kg) or vehicle was administered peritoneally to adult male rats 2 h after MCAO surgery, and animals were sacrificed 24 h after MCAO surgery. Neurobehavioral tests were performed, and brain tissues were isolated. The cerebral cortex was collected for Western blot and immunoprecipitation analyses. Results: MCAO damage caused severe neurobehavioral disorders and chlorogenic acid improved the neurological disorders. Chlorogenic acid alleviated the MCAO-induced histopathological changes and decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells. Furthermore, MCAO-induced damage reduced the expression of phospho-PDK1, phospho-Akt, and phospho-Bad, which was alleviated with administration of chlorogenic acid. The interaction between phospho-Bad and 14-3-3 levels was reduced in MCAO animals, which was attenuated by chlorogenic acid treatment. In addition, chlorogenic acid alleviated the increase of cytochrome c and caspase-3 expression caused by MCAO damage. Conclusions: The results of the present study showed that chlorogenic acid activates phospho-Akt and phospho-Bad and promotes the interaction between phospho-Bad and 14-3-3 during MCAO damage. In conclusion, chlorogenic acid exerts neuroprotective effects by activating the Akt-Bad signaling pathway and maintaining the interaction between phospho-Bad and 14-3-3 in ischemic stroke model.

• Biomolecules & Therapeutics
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• v.8 no.2
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• pp.160-166
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• 2000

The present study examined influence of various ischemic duration on extent of focal ischemic brain injury induced by middle cerebral artery occlusion (MCAO) in rats. The MCAO was produced by insertion of a 17 mm silicone-coated 4-0 nylon surgical thread to the origin of MCA through the internal carotid artery for 30, 60, 90, 120 min (transient) or 24 hr (permanent) in male Sprague-Dawley rats under isoflurane anesthesia. Reperfusion in transient MCAO models was achieved by pulling the thread out of the internal carotid artery. Only rats showing neurological deficits characterized by left hemiparesis and/or circling to the left, were included in cerebral ischemic groups. The rats were sacrificed 24 hr after MCAO and seven serial coronal slices of the brain were stained with 2,3,5-triphenyltetrazolium chloride. Infarct size was measured using a computerized image analyzer. Ischemic damage was common in the frontoparietal cortex (somatosensory area) and the lateral segment of the striatum while damage to the medial segment of the striatum depended on the duration of the occlusion. In the 30-min MCAO grouts, however, infarcted region was primarily confined to the striatum and it was difficult to clearly delineate the region since there was mixed population of live and dead cells in the nucleus. Infarct volume was generally increased depending on the duration of MCAO, showing the most severe damage in the permanent MCAO group. However, there was no significant difference in infarct size between the 90-min and 120-min MCAO groups. % Edema also tended to increase depending on the duration of MCAO. The results suggest that the various focal ischemic rat models established in the present study can be used to evaluate in vivo neuroprotective activities of candidate compounds or to elucidate pathophysiological mechanisms of ischemic neuronal cell death.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.14 no.1
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• pp.10-18
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• 2014

Recent advances in the diagnosis and treatment of inborn errors of metabolism have improved substantially the prognosis of many of these diseases, if diagnosed early enough before irreversible damage occurs. This makes it essential that the practicing pediatrician, especially neonatologists be familliar with the clinical presentations and systematic approaches of these disorders. Characteristic clinical presentations, methods of systematic approach and typing of various disorders is discussed in this review. The signs of neurological dysfunctions of many IEMs manifesting in the neonatal period is very nonspecific, such as poor feeding, poor sucking, apnea or tachypnea, vomiting, hypertonia, hypotonia, seizure, letharginess, consciousness change and coma. Many other non-metabolic severe disorders of neonatal period such as neonatal sepsis and intracerebral hemorrhage share these nonspecific symptoms. Hyperammonemia, metabolic acidosis, ketosis and hyperlatic acidemia are observed in many of these conditions but there are exceptions in which conditions all basal laboratory tests are normal, such as NKH, sulfite oxidase deficiency and peroxisomal disorders. According to the results of basal laboratory tests, IEMs in the neonatal period can be categorized in to 6 types. Grouping of IEMs into 6 types will make confirmatory tests and early emergency treatment more efficient.