Brain Glucose Metabolism In Patients Research Articles

Frontal-striatal glucose metabolism and fatigue in patients with multiple sclerosis, long COVID, and COVID-19 recovered controls.

This study compared brain glucose metabolism using FDG-PET in the caudate nucleus, putamen, globus pallidus, thalamus, and dorsolateral prefrontal cortex (DLPFC) among patients with Long COVID, patients with fatigue, people with multiple sclerosis (PwMS) patients with fatigue, and COVID recovered controls. PwMS exhibited greater hypometabolism compared to long COVID patients with fatigue and the COVID recovered control group in all studied brain areas except the globus pallidus (effect size range 0.7-1.5). The results showed no significant differences in glucose metabolism between patients with Long COVID and the COVID recovered control group in these regions. These findings suggest that long COVID fatigue may involve non-CNS systems, neurotransmitter imbalances, or psychological factors not captured by FDG-PET, while MS-related fatigue is associated with more severe frontal-striatal circuit dysfunction due to demyelination and neurodegeneration. Symmetrical standardized uptake values (SUVs) between hemispheres in all groups imply that fatigue in these conditions may be related to global or network-level alterations rather than hemisphere-specific changes. Future studies should employ fine-grained analysis methods, explore other brain regions, and control for confounding factors to better understand the pathophysiology of fatigue in MS and long COVID. Longitudinal studies tracking brain glucose metabolism in patients with Long COVID could provide insights into the evolution of metabolic patterns as the condition progresses.

The clinical application value of brain 18F-FDG PET/CT in the diagnostics of Parkinsonian syndromes

Objective: To analyze the PET/CT imaging features of fluoride 18F-fluorodeoxyglucose (18F-FDG) in patients with various types of Parkinson's syndrome (PS), and to establish a "diagnostic tree" model of 18F-FDG PET/CT for PS. Methods: Data of patients with Parkinson's disease (PD), patients with multiple system atrophy cerebellar type (MSA-C), and patients with multiple system atrophy Parkinson's type (MSA-P)admitted to the Neurology Department of Huashan Hospital affiliated to Fudan University from January 2019 to December 2021. 18F-FDG PET/CT examination was conducted in all patients. Clinical and follow-up data was collected to determine clinical diagnosis. The specific patterns of brain glucose metabolism in patients with various types of Parkinsonism were observed and their utility in the differential diagnosis of the disease was analyzed. 18F-FDG PET/CT imaging"diagnostic tree"model was established and its value in the differential diagnosis of Parkinsonism was verified. Results: A total of 320 patients, 187 males and 133 females, aged (62±9) years, were enrolled in our study, including 80 PD, 90 PSP, 114 MSA-C and 36 MSA-P patients. The differential diagnostic features of cerebral glucose metabolism of Parkinsonism were as follows: the metabolism of putamen increased in PD patients, the metabolism of caudate nucleus, thalamus, midbrain, and frontal lobe decreased in PSP patients, the metabolism of cerebellum decreased in MSA-C patients, and the metabolism of putamen and cerebellum decreased in MSA-P patients. The sensitivity and specificity of the"diagnostic tree"model are 88.75% and 91.25% for PD diagnosis, 54.44% and 96.96% for PSP diagnosis, 87.72% and 86.41% for MSA-C diagnosis, and 55.56% and 91.55% for MSA-P diagnosis, respectively. It could correctly classify 75%(240/320) of patients. Conclusions: Characteristic metabolism patterns of brain in 18F-FDG PET/CT imaging is significant for the differential diagnosis of PD, PSP, MSA-C and MSA-P. The"diagnostic tree"model is valuable for clinical diagnosis.

Applications of PET and SPECT in Patients with Autism Spectrum Disorder.

Autism spectrum disorder (ASD) consists of neurological development disorders that manifest before three years of age and affect social interactions, markedly restricting range of interests and activities, often associated with some degree of intellectual disability. Single-photon emission computed tomography (SPECT) and positron emission tomography (PET) are non-invasive imaging tools to investigate the function of the brain in vivo. SPECT and PET studies exploring rCBF and brain glucose metabolism in patients with ASD have been performed, providing important insights into the brain regions involved in ASD. Abnormalities in serotonergic, dopaminergic, GABAergic, cholinergic, and glutamatergic systems have been suggested to contribute to the observed distorted brain circuitry associated with ASD. However, the specificity of such abnormalities needs to be fully clarified because schizophrenia and other psychiatric diseases have been shown to present with comparable changes in neurotransmitter systems. Neuroinflammation could also play a role in the development of autism. Therefore, ASD is a complicated process involving a number of factors. It is mandatory to perform more research studies to determine the molecular cornerstone of ASD and to improve our comprehension of the clinical correlates of ASD.

A study of brain glucose metabolism in obsessive-compulsive disorder patients.

Obsessive-compulsive disorder (OCD) is a chronic neural psychological condition. Its pathogenesis is not yet completely understood. This current research used fluorine-18 fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) imaging to examine the changes in brain glucose metabolism in patients with OCD during the course of treatment, and analyzed its relationship with clinical efficacy. A total of 23 patients with OCD were enrolled and divided into case group 1, consisting of patients who received no drug treatment or those who recently stopped drug treatment for more than five half-life periods (OCD1 group, N=10), and case group 2, consisting of patients who were receiving drug treatment before enrollment (OCD2 group, N=13). Ten healthy volunteers were selected as controls. All patients and healthy controls were subjected to head PET-computed tomography (CT) examination. Seven patients in case group 2 underwent scanning again after 3 months of drug treatment, namely, case group 3 (OCD3 group, N=7). Statistical Parametric Mapping (SPM) 8 software was used to analyze the PET-CT results. OCD patients had abnormally enhanced glucose metabolism in the medium orbito-frontal region of the brain, and abnormally reduced glucose metabolism in brain areas including the insula, caudate nucleus, and middle temporal gyrus. No changes in brain glucose metabolism related to curative effect was found. In OCD patients, abnormal brain function may not only be limited to the usual cortico-striato-thalamo-cortical (CSTC) loop model, but may involve a wide range of brain regions simultaneously.

Evaluation of the Effects of R-CHOP Chemotherapy on Brain Glucose Metabolism in Patients with Diffuse Large B Cell Lymphoma: A Baseline, Interim, and End-of-Treatment PET/CT Study.

Background: To investigate the effect of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy on brain glucose metabolism in patients with diffuse large B cell lymphoma (DLBCL). Methods: Seventy-two patients with newly diagnosed DLBCL underwent FDG PET/CT brain and whole-body scans at baseline (PET0), in the interim of chemotherapy (PET2), and at the end (PET6) of chemotherapy. All three brain scans of each patient were analyzed using statistical parametric mapping software. Results: Compared with the PET0 scan, the PET2 and PET6 scans revealed a significantly higher glucose metabolism throughout the whole brain, with the PET6 scan revealing a higher metabolism than the PET2 scan. Patients with a complete response (CR) displayed decreased glucose metabolism in the lingual gyrus and increased glucose metabolism in the pons after chemotherapy compared with the findings in patients with partial responses or progressive disease. Conclusions: Brain glucose metabolism was affected by R-CHOP treatment throughout the entire chemotherapy protocol.

Brain Metabolic Correlates of Dopaminergic Denervation in Prodromal and Early Parkinson's Disease.

It remains unclear how brain metabolic activities transform in response to dopamine deficiency in the prodromal and early phases of Parkinson's disease (PD). To investigate the relationship between nigrostriatal dopaminergic denervation and brain glucose metabolism in patients with isolated rapid eye movement sleep behavior disorder (iRBD) and early PD. This cohort study included 28 patients with polysomnography-confirmed iRBD, 24 patients with de novo PD with probable rapid eye movement sleep behavior disorder (denovo PD), and 28 healthy controls (HCs) who underwent two positron emission tomography scans with 18 F-fluorodeoxyglucose (all participants) and 18 F-N-3-fluoropropyl-2β-carboxymethoxy-3β-(4-iodophenyl)-nortropane (except for one denovo PD patient and 15 HCs). We analyzed striatal and voxel-wise whole-brain glucose metabolism in relation to nigrostriatal dopaminergic integrity and comparatively investigated the whole-brain metabolic connectivity among the groups. We also assessed longitudinal metabolic changes against progressive dopaminergic denervation over 4 years in the iRBD group. From HCs to iRBD and finally to the denovo PD, dopaminergic integrity positively correlated with metabolic activity in the caudate, whereas a negative correlation was observed in the posterior putamen. In the iRBD group, there was a metabolic increase in the inferior orbitofrontal cortex against putaminal dopaminergic denervation at baseline, but negative correlations were newly observed in the superior orbitofrontal cortex and superior frontal gyrus at the 4-year follow-up. The denovo PD group showed negative correlations in the cerebellum and fusiform gyrus. Intra- and inter-regional metabolic connectivities in the parieto-occipital cortices were enhanced in the iRBD group compared with the denovo PD and HC groups. In the iRBD group, overall metabolic connectivity was strengthened along with enhanced basal ganglia-frontal connection by advancing dopaminergic denervation. Our findings suggest diverse trajectories of metabolic responses associated with dopaminergic denervation between individual brain areas in the prodromal and early PD stages. © 2022 International Parkinson and Movement Disorder Society.

Correlation Between Brain 18F-AV45 and 18F-FDG PET Distribution Characteristics and Cognitive Function in Patients with Mild and Moderate Alzheimer's Disease.

Florbetapir (AV45) and fluorodeoxyglucose (FDG) PET imaging are valuable techniques to detect the amyloid-β (Aβ) load and brain glucose metabolism in patients with Alzheimer's disease (AD). The purpose of this study is to access the characteristics of Aβ load and FDG metabolism in brain for further investigating their relationships with cognitive impairment in AD patients. Twenty-seven patients with AD (average 70.6 years old, N = 13 male, N = 14 female) were enrolled in this study. These AD patients underwent the standard clinical assessment and received detailed imaging examinations of the nervous system by using Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MOCA), 18F-AV45, and 18F-FDG PET scans. Of 27 AD patients, 22 patients (81.5%) showed significantly increases in Aβ load and 26 patients (96.3%) had significantly reductions in FDG metabolism. The moderate AD patients had more brain areas of reduced FDG metabolism and more severe reductions in some regions compared to mild AD patients, with no differences in Aβ load observed. Moreover, the range and degree of reduced FDG metabolism in several regions were positively correlated with the total score of MMSE or MOCA, whereas the range of Aβ load did not. No correlation was found between the range of Aβ load and the range of reduced FDG metabolism in this study. The reduction in FDG metabolisms captured by 18F-FDG imaging can be used as a potential biomarker for AD diagnosis in the future. 18F-AV45 imaging did not present valuable evidence for evaluating AD patient in this study.

Imaging Cerebral Glucose Metabolism during Dual-Task Walking in Patients with Parkinson's disease.

Gait impairment is a hallmark of Parkinson's disease (PD). Natural walking involves more cognitive demand than treadmill walking or in-laboratory walking tests because patients have to actively work on navigation and top-down cognitive control which taxes cognitive reserve in the prefrontal cortex. To mimic the prefrontal engagement occurring with natural walking in a controlled and safe environment, dual-task (DT) treadmill walking has been developed. In this study, we tested the feasibility of imaging DT walking-related changes in brain glucose metabolism in patients with PD. Fifteen patients with PD were scanned with fluorodeoxyglucose (FDG) positron emission tomography. Five patients performed DT walking, and 10 patients were rested during the FDG uptake period. First, the images were contrasted between the groups. Second, the walking-related brain glucose metabolism was inspected at the individual level. Consistently increased glucose metabolism was identified in DT walking versus rest in the primary visual/sensorimotor areas, thalamus, superior colliculus, and cerebellum. In individual level analysis, patients with less progressed disease (n = 3) showed prefrontal activity during DT walking while patients with more progressed disease (n = 2) did not. This study confirms the feasibility of imaging glucose metabolism during DT walking in patients with PD. We also report that during DT walking, there is a lesser degree of prefrontal engagement in the patients with more progressed disease compared to those with less progressed disease, implying increased degrees of frontal dysfunction with PD progression.

Identifying the characteristics of brain glucose metabolism using normal 18F-FDG PET database in patients with temporal lobe epilepsy

This study aimed to measure the global brain glucose metabolism of patients with temporal lobe epilepsy (TLE) using MIMneuro software based on the normal brain glucose metabolism database. In this cross-sectional study, 23 patients (11 males and 12 females, mean age 25.6 ± 10.1years) with TLE who underwent 18F-labeled fluoro-2-deoxyglucose positron emission tomography (18F-FDG PET) were enrolled. 18F-FDG PET images were then imported into MIMneuro software, which can automatically analyze the differences in regional brain glucose metabolism between patients and a normal database, and the results of different brain regions were presented by values of Z-score. In patients with TLE, 18F-FDG PET imaging showed that in addition to the presence of temporal lobe hypometabolism, there was hypometabolism in the ipsilateral hippocampus, parahippocampal gyrus, insula, amygdala, temporal operculum, and bilateral cerebellar hemisphere, while hypermetabolism was found in the contralateral temporal lobe, frontal lobe, parietal lobe, parietal lobule, angular gyrus, and precentral gyrus. There was no significant difference in brain areas between the left and the right temporal lobe seizures (P > 0.05). We found that TLE has a specific characteristic in terms of brain glucose metabolism, and the underlying mechanism needs to be further studied that may be helpful to localize seizure focus.

Brain glucose metabolism in patients with newly diagnosed multiple myeloma significantly decreases after high-dose chemotherapy followed by autologous stem cell transplantation.

The aim of this study was to compare the effect of intensive therapy [consisting of high-dose chemotherapy followed by autologous stem cell transplantation (HDC/ASCT)] and conventional standard-dose chemotherapy (CDC) on brain FDG uptake, as an indicator of glucose metabolism, in multiple myeloma patients. Twenty-four patients with newly diagnosed multiple myeloma were included. Sixteen patients received HDC/ASCT, including bortezomib-based induction therapy, and eight patients received CDC. F-fluorodeoxyglucose (FDG)-PET/computed tomography (CT) was performed 1 and 3 hours following tracer administration before and after the treatment. The manual segmentation of supratentorial and cerebellum of each patient was performed by two independent observers. The data were expressed as global mean standardized uptake values (GSUVmean). Wilcoxon signed-rank test was used to compare changes from before to after treatment. A significant decrease in the GSUVmean of supratentorial brain and cerebellum was observed after treatment in the patients who received HDC/ASCT (1 hour scans: 7.03 ± 1.18 vs. 6.56 ± 0.94; P = 0.03 and 7.01 ± 1.08 vs. 6.34 ± 0.93; P = 0.01, respectively). GSUVmean changes in the patients who received CDC were not significantly different after treatment (1 hour scans: 6.47 ± 1.16 vs. 6.21 ± 0.91; P = 0.40 and 6.30 ± 1.21 vs. 6.09 ± 0.86; P = 0.62, respectively). The same findings were observed for 3 hours scans. A high level of agreement was observed between two operators. Multiple myeloma patients who received HDC/ASCT demonstrated a significant decrease in FDG uptake in the supratentorial brain and cerebellum, while patients who received CDC did not demonstrate significant changes in the brain FDG uptake.

Effects of Amisulpride Adjunctive Therapy on Working Memory and Brain Metabolism in the Frontal Cortex of Patients with Schizophrenia: A Preliminary Positron Emission Tomography/Computerized Tomography Investigation.

ObjectiveDopamine plays a significant role in working memory by acting as a key neuromodulator between brain networks. Additionally, treatment of patients with schizophrenia using amisulpride, a pure dopamine class 2/3 receptor antagonist, improves their clinical symptoms with fewer side effects. We hypothesized that patients with schizophrenia treated with amisulpride and aripiprazole show increased working memory and glucose metabolism compared with those treated with cognitive behavioral therapy (CBT) and aripiprazole instead.MethodsSixteen patients with schizophrenia (eight in the amisulpride group [aripiprazole+amisulpride] and eight in the CBT group [aripiprazole+CBT]) and 15 age- and sex-matched healthy control subjects were recruited for a 12-week-long prospective trial. An [18F]-fluorodeoxyglucose-positron emission tomography/computerized tomography scanner was used to acquire the images.ResultsAfter 12 weeks of treatment, the amisulpride group showed greater improvement in the Letter-Number Span scores than the CBT group. Additionally, although brain metabolism in the left middle frontal gyrus, left occipital lingual gyrus, and right inferior parietal lobe was increased in all patients with schizophrenia, the amisulpride group exhibited a greater increase in metabolism in both the right superior frontal gyrus and right frontal precentral gyrus than the CBT group.ConclusionThis study suggests that a small dose of amisulpride improves the general psychopathology, working memory performance, and brain glucose metabolism of patients with schizophrenia treated with aripiprazole.

Brain Glucose Metabolism Heterogeneity in Idiopathic REM Sleep Behavior Disorder and in Parkinson's Disease.

Idiopathic REM sleep behavior disorder (iRBD) often precedes Parkinson's disease (PD) and other alpha-synucleinopathies. The aim of the study is to investigate brain glucose metabolism of patients with RBD and PD by means of a multidimensional scaling approach, using18F-FDG-PET as a biomarker of synaptic function. Thirty-six iRBD patients (64.1±6.5 y, 32 M), 72 PD patients, and 79 controls (65.6±9.4 y, 53 M) underwent brain 18F-FDG-PET. PD patients were divided according to the absence (PD, 32 subjects; 68.4±8.5 y, 15 M) or presence (PDRBD, 40 subjects; 71.8±6.6 y, 29 M) of RBD. 18F-FDG-PET scans were used to independently discriminate subjects belonging to four categories: controls (RBD no, PD no), iRBD (RBD yes, PD no), PD (RBD no, PD yes) and PDRBD (RBD yes, PD yes). The discriminant analysis was moderately accurate in identifying the correct category. This is because the model mostly confounds iRBD and PD, thus the intermediate classes. Indeed, iRBD, PD and PDRBD were progressively located at increasing distance from controls and are ordered along a single dimension (principal coordinate analysis) indicating the presence of a single flux of variation encompassing both RBD and PD conditions. Data-driven approach to brain 18F-FDG-PET showed only moderate discrimination between iRBD and PD patients, highlighting brain glucose metabolism heterogeneity among such patients. iRBD should be considered as a marker of an ongoing condition that may be picked-up in different stages across patients and thus express different brain imaging features and likely different clinical trajectories.

The Neural Basis of Postural Instability Gait Disorder Subtype of Parkinson's Disease: A PET and fMRI Study.

The aim of this study is to further uncover the neural basis of postural instability gait disorder (PIGD) subtype of Parkinson's disease. With F-18 fluorodeoxyglucose PET (FDG-PET), brain glucose metabolism of patients with PIGD (n = 15) was compared with healthy controls (n = 17) and tremor-dominant (TD) patients (n = 15), and the correlation between metabolism and PIGD symptoms was also assessed. Within PIGD symptom-correlated hypometabolic areas, the relationship of functional connectivity (FC) with motor and cognitive symptoms was examined by using functional MRI. Compared with controls, patients with PIGD displayed a distributed pattern of brain hypometabolism including striatal, frontal, and parietal areas. Relative to the pattern of TD patients, the pattern of patients with PIGD had additional metabolic decreases in caudate and inferior parietal lobule (IPL, Brodmann area [BA] 40). In PIGD group, the metabolic reductions in IPL (BA 40), middle frontal gyrus (MFG, BA 9) and fusiform gyrus (FG, BA 20) were associated with severe PIGD symptoms. Regions showing such correlation were chosen for further seed-based FC analysis. Decreased FC within the prefrontal-parietal network (between the MFG and IPL) was associated with severe PIGD symptoms. The involvement of the caudate, FG, and prefrontal-parietal network may be associated with the prominent gait impairments of PIGD subtype. Our findings expand the pathophysiological knowledge of PIGD subtype and provide valuable information for potential neuromodulation therapies alleviating gait disorders.

Dissociable Effects of Alzheimer Disease and White Matter Hyperintensities on Brain Metabolism

Cerebrovascular disease and Alzheimer disease (AD) frequently co-occur and seem to act through different pathways in producing dementia. To examine cerebrovascular disease and AD markers in relation to brain glucose metabolism in patients with mild cognitive impairment. Cohort study among the Alzheimer Disease Neuroimaging Initiative clinical sites in the United States and Canada. Two hundred three patients having amnestic mild cognitive impairment (74 of whom converted to AD) with serial imaging during a 3-year follow-up period. Quantified white matter hyperintensities (WMHs) represented cerebrovascular disease, and cerebrospinal fluid β-amyloid represented AD pathology. Brain glucose metabolism in temporoparietal and frontal brain regions was measured using positron emission tomography with fluorodeoxyglucose F18. In converters, greater WMHs were associated with decreased frontal metabolism (-0.048; 95% CI, -0.067 to -0.029) but not temporoparietal metabolism (0.010; 95% CI, -0.010 to 0.030). Greater cerebrospinal fluid β-amyloid (per 10-pg/mL increase) was associated with increased temporoparietal metabolism (0.005; 95% CI, 0.000-0.010) but not frontal metabolism (0.002; 95% CI, -0.004 to 0.007) in the same patients. In nonconverters, similar relationships were observed except for a positive association of greater WMHs with increased temporoparietal metabolism (0.051; 95% CI, 0.027-0.076). The dissociation of WMHs and cerebrospinal fluid β-amyloid in relation to regional glucose metabolism suggests that these pathologic conditions operate through different and independent pathways in AD that reflect dysfunction in different brain systems. The positive association of greater WMHs with temporoparietal metabolism suggests that these pathologic processes do not co-occur in nonconverters.

Is cerebral glucose metabolism affected by chemotherapy in patients with Hodgkin’s lymphoma?

The aim of the study was to investigate the effect of chemotherapy treatment with ABVD on brain glucose metabolism in patients with Hodgkin's disease (HD). A total of 49 patients (23 men, 26 women; mean age 32±9 years) diagnosed with HD were included in the study. All of them underwent a baseline (PET0) and an interim (PET2) 2-deoxy-2-[(18)F]fluoro-D-glucose ((18)F-FDG) PET/computed tomography (CT) brain scan. All patients were treated after PET0 with two cycles of ABVD consisting of doxorubicin (adriamycin), bleomycin, vinblastine, and dacarbazine for 2 months. Thirty-five patients were evaluated further 15±6 days after four additional cycles (PET6). Differences in brain (18)F-FDG uptake were analyzed by statistical parametric mapping (SPM2). Compared with PET0, PET2 showed a significantly higher metabolic activity in the right angular gyrus (Brodmann area 39) and a significant metabolic reduction in Brodmann areas 10, 11, and 32 bilaterally. All these changes disappeared at PET6. Our results support the conclusion of a very limited impact of ABVD chemotherapy on brain metabolism in patients with HD.

Positron emission computed tomography analysis of hyperbaric oxygen therapy on patients with severe brain injury

Objective By using 18F-deoxyglucose (18F-FDG) positron emission computed tomography (PET-CT) to measure the brain glucose metabolism of patients with severe traumatic brain injury before and after hyperbaric oxygen (HBO) therapy,and to investigate the mechanisms of H BO treating patients with traumatic brain injury.Methods Twenty-six patients suffered form severe traumatic brain injury with stable vital signs within 2 weeks were randomly divided into the HBO group and the control group.The patients of both groups received routine clinical interventions (including neuroprotection,dehydration,reducing intracranial pressure,anti-infection and other symptomatic treatments).Patients of the HBO group received the basic treatment combined with HBO therapy one tine per day for 7 days per week.In early stage and 4 weeks after treatment,all patients were examined with PET-CT scanning and Glasgow coma scale (GCS),disability rating scale (DRS) at the same time.Results There was standard uptake value (SUV) of significant difference between affected and unaffected brain areas in two groups before treatment(P＜0.01),but no significant difference between two groups (P＞0.05).After 4-week of treatment,SUV of affected and unaffected brain areas of two groups improved,the damaged area of HBO group improved obviously and the SUV was much better than before treatment and the control group (P＜0.0l).The GCS and DRS scores of HBO group were also significantly better than that of control group (P＜0.05).Conclusion The 18F-FDG PET-CT examination showed that HBO therapy can significantly improve glucose metabolism function of the brain damaged area,promote the brain functional recovery and awakening,and improve the prognosis in patients with severe traumatic brain injury. Key words: Hyperbaric oxygenation; Craniocerebral trauma; Positron emission tomography

P4‐362: Brain glucose metabolism in patients with mild to moderate Alzheimer's disease before and after six months treatment with intravenous immunoglobulin (octagam 10%): A phase II double blind, placebo‐controlled multi‐center study

P4‐362: Brain glucose metabolism in patients with mild to moderate Alzheimer's disease before and after six months treatment with intravenous immunoglobulin (octagam 10%): A phase II double blind, placebo‐controlled multi‐center study

Effects of disease duration on the clinical features and brain glucose metabolism in patients with mixed type multiple system atrophy

To study the effect of disease duration on the clinical, neuropsychological and [(18)F]-deoxyglucose (FDG) PET findings in patients with mixed type multiple system atrophy (MSA), this study included 16 controls and 37 mixed-type MSA patients with a shorter than a 3-year history of cerebellar or parkinsonian symptoms. We classified the patients into three groups according to the duration of parkinsonian or cerebellar symptoms (Group I = <or=1 year; II = 13-24 months; III = 25-36 months). We performed UPDRS, international cooperative ataxia rating scale (ICARS), and a neuropsychological test battery. We compared the FDG PET findings of each group of patients with controls. Group I patients frequently had memory and frontal executive dysfunction. They showed hypometabolism in the frontal cortex, anterior cerebellar hemisphere and vermis. They had parkinsonian motor deficits, but no basal ganglia hypometabolism. Group II and III patients frequently had multiple domain cognitive impairments, and showed hypometabolism in the frontal and parieto-temporal cortices. Hypometabolism of the bilateral caudate and the left posterolateral putamen was observed in Group II, and whole striatum in Group III. In summary, the cortical hypometabolism begins in the frontal cortex and spreads to the parieto-temporal cortex in MSA. This spreading pattern coincides with the progressive cognitive decline. Early caudate hypometabolism may also contribute to the cognitive impairment. Parkinsonian motor deficits precede putaminal hypometabolism that begins in its posterolateral part. Cerebellar hypometabolism occurs early in the clinical courses and seems to be a relevant metabolic descriptor of cerebellar deficits.

Positron emission tomography in epileptogenic hypothalamic hamartomas

ABSTRACT Whether the intrinsic epileptogenicity of hypothalamic hamartomas (HH) is responsible for the entire clinical spectrum of epileptic, neuropsychological and behavioural disorders associated with HH, remains an open issue, in as much as morphologically similar HH can be associated with dramatically different seizure types and cognitive outcomes. The aim of this study was to investigate brain glucose metabolism in patients with epileptogenic HH, in an attempt to identify signs of focal cortical and subcortical dysfunction which might correlate with other clinical data. We have studied five patients with epileptogenic HH using [ 18 F]‐fluorodesoxyglucose and positron emission tomography (FDG‐PET). All our patients also underwent an optimal MRI and a video‐EEG monitoring, as well as an intra‐cranial EEG recording in one of them. The anatomical distribution of FDG‐PET abnormalities was compared to that of interictal and ictal electroclinical findings. All five patients demonstrated focal hypometabolism, ipsilateral to the predominant EEG abnormalities and side of HH. Hypometabolic areas greatly varied between patients, but were grossly concordant with the cortical regions suspected to participate in the ictal discharges in each individual. Epileptogenic hypothalamic hamartomas are usually associated with focal cortical hypometabolism in regions which might participate in the overall HH‐driven epileptic network. Whether these cortical abnormalities only reflect the propagation of ictal discharges, or a potentially independent seizure onset zone remains unknown.

A preliminary study of the effects of electroconvulsive therapy on regional brain glucose metabolism in patients with major depression.

Animal studies have shown that a course of electroconvulsive shock (ECS) leads to a significant reduction in glucose metabolism in rat brains 1 day after the last ECS. In humans, of the two positron emission tomography (PET) studies that assessed the effects of a course of electroconvulsive therapy (ECT) on brain glucose metabolism in depressed patients, one reported no change while the other found a trend for reduction in glucose metabolism in frontal cortical region 24 hours after last ECT. The changes in glucose metabolism detected 24 hours after the last ECS/ECT treatment might simply be due to subacute effects of a seizure. We hypothesized that the changes in brain metabolism that persist 1 week after a course of ECT are more likely to underlie the therapeutic effects of ECT. We, therefore, investigated the effects of a course of ECT on brain glucose metabolism 1 week after last ECT by using PET and [18F]fluorodeoxyglucose (FDG). Six patients who met DSM-IV criteria for a diagnosis of major depressive disorder (unipolar), and were referred for ECT as the clinically indicated treatment were recruited. They underwent two PET scans, one prior to first ECT and the second a week after last ECT. The number of ECT treatments subjects received ranged from 8 to 12 with a mean of 11. Five out of six patients responded to the ECT treatment. Cerebral metabolic rates for glucose were slightly lower in most regions post treatment compared with pretreatment but the differences were not statistically significant. Similarly, there was no significant correlation between changes in regional cerebral metabolic rates for glucose (rCMRglc) and changes in Hamilton Depression Rating Scale (HAM-D 21-item) scores. Our results might suggest that rCMRglc rates are not altered 1 week after a therapeutic course of ECT in depressed patients. Further studies using new generation PET scanners, which have a higher resolution, in larger numbers of depressed patients, are clearly needed before firm conclusions can be drawn.