Hyug-Gi Kim

Texture analyses of quantitative susceptibility maps to differentiate Alzheimer's disease from cognitive normal and mild cognitive impairment

PURPOSE Although a number of studies have focused on finding anatomical regions in which iron concentrations are high, no study has been conducted to examine the overall variations in susceptibility maps of Alzheimers disease (AD). The objective of this study, therefore, was to differentiate AD from cognitive normal (CN) and mild cognitive impairment (MCI) using a texture analysis of quantitative susceptibility maps (QSMs). METHODS The study was approved by the local institutional review board, and informed consent was obtained from all subjects. In each participant group-CN, MCI, and AD-18 elderly subjects were enrolled. A fully first-order flow-compensated 3D gradient-echo sequence was run to obtain axial magnitudes and phase images and to produce QSM data. Sagittal structural 3D T1-weighted (3DT1W) images were also obtained with the magnetization-prepared rapid acquisition of gradient-echo sequence to obtain brain tissue images. The first- and second-order texture parameters of the QSMs and 3DT1W images were obtained to evaluate group differences using a one-way analysis of covariance. RESULTS For the first-order QSM analysis, mean, standard deviation, and covariance of signal intensity separated the subject groups (F = 5.191, p = 0.009). For the second-order analysis, angular second moment, contrast, and correlation separated the subject groups (F = 6.896, p = 0.002). Finally, a receiver operating characteristic curve analysis differentiated MCI from CN in white matter on the QSMs (z = 3.092, p = 0.0020). CONCLUSIONS This was the first study to evaluate the textures of QSM in AD, which overcame the limitations of voxel-based analyses. The QSM texture analysis successfully distinguished both AD and MCI from CN and outperformed the voxel-based analysis using 3DT1-weighed images in separating MCI from CN. The first-order textures were more efficient in differentiating MCI from CN than did the second-order.

Glutamine and Glutamate Complex, as Measured by Functional Magnetic Resonance Spectroscopy, Alters During Face-Name Association Task in Patients with Mild Cognitive Impairment and Alzheimer’s Disease

BACKGROUND The metabolite response during a memory task in Alzheimers disease (AD) patients is unknown. OBJECTIVE To investigate the metabolite changes in subjects with AD, amnestic mild cognitive impairment (aMCI), and cognitively normal (CN) elderly during a memory task using functional magnetic resonance spectroscopy (fMRS). METHODS This study involved 23 young normal controls (YC), 24 CN elderly, 24 aMCI, and 24 mild and probable AD individuals. fMRS data were acquired at the precuneus and posterior cingulate brain regions during a face-name association task. Statistical analyses of quantified metabolites were performed to evaluate differences of the metabolite values between the stimulation conditions and among the four subject groups. Receiver operating curve analysis was performed to evaluate whether the metabolic changes after functional activations can differentiate the subject groups. RESULT Glutamine and glutamate complex (Glx) was statistically significantly different between the fixation and repeat conditions in aMCI (p = 0.0492) as well as between the fixation and the novel conditions in the AD (p = 0.0412) group. The total N-acetylaspartate (tNAA) was statistically significantly different among the four subject groups in the fixation condition (DF = 3, F = 7.673, p <  0.001), the novel condition (DF = 3, F = 6.945, p <  0.001), and the repeat condition (DF = 3, F = 7.127, p <  0.001). tNAA, tCr, and mIns could be used to differentiate CN from aMCI. Furthermore, tNAA, tCr, Glx, and Glu could also differentiate CN from AD, and aMCI from AD. CONCLUSION Glx was altered during a stimulation that may be used to evaluate neuronal dysfunction in a demented patient. tNAA and tCr were reduced in patients with AD.

Quantitative susceptibility mapping to evaluate the early stage of Alzheimer's disease☆

The objective of this study was to evaluate susceptibility changes caused by iron accumulation in cognitive normal (CN) elderly, those with amnestic mild cognitive impairment (aMCI), and those with early state AD, and to compare the findings with gray matter volume (GMV) changes caused by neuronal loss. The participants included 19 elderly CN, 19 aMCI, and 19 AD subjects. The voxel-based quantitative susceptibility map (QSM) and GMV in the brain were calculated and the differences of those insides were compared among the three groups. The differences of the QSM data and GMVs among the three groups were investigated by voxel-based and region of interest (ROI)-based comparisons using a one-way analysis of covariance (ANCOVA) test with the gender and age as covariates. Finally, a receiver-operating-characteristic (ROC) curve analysis was performed. The voxel-based results showed that QSM demonstrated more areas with significant difference between the CN and AD groups compared to GMV. GMVs were decreased, but QSM values were increased in aMCI and AD groups compared with the CN group. QSM better differentiated aMCI from CN than GMV in the precuneus and allocortex regions. In the accumulation regions of iron and amyloid β, QSM can be used to differentiate between CN and aMCI groups, indicating a useful an auxiliary imaging for early diagnosis of AD.

Ionic cellulose-stabilized gold nanoparticles and their application in the catalytic reduction of 4-nitrophenol

A novel strategy for the synthesis of highly stable gold nanoparticles (GNPs) was designed by reducing HAuCl4 with NaBH4 in an aqueous solution of water-soluble ionic cellulose composed of dimethylimidazolium cations and phosphite-bound cellulose anions. NMR and UV-Vis analysis along with the measurement of the zeta potential suggest that the exceptionally high stability of GNPs originates from the strong interaction of GNPs with the phosphite groups of the ionic cellulose. The thus prepared GNPs exhibit excellent catalytic activity for the reduction of 4-nitrophenol to 4-aminophenol, a model hydrogenation reaction.

CT pattern analysis of necrotizing and nonnecrotizing lymph nodes in Kikuchi disease

Objective The purpose of this study was to determine whether a CT interpretation with imaging pattern analysis differentiates Kikuchi disease (KD) from the two more frequently encountered differential lymph nodes diagnoses of tuberculous lymphadenopathy (TL) and reactive hyperplasia (RH). Materials and methods Between January 2012 and July 2015, 20 patients with KD (6 men, 14 women; mean age, 27.80 years), 36 patients with RH (10 men, 26 women; mean age, 33.08 years) and 34 patients with TL (17 men, 17 women; mean age, 39.82 years) were pathologically diagnosed using US-guided fine needle aspiration biopsy, core needle biopsy, or surgical excisional biopsy. We recorded the total number, location, and size of the affected cervical lymph nodes, and two radiologists reviewed the characteristic imaging findings, including the presence of necrosis, cortical enhancement pattern, perinodal infiltration, conglomeration and nodal calcification, to form a consensus. In addition, we compared two attenuation indices on the nonnecrotic portion of the affected lymph nodes, nodal cortical attenuation (NCA) and the ratio of NCA to the adjacent muscle (NCA/M). Results Conglomeration, enhancement pattern and NCA/M values were independent predictive CT features to distinguish KD from RH. Age and enhancement pattern discriminated KD from TL. Only the mean NCA/M value was a statistically significant CT feature (p = .008) in differentiating KD from both RH+TL. The mean NCA/M of KD (1.67 ± 0.20) was significantly higher than that of RH (1.49 ± 0.20) or TL (1.47 ± 0.21). Conclusion Our results indicate that in case of nonnecrotic lymphadenopathy, a higher NCA/M index can differentiate KD from RH and TL. In addition, the enhancement pattern according to the degree of necrosis discriminated between KD and TL in the case of necrotic lymphadenopathy.

Orofacial complex regional pain syndrome: pathophysiologic mechanisms and functional MRI

Complex regional pain syndrome (CRPS) is one of the most challenging chronic pain conditions and is characterized by burning pain, allodynia, hyperalgesia, autonomic changes, trophic changes, edema, and functional loss involving mainly the extremities. Until recently, very few reports have been published concerning CRPS involving the orofacial area. We report on a 50-year-old female patient who presented with unbearable pain in all of her teeth and hypersensitivity of the facial skin. She also reported intractable pain in both extremities accompanied by temperature changes and orofacial pain that increased when the other pains were aggravated. In the case of CRPS with trigeminal neuropathic pain, protocols for proper diagnosis and prompt treatment have yet to be established in academia or in the clinical field. We performed functional magnetic resonance imaging for a thorough analysis of the cortical representation of the affected orofacial area immediately before and immediately after isolated light stimulus of the affected hand and foot and concluded that CRPS can be correlated with trigeminal neuropathy in the orofacial area. Furthermore, the patient was treated with carbamazepine administration and stellate ganglion block, which can result in a rapid improvement of pain in the trigeminal region.

A case of recurrent transient ischemic attacks: carotid stump syndrome or posterior cerebral artery syndrome?

Dear Editor: A 71-year-old woman presented with two episodes of a transient right hemiparesis, lasting approximately 2–3 min, over the course of 1 week. Her medical history was unremarkable. The patient’s blood pressure was 125/78 mmHg, and her heart rate was 80 beats per minute. On neurological examination, the cranial nerves were intact, including normal movements of the extraocular muscles. Motor examination revealed normal muscle strength and tone; deep tendon reflexes were also normal. The Babinski sign was not elicited. Sensory examination results were normal for all modalities. No triggers for the observed neurological events were identified. Recurrent transient ischemic attacks (TIAs) were suspected, and a laboratory and imaging diagnosticworkupwas performed. Hematological and biochemical profiles were normal. Thrombophilia, vasculitis, and infection screeningswere all negative. Brainmagnetic resonance imaging (MRI) showed delayed arterial transit (DAT) effects of the left posterior cerebral artery (PCA) territory when using arterial spin labeling (ASL) technique without diffusion restriction or T2 signal abnormality (Fig. 1a, b, c). Magnetic resonance angiography (MRA) revealed occlusion of the left PCA (Fig. 1d). Notably, the patient had an unusual vascular variation, which was diagnosed as an anomalous external carotid artery (ECA)-internal carotid artery (ICA) anastomosis with proximal ICA stump in the left side (Fig. 1e). The cranial distribution of the left ICA, distal to the anastomosis level, was otherwise normal. The occipital artery originated from the main trunk of the left ECA, just past the anomalous connection. Therewas no evidence of atherosclerotic plaque in the carotid stump. Four-dimensional (4D) flow MRI revealed turbulent flow within the ICA stump during the venous phase and a relatively high velocity of flow signal in the left ECA-ICA anastomosis, compared with the contralateral ICA at the same level (Fig. 1f and Supplementary Data). In addition, transcranial doppler with bubble study revealed normal findings. Investigation of the cardioembolic source of stroke included an echocardiogram, which showed normal left ventricular function without structural abnormalities. No arrhythmias were found on routine electrocardiography and 24-h Holter monitoring. A diagnosis of TIAwas made, and she was given 100 mg of aspirin for secondary prevention. Based on the neuroimaging findings of the patient, we suspect two potential causes for her episodes of transient right hemiparesis. First, an ICA stump could be a possible source of the embolism in recurrent TIAs. When all other sources of emboli are excluded, ipsilateral ischemic stroke, caused by microembolization arising from the ICA stump, is known as carotid stump syndrome (CSS). CSS is a recognized cause of recurrent cerebrovascular events [1], and the related pathophysiological causes can be attributed to microemboli originating from the carotid stump, or the ipsilateral ECA can enter the intracranial circulation due to the existence of patent anomalous ECA-ICA anastomotic channels [2]. To the best of our knowledge, no studies have investigated the hemodynamic mechanisms of anomalous ECA-ICA anastomosis with the ICA stump. Previous studies presented the digital subtraction angiography in cases of CSS; however, in our case, we visualized the hemodynamic parameters at the level of the ICA stump by using 4D flow MRI. Applying 4D flow MRI in a systematic study with a large number of samples will reveal the hemodynamic characteristics and mechanisms in patients with CSS. Since her past medical history was unremarkable, we speculated that the etiology of the ICA stump would be considered as developmental variants or multiple artery dissection. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s10072-018-3509-9) contains supplementary material, which is available to authorized users.

Ethnic Differences in Intracranial Artery Tortuosity: A Possible Reason for Different Locations of Cerebral Atherosclerosis

Department of Neurology, Kyung Hee University Hospital, Kyung Hee University School of Medicine, Seoul, Korea Department of Radiology, Kyung Hee University Hospital, Kyung Hee University School of Medicine, Seoul, Korea Department of Neurosurgery, Kyung Hee University Hospital, Kyung Hee University School of Medicine, Seoul, Korea Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea

A case report of multiple cervical artery dissection after peripheral type facial palsy and use of steroids.

BackgroundCervical artery dissection is one of the most important causes of ischemic stroke in young age patients. However, multiple cervical artery dissection simultaneously involving the anterior and posterior circulation is uncommon. Here, we would like to report a case of a patient with bilateral vertebral artery (VA) and internal carotid artery dissection (ICA) after a use of systemic steroid due to peripheral facial palsy.Case presentationA 44-year-old man with hypertension visited emergency department due to recurrent vertigo. He was receiving methyl prednisolone for two weeks for the treatment of right peripheral type facial palsy which occurred after retro-orbital headache. Neurologic examination revealed severe ataxia at left side. Sensory for pain and temperature was declined in the right arm and leg. Diffusion-weighted image showed an acute ischemic lesion at the whole territory of posterior-inferior cerebellar artery. Severe stenosis was observed from bilateral VAs and ICAs on conventional magnetic resonance angiography. Intramural hematoma and intimal flap was observed from the high-resolution MRI.ConclusionsPeripheral type facial palsy is an unusual presentation of carotid dissection. Steroids aggravate arterial dissection by increasing blood pressure and blood vessel fragility by its negative effect on connective tissue strength. Use of steroid in patients with peripheral type facial palsy with severe headache may need caution.

INDIVIDUAL EVALUATION SYSTEM FOR WHITE MATTER HYPERINTENSITY RECOGNITION USING DEEP CONVOLUTIONAL NEURAL NETWORK

linear mixed effect model.Results:Among 65 CAApatients, 43 (66.2 %) showed A}