Search

Visceral adipose tissue (VAT) dysfunction has been recently recognized as a potential contributor to the development of Alzheimer's disease (AD). This study aimed to explore the relationship between VAT metabolism and cerebral glucose metabolism in patients with cognitive impairment. This cross-sectional prospective study included 54 patients who underwent 18F-fluorodeoxyglucose (18F-FDG) brain and torso positron emission tomography/computed tomography (PET/CT), and neuropsychological evaluations. VAT metabolism was measured by 18F-FDG torso PET/CT, and cerebral glucose metabolism was measured using 18F-FDG brain PET/CT. A voxel-based analysis revealed that the high-VAT-metabolism group exhibited a significantly lower cerebral glucose metabolism in AD-signature regions such as the parietal and temporal cortices. In the volume-of-interest analysis, multiple linear regression analyses with adjustment for age, sex, and white matter hyperintensity volume revealed that VAT metabolism was negatively associated with cerebral glucose metabolism in AD-signature regions. In addition, higher VAT metabolism was correlated with poorer outcomes on cognitive assessments, including the Korean Boston Naming Test, Rey Complex Figure Test immediate recall, and the Controlled Oral Word Association Test. In conclusion, our study revealed significant relationships among VAT metabolism, cerebral glucose metabolism, and cognitive function. This suggests that VAT dysfunction actively contributes to the neurodegenerative processes characteristic of AD, making VAT dysfunction targeting a novel AD therapy approach. [ABSTRACT FROM AUTHOR]

The visceral adipose tissue (VAT) has been recognized as an endocrine organ, and VAT dysfunction could be a risk factor for Alzheimer's disease (AD). We aimed to evaluate the association of VAT metabolism with AD pathology. This cross-sectional study included 54 older subjects with cognitive impairment who underwent 2-deoxy-2-[fluorine-18]-fluoro-D-glucose (18F-FDG) torso positron emission tomography (PET) and 18F-florbetaben brain PET. 18F-FDG uptake in VAT on 18F-FDG PET images was used as a marker of VAT metabolism, and subjects were classified into high and low VAT metabolism groups. A voxel-based analysis revealed that the high VAT metabolism group exhibited a significantly higher cerebral amyloid-β (Aβ) burden than the low VAT metabolism group. In the volume-of-interest analysis, multiple linear regression analyses with adjustment for age, sex, and white matter hyperintensity volume revealed that 18F-FDG uptake in VAT was significantly associated with the cerebral Aβ burden (β = 0.359, p = 0.007). In conclusion, VAT metabolism was associated with AD pathology in older subjects. Our findings suggest that VAT dysfunction could contribute to AD development. [ABSTRACT FROM AUTHOR]

Background: Diabetes mellitus (DM) increases the risk of brain atrophy and dementia. We aimed to reveal whether DM could affect cognitive function and the pattern of amyloid retention in cognitively impaired patients. Also we tried to show whether the existence of DM could cause subcortical structural abnormalities with cognitive dysfunction. Method: We included consecutive 56 controls and 145 cognitively impaired people (CI, 50 MCI and 95 mild to moderate Alzheimer's disease (AD) patients). All participants of this cross‐sectional study underwent blood tests, detailed neuropsychological evaluations, 3D T1‐weighted MRI at 3‐Tesla and 18F‐FBB‐PET. We estimated the cerebral Aβ burden quantitatively using volume‐of‐interest analysis and segmented the volumes of six subcortical structures, using FMRIBs integrated registration and segmentation tool Multiple linear regression analysis adjusted for age and gender was performed to evaluate the relationship among cerebral Aβ burden, cognitive function and diabetes. Result: All subcortical structures, except for the globus pallidus, were smaller in CI compared with controls on adjusting for age and gender. CI with DM was associated with the lower volumes of caudate nucleus and putamen than CI without DM patients. Although there was no significant difference of MMSE score within two groups, the performance of frontal‐executive and memory functions was negatively correlated with subcortical structural volume loss in CI with DM. There was no difference between cerebral Aβ burden using composite SUVR and MMSE score in CI patients. However we found higher amyloid retention in CI with DM patients. Conclusion: The co‐morbidity of DM in AD patients might cause more specific subcortical volume loss beyond diffuse cerebral atrophy and the resultant cortical‐subcortical dysfunction could make cognitive dysfunction worse, especially frontal‐executive and memory functions. Also, CI with DM patients showed higher cerebral amyloid retention, which might be the accelerating factor of cognitive deterioration. [ABSTRACT FROM AUTHOR]

Background: Although several studies have reported an association between thyroid dysfunction and Alzheimer's disease (AD), the effect of mild thyroid dysfunction within the normal range of thyrotropin (TSH) on the development of AD remains unclear. The aim of this study was to evaluate the association between thyroid hormones and the pathology of AD in euthyroid subjects. Methods: Sixty-nine subjects with a TSH level between 0.5 and 4.5 μIU/L who underwent 18F-florbetaben positron emission tomography were included in this prospective cross-sectional study. The levels of serum free thyroxine (fT4) and TSH were quantified using radioimmunoassay. Neuropsychological tests were performed to assess cognitive function. Differences in cerebral amyloid-β (Aβ) burden were compared between high-normal TSH (TSH ≥2.5 μIU/mL) and low-normal TSH (TSH <2.5 μIU/mL) groups. Multiple linear regression analyses, adjusted for age, sex, education level, and Neuropsychiatric Inventory scores, were performed to evaluate relationships between thyroid hormone levels and both cerebral Aβ burden and cognitive function. Results: The cerebral Aβ burden in the high-normal TSH group was significantly higher than in the low-normal TSH group (1.53 ± 0.31 vs. 1.35 ± 0.22, p = 0.009). The fT4 levels were negatively correlated with cerebral Aβ burden (β = −0.240, p = 0.035), and TSH levels were positively correlated with cerebral Aβ burden (β = 0.267, p = 0.020). The fT4 level was also positively associated with cognitive function, as inferred from neuropsychological test scores. Conclusions: Thyroid hormone concentrations were associated with AD pathology in euthyroid subjects. Our findings suggest that AD is likely to occur even in individuals with high-normal TSH levels. [ABSTRACT FROM AUTHOR]

Los daños en la sustancia blanca (DSB), detectados como hiperintensidades en las imágenes de RM ponderadas en T2, representan la enfermedad de pequeños vasos cerebrales, y están considerados como un factor de riesgo potencial de trastornos de la memoria y disfunción cognitiva. No se ha evidenciado suficientemente que la disfunción cognitiva en pacientes con enfermedad de Alzheimer esté causada por DSB y la patología β-amiloide (Aβ). El objetivo de estudio fue evaluar la relación entre los DSB y el metabolismo de la glucosa cerebral en pacientes con disfunción cognitiva, tras el ajuste de la carga cerebral de Aβ. Incluimos en este estudio transversal a ochenta y tres sujetos con desempeño cognitivo que oscilaba entre normal y demencia, a quienes se realizó RM cerebral y PET con Florbetaben (18F) y PET con 18F-FDG. Utilizamos la escala Fazekas para cuantificar los DSB en la RM cerebral ponderada en T2. Estimamos cuantitativamente la carga cerebral de Aβ y el metabolismo de la glucosa cerebral utilizando el análisis del volumen de interés. Evaluamos las diferencias del metabolismo de la glucosa cerebral regional entre los grupos de bajo DSB (escala Fazekas < 2) y alto DSB (escala Fazekas ≥ 2). Realizamos un análisis de regresión lineal múltiple ajustado por edad, sexo y carga cerebral de Aβ, para evaluar la relación entre la puntuación de la escala Fazekas y el metabolismo de la glucosa cerebral. El metabolismo de la glucosa cerebral regional para los lóbulos bilateral frontal, temporal, córtices parietales, y lóbulos límbicos en el grupo de alto DSB fueron significativamente menores que los del grupo de bajo DSB. Existieron correlaciones negativas significativas entre la puntuación de la escala Fazekas y el metabolismo de la glucosa cerebral regional en los córtices bilateral frontal, bilateral temporal y córtices parietales izquierdos, y lóbulos límbicos bilaterales. Los análisis de regresión lineal múltiple revelaron que la puntuación de la escala Fazekas era un determinante independiente del metabolismo de la glucosa en los córtices bilateral frontal y temporal y los lóbulos límbicos. Los DSB están asociados a un descenso del metabolismo de la glucosa cerebral. Nuestros hallazgos sugieren que la enfermedad de los pequeños vasos, así como lo patología de Aβ, pueden contribuir a la disfunción cognitiva en pacientes con enfermedad de Alzheimer. White matter lesions (WMLs), detected as hyperintensities on T2-weighted MRI, represent small vessel disease in the brain and are considered a potential risk factor for memory and cognitive impairment. It has not been sufficiently evident that cognitive impairment in patients with Alzheimer's disease is caused by WMLs as well as β-amyloid (Aβ) pathology. The aim of this study was to evaluate relationship between WMLs and cerebral glucose metabolism in patients with cognitive impairment after adjustment of cerebral Aβ burden. Eighty-three subjects with cognitive performance ranging from normal to dementia, who underwent brain MRI and 18F-florbetaben positron emission tomography (PET) and 18F-fluorodeoxyglucose PET, were included in this cross-sectional study. The Fazekas scale was used to quantify WMLs on brain T2-weighted MRI. The cerebral Aβ burden and cerebral glucose metabolism were quantitatively estimated using volume-of-interest analysis. Differences in the regional cerebral glucose metabolism were evaluated between low-WML (Fazekas scale < 2) and high-WML (Fazekas scale ≥ 2) groups. Multiple linear regression analysis adjusted for age, sex and cerebral Aβ burden was performed to evaluate the relationship between the Fazekas scale score and cerebral glucose metabolism. The regional cerebral glucose metabolism for the bilateral frontal, temporal, and parietal cortices, and limbic lobes in the high-WML group were significantly lower than those in the low-WML group. There were significant negative correlations between the Fazekas scale score and regional cerebral glucose metabolism in the bilateral frontal, bilateral temporal and left parietal cortices, and bilateral limbic lobes. Multiple linear regression analysis revealed that the Fazekas scale score was an independent determinant of the glucose metabolism in the bilateral frontal and temporal cortices and limbic lobes. WMLs are associated with decreased cerebral glucose metabolism. Our findings suggest that small vessel disease, as well as Aβ pathology, may contribute to cognitive impairment in patients with Alzheimer's disease. [ABSTRACT FROM AUTHOR]

Introduction: White matter lesions (WMLs), detected as hyperintensities on T2-weighted MRI, represent small vessel disease in the brain and are considered a potential risk factor for memory and cognitive impairment in older adults. The purpose of this study was to evaluate the association between WMLs and cerebral amyloid-β (Aβ) burden in patients with cognitive impairment. Methods: A total of 83 patients with cognitive impairment, who underwent brain MRI and F-18 florbetaben PET, were included prospectively: 19 patients were cognitively unimpaired, 30 exhibited mild cognitive impairment (MCI), and 34 exhibited dementia. The Fazekas scale was used to quantify WMLs on T2-weighted brain MR images. Cerebral Aβ burden was quantitatively estimated using volume-of-interest analysis. Differences in cerebral Aβ burden were evaluated between low-WML (Fazekas scale ≤1) and high-WML (Fazekas scale ≥2) groups. The relationship between the Fazekas rating and cerebral Aβ burden was evaluated using linear regression analysis after adjusting for age and sex. Results: In the overall cohort, the high-WML group exhibited significantly higher Aβ burden compared with the low-WML group (P = 0.011) and cerebral Aβ burden was positively correlated with Fazekas rating (β = 0.299, P = 0.006). In patients with MCI, the high-WML group exhibited significantly higher Aβ burden compared with the low-WML group (P = 0.019) and cerebral Aβ burden was positively correlated with Fazekas rating (β = 0.517, P = 0.003). Conclusion: The presence of WMLs was associated with cerebral Aβ burden in patients with MCI. Our findings suggest that small vessel disease in the brain is related to Alzheimer’s disease pathology. [ABSTRACT FROM AUTHOR]

Background and objective: Studies investigating the impact of white matter hyperintensities (WMHs) on the response of acetylcholinesterase inhibitors in patients with Alzheimer’s disease (AD) have presented inconsistent results. We aimed to compare the effects of the rivastigmine patch between patients with AD with minimal WMHs and those with moderate WMHs. Methods: Three hundred patients with mild to moderate AD were enrolled in this multicenter prospective open-label study and divided into two groups. Group 1 comprised patients with AD with minimal WMHs and group 2 comprised those with moderate WMHs. The patients were treated with a rivastigmine patch for 24 weeks. Efficacy measures were obtained at baseline and after 24 weeks. The primary endpoint was the change in the AD Assessment Scale-Cognitive subscale (ADAS-Cog) from the baseline to the end of the study. Results: Of the 300 patients, there were 206 patients in group 1 and 94 patients in group 2. The intention-to-treat group comprised 198 patients (group 1, n = 136; group 2, n = 46) during the 24-week study period. Demographic factors did not differ between group 1 and group 2. There were no significant differences in change in ADAS-cog between group 1 (-0.62±5.70) and group 2 (-0.23±5.98) after the 24-week rivastigmine patch therapy (p = 0.378). The patients in group 1 had a 0.63-point improvement from baseline on the Frontal Assessment Battery, while group 2 had a 0.16-point decline compared to baseline at the end of the study (p = 0.037). The rates of adverse events (AEs) (42.6 vs. 40.3%) and discontinuation due to AEs (10.3% vs. 4.3%) did not differ between the groups. Conclusions: Although the efficacy and tolerability of rivastigmine patch therapy were not associated with WMH severity in patients with AD, some improvement in frontal function was observed in those with minimal WMHs. Trial registration: ClinicalTrials.gov [ABSTRACT FROM AUTHOR]

Objective: To investigate whether subcortical grey matter atrophy predicts progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD), and to compare subcortical volumes between AD, MCI and controls. To assess the correlation between subcortical grey matter volumes and severity of cognitive impairment.Methods: We included 773 participants with three-dimensional T1-weighted MRI at 3 T, made up of 181 controls, who had subjective memory symptoms with normal cognition, 201 MCIs and 391 AD. During follow-up (2.0 ± 0.9 years), 35 MCIs converted to AD (progressive MCI) and 160 MCIs remained stable (stable MCI). We segmented volumes of six subcortical structures of the amygdala, thalamus, caudate nucleus, putamen, globus pallidus and nucleus accumbens, and of the hippocampus, using FMRIBs integrated registration and segmentation tool.Results: Analysis of variances, adjusted for sex and age, showed that all structures, except the globus pallidus, were smaller in AD than in controls. In addition, the amygdala, thalamus, putamen, nucleus accumbens and hippocampus were smaller in MCIs than in controls. Across groups, all subcortical greymatter volumes, except the globus pallidus, showed a positive correlation with cognitive function, as measured by Mini Mental State Examination (MMSE) (0.16Conclusions: In addition to the hippocampus, the nucleus accumbens volume loss was also associated with increased risk of progression from MCI to AD. Furthermore, volume loss of subcortical grey matter structures was associated with severity of cognitive impairment. [ABSTRACT FROM AUTHOR]

Highlights: [•] This study investigated the frequency and detailed spectrum of autonomic dysfunction in patients with orthostatic dizziness. [•] Approximately 83% (180/217) of patients showed at least one abnormal autonomic testing result. We classified orthostatic dizziness into 11 groups according to the patterns of autonomic dysfunctions. [•] This study helps clinicians to understand the pattern and mechanism of autonomic dysfunction associated with orthostatic dizziness. [ABSTRACT FROM AUTHOR]

Background: It was the aim of this study to investigate the pattern of evolution of hyperventilation-induced nystagmus (HIN) in vestibular neuritis (VN) and to determine whether HIN influences the dizziness outcome at the last follow-up visit. Methods: Fifty-three consecutive patients with VN underwent a quantitative vestibular function test including hyperventilation and the Korean version of the Dizziness Handicap Inventory during the acute period and the follow-up visit. Results: The incidence of HIN was higher in the acute (62%, 33/53) than in the chronic (17%, 9/53) stages of VN. Approximately 70% (6/9) of patients who continued to have persistent HIN at the last follow-up reported dizziness compared to only 27% (12/44) of patients who had no HIN. Patients who complained of persistent dizziness were significantly more likely to have persistent HIN and high Korean Dizziness Handicap Inventory scores at the last follow-up compared with patients who did not suffer from dizziness. In terms of the degree of recovery of dizziness, patients with HIN initially beating toward the contralesional side exhibited significantly more improvement than patients with HIN initially beating toward the ipsilesional side. Conclusions: The presence of either HIN beating toward the ipsilesional side at the acute stage of VN or persistent HIN at the follow-up visit is associated with persistent dizziness. Copyright © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Abstract: Impairment of gaze holding mechanism and gaze-evoked nystagmus (GEN) in the vertical plane due to a focal brain lesion is usually caused by a failure of the vertical neural integrator, which is known to be localized in the interstitial nucleus of the Cajal in the upper midbrain. We report a patient with hemorrhagic stroke involving the paramedian pontine tegmentum who presented with vertical GEN due to a failure of vertical gaze holding mechanism and unilateral internuclear ophthalmoplegia. The possible structure taking a role as a vertical neural integrator in this patient might be the paramedian tract (PMT) neuron. [Copyright &y& Elsevier]

Background/Aims: The apolipoprotein E (APOE) genotype in response to pharmacological treatments in patients with Alzheimer's disease (AD) remains a matter of controversy. This analysis investigated the effect of the APOE genotype on the clinical response to rivastigmine transdermal patch monotherapy or memantine plus rivastigmine patch in patients with mild to moderate AD. Methods: Two hundred and six (n = 206) patients with probable AD and Mini-Mental State Examination (MMSE) scores of 10-20 were randomized to rivastigmine patch monotherapy or memantine plus rivastigmine patch for 24 weeks. Of the 206 patients with probable AD, 146 patients who consented to genetic testing for APOE were included and assessed for this subgroup study. Results: There were no significant differences on MMSE, NPI, ADAS-cog, ADCS-ADL, CDR-SB, NPI and FAB between rivastigmine patch monotherapy and memantine plus rivastigmine patch according to the APOE genotype. However, patients with moderately severe AD (MMSE ≤15) who were APOE ε4 carriers showed higher responder rates on ADCS-ADL with memantine plus rivastigmine patch compared to rivastigmine patch monotherapy. Conclusion: Moderately severe AD patients with the APOE ε4 allele may respond more favorably to memantine plus rivastigmine patch than ε4 noncarriers. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The outbreak of the COVID-19 pandemic is a substantial threat to the health of all populations worldwide, and old age is a robust risk factor for poor prognosis of COVID-19 infection. To reduce the fatality rate of COVID-19 infection, further understanding of elderly patients with COVID-19 is necessary. We aimed to investigate the prognostic factors in elderly patients with COVID-19. This was a multicenter and retrospective study. Overall, 340 elderly patients with COVID-19 were enrolled in 3 hospitals in Daegu, South Korea. Death and severe pneumonia requiring oxygen treatment were defined as poor clinical outcomes. Of the patients studied, 15% died and 35.2% were classified as having severe pneumonia. In binary logistic regression analysis, activities of daily living (ADL) impairment, fever during hospitalization, initial infiltration on chest radiograph, and initial increased C-reactive protein (CRP) were significantly associated with severe pneumonia (OR = 5.33, p < 0.001; OR = 3.2, p = 0.002; OR = 2.32, p = 0.044; and OR = 1.33, p < 0.001, respectively). ADL impairment, comorbidity, fever during hospitalization, and initial increased CRP were significantly associated with death (OR = 7.13, p < 0.001; OR = 3.28, p = 0.005; OR = 3.15, p = 0.032, and OR = 1.18, p < 0.001, respectively). ADL impairment, fever, and initial CRP were poor prognostic factors in elderly patients with COVID-19. Understanding these poor prognostic factors is necessary to control the disease in elderly patients. [ABSTRACT FROM AUTHOR]

Abstract: A 70-year-old man presented with left-sided weakness and dysarthria. His brain MRI and magnetic resonance angiography demonstrated acute infarctions in the bilateral middle cerebral artery territories in a setting of agenesis of the right internal carotid artery (ICA) with transcavernous anastomosis, a rare developmental anomaly. In this setting, atherosclerotic disease in the unilateral common carotid artery or ICA can induce acute infarctions in the bilateral anterior circulation. [Copyright &y& Elsevier]

Abstract: Upbeat nystagmus (UBN) is typically increased with upward gaze and decreased with downward gaze. We describe a patient with acute multiple sclerosis who developed primary position UBN with a linear slow phase waveform, in which the velocity of nystagmus was intensified in downward gaze and decreased during upward gaze. Brain MRI showed high signal lesions in the paramedian dorsal area of the caudal medulla encompassing the most caudal part of the perihypoglossal nuclei. Clinicians should be aware of possibility of a caudal medullary lesion in a patient with UBN, especially when the velocity of the UBN is increased in downward gaze. [Copyright &y& Elsevier]

Abstract: Background and purpose: Vertebrobasilar ischemic stroke (VBIS) can cause acute hearing loss (AHL) because the vertebrobasilar system supplies most of the auditory system including the inner ear. The aim of this study was to assess the long-term prognosis of AHL associated with VBIS. Methods: Over 12.5years, 62 patients with AHL of a vascular cause who were followed for at least 1year (mean, 49.2months; SD, 24.4months) were enrolled in this study. Quantitative audiovestibular function testing was performed during the acute (mostly within 10days after symptom onset) and last follow-up periods in all patients. Results: On the last follow-up, approximately 65% (39/62) of the patients showed a partial (n=24) or complete (n=15) hearing recovery. All but 2 (97%) patients had acute vertigo and 56 (56/62, 90%) had a unilateral canal paresis to caloric stimulation on the side of the AHL. The most commonly infarcted territory on brain MRI was in the distribution of the anterior inferior cerebellar artery (55/62, 89%). Multivariable analysis showed that multiple risk factors for stroke [odds ratio (OR) 10.46, 95% confidence interval (CI) 1.72 to 13.7, p=0.011] and profound hearing loss [OR 3.92, 95% CI 1.03 to 14.97, p<0.046] predicted a poor outcome for recovery of hearing loss. Conclusions: Acute hearing loss associated with posterior circulation ischemic stroke exhibits a relatively good long-term outcome. Two or more risk factors for stroke and profound hearing loss are adverse prognostic factors for recovery of hearing loss of a vascular cause. [Copyright &y& Elsevier]

Aim: White matter lesions (WMLs), detected as hyperintensities on T2-weighted MRI, represent small vessel disease in the brain and are considered a potential risk factor for memory and cognitive impairment. It has not been sufficiently evident that cognitive impairment in patients with Alzheimer's disease is caused by WMLs as well as β-amyloid (Aβ) pathology. The aim of this study was to evaluate relationship between WMLs and cerebral glucose metabolism in patients with cognitive impairment after adjustment of cerebral Aβ burden., Materials and Methods: Eighty-three subjects with cognitive performance ranging from normal to dementia, who underwent brain MRI and 18 F-florbetaben positron emission tomography (PET) and 18 F-fluorodeoxyglucose PET, were included in this cross-sectional study. The Fazekas scale was used to quantify WMLs on brain T2-weighted MRI. The cerebral Aβ burden and cerebral glucose metabolism were quantitatively estimated using volume-of-interest analysis. Differences in the regional cerebral glucose metabolism were evaluated between low-WML (Fazekas scale<2) and high-WML (Fazekas scale≥2) groups. Multiple linear regression analysis adjusted for age, sex and cerebral Aβ burden was performed to evaluate the relationship between the Fazekas scale score and cerebral glucose metabolism., Results: The regional cerebral glucose metabolism for the bilateral frontal, temporal, and parietal cortices, and limbic lobes in the high-WML group were significantly lower than those in the low-WML group. There were significant negative correlations between the Fazekas scale score and regional cerebral glucose metabolism in the bilateral frontal, bilateral temporal and left parietal cortices, and bilateral limbic lobes. Multiple linear regression analysis revealed that the Fazekas scale score was an independent determinant of the glucose metabolism in the bilateral frontal and temporal cortices and limbic lobes., Conclusions: WMLs are associated with decreased cerebral glucose metabolism. Our findings suggest that small vessel disease, as well as Aβ pathology, may contribute to cognitive impairment in patients with Alzheimer's disease., (Copyright © 2019 Sociedad Española de Medicina Nuclear e Imagen Molecular. Publicado por Elsevier España, S.L.U. All rights reserved.)

The relationship between postural instability and subcortical structure in AD has received less attention. The aims of this study were to assess whether there are differences in the ability to control balance between Alzheimer's disease (AD) and controls, and to investigate the association between subcortical gray matter volumes and postural instability in AD.We enrolled 107 consecutive AD patients and 37 controls. All participants underwent detailed neuropsychological evaluations, T1-weighted MRI at 3 T, and posture assessment using computerized dynamic posturography. We segmented the volumes of 6 subcortical structures of the amygdala, thalamus, caudate nucleus, putamen, globus pallidus and nucleus accumbens, and of hippocampus, using the FMRIBs integrated registration and segmentation tool.All subcortical structures, except for the globus pallidus, were smaller in AD compared with controls on adjusting for age and gender. Falling frequencies in unilateral stance test (UST) and composite scores in sensory organization test (SOT) were worse in AD than in controls. The motor control test did not reveal any differences between groups. On subgroup analyses in AD, the groups with poor performance in UST or SOT exhibited significantly reduced nucleus accumbens and putamen volumes, and nucleus accumbens volume, respectively. The smaller volume of the nucleus accumbens was associated with postural instability in AD (OR [95% CI] 17.847 [2.59-122.80] for UST, 42.827[6.06-302.47] for SOT, all P < .05).AD patients exhibited reduced ability to control balance compared with controls, and this postural instability was associated with nucleus accumbens volume loss. Furthermore, cognitive dysfunction was more prominent in the group with severe postural instability.

Although the head-up tilt (HUT) test and Valsalva maneuver (VM) have been widely used to identify sympathetic adrenergic impairment, the detailed relationship between the degree of orthostatic hypotension (OH) during the HUT test and the pattern of blood pressure (BP) change during the VM remains unknown. This study was performed to investigate the relationship between the degree of OH during the HUT test and the pattern of BP change during the VM. During a 4-year period, a total of 132 consecutive patients with neurogenic OH and 60 healthy controls were enrolled. The degree of OH was defined as mild (associated with a fall in systolic BP [SBP] ≥ 20 < 30 on tilting, n = 49), moderate (associated with a fall in SBP ≥ 30 < 40 on tilting, n = 43), and severe (associated with a fall in SBP ≥ 40 on tilting, n = 40). A standardized battery of autonomic tests, including the HUT test and VM using Finometer devices for recording beat-to-beat BP and heart rate response, and a quantitative sudomotor axon reflex test, was performed. Sympathetic indexes (SIs 1-6) were calculated from the VM. A composite autonomic severity score (CASS) was also obtained to evaluate the severity and distribution of autonomic dysfunction. The degree of OH was compared with the BP decline and recovery during the VM. All indexes exhibited overall significant differences among tested groups (P < 0.001). Only SI 3 differentiated all subject groups. Compared with other SIs, SI 3 was best correlated with the amount of decrease in the mean SBP (R = 0.473, P < 0.001) on tilting. The decrease in mean SBP on tilting was best correlated with CASS adrenergic subscore. SI 3 can differentiate between groups with different degrees of OH. The SI 3 obtained during VM can improve the diagnostic accuracy of autonomic dysfunction in patients with different degree of OH.

Objectives: To evaluate the efficacy and tolerability of donepezil in patients with Binswanger type subcortical vascular dementia., Methods: Patients (n = 34, mean age = 71.8 + 7.12) with Binswanger type subcortical vascular dementia from 8 multicenter, according to clinical and neuroradiological working criteria, were selected to receive donepezil 5 mg/day (n = 2) or donepezil 10 mg/day (n = 32, after 5 mg/day) for 24 weeks. Our primary endpoints were change from baseline to weeks 12 and 24 in the Seoul Neuropsychological Screening Battery-Dementia version (SNSB-D) and the Korean version of neuropsychiatric inventory (K-NPI)., Results: A total of 24 patients received donepezil completed the study (mean age = 72.0 + 7.5 K-Mini-Mental State Examination [MMSE] = 21.0 + 5.1). After 12 weeks and 24 weeks, patients showed improvements in cognitive function on the SNSB-D compared baseline of 16.29 points at 12 weeks (P < .05) and 12.44 points at 24 weeks (P < .05). Significant improvements were shown in only memory domain, immediate verbal recall and delayed recall tests. Subgroup with better cognitive function (SNSB-D > 100) were more effective in frontal and memory domains than the other subgroup (SNSB-D < 100). Withdrawal rates due to adverse events were very low (4.16%)., Conclusions: Donepezil-treated patients with Binswanger type subcortical vascular dementia demonstrated significant improvement in cognition compared with baseline, and donepezil was well tolerated.

Chronic recurrent attacks of vertigo, not associated with any auditory or neurological symptoms, are a common reason for referral to our neurotology clinic. Even after an extensive neurotological evaluation, some cases remain undiagnosed. We prospectively evaluated 72 consecutive patients who presented to the clinic with isolated recurrent vertigo of unknown cause. All patients underwent diagnostic evaluation to exclude identifiable causes of isolated recurrent vertigo. We compared the prevalence of migraine, according to the International Headache Society (IHS) criteria, in the isolated recurrent vertigo group, with a sex- and age-matched control group of orthopedic patients. The prevalence of migraine according to IHS criteria was higher in the isolated recurrent vertigo group (61.1%) than in the control group (10%; p < 0.01). Only 16.7% of patients had an abnormal vestibular function test. The most common abnormal finding was a unilateral vestibular weakness to caloric stimulation. Our results suggest that migraine should be considered in the differential diagnosis of isolated recurrent vertigo of unknown cause.