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Objectives: This study aimed to identify predictors for the recurrence of spontaneous intracranial hypotension (SIH) after epidural blood patch (EBP). Background: Epidural blood patch is the main treatment option for SIH; however, the characteristics of patients who experience relapse after successful EBP treatment for SIH remain understudied. Methods: In this exploratory, retrospective, case–control study, we included 19 patients with SIH recurrence after EBP and 36 age‐ and sex‐matched patients without recurrence from a single tertiary medical institution. We analyzed clinical characteristics, neuroimaging findings, and volume changes in intracranial structures after EBP treatment. Machine learning methods were utilized to predict the recurrence of SIH after EBP treatment. Results: There were no significant differences in clinical features between the recurrence and no‐recurrence groups. Among brain magnetic resonance imaging signs, diffuse pachymeningeal enhancement and cerebral venous dilatation were more prominent in the recurrence group than no‐recurrence group after EBP (14/19 [73%] vs. eight of 36 [22%] patients, p = 0.001; 11/19 [57%] vs. seven of 36 [19%] patients, p = 0.010, respectively). The midbrain–pons angle decreased in the recurrence group compared to the no‐recurrence group after EBP, at a mean (standard deviation [SD]) of –12.0 [16.7] vs. +1.8[18.3]° (p = 0.048). In volumetric analysis, volume changes after EBP were smaller in the recurrence group than in the no‐recurrence group in intracranial cerebrospinal fluid (mean [SD] −11.6 [15.3] vs. +4.8 [17.1] mL, p = 0.001) and ventricles (mean [SD] +1.0 [2.0] vs. +2.0 [2.5] mL, p = 0.003). Notably, the random forest classifier indicated that the model constructed with brain volumetry was more accurate in discriminating SIH recurrence (area under the curve = 0.80 vs. 0.52). Conclusion: Our study suggests that volumetric analysis of intracranial structures may aid in predicting recurrence after EBP treatment in patients with SIH. Plain Language Summary: There is not much research about patients who experience symptom relapse after successful epidural blood patch (EBP) treatment for spontaneous intracranial hypotension (SIH). We used machine learning (an analysis that helps us understand patterns in data) to learn about medical records from 19 patients with SIH whose symptoms came back and 36 patients whose symptoms did not recur after EBP treatment. Our results suggest that changes in the amount of cerebrospinal fluid in the brain and the size of the ventricles can help predict the recurrence of SIH after EBP treatment. [ABSTRACT FROM AUTHOR]

Background and purpose: As part of network‐specific neurodegeneration, changes in cerebellar gray matter (GM) volume and impaired cerebello–cerebral functional networks have been reported in Alzheimer disease (AD). Compared with healthy controls, a volume loss in the cerebellum has been observed in patients with continuum of AD. However, little is known about the anatomical or functional changes in patients with clinical AD but no brain amyloidosis. We aimed to identify the relationship between cerebellar volume and dementia conversion of amyloid‐negative mild cognitive impairment (MCI). Methods: This study was a retrospective cohort study of patients over the age 50 years with amyloid‐negative amnestic MCI who visited the memory clinic of Asan Medical Center with no less than a 36‐month follow‐up period. All subjects underwent detailed neuropsychological tests, 3 T brain magnetic resonance imaging scans including three‐dimensional T1 imaging, and fluorine‐18[F18]‐florbetaben amyloid positron emission tomography scans. A spatially unbiased atlas template of the cerebellum and brainstem was used for analyzing cerebellar GM volume. Results: During the 36 months of follow‐up, 39 of 107 (36.4%) patients converted to dementia from amnestic MCI. The converter group had more severe impairments in all visual memory tasks. In terms of volumetric analysis, reduced crus I/II volume adjusted with total intracranial volume, and age was observed in the converter group. Conclusions: Significant cerebellar GM atrophy involving the bilateral crus I/II may be a novel imaging biomarker for predicting dementia progression in amyloid‐negative amnestic MCI patients. [ABSTRACT FROM AUTHOR]

Background: Amyloid positron emission tomography (PET) imaging is appropriate for patients with atypical presentation, unusually rapid course and very early onset of dementia. Standardized uptake value ratios (SUVr) are used for relative quantification of 18F‐florbetaben (18F‐FBB) PET scans and cerebellar cortex can be used as reference region for quantification. Previous study showed that 18F‐FBB PET demonstrated a diffuse cortical uptake and in particular an intense uptake in the basal ganglia in familial Alzheimer’s disease with presenilin‐1(PS‐1) mutation. Method: This report describes the case of a young woman with early‐onset familial Alzheimer’s disease(EOfAD), who has atypical pattern of uptake on amyloid PET. Result: A 37‐year‐old woman with a college level educational background was brought in by her family for further evaluation of cognitive impairment, personality and behavioral changes. At age 30 years of age, the patient presented memory impairment and she had difficulty serving guests in bakery. Patient had positive family history of early onset dementia; her father, grand mother, and two sisters of grand mother. (Fig. 1 Pedigree showing autosomal dominant inheritance trait of early‐onset dementia. (nn/nn) Age at onset/age at death). She had an initial Mini‐Mental State Examination score of 22/30 (time disorientation, dyscalculia, poor delayed recall). Neuropsychological assessment showed global cerebral dysfunction and revealed dementia with psychiatric symptoms. Brain magnetic resonance imaging showed no significant abnormality. On genetic testing, homozygotes for the apolipoprotein E ε3 allele and a PS‐1 mutation (c.616G>A , p.G602S) was identified. 18F‐FBB PET revealed diffusely increased amyloid deposition including not only bilateral frontal, parietal, posterior cingulate gyrus/precuneus, anterior striatum but also bilateral cerebellar cortex. (Fig. 2 18F‐florbetaben PET, at age 37) Conclusion: This will be the first case report of EOfAD with increased bilateral cerebellar cortical uptake on 18F‐ FBB PET, we present the case to increase awareness of this unusual entity. [ABSTRACT FROM AUTHOR]

Background: Around 15–20% of patients with clinically probable Alzheimer’s disease have been found to have no significant Alzheimer’s pathology on amyloid PET. A previous study shows that conversion to dementia from amyloid‐negative mild cognitive impairment (MCI) was observed in up to 11% of patients, drawing attention to this condition. We gathered the detailed neuropsychological and neuroimaging data of this population to elucidate factors for conversion to dementia from amyloid‐negative amnestic MCI. Method: This study was a retrospective cohort study of patients over the age 50 with amyloid‐negative amnestic MCI who visited the memory clinic of Asan Medical Center with no less than a 36 months follow‐up period. All subjects underwent detailed neuropsychologic tests, three tesla brain magnetic resonance imaging (MRI) scans including 3‐dimensional T1 imaging, and fluorine‐18[F18]‐florbetaben amyloid PET scans. Result: During the 36 months of follow‐up, 39 of 107 (36.4%) patients converted to dementia from amnestic MCI. The volumetric analysis revealed that the converter group had significantly reduced total hippocampal volume on the right side, gray matter volume in the right lateral temporal, lingual gyri, and occipital pole. In terms of cerebellar gray matter (GM) volumetric analysis, reduced Crus I/II volume adjusted with total intracranial volume (TIV) and age was observed in the converter group. The converter group had also more severe impairments in all visual memory tasks. Conclusion: Our study showed that the reduced gray matter volume related to visual memory processing in the cerebrum and Significant cerebellar GM atrophy involving the bilateral Crus I/II may predict the clinical progression in this amyloid‐negative MCI population. [ABSTRACT FROM AUTHOR]

Background: Pathophysiology of cognitive decline in CAA is multifactorial, because microbleeds, white matter hyperintensities, and combined concomitant parenchymal Alzheimer’s disease (AD) pathology have been suggested to cause cognitive impairment. The mechanism by which microbleeds affect cognitive impairment is still under investigation. We aimed to investigate the mechanism of how microbleeds contribute to cognitive impairment, in association with white matter tract abnormalities or cortical thickness in CAA with significant amyloid deposition. Method: We retrospectively investigated 30 patients with probable CAA according to Boston criteria and 30 patients with Alzheimer’s disease (AD), all of whom showed severe amyloid deposition on amyloid PET (Aβ+). Age, sex, and clinical deteriorating scale were matched. Using MRI, cortical thickness and white matter tract abnormalities as fractional anisotropy (FA) were obtained. We compared cortical thickness, FA, and cognitive scores of five domains between Aβ+ CAA and Aβ+ AD. Using path analysis, we investigated the correlation between number of regional microbleeds, cortical thickness, FA, and cognitive impairments. Result: Both CAA and AD group showed similar cortical amyloid deposition in AD related regions such as precuneus, and posterior cingulate cortex suggesting that CAA in this study might have AD pathology. Patients with Aβ+ CAA presented with significantly lower FA in clusters of posterior area than patients with Aβ+ AD (FWE‐corrected p value <0.05) Importantly, total number of microbleeds were associated with decreased FA in tapetum of corpus callosum (r=‐0.429, p<0.001), which were consequently associated with visuospatial function (r=0.466, p<0.001). Cortical thickness was not significantly different between CAA and AD, and it did not mediate the association between regional microbleeds and cognition. Conclusion: This study suggests that lobar microbleeds may impact cognitive decline through the mediation of white matter tract abnormalities in CAA. [ABSTRACT FROM AUTHOR]