• Journal of Physiology & Pathology in Korean Medicine
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• v.28 no.2
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• pp.200-205
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• 2014

Based on the way we have created to measure the brain atrophy of pons, frontal lobe, sylvian fissure, ventricle, cerebellum, we analyzed the correlation with age. We confirmed whether the brain atrophy due to hypertension, diabetes, hyperlipidemia, drinking, smoking is increasing. Brain deficiency(髓海不足), Brain dissatisfied(腦爲之不滿), Brain Consume(腦髓消烁) listed in Donguibogam(東醫寶鑑) have to be diagnosed with brain atrophy induced by developmental disorders, diseases, aging. Sylvian fissure is well reflected brain atrophy progressed by aging. And brain atrophy increased in hypertension, diabetes, hyperlipidemia, drinking, smoking is well reflected at Sylvian fissure.

• The Korea Journal of Herbology
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• v.21 no.4
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• pp.197-205
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• 2006

Objectives: Anti-oxidants are known to prevent neuronal diseases with pathological and physiological changes such as the brain atrophy and cognitive impairment. This study was designed to investigate the protective effects of Korean ginseng on the oxidative stress induced pathologic changes, and develop new animal model for the brain atrophy. Korean ginseng has anti-oxidant, anti-aging, and protective effects on the brain ischemia. Methods : The intracerebroventricular (ICV) hydrogen peroxide ($H_2O_2$) injection into mice was conducted to generate oxidative stress. Results : The ICV $H_2O_2$ (1 M, $5\;{\mu}l$ injection did not induce either convulsion or death in the acute phase. At the end of second week, cognitive impairment and pathologic change of the brain were observed. The massive brain atrophy was found in the $H_2O_2-injected$ mice, especially in the hippocampus and thalamus. Treatment with Korean ginseng showed a protective effect against the brain atrophy. The $H_2O_2$ injected mice revealed cognitive impairment in the passive avoidance test, and Korean ginseng alleviated cognitive impairment. Conclusion : The results indicate that Korean ginseng has a protective effect on the oxidative stress-induced neuronal damages.

• The Journal of Korean Medicine
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• v.21 no.4
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• pp.9-15
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• 2000

Objective : The aim of this study was to investigate the neuroprotection effect of estrogen on brain atrophy following cerebral infarction. Method : All animals in this study were classified into 4 groups; ovariectomy group (OVXgroup), cerebral infarction group (INF group), combination ovariectomy and cerebral infarction group (OVX + INF group), and naturally intact group for control data (NOR group). Cerebral infarction was made by Chen's method with some modification. Ovariectomy was performed by Wayforth's method. Experimental data for each group was collected at 15 days, month, 3 months, and 6 months after starting observation. Serum $17{\beta}-estradiol(E2)$ was determined by radioimmunoassay. Brain volume was measured and calculated with image analysis. Each brain was sliced at intervals of 2mm in chamber after 30 min of freezing in refregerater. Cerebral volume was obtained by sum of volume of each slice level, which was mean $area{\;}{\times}{\;}2mm$. Results : Cerebral ischemia was found to decrease the serum concentration of $17{\beta}-{\;}estradiol(E2)$ and to inhibit the physiologically conpensatary function of the ovariectomized rats. Also we found that deprivation of estrogen have resulted in more severe cerebral atrophy followed by cerebral infarction. Conclusion : It is suggested that estrogen has a neuroprotection effect on cerebral atrophy following cerebral infarction.

• Journal of Oral Medicine and Pain
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• v.47 no.4
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• pp.217-221
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• 2022

Neurogenic muscular atrophy is muscle wasting and weakness caused by trauma or disease of the nerve that innervates the muscle. We describe a case of unilateral trigeminal neuropathy and neurogenic muscular atrophy of the masticatory muscle caused by a tumor in the foramen ovale. A 59-year-old man visited our clinic complaining of difficulty in right-sided mastication. There were no evident clinical signs and symptoms of temporomandibular disorder. However, severe atrophy of the right masseter and temporalis muscles and hypesthesia of the right side mandibular nerve area were confirmed. Through T1 and T2 signals on magnetic resonance imaging (MRI), a mass suspected of a neurogenic tumor was observed in the foramen ovale and cavernous sinus. Severe atrophy of all masticatory muscles on the right side was observed. This rare case shows trigeminal neuropathy caused by a tumor around the foramen ovale and atrophy of the ipsilateral masticatory muscles. For an accurate diagnosis, it is essential to identify the underlying cause of muscle atrophy with neurologic symptoms present. This can be done through a more detailed clinical examination, including sensory testing and brain MRI, and consider a referral to neurology or neurosurgery for the differential diagnosis of the intracranial disorder.

• Korean Journal of Biological Psychiatry
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• v.3 no.2
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• pp.203-210
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• 1996

Objects : To investigate the relationship between the age of onset with the atrophy and the white matter hyperintensities observed in the brain MRI of Alzheimer patients. Methods : The authors measured volumetrically cortical and ventricular brain atrophy and rated semiquantitatively white matter signal hyperintensities in nine presenile and 18 senile Alzheimer patients, who were matched for dementia severity, according to NINCDS-ADRDA criteria and in age-matched 10 presenile and 11 senile control subjects. Results : Presenile Alzheimer patients showed significantly greater cortical and ventricular atrophy indices(p<0.05) but no difference in white matter hyperintensity scores compared to the age-matched control group. On the contrary, senile Alzheimer patients showed significantly greater white matter hyperintensity scores(p<0.05) but no difference in cortical and ventricular atrophy indices compared to the age-matched control group. Conclusion : An earlier onset was related to marked brain atrophy with less white matter lesions and a later onset is related to marked white matter lesions with less brain atrophy in Alzheimer's disease. Our results suggested the passible difference in the pathophysiology between the presenile and the senile-onset Alzheimer's disease.

• Communications for Statistical Applications and Methods
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• v.23 no.6
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• pp.531-541
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• 2016

Cerebral atrophy affects the brain and is a common feature of patients with mild cognitive impairment or Alzheimer's diseases. It is evaluated by the radiologist or reader based on patient's history, age and the space between the brain and the skull as indicated by magnetic resonance (MR) images. A total of 70 patients were scanned in the supine and prone positions before three radiologist assessed their atrophy level. This study examined the radiologist's assessment of the cerebral atrophy level using a graded response model of item response theory (IRT). A graded response model (GRM) is fitted to our data and then item-fit and person-fit statistics are evaluated to assess the fitted model. Our analysis found that the cerebral atrophy level is better discriminated by readers in the prone position because all item slopes were greater than 2 at this position, versus the supine position where all the slope parameters were less than 1. However, the thresholds are very similar for the first reader and are quite different for the second and third readers because the scanning position affects readers differently as the category threshold estimates vary considerably between the readers..

• Anatomy and Cell Biology
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• v.57 no.1
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• pp.45-60
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• 2024

Morphologic changes in the brain through aging, as a physiologic process, may involve a wide range of variables including ventricular dilation, and sulcus widening. This study reports normal ranges of these changes as standard criteria. Normal brain computed tomography scans of 400 patients (200 males, 200 females) in every decade of life (20 groups each containing 20 participants) were investigated for subcortical/cortical atrophy (bicaudate width [BCW], third ventricle width [ThVW], maximum length of lateral ventricle at cella media [MLCM], bicaudate index [BCI], third ventricle index [ThVI], and cella media index 3 [CMI3], interhemispheric sulcus width [IHSW], right hemisphere sulci diameter [RHSD], and left hemisphere sulci diameter [LHSD]), ventricular symmetry. Distribution and correlation of all the variables were demonstrated with age and a multiple linear regression model was reported for age prediction. Among the various parameters of subcortical atrophy, BCW, ThVW, MLCM, and the corresponding indices of BCI, ThVI, and CMI3 demonstrated a significant correlation with age (R²≥0.62). All the cortical atrophy parameters including IHSW, RHSD, and LHSD demonstrated a significant correlation with age (R²≥0.63). This study is a thorough investigation of variables in a normal brain which can be affected by aging disclosing normal ranges of variables including major ventricular variables, derived ventricular indices, lateral ventricles asymmetry, cortical atrophy, in every decade of life introducing BW, ThVW, MLCM, BCI, ThVI, CMI3 as most significant ventricular parameters, and IHSW, RHSD, LHSD as significant cortical parameters associated with age.

• Journal of Oral Medicine and Pain
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• v.43 no.4
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• pp.147-151
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• 2018

Disuse atrophy involves gradual muscle weakening due to inadequate usage and can cause temporomandibular disorder (TMD). A 45-year old man with TMD symptoms on the left side, who had disuse atrophy of the masticatory muscles on the right side following surgical removal of a trigeminal schwannoma on the right side, first visited the Department of Orofacial Pain and Oral Medicine at Kyung Hee University Dental Hospital with left jaw pain and difficulty in opening mouth and chewing. He had been experiencing difficulties in cognitive function, decrease in visual acuity, impaired speech, and writing deficits after brain surgery. Furthermore, he complained of abnormal occlusion on the right side, which interfered with his ability to chew comfortably and open his mouth effectively. Herein, we describe a contralateral TMD case due to ipsilateral disuse atrophy after brain surgery for a trigeminal schwannoma and our successful treatment with medication, physical therapy, and stabilization splint.

• Proceedings of the Korea Contents Association Conference
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• 2016.05a
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• pp.433-434
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• 2016

Cerebellar atrophy was found that a patient was taking oral phenytoin for 3 years. 53 years old female patient with General tonic clonic(GTC) type seizure was prescribed phenytoin. In the process, she developed ataxic gate, dysarthria. Brain magnetic resonance imaging(MRI) finding was revealed differential diagnosis cerebellar atrophy. She was prescribed epileptol instead of phenytoin. But leukopenia, thrombocytopenia occurred. As a result, phenytoin restarted. Development of medical state decreased abuse of anticonvulsants. Considering various convulsive disorders, we must give attention to using anticonvulsants.

• The Korea Journal of Herbology
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• v.23 no.2
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• pp.159-168
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• 2008

Objectives : The present study has been undertaken to investigate the effects of Dipsaci Radix on Muscle Fiber Atrophy and MyoD Expression in Gastrocnemius of MCAO Rats Methods : In order to investigate effects of Dipsaci radix on the skeletal muscle atrophy following stroke, cerebral infarct was induced by the middle cerebral artery occlusion (MCAO) in the rats. Water extract of Dipsaci radix (184.4 mg/100 g) was treated for 4 weeks, once a day orally, after the MCAO. Effects were evaluated with muscle fiber type composition and cross-sectioned area of muscle fibers in gastrocnemius of the unaffected & affected hind limbs. And MyoD protein expression in gastrocnemius was demonstrated with immunohistochemistry and western blotting. Results : Obtained results were as follows; 1. Infarct volume was not attenuated by Dipsaci radix treatment in the MCAO rats. 2. At the affected-side hind limb of the MCAO rats, the increase of type-I fibers and the decrease of type-II fibers were induced by Dipsaci radix treatment. 3. At the affected-side hind limb of the MCAO rats, decreases of cross-sectioned areas of type-I and type-II fibers were attenuated by Dipsaci radix treatment. 4. At the affected-side hind limb of the MCAO rats, MyoD positive cells were increased by Dipsaci radix treatment. 5. At the affected-side hind limb of the MCAO rats, MyoD expressions were increased by Dipsaci radix treatment. Conclusions : These results suggest that Dipsaci radix has a protective effect against muscle atrophy, through the inhibition of the muscle cell apoptosis, following the central nervous system demage.