Yong-Duk Kim

Comparison of diffusion tensor imaging and voxel-based morphometry to detect white matter damage in Alzheimer's disease.

Regional atrophy of gray matter (GM) in Alzheimers disease (AD) is well known; however, the relationship between macroscopic and microscopic changes of cerebral white matter (WM) is uncertain. The aim of this study was to investigate the pattern of GM, WM atrophy, and microscopic WM changes in the same individuals with AD. All subjects (10AD and 15 healthy controls [HC]) underwent a MRI scanning at 1.5 T, including a 3-dimensional volumetric scan and diffusion tensor imaging (DTI). We performed statistical parametric mapping (SPM) with DTI to evaluate the patterns of the microscopic WM changes, as well as voxel-based morphometry (VBM) for GM and WM volume changes between patients with AD and HC. GM atrophy was detected, mainly in posterior regions, and WM atrophy was similarly distributed, but less involved on VBM analysis. Unlike WM atrophy on VBM analysis, microscopic WM changes were shown in the medial frontal, orbitofrontal, splenium of the corpus callosum, and cingulum on DTI analysis with SPM. We demonstrated that the pattern of macroscopic WM atrophy was similar to GM atrophy, while microscopic WM changes had a different pattern and distribution. Our findings suggest that WM atrophy may preferentially reflect the secondary changes of GM atrophy, while microscopic WM changes start earlier in frontal areas before GM and WM atrophy can be detected macroscopically.

Pattern of Voiding Dysfunction after Acute Brainstem Infarction

Background: The purpose of this study is to compare the patterns of voiding dysfunction according to the locations of brainstem lesions. Methods: Between November 2008 and December 2011, a total of 30 patients participated in this study. All 30 subjects, consisting of 16 men and 14 women, aged between 41 and 82 years (mean age, 63.0 ± 11.0 years) underwent a urodynamic study within 7 days after the onset of a stroke. Results: Twenty-one (70%) patients had a pontine lesion and 9 (30%) had a medullary lesion. Fourteen of these patients (46.7%) had bladder storage disorder, 7 patients (23.3%) had bladder emptying disorder, and 9 patients (30%) had a normal report. Five of the patients who had a medullary lesion (55.6%) had bladder emptying disorder, whereas only 2 patients who had a pontine lesion (9.5%) had bladder emptying disorder. Thirteen patients who had a pontine lesion (61.9%) showed bladder storage disorder. Discussion: The descending pathway from the midbrain tegmentum is inhibitory, and the pathway from the pontine tegmentum is stimulatory. Because of their location pontine lesions could disrupt the descending fibers of the midbrain tegmentum and medullary lesions could disrupt the descending fibers of the pontine tegmentum.

Brain perfusion alterations in depressed patients with Parkinson’s disease

ObjectiveAlthough Parkinson’s disease (PD) is frequently accompanied by depression, brain perfusion deficits in PD with depression remain unclear. This study aimed to assess alterations in regional cerebral blood flow (rCBF) in depressed PD patients using 99mTc hexamethyl-propylene-amine-oxime single-photon emission computed tomography (SPECT).MethodsAmong 78 patients with PD, 35 patients were classified into the depressed PD group, while the rest (43 patients) was assigned to the nondepressed PD group based on the scores of the Geriatric Depressive Scale (GDS). All participants underwent brain SPECT imaging. The voxel-wise whole-brain analysis and region-of-interest (ROI) analysis of the limbic areas were conducted to compare rCBF between the depressed and nondepressed PD groups.ResultsThe depressed PD patients demonstrated higher GDS scores than nondepressed patients, whereas between-group differences in the PD severity and cognitive function were not significant. Perfusion in the left cuneus was increased, while that in the right superior temporal gyrus and right medial orbitofrontal cortex was reduced in the depressed PD patients as compared with nondepressed PD patients. In addition, the ROI analysis demonstrated rCBF decreases in the amygdala, anterior cingulate cortex, hippocampus, and parahippocampal gyrus in the depressed PD group. A positive correlation was found between the GDS scores and rCBF in the left cuneus cluster in the depressed PD patients.ConclusionThis study identified the regional pattern of brain perfusion that distinguished depressed from nondepressed PD patients. Hyperperfusion in the occipital areas and hypoperfusion in the fronto-temporo-limbic regions may be potential imaging biomarkers for depression in PD.

Interaction of white matter hyperintensities (WMHs) and apolipoprotein E (APOE) genotypes on cognition in patients with amnestic mild cognitive impairment (aMCI)

The clinical implications of WMHs in aMCI are inconclusive. Moreover, clinical interactions between APOE genotypes and WMHs remain unclear. This study was conducted to investigate the relationship between WMHs and cognitive functions and how this relationship interacted with APOE genotype in people with aMCI. This study included a total of 1472 patients with aMCI from the Clinical Research Center for Dementia of South Korea (CREDOS) and divided them into 3 groups according to the severity of WMHs as assessed by visual ratings of brain magnetic resonance images. The associations of WMHs with the various cognitive domains and with APOE epsilon 4 (ɛ4) status were evaluated. After multivariable adjustments, the severity of WMHs was independently associated with semantic/phonemic verbal fluency and Stroop test-color reading, while APOE ɛ4 status was associated with verbal and visual memory-immediate, delayed recall, and recognition. Moreover, there were interaction between WMHs and APOE ɛ4 status in semantic verbal fluency (animal, P=0.033; supermarket, P=0.047)/Stroop test-color reading (P=0.024). WMHs independently deleteriously affected frontal executive functions in aMCI patients, regardless of APOE ɛ4 presence. Furthermore, APOE ɛ4 possession caused a rapid decline in frontal executive functions with the increase in the WMHs severity (vs. absence), suggesting that WMHs and APOE ɛ4 genotypes synergistically contribute to frontal executive dysfunctions in aMCI.

A case of cerebral erdheim-chester disease with progressive cerebellar syndrome.

Erdheim-Chester disease (ECD) is a rare non-Langerhans form of histiocytosis. Cerebellar involvement is rare in this syndrome. We report a 37-year-old woman with slowly progressive cerebellar ataxia, dysmetria of limbs, nystagmus, and dysarthria, bilateral painful axillary masses, and generalized arthralgia. Brain MRI revealed cerebellar atrophy with focal lesions in the pons, middle cerebellar peduncle, and the cerebellum. She underwent incisional biopsy of her axillary masses which showed findings consistent with ECD. An MRI of her lower extremities revealed lesions in the diaphyses, metaphyses, and epiphyses of the proximal tibia and distal femur bilaterally. This is a rare case of cerebral ECD with progressive cerebellar syndrome associated with cerebellar atrophy.

Correlation between instrumental activities of daily living and white matter hyperintensities in amnestic mild cognitive impairment: results of a cross-sectional study

Although some studies have supported the association between white matter hyperintensities (WMH) and cognitive impairment, whether WMH are associated with the impairments in instrumental activities of daily living (IADLs) remains unknown. This cross-sectional study investigated differences in basic ADLs and IADLs among different severity of WMH in a large, well-defined registry of patients with amnestic mild cognitive impairment (aMCI). 1,514 patients with aMCI were divided into three groups according to the degree of WMH (1,026 mild, 393 moderate, and 95 severe). We compared the total IADL scores and analyzed the prevalence of the impairment for each IADL item for each group. The severity of WMH was associated with the impairments in IADLs. Among 15 Seoul IADL items, “using public transportation”, “going out (short distance)”, “grooming” and “participating in leisure activities/hobbies” showed greater positive association with the severity of WMH. WMH in patients with aMCI were associated with the impairments in IADLs but not in basic ADLs. These findings are likely to be more obvious with respect to using public transportation, going out (short distances), shopping, grooming and participating in leisure activities/hobbies.

A case of acute motor and sensory axonal neuropathy following hepatitis a infection.

Acute motor and sensory axonal neuropathy (AMSAN) are recently described subtypes of Guillain-Barre syndrome characterized by acute onset of distal weakness, loss of deep tendon reflexes, and sensory symptoms. A 21-yr-old male was transferred to our hospital due to respiration difficulties and progressive weakness. In laboratory findings, immunoglobulin M antibodies against hepatitis A were detected in blood and cerebrospinal fluid. The findings of motor nerve conduction studies showed markedly reduced amplitudes of compound muscle action potentials in bilateral peroneal, and posterior tibial nerves, without evidence of demyelination. Based on clinical features, laboratory findings, and electrophysiologic investigation, the patient was diagnosed the AMSAN following acute hepatitis A viral infection. The patient was treated with intravenous immunoglobulin and recovered slowly. Clinicians should consider this rare but a serious case of AMSAN following acute hepatitis A infection.

Isolated Bilateral Hippocampal Lesions following Carbon Monoxide Poisoning

noted except short-term memory disturbance. MRI revealed ischemic changes in the bilateral hippocampus ( fig. 1 ). In hypoxicischemic encephalopathy, the hippocampus is a particularly vulnerable site to injury, and as a result, pure amnesic syndrome may occur [1] . Hippocampal involvement following CO poisoning has been reported in several previous cases, but it was always accompanied by other lesions [2] . To our knowledge, this is the first report of isolated bilateral hippocampal lesions following carbon monoxide poisoning.

A case of cerebellar infarction presenting as thunderclap headache

Thunderclap headache (TCH) refers to a sudden-onset, severe headache that features in subarachnoid hemorrhage, unruptured intracranial aneurysm, cerebral venous thrombosis, pituitary apoplexy, cervical artery dissection, and hypertensive reversible posterior leukoencephalopathy. TCH is a rare manifestation in cerebral or cerebellar infarctions. Herein, we report on a 60-year-old woman with a thunderclap headache as the first symptom of cerebellar infarction, in the absence of abnormal findings in the brain computed tomography (CT), CT angiography, and lumbar puncture. An urgent brain MRI showed an acute infarction of the right cerebellar hemisphere. The next day, the patient presented with right side ataxia. In emergency cases presenting with thunderclap headache, one should consider an expanded evaluation and/or close observation, with frequent neurological examinations, even though the findings are normal on the initial neurological examination, cerebrospinal fluid analysis, and brain CT.

Hemichorea caused by intracranial hemorrhage following contralateral herpes zoster ophthalmicus

A healthy, 66-year-old, right-handed man was admitted to our university hospital and diagnosed with herpes zoster ophthalmicus (HZO). After 4 weeks, he complained of hemichorea on his left side. Brain MRI showed a focal hemorrhage in the right subthalamic area. No evidence of aneurysmal lesion or cerebral angiitis was observed on cerebral angiography.