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author:("Ahn, Tae-beam")
1.  Apparently Ipsilateral Parkinsonism in a Patient with Chronic Subdural Hematoma 
Journal of Movement Disorders  2012;5(1):18-20.
Symptomatic parkinsonism secondary to ipsilateral lesion is rarely reported. Although the contribution of the contralateral lesions was assumed in some cases, the pathomechanism remains undetermined. Herein we report a patient with a subdural hematoma, who developed parkinsonism in the ipsilateral hemibody. Structural and functional imaging suggests the contralateral dopaminergic dysfunction as the major culprit of apparently ipsilateral parkinsonism.
PMCID: PMC4027679  PMID: 24868408
Symptomatic ipsilateral parkinsonism; Subdural hematoma
2.  Clinicopathological Correlates of Lewy Body Disease: Fundamental Issues 
Journal of Movement Disorders  2010;3(1):11-14.
Lewy body pathology (LBP) is the pathological hallmark of Lewy body diseases, such as Parkinson’s disease and Lewy body dementia. Recent studies have shed new light on the role of LBP, the interactions of LBP with concomitant pathologies, and the propagation of LBP from the olfactory bulb and enteric nervous system to the central nervous system. The intrinsic difficulty with identifying clinicopathological correlates could be overcome by improving our understanding of the pathological evolution of LBP.
PMCID: PMC4027657  PMID: 24868372
Lewy body; Lewy body disease; Parkinson’s disease; Lewy body dementia
3.  Polyneuropathy and Cerebral Infarction Complicating Scrub Typhus 
We describe a 64-year-old man with scrub typhus who presented with both polyneuropathy and cerebral infarction. A eurological examination revealed a confused mental state, stiff neck, hearing impairment, symmetric weakness, sensory loss, and ataxia. Electrophysiologic studies showed demyelinating sensorimotor polyneuropathy and sensorineural hearing loss. Brain magnetic resonance imaging showed multiple infarctions. Brain involvement or polyneuropathy associated with scrub typhus has been rarely reported, and the pathogenic mechanism underlying the multiple neurological complications remains to be elucidated.
PMCID: PMC2686884  PMID: 19513323
Scrub typhus; Guillain-Barré syndrome; Cerebral infarction
4.  Nanomolar concentration of alpha-synuclein enhances dopaminergic neuronal survival via Akt pathway 
Neural Regeneration Research  2013;8(35):3269-3274.
Although alpha-synuclein is generally thought to have a pathological role in Parkinson's disease, accumulative evidence exists that alpha-synuclein has a neuroprotective effect. The aim of this study was to evaluate the effect of extracellular alpha-synuclein on dopaminergic cell survival. We assessed cell viability using the 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltertazolium bromide (MTT) assay both in undifferentiated SH-SY5Y (SHSY) cells and neuronally-differentiated SH-SY5Y (ndSHSY) cells after 24 hour treatment with monomeric alpha-synuclein at various concentrations (0 [control], 50, 100 nmol/L, 1 μmol/L). To determine whether cell viability assessed by MTT assay was affected by cell proliferation, 5-bromo-2’-deoxyuridine (BrdU) incorporation assay was performed. Level of both Akt and phosphorylated Akt was measured using western blot method in ndSHSY cells with or without 24 hour alpha-synuclein treatment. Cell viability was increased in ndSHSY cells at the nanomolar concentration of alpha-synuclein, but not in SHSY cells. Proportion of BrdU-positive ndSHSY cells was decreased in alpha-synuclein-treated group compared with control group. Level of phosphorylated Akt in alpha-synuclein-treated group was higher compared with the control group. Our study shows that extracellular alpha-synuclein at nanomolar concentration benefits dopaminergic cell survival via Akt pathway.
PMCID: PMC4145947  PMID: 25206648
neural regeneration; alpha-synuclein; neuronal survival; nanomolar; extracellular; phosphorylated Akt; SH-SY5Y cell; neuronal differentiation; proliferation; dopaminergic; 5-bromo-2’-deoxyuridine; grants-supported paper; neuroregeneration
5.  Translation and Validation of the Korean Version of the 39-Item Parkinson's Disease Questionnaire 
Background and Purpose
The importance of health-related quality of life (HrQoL) has been increasingly emphasized when assessing and providing treatment to patients with chronic, progressive, degenerative disorders. The 39-item Parkinson's disease questionnaire (PDQ-39) is the most widely used patient-reporting scale to assess HrQoL in Parkinson's disease (PD). This study evaluated the validity and reliability of the translated Korean version of the PDQ-39 (K-PDQ-39).
One hundred and two participants with PD from 10 movement disorder clinics at university-affiliated hospitals in South Korea completed the K-PDQ-39. All of the participants were also tested using the Unified Parkinson's Disease Rating Scale (UPDRS), Korean version of the Mini-Mental State Examination (K-MMSE), Korean version of the Montgomery-Asberg Depression Scale (K-MADS), Epworth Sleepiness Scale (ESS) and non-motor symptoms scale (NMSS). Retests of the K-PDQ-39 were performed over time intervals from 10 to 14 days in order to assess test-retest reliability.
Each K-PDQ-39 domain showed correlations with the summary index scores (rS=0.559-0.793, p<0.001). Six out of eight domains met the acceptable standard of reliability (Cronbach's α coefficient ≥0.70). The Guttman split-half coefficient value of the K-PDQ-39 summary index, which is an indicator of test-retest reliability, was 0.919 (p<0.001). All of the clinical variables examined except for age, comprising disease duration, levodopa equivalent dose, modified Hoehn and Yahr stage (H&Y stage), UPDRS part I, II and III, mood status (K-MADS), cognition (K-MMSE), daytime sleepiness (ESS) and (NMSS) showed strong correlations with the K-PDQ-39 summary index (p<0.01).
The K-PDQ-39 has been validated for use in the Korean-speaking PD population. The questionnaire is a valid and reliable assessment tool for assessing the HrQoL of Korean PD patients.
PMCID: PMC3543906  PMID: 23346157
Parkinson's disease; quality of life; validation
6.  Validation of the Korean-Version of the Nonmotor Symptoms Scale for Parkinson's Disease 
Background and Purpose
Non-motor symptoms are common in Parkinson's disease (PD), and are the primary cause of disability in many PD patients. Our aim in this study was to translate the origin non-motor symptoms scale for PD (NMSS), which was written in English, into Korean (K-NMSS), and to evaluate its reliability and validity for use with Korean-speaking patients with PD.
In total, 102 patients with PD from 9 movement disorders sections of university teaching hospitals in Korea were enrolled in this study. They were assessed using the K-NMSS, the Unified Parkinson's Disease Rating Scale (UPDRS), the Korean version of the Mini-Mental Status Examination (K-MMSE), the Korean version of the Montgomery-Asberg Depression Rating Scale (K-MADS), the Epworth Sleepiness Scale (ESS), and Parkinson's Disease Questionnaire 39 (PDQ39). Test-retest reliability was assessed over a time interval of 10-14 days in all but one patient.
The K-NMSS was administered to 102 patients with PD. The internal consistency and reliability of this tool was 0.742 (mean Cronbach's α-coefficient). The test-retest correlation reliability was 0.941 (Guttman split-half coefficient). There was a moderate correlation between the total K-NMSS score and the scores for UPDRS part I [Spearman's rank correlation coefficient, (rS)=0.521, p<0.001] and UPDRS part II (rS=0.464, p=0.001), but there was only a weak correlation between the total K-NMSS score and the UPDRS part III score (rS=0.288, p=0.003). The total K-NMSS score was significantly correlated with the K-MADS (rS=0.594, p<0.001), K-MMSE (rS=-0.291, p=0.003), and ESS (rS=0.348, p<0.001). The total K-NMSS score was also significantly and positively correlated with the PDQ39 score (rS=0.814, p<0.001).
The K-NMSS exhibited good reliability and validity for the assessment of non-motor symptoms in Korean PD patients.
PMCID: PMC3540287  PMID: 23323136
Parkinson's disease; non-motor symptoms scale; validation
7.  Incidental Lewy Body Disease: Do some cases represent a preclinical stage of Dementia with Lewy Bodies? 
Neurobiology of Aging  2009;32(5):857-863.
Lewy pathology occurs in 8–17% of neurologically-normal people >age 60, termed incidental Lewy body disease, (iLBD). It is often assumed to represent preclinical Parkinson disease (PD). However, some iLBD cases have diffuse pathology inconsistent with preclinical PD. We analyzed iLBD cases (α-synuclein immunohistochemistry) using the Braak PD staging scheme and determined if some had a neuropathological pattern suggestive of preclinical Dementia with Lewy bodies (DLB). Of the 235 brains examined, 34 had iLBD (14.5%) and all but one could be assigned a Braak PD stage. The distribution of α-synuclein pathology in the 33 cases fell into three patterns: (1) Diffuse cortical and subcortical α-synuclein pathology; (2) No cortical a-synuclein pathology, but a caudal-to-rostral ascending pattern, primarily involving brainstem; (3) Intermediate between these two categories. Also, 6/33 cases failed to follow the pattern of contiguous spread proposed by Braak. These findings suggest dichotomy in the distribution of iLBD: some cases fit the Braak ascending scheme, conceptually consistent with preclinical PD, whereas others displayed prominent cortical involvement that might represent preclinical DLB.
PMCID: PMC3366193  PMID: 19560232
incidental Lewy body disease; parkinson disease; dementia with Lewy bodies
8.  Relationship of neighboring tissue and gliosis to α-synuclein pathology in a fetal transplant for Parkinson’s disease 
Background: Fetal transplantation for Parkinson disease (PD) had been considered a promising therapeutic strategy; however, reports of Lewy bodies (LBs) and Lewy neurites (LNs) in engrafted tissue adds to controversy surrounding this treatment for PD. Methods: The brain of a PD patient who had fetal transplantation 14 years before death was evaluated. The graft was studied with routine histologic methods, as well as immunohistochemistry for α-synuclein, neurofilament, synaptophysin and tyrosine hydroxylase (TH), as well as glial fibrillary acidic protein (GFAP) for astrocytes and ionized calcium-binding adaptor molecule 1 (IBA-1) for microglia. Results: On coronal sections of the brain, the graft extended from the putamen to the amygdala, abutting the anterior hippocampus. Microscopically, the graft consisted of neuron-rich and glia-rich portions. Neuron-rich portions, resembling a neuronal heterotopia, were located in the putamen, whereas the glia-rich portion was more ventral near the amygdala. LBs and LNs were detected in the ventral portion of the graft, especially that part of the graft within the amygdala. Areas with LBs and LNs also had astrogliosis and microgliosis. TH positive neurons were rare and their distribution did not overlap with LBs or LNs. Comments: LBs and LNs were detected in the transplanted tissue with α-synuclein immunohistochemistry. Unexpected outgrowth of the graft into the amygdala was accompanied by skewed distribution of LBs and gliosis, more abundant in the graft within the amygdala. The distribution of LBs within the graft may suggest the potential role of the local environment as well as gliosis in formation of α-synuclein pathology.
PMCID: PMC3560449  PMID: 23383381
Fetal transplantation; Parkinson disease (PD); therapy; α-synuclein pathology; gliosis
9.  Overnight switch from ropinirole to transdermal rotigotine patch in patients with Parkinson disease 
BMC Neurology  2011;11:100.
A recent trial involving predominantly Caucasian subjects with Parkinson Disease (PD) showed switching overnight from an oral dopaminergic agonist to the rotigotine patch was well tolerated without loss of efficacy. However, no such data have been generated for Korean patients.
This open-label multicenter trial investigated PD patients whose symptoms were not satisfactorily controlled by ropinirole, at a total daily dose of 3 mg to 12 mg, taken as monotherapy or as an adjunct to levodopa. Switching treatment from oral ropinirole to transdermal rotigotine was carried out overnight, with a dosage ratio of 1.5:1. After a 28-day treatment period, the safety and tolerability of switching was evaluated. Due to the exploratory nature of this trial, the effects of rotigotine on motor and nonmotor symptoms of PD were analyzed in a descriptive manner.
Of the 116 subjects who received at least one treatment, 99 (85%) completed the 28-day trial period. Dose adjustments were required for 11 subjects who completed the treatment period. A total of 76 treatment-emergent adverse events (AEs) occurred in 45 subjects. No subject experienced a serious AE. Thirteen subjects discontinued rotigotine prematurely due to AEs. Efficacy results suggested improvements in both motor and nonmotor symptoms and quality of life after switching. Fifty-two subjects (46%) agreed that they preferred using the patch over oral medications, while 31 (28%) disagreed.
Switching treatment overnight from oral ropinirole to transdermal rotigotine patch, using a dosage ratio of 1.5:1, was well tolerated in Korean patients with no loss of efficacy.
Trial registration
This trial is registered with the Registry (NCT00593606).
PMCID: PMC3166898  PMID: 21831297
10.  Plaque Rupture is a Determinant of Vascular Events in Carotid Artery Atherosclerotic Disease: Involvement of Matrix Metalloproteinases 2 and 9 
Background and Purpose
Unstable carotid atherosclerotic plaques are characterized by cap rupture, leading to thromboembolism and stroke. Matrix metalloproteinases (MMPs) have been implicated in the progression of atherosclerosis and plaque rupture. The aim of this study was to assess the relationship between the expressions of MMP-2 and MMP-9 and carotid plaque instability.
Eighty atherosclerotic plaques were collected from 74 patients undergoing carotid endarterectomy. Clinical information was obtained from each patient, and plaque morphology was examined at the macroscopic and microscopic levels. The immunohistochemical expressions of MMPs were graded using semiquantitative scales.
Macroscopic ulceration (84.6% versus 63.4%, p=0.042) and microscopic cap rupture (79.5% versus 51.2%, p=0.010) were more common in symptomatic than in asymptomatic patients. Immunoreactivities of MMP-2 and MMP-9 were increased in 40 and 36 atheromatous plaques, respectively. Macroscopic ulceration was strongly correlated with the expressions of MMP-2 (p<0.001) and MMP-9 (p=0.001). There were significant correlations between increased MMP-2 expression and cap rupture (p=0.002), intraplaque hemorrhage (p=0.039), and a thin fibrous cap (p=0.002), and between increased MMP-9 expression and cap rupture (p=0.010) and a large lipid core (p=0.013).
Plaque rupture was significantly associated with the development of vascular events in carotid atherosclerotic disease. MMP-2 and MMP-9 are strongly correlated with plaque instability.
PMCID: PMC3131541  PMID: 21779294
metalloproteinase; carotid plaque; instability
11.  Glial cytoplasmic inclusions in neurologically normal elderly: Prodromal multiple system atrophy? 
Acta neuropathologica  2008;116(3):269-275.
In this study we used immunohistochemistry to screen for α-synuclein pathology in the brains of 241 individuals without clinical evidence of neurologic disease, and discovered 36 cases (15%) with incidental Lewy bodies (LBs) and one case, a 96-year-old woman (0.4%), with inclusions similar to those seen in multiple system atrophy (MSA), a nonfamilial neurodegenerative disorder characterized by parkinsonism, cerebellar ataxia and autonomic dysfunction and α-synuclein immunoreactive glial cytoplasmic inclusions (GCI). In a routine hospital autopsy series of 125 brains, we detected GCI in a neurologically normal 82-year-old man (0.8%). Both cases showed widespread GCI in the central nervous system, as well as a few neuronal cytoplasmic inclusions, but no neuronal loss or gliosis in vulnerable brain regions, including the substantia nigra, putamen, inferior olive and pontine base. Applying a recently proposed grading scale for MSA, the two cases showed pathology far below that detected in patients with clinically overt MSA, suggesting the possibility that these two individuals had preclinical MSA. The prevalence of clinically overt MSA is estimated to be about 4 per 100,000 persons (0.004%), which is far less than the frequency of GCI in this series (0.4%–0.8%). Further studies are needed to determine is GCI in neurologically normal elderly represents prodromal MSA or a rare non-progressive age-related α-synucleinopathy.
PMCID: PMC2880173  PMID: 18553090
α-synuclein; clinicopathologic; glial cytoplasmic inclusion; multiple system atrophy; preclinical
12.  Amnesic Syndrome in a Mammillothalamic Tract Infarction 
Journal of Korean Medical Science  2007;22(6):1094-1097.
It is controversial whether isolated lesions of mammillothalamic tract (MTT) produce significant amnesia. Since the MTT is small and adjacent to several important structures for memory, amnesia associated with isolated MTT infarction has been rarely reported. We report a patient who developed amnesia following an infarction of the left MTT that spared adjacent memory-related structures including the anterior thalamic nucleus. The patient's memory deficit was characterized by a severe anterograde encoding deficit and retrograde amnesia with a temporal gradient. In contrast, he did not show either frontal executive dysfunction or personality change that is frequently recognized in the anterior or medial thalamic lesion. We postulate that an amnesic syndrome can develop following discrete lesions of the MTT.
PMCID: PMC2694637  PMID: 18162731
Amnesia; Cerebral Infarction; Mammillothalamic Tract
13.  One-Year Open-Label Study of Entacapone in Patients with Advanced Parkinson Disease 
Background and purpose
A carboxy-O-methyl transferase inhibitor entacapone has been introduced as an adjuvant drug for Parkinson disease (PD) patients. Although clinical trials reported beneficial role of entacapone, a long-term trial over 3 years failed to show significant effect. The goals of this study were to evaluate the clinical benefit and the efficacy of entacapone in an open clinical practice.
After the completion of a double-blind placebo-controlled entacapone study, 149 patients from 4 centers were included. Antiparkinsonian medications were optimized by the judgment of the neurologists in charge. The clinical global impression (CGI) scale was obtained at 6 months and 1 year after the initiation of entacapone treatment.
Of the 149 patients, 117 patients chose to try entacapone in an open-label fashion. Sixty-nine (59%) patients completed the 1-year trial. Twenty-nine patients discontinued entacpaone before 6 months, and 19 between 6 months and 1 year during trial. Twelve patients out of 48 patients discontinued entacapone because of its poor efficacy. The CGI scale was 3.9 (±1.5) at the beginning of the trial, 4.3 (±1.1) at 6 month, and 3.8 (±1.3) at 1 year, respectively. The CGI scale of those who discontinued between 6 month and 1 year was 3.4 (±1.7), which was worse, but insignificantly, than that of the continuer.
The dropout at 1 year of our study was very high at 41%. Even though entacapone is indicated for advanced PD patients with motor fluctuation, the fluctuators commonly have dyskinesia and mental symptoms, which can become more troublesome with entacapone. In the patients with advanced PD, the clinical efficacy and side effects should be carefully considered in a long-term use of entacapone.
PMCID: PMC2686863  PMID: 19513296
Parkinson disease; Entacapone; Long-term efficacy

Results 1-13 (13)