Cerebral Hypometabolism Research Articles

Different FDG-PET metabolic patterns at single-subject level in the behavioral variant of fronto-temporal dementia

BackgroundThe diagnosis of probable behavioral variant of fronto-temporal dementia (bvFTD) according to current criteria requires the imaging evidence of frontal and/or anterior temporal atrophy or hypoperfusion/hypometabolism. Different variants of this pattern of brain involvement may, however, be found in individual cases, supporting the presence of heterogeneous phenotypes. ObjectiveWe examined in a case-by-case approach the FDG-PET metabolic patterns of patients fulfilling clinical criteria for probable bvFTD, assessing the presence and frequency of specific FDG-PET features. Materials and methodsFifty two FDG-PET scans of probable bvFTD patients were retrospectively analyzed together with clinical and neuropsychological data. Neuroimaging experts rated the FDG-PET hypometabolism maps obtained at the single-subject level with optimized voxel-based Statistical Parametric Mapping (SPM). The functional metabolic heterogeneity was further tested by hierarchical cluster analysis and principal component analysis (PCA). ResultsBoth the SPM maps and cluster analysis identified two major variants of cerebral hypometabolism, namely the “frontal” and the “temporo-limbic”, which were correlated with different cognitive profiles. Executive and language deficits were the cognitive hallmark in the “frontal” subgroup, while poor encoding and recall on long-term memory tasks was typical of the “temporo-limbic” subgroup. DiscussionSPM single-subject analysis indicates distinct patterns of brain dysfunction in bvFTD, coupled with specific clinical features, suggesting different profiles of neurodegenerative vulnerability. These findings have important implications for the early diagnosis of bvFTD and for the application of the recent international consensus criteria.

Cerebral glucose hypometabolism in Tick-Borne Encephalitis, a pilot study in 10 Patients

BackgroundTick borne encephalitis (TBE) is an acute meningoencephalitis with or without myelitis caused by an RNA virus from the flavivirus family transmitted by Ixodes spp ticks. The neurotropic TBE virus infects preferentially large neurons in basal ganglia, anterior horns, medulla oblongata, Purkinje cells and thalamus. Brain metabolic changes related to radiologic and clinical findings have not been described so far. MethodsHere we describe the clinical course of 10 consecutive TBE patients with outcome assessment at discharge and after 12 month using a modified Rankin Scale. Patients underwent cerebral MRI after confirmation of diagnosis and before discharge. 18F-FDG PET/CT scans were performed within day 5 to day 14 after TBE diagnosis. Extended analysis of coagulation parameters by thrombelastometry (ROTEM® InTEM, ExTEM, FibTEM) was performed every other day after confirmation of TBE diagnosis up to day 10 after hospital admission or discharge. ResultsAll patients presented with a meningoencephalitic course of disease. Cerebral MRI scans showed unspecific findings at predilection areas in 3 patients. 18F-FDG PET/CT showed increased glucose utilization in one patient and decreased 18F-FDG uptake in seven patients. Changes in coagulation measured by standard parameters and thrombelastometry were not found in any of the patients. DiscussionGlucose hypometabolism was present in 7 out of 10 TBE patients reflecting neuronal dysfunction in predilection areas of TBE virus infiltration responsible for development of clinical signs and symptoms.

DIFFERENTIAL REGIONAL CEREBRAL HYPOMETABOLISM PATTERNS ACCORDING TO THE LEVEL OF CEREBRAL AMYLOID DEPOSITION IN MILD COGNITIVE IMPAIRMENT

DIFFERENTIAL REGIONAL CEREBRAL HYPOMETABOLISM PATTERNS ACCORDING TO THE LEVEL OF CEREBRAL AMYLOID DEPOSITION IN MILD COGNITIVE IMPAIRMENT

DIFFERENTIAL REGIONAL CEREBRAL HYPOMETABOLISM PATTERNS ACCORDING TO THE LEVEL OF CEREBRAL AMYLOID DEPOSITION IN MILD COGNITIVE IMPAIRMENT

DIFFERENTIAL REGIONAL CEREBRAL HYPOMETABOLISM PATTERNS ACCORDING TO THE LEVEL OF CEREBRAL AMYLOID DEPOSITION IN MILD COGNITIVE IMPAIRMENT

Cerebral hypoperfusion and glucose hypometabolism: Key pathophysiological modulators promote neurodegeneration, cognitive impairment, and Alzheimer's disease.

Aging, hypertension, diabetes, hypoxia/obstructive sleep apnea (OSA), obesity, vitamin B12/folate deficiency, depression, and traumatic brain injury synergistically promote diverse pathological mechanisms including cerebral hypoperfusion and glucose hypometabolism. These risk factors trigger neuroinflammation and oxidative-nitrosative stress that in turn decrease nitric oxide and enhance endothelin, Amyloid-β deposition, cerebral amyloid angiopathy, and blood-brain barrier disruption. Proinflammatory cytokines, endothelin-1, and oxidative-nitrosative stress trigger several pathological feedforward and feedback loops. These upstream factors persist in the brain for decades, upregulating amyloid and tau, before the cognitive decline. These cascades lead to neuronal Ca2+ increase, neurodegeneration, cognitive/memory decline, and Alzheimer's disease (AD). However, strategies are available to attenuate cerebral hypoperfusion and glucose hypometabolism and ameliorate cognitive decline. AD is the leading cause of dementia among the elderly. There is significant evidence that pathways involving inflammation and oxidative-nitrosative stress (ONS) play a key pathophysiological role in promoting cognitive dysfunction. Aging and several comorbid conditions mentioned above promote diverse pathologies. These include inflammation, ONS, hypoperfusion, and hypometabolism in the brain. In AD, chronic cerebral hypoperfusion and glucose hypometabolism precede decades before the cognitive decline. These comorbid disease conditions may share and synergistically activate these pathophysiological pathways. Inflammation upregulates cerebrovascular pathology through proinflammatory cytokines, endothelin-1, and nitric oxide (NO). Inflammation-triggered ONS promotes long-term damage involving fatty acids, proteins, DNA, and mitochondria; these amplify and perpetuate several feedforward and feedback pathological loops. The latter includes dysfunctional energy metabolism (compromised mitochondrial ATP production), amyloid-β generation, endothelial dysfunction, and blood-brain-barrier disruption. These lead to decreased cerebral blood flow and chronic cerebral hypoperfusion- that would modulate metabolic dysfunction and neurodegeneration. In essence, hypoperfusion deprives the brain from its two paramount trophic substances, viz., oxygen and nutrients. Consequently, the brain suffers from synaptic dysfunction and neuronal degeneration/loss, leading to both gray and white matter atrophy, cognitive dysfunction, and AD. This Review underscores the importance of treating the above-mentioned comorbid disease conditions to attenuate inflammation and ONS and ameliorate decreased cerebral blood flow and hypometabolism. Additionally, several strategies are described here to control chronic hypoperfusion of the brain and enhance cognition. © 2016 Wiley Periodicals, Inc.

Evaluation of metabolic changes in Parkinson's disease patients with different severities of cognitive impairments by 18F-FDG PET/CT brain imaging

Objective To investigate the characteristics of cerebral glucose metabolism (CGM) in PD patients with cognitive impairment (PD-CI) using 18F-FDG PET/CT, and to analyze the correlation between the progress of PD-CI and CGM changes. Methods A total of 31 idiopathic PD patients (14 males, 17 females, aged 37-77 years) from May 2013 to February 2014 were divided into 3 groups based on Montreal cognitive assessment (MOCA): none CI in PD (PD-NC) group (MOCA>26 scores), mild CI in PD (PD-MCI) group (MOCA 21-26 scores), PD with dementia (PDD) group (MOCA<21 scores). The normal controls (NC) group included 12 age- and gender-matched healthy adults (7 males, 5 females, aged 40-76 years). All subjects underwent PET/CT imaging after intravenous injection of 18F-FDG(5.55 MBq/kg). MIMneuro software was used to analyze the data. The correlation between the CGM and cognitive function was analyzed using Pearson or Spearman correlation analysis. Results (1) Compared with NC group, PDD group presented a widespread cortical metabolism decrease in frontal, parietal, temporal, occipital lobes and the limbic lobe; PD-MCI group showed hypometabolic areas in the parietal and occipital lobes, and with less extent in the frontal and temporal lobes; PD-NC group showed no significant cerebral hypometabolism. (2) Compared with PD-NC group, PDD group showed widespread cortical metabolism decrease in occipital lobe, temporal lobe, partial parietal cortex and the posterior cingulated cortex. Compared with PD-MCI group, PDD group had lower metabolism, mainly in posterior brain areas (parietal, occipital and temporal lobes). Compared with PD-NC group, PD-MCI group showed hypometabolism in right supramarginal gyrus and the left parahippocampal gyrus. (3) There were positive correlations between visuospatial/executive function and visual cortex metabolism, angular gyrus metabolism or superior parietal lobule metabolism (r=0.535, 0.443, 0.395; all P<0.05). A positive correlation was also found between delayed memory and heschl's gyrus metabolism (r=0.337, P<0.05). Conclusions The cerebral glucose metabolism detected with 18F-FDG PET/CT is well correlated with MOCA assessments. Thus it may be helpful in evaluation of the progress of cognitive impairments in PD. Key words: Parkinson disease; Cognition disorders; Tomography, emission-computed; Tomography, X-ray computed; Deoxyglucose

Periventricular hyperintensities are associated with elevated cerebral amyloid

To investigate the association between periventricular white mater hyperintensities (PVWMH) and biomarkers of elevated cerebral β-amyloid (Aβ) in the Alzheimer's Disease Neuroimaging Initiative, a large prospective multicenter observational study. The burden of frontal, parietal, and occipital PVWMH on 3T fluid-attenuated inversion recovery MRI was evaluated in 698 cognitively normal participants and participants with mild cognitive impairment (MCI) using a novel semiquantitative visual rating scale. Results were correlated with CSF-Aβ, florbetapir-PET, and fluorodeoxyglucose (FDG)-PET. Increased burden of parietal, occipital, and frontal PVWMH was associated with elevated cerebral amyloid evidenced by high florbetapir-PET signal (p < 0.01) and low CSF-Aβ (p < 0.01). In logistic regression models, including PVWMH, age, sex, APOE status, vascular risk factors, pulse pressure, vascular secondary prevention medications, education, ethnicity, and race, parietal, occipital, and frontal PVWMH burden was independently associated with high florbetapir-PET uptake (p < 0.05). In a similar logistic regression model, parietal and occipital (p < 0.05) but not frontal (p = 0.05) PVWMH were independently associated with CSF-Aβ. Weaker associations were found between parieto-occipital PVWMH and elevated CSF-tau (p < 0.05) and occipital PVWMH and elevated CSF-phospho-tau (p < 0.05). PVWMH were associated with cerebral hypometabolism on FDG-PET independent of CSF-Aβ levels (p < 0.05). Absolute and consistency of agreement intraclass correlation coefficients were, respectively, 0.83 and 0.83 for frontal, 0.78 and 0.8 for parietal, and 0.45 and 0.75 for occipital PVWMH measurements. Increased PVWMH were associated with elevated cerebral amyloid independent of potential confounders such as age, APOE genotype, and vascular risk factors. The mechanisms underlying the association between PVWMH and cerebral amyloid remain to be clarified.

Multiple Effect of APOE Genotype on Clinical and Neuroimaging Biomarkers Across Alzheimer’s Disease Spectrum

The apolipoprotein E ε4 (APOE ε4) allele is the most important genetic risk factor for Alzheimer's disease (AD); however, the underlying mechanisms responsible for it remain controversial. We used the Alzheimer's Disease Neuroimaging Initiative (ADNI) database to examine the influence of APOE ε4 dose on clinical and neuroimaging biomarkers across the AD spectrum (from cognitive normal to AD patients with severe cognitive impairment). A total of 1718 participants from the ADNI cohort were selected, and we evaluated the impact of ε4 dose on cerebrospinal fluid (CSF) levels' Abeta1-42 (Aβ1-42), tau, and phosphorylated-tau (p-tau); cortical amyloid deposition (Florbetapir-PET-AV45); brain atrophy (MRI); brain metabolism (FDG-PET); hippocampal metabolism; and cognitive declines, through different cognitive subgroups. We found that (1) ε4 was associated with decreased CSF beta-amyloid (Aβ1-42) and increased cerebral Aβ deposition across the AD spectrum; (2) increased CSF tau, P-tau and cerebral hypometabolism, hippocampal atrophy, and cognition decline were all associated with APOE ε4 in prodromal AD stage; (3) increased CSF tau, P-tau and cerebral hypometabolism appear to begin earlier than hippocampal atrophy and cognitive decline. We hypothesized that APOE ε4 increases cerebral amyloid-β (Aβ) deposition in all the stages of AD development, and also influences Aβ-initiated cascade of downstream neurodegenerative effects, thereby increasing the risk of AD.

Simultaneous PET-MRI Studies of the Concordance of Atrophy and Hypometabolism in Syndromic Variants of Alzheimer's Disease and Frontotemporal Dementia: An Extended Case Series.

Simultaneous PET-MRI is used to compare patterns of cerebral hypometabolism and atrophy in six different dementia syndromes. The primary objective was to conduct an initial exploratory study regarding the concordance of atrophy and hypometabolism in syndromic variants of Alzheimer's disease (AD) and frontotemporal dementia (FTD). The secondary objective was to determine the effect of image analysis methods on determination of atrophy and hypometabolism. PET and MRI data were acquired simultaneously on 24 subjects with six variants of AD and FTD (n = 4 per group). Atrophy was rated visually and also quantified with measures of cortical thickness. Hypometabolism was rated visually and also quantified using atlas- and SPM-based approaches. Concordance was measured using weighted Cohen's kappa. Atrophy-hypometabolism concordance differed markedly between patient groups; kappa scores ranged from 0.13 (nonfluent/agrammatic variant of primary progressive aphasia, nfvPPA) to 0.49 (posterior cortical variant of AD, PCA). Heterogeneity was also observed within groups; the confidence intervals of kappa scores ranging from 0-0.25 for PCA to 0.29-0.61 for nfvPPA. More widespread MRI and PET changes were identified using quantitative methods than on visual rating. The marked differences in concordance identified in this initial study may reflect differences in the molecular pathologies underlying AD and FTD syndromic variants but also operational differences in the methods used to diagnose these syndromes. The superior ability of quantitative methodologies to detect changes on PET and MRI, if confirmed on larger cohorts, may favor their usage over qualitative visual inspection in future clinical diagnostic practice.

Cerebral Hypoperfusion and Hypometabolism Detected by Arterial Spin Labeling MRI and FDG-PET in Early-Onset Alzheimer's Disease.

Early-onset Alzheimer's disease (EOAD) is frequently associated with atypical clinical presentations and its early detection remains a challenging issue. In this study, we used arterial spin labeling (ASL), a noninvasive perfusion MRI sequence, and [(18)F]-FDG-PET to detect the perfusion and metabolic features in patients with EOAD. All patients were investigated in the French reference center for young-onset dementia and were assessed by MRI, including a pseudo-continuous ASL (pCASL) sequence, and [(18)F]-FDG-PET. Quantitative analyses and intermodality comparison with correlation analysis were made after data processing including correction of partial volume effects, cortical projection, and specific intensity normalization. We prospectively included 37 patients with EOAD with a mean age of 58.3 years. The areas of most severe hypoperfusion detected with ASL were located in the parietal lobes, the precuneus, the right posterior cingulate cortex, and the frontal lobes (P < .05). The areas of lowest glucose metabolism detected by [(18)F]-FDG-PET were identified in the temporoparietal cortex and the precuneus (P < .05). Hypometabolic regions were more extensive than hypoperfused regions on ASL maps whereas ASL highlighted alterations in the frontal lobes without apparent hypometabolism on [(18)F]-FDG-PET maps. ASL and [(18)F]-FDG-PET detected pathological areas of similar distribution mainly located in the inferior parietal lobules and local zones in the temporal cortex in patients with EOAD. Our preliminary study showed that ASL and [(18)F]-FDG-PET may have a complementary role in combination with structural MRI for the assessment of suspected EOAD.

Cortical Hypometabolism in Opsoclonus-Myoclonus Syndrome

Opsoclonus-myoclonus syndrome (OMS) is characterized by opsoclonus and arrhythmic myoclonic jerks predominantly involving the trunk, limbs, and head. We present two patients with OMS after respiratory tract infection who exhibited diffuse cerebral hypometabolism, particularly in the parieto-occipital cortex on 18 F-fluorodeoxyglucose positron-emission tomography (F-FDG PET). This metabolic change might be a consequence rather than a direct cause of motor symptoms, which may be attributable to brainstem or cerebellar pathology. J Korean Neurol Assoc 33(2):103-105, 2015

Progression of Cerebral Atrophy and Hypometabolism in the presence of β-amyloidosis in mild cognitive impairment (S41.007)

Progression of Cerebral Atrophy and Hypometabolism in the presence of β-amyloidosis in mild cognitive impairment (S41.007)

The semantic variant of primary progressive aphasia: clinical and neuroimaging evidence in single subjects.

Background/AimWe present a clinical-neuroimaging study in a series of patients with a clinical diagnosis of semantic variant of primary progressive aphasia (svPPA), with the aim to provide clinical-functional correlations of the cognitive and behavioral manifestations at the single-subject level.MethodsWe performed neuropsychological investigations, 18F-FDG-PET single-subject and group analysis, with an optimized SPM voxel-based approach, and correlation analyses. A measurement of white matter integrity by means of diffusion tensor imaging (DTI) was also available for a subgroup of patients.ResultsCognitive assessment confirmed the presence of typical semantic memory deficits in all patients, with a relative sparing of executive, attentional, visuo-constructional, and episodic memory domains. 18F-FDG-PET showed a consistent pattern of cerebral hypometabolism across all patients, which correlated with performance in semantic memory tasks. In addition, a majority of patients also presented with behavioral disturbances associated with metabolic dysfunction in limbic structures. In a subgroup of cases the DTI analysis showed FA abnormalities in the inferior longitudinal and uncinate fasciculi.DiscussionEach svPPA individual had functional derangement involving an extended, connected system within the left temporal lobe, a crucial part of the verbal semantic network, as well as an involvement of limbic structures. The latter was associated with behavioral manifestations and extended beyond the area of atrophy shown by CT scan.ConclusionSingle-subject 18F-FDG-PET analysis can account for both cognitive and behavioral alterations in svPPA. This provides useful support to the clinical diagnosis.

Intracerebroventricular Streptozotocin Injections as a Model of Alzheimer's Disease: in Search of a Relevant Mechanism.

Streptozotocin (STZ), a glucosamine-nitrosourea compound derived from soil bacteria and originally developed as an anticancer agent, in 1963 has been found to induce diabetes in experimental animals. Since then, systemic application of STZ became the most frequently studied experimental model of insulin-dependent (type 1) diabetes. The compound is selectively toxic toward insulin-producing pancreatic beta cells, which is explained as the result of its cellular uptake by the low-affinity glucose transporter 2 (GLUT2) protein located in their cell membranes. STZ cytotoxicity is mainly due to DNA alkylation which results in cellular necrosis. Besides pancreatic beta cells, STZ applied systemically damages also other organs expressing GLUT2, such as kidney and liver, whereas brain is not affected directly because blood-brain barrier lacks this transporter protein. However, single or double intracerebroventricular (icv) STZ injection(s) chronically decrease cerebral glucose uptake and produce multiple other effects that resemble molecular, pathological, and behavioral features of Alzheimer’s disease (AD). Taking into consideration that glucose hypometabolism is an early and persistent sign of AD and that Alzheimer’s brains present features of impaired insulin signaling, icv STZ injections are exploited by some investigators as a non-transgenic model of this disease and used for preclinical testing of pharmacological therapies for AD. While it has been assumed that icv STZ produces cerebral glucose hypometabolism and other effects directly through desensitizing brain insulin receptors, the evidence for such mechanism is poor. On the other hand, early data on insulin immunoreactivity showed intense insulin expression in the rodent brain, and the possibility of local production of insulin in the mammalian brain has never been conclusively excluded. Also, there are GLUT2-expressing cells in the brain, in particular in the circumventricular organs and hypothalamus; some of these cells may be involved in glucose sensing. Thus, icv STZ may damage brain glucose insulin producing cells and/or brain glucose sensors. Mechanistic explanation of the mode of action of icv STZ, which is currently lacking, would provide a valuable contribution to the field of animal models of Alzheimer’s disease.

The neural correlates of road sign knowledge and route learning in semantic dementia and Alzheimer's disease

BackgroundAlthough there is a growing body of research on driving and Alzheimer's disease (AD), focal dementias have been understudied. Moreover, driving has never been explored in semantic dementia (SD).MethodsAn experimental...

Topography of brain glucose hypometabolism and epileptic network in glucose transporter 1 deficiency

(18)F fluorodeoxyglucose positron emission tomography ((18)F FDG-PET) facilitates examination of glucose metabolism. Previously, we described regional cerebral glucose hypometabolism using (18)F FDG-PET in patients with Glucose transporter 1 Deficiency Syndrome (Glut1 DS). We now expand this observation in Glut1 DS using quantitative image analysis to identify the epileptic network based on the regional distribution of glucose hypometabolism. (18)F FDG-PET scans of 16 Glut1 DS patients and 7 healthy participants were examined using Statistical parametric Mapping (SPM). Summed images were preprocessed for statistical analysis using MATLAB 7.1 and SPM 2 software. Region of interest (ROI) analysis was performed to validate SPM results. Visual analysis of the (18)F FDG-PET images demonstrated prominent regional glucose hypometabolism in the thalamus, neocortical regions and cerebellum bilaterally. Group comparison using SPM analysis confirmed that the regional distribution of glucose hypo-metabolism was present in thalamus, cerebellum, temporal cortex and central lobule. Two mildly affected patients without epilepsy had hypometabolism in cerebellum, inferior frontal cortex, and temporal lobe, but not thalamus. Glucose hypometabolism did not correlate with age at the time of PET imaging, head circumference, CSF glucose concentration at the time of diagnosis, RBC glucose uptake, or CNS score. Quantitative analysis of (18)F FDG-PET imaging in Glut1 DS patients confirmed that hypometabolism was present symmetrically in thalamus, cerebellum, frontal and temporal cortex. The hypometabolism in thalamus correlated with the clinical history of epilepsy.

Cerebral glucose hypometabolism is associated with mitochondrial dysfunction in patients with intractable epilepsy and cortical dysplasia.

Metabolic imaging studies, such as positron emission tomography (PET), allow for an assessment of physiologic functioning of the brain, and [(18)F]fluoro-2-deoxyglucose (FDG)-PET is now a commonly used technique in presurgical epilepsy evaluations. Focal interictal decreases in glucose consumption are often but inconsistently concordant with the ictal onset area, and the underlying mechanisms are poorly understood. The current study tests the hypothesis that areas of glucose hypometabolism, determined by FDG-PET, are associated with mitochondrial dysfunction in patients with medically intractable epilepsy associated with isolated focal cortical dysplasia (FCD). Measures of electron transport chain (ETC) functioning and mitochondrial abnormalities (ETC complex biochemistry, protein kinase B subtype 1 (Akt1), glial fibrillary acidic protein (GFAP)) were assessed in surgical resection specimens that had hypometabolic abnormalities and those that were normal on FDG-PET. Determination of FDG-PET abnormalities was based on coregistration of statistical parametric mapping (SPM) results with postsurgical images. Twenty-two patients (11 male, 11 female; mean age at the time of surgery 10.5 ± 4.4 years), with pathologically confirmed FCD, were included in this retrospective review. Complex IV function was found to be significantly reduced in areas of hypometabolism (p = 0.014), whereas there was a trend toward a significant reduction in complex II and III function in areas of hypometabolism (p = 0.08, p = 0.059, respectively). These decreases were independent of cortical dysplasia severity (p = 0.321) and other clinical epilepsy measures. This study suggests an association between glucose hypometabolism and reduced mitochondrial complex IV functioning, which is independent of the degree of cortical dysplasia. This supports the role of cellular energy failure as a potential mechanism for intractable epilepsy.

Altered Serum Levels of Adipokines and Insulin in Probable Alzheimer's Disease

Cerebral hypometabolism of glucose, weight loss, and decreased food intake are characteristic features of sporadic Alzheimer's disease (AD). A systematic study on the serum levels of adipokines and insulin, the major hormones regulating energy metabolism, food intake, and body weight, in sporadic AD is necessary. The present study compares the serum levels of leptin, adiponectin, and insulin, measured by commercially available immuno-assay kits, between controls and sporadic AD subjects. The results show a conspicuous decrease in the level of leptin, a dramatic rise in the level of adiponectin, and also a statistically significant increase in insulin level, in the blood of AD subjects, with respect to controls. The changes in the serum levels of adiponectin and insulin in AD are positively correlated with the severity of dementia. Likewise, the serum level of leptin in AD subjects is negatively correlated with the degree of dementia. The changes in the levels of adipokines and insulin have implications in the amyloid pathology, neurodegeneration, and hypometabolism of glucose existing in the AD brain.

APOE genotype and neuroimaging markers of Alzheimer's disease: systematic review and meta-analysis

ObjectiveWe aimed to examine the association of apolipoprotein E (APOE) ɛ4 genotype with neuroimaging markers of Alzheimer's disease: hippocampal volume, brain amyloid deposition and cerebral metabolism.MethodsWe performed a systematic review...

Saccadic Palsy after Cardiac Surgery: Serial Neuroimaging Findings during a 6-Year Follow-Up.

BackgroundPatients who develop horizontal and vertical saccadic palsy after cardiac surgery have rarely been described. Although most such patients exhibit distinct neurological deficits, their brain MRI findings are almost normal. In addition, functional neuroimaging of such patients has never been reported.Case ReportA 43-year-old woman with dysarthria, dysphagia, and horizontal and vertical saccadic palsy after cardiac surgery was followed up for about 6 years; serial brain MRIs has been performed during this period, including susceptibility-weighted imaging (SWI) and [18F]-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET). Multiple microbleeds in the cerebral cortex, cerebellum, and brainstem, and glucose hypometabolism in the brainstem, cerebellum, and multiple cortical areas.ConclusionsTo the best of our knowledge, this is the first reported case of saccadic palsy after cardiac surgery with serial SWI and [18F]-FDG-PET performed to explore the possible cerebral lesions.