The metabolic anatomy of Parkinson's disease: complementary [18F]fluorodeoxyglucose and [18F]fluorodopa positron emission tomographic studies

We studied the metabolic anatomy of typical Parkinson's disease (PD) using [18F]fluorodeoxyglucose (FDG) and [18F]fluorodopa (FDOPA) and positron emission tomography (PET). Fourteen PD patients (mean age 49 years) had FDG/PET scans, of which 11 were scanned with both FDOPA and FDG. After the injection of FDOPA, brain uptake and arterial plasma radioactivity were monitored for 2 h. Striatal FDOPA uptake was analyzed with regard to a two-compartment model, and target-to-background ratios (TBRs) and TBR-versus-time slopes were also calculated. Regional patterns of metabolic covariation were extracted from FDG/PET data using the Scaled Subprofile Model (SSM). SSM pattern weights, FDOPA uptake constants (Ki), TBRs, and TBR slopes were correlated with clinical measures for bradykinesia, rigidity, tremor, gait disturbance, left-right asymmetry, dementia, and overall disease severity. In PD patients, rate constants for FDOPA uptake correlated with individual measures of bradykinesia (p = 0.001) and gait disability (p less than 0.05). SSM analysis revealed a distinct pattern of regional metabolic asymmetries, which correlated with motor asymmetries (p less than 0.001) and left-right differences in Ki (p less than 0.01). Our data suggest that in PD patients, FDG/PET and FDOPA/PET may provide unique and complementary information about underlying disease processes.     

Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the off and on conditions with [(18)F]FDG-PET.

Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson's disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [(18)F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 11 nondemented PD patients with advanced disease and 10 age-matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time 1 hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [(18)F] activity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus. Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [(18)F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment.     

Objective PET study of glucose metabolism asymmetries in children with epilepsy: Implications for normal brain development

Clinical interpretation of cerebral positron emission tomography with 2‐deoxy‐2[F‐18]fluoro‐d ‐glucose (FDG‐PET) images often relies on evaluation of regional asymmetries. This study was designed to establish age‐related variations in regional cortical glucose metabolism asymmetries in the developing human brain. FDG‐PET scans of 58 children (age: 1–18 years) were selected from a large single‐center pediatric PET database. All children had a history of epilepsy, normal MRI, and normal pattern of glucose metabolism on visual evaluation. PET images were analyzed objectively by statistical parametric mapping with the use of age‐specific FDG‐PET templates. Regional FDG uptake was measured in 35 cortical regions in both hemispheres using an automated anatomical labeling atlas, and left/right ratios were correlated with age, gender, and epilepsy variables. Cortical glucose metabolism was mostly symmetric in young children and became increasingly asymmetric in older subjects. Specifically, several frontal cortical regions showed an age‐related increase of left > right asymmetries (mean: up to 10%), while right > left asymmetries emerged in posterior cortex (including portions of the occipital, parietal, and temporal lobe) in older children (up to 9%). Similar trends were seen in a subgroup of 39 children with known right‐handedness. Age‐related correlations of regional metabolic asymmetries showed no robust gender differences and were not affected by epilepsy variables. These data demonstrate a region‐specific emergence of cortical metabolic asymmetries between age 1–18 years, with left > right asymmetry in frontal and right > left asymmetry in posterior regions. The findings can facilitate correct interpretation of cortical regional asymmetries on pediatric FDG‐PET images across a wide age range.     

Subthalamic nucleus stimulation restores glucose metabolism in associative and limbic cortices and in cerebellum: evidence from a FDG-PET study in advanced Parkinson's disease.

Deep brain stimulation of the subthalamic nucleus (STN-DBS) is a highly effective surgical treatment in patients with advanced Parkinson's disease (PD). Because the STN has been shown to represent an important relay station not only in motor basal ganglia circuits, the modification of brain areas also involved in non-motor functioning can be expected by this intervention. To determine the impact of STN-DBS upon the regional cerebral metabolic rate of glucose (rCMRGlc), we performed positron emission tomography (PET) with 18-fluorodeoxyglucose (FDG) in eight patients with advanced PD before surgery as well as in the DBS on- and off-conditions 4 months after electrode implantation and in ten age-matched healthy controls. Before surgery, PD patients showed widespread bilateral reductions of cortical rCMRGlc versus controls but a hypermetabolic state in the left rostral cerebellum. In the STN-DBS on-condition, clusters of significantly increased rCMRGlc were found in both lower thalami reaching down to the midbrain area and remote from the stimulation site in the right frontal cortex, temporal cortex, and parietal cortex, whereas rCMRGlc significantly decreased in the left rostral cerebellum. Therefore, STN-DBS was found to suppress cerebellar hypermetabolism and to partly restore physiologic glucose consumption in limbic and associative projection territories of the basal ganglia. These data suggest an activating effect of DBS upon its target structures and confirm a central role of the STN in motor as well as associative, limbic, and cerebellar basal ganglia circuits.     

Regional metabolic changes in parkinsonian patients with normal dopaminergic imaging.

Dopaminergic imaging has been found to be normal in approximately 15% of parkinsonian patients enrolled in neuroprotective trials. We used (18)F-fluorodeoxyglucose positron emission tomography (FDG PET) to determine the metabolic basis for this finding. We reviewed scans from 185 patients with clinical signs of Parkinson's disease (PD) who underwent (18)F-fluorodopa PET imaging for diagnostic confirmation. Of this group, 27 patients (14.6%) had quantitatively normal scans; 8 of these patients were additionally scanned with FDG PET. Pattern analysis was performed on an individual scan basis to determine whether the metabolic changes were consistent with classic PD. Computer-assisted single-case assessments of the FDG PET scans of these 8 patients did not disclose patterns of regional metabolic change compatible with classical PD or an atypical parkinsonian variant. Similarly, network quantification revealed that PD-related pattern expression was not elevated in these patients as it was in an age- and duration-matched cohort with classical PD (P < 0.0001). None of these patients developed clinical signs of classical PD or of an atypical parkinsonian syndrome at a follow-up visit conducted 3 years after imaging. The results suggest that parkinsonian subjects with normal dopaminergic imaging do not have evidence of classical PD or an atypical parkinsonian syndrome.     

Positron emission tomography in degenerative disorders of the dopaminergic system

Summary 21 patients who had Parkinson's disease (PD), PD plus dementia of Alzheimer type (PDAT) or progressive supranuclear palsy (PSP), were studied with positron emission tomography (PET) using (¹⁸F)-2-fluoro-2-deoxy-D-glucose (FDG). In one patient with strictly unilateral PD side differences in striatal dopa uptake were studied with 6-(¹⁸F)fluoro-L-dopa (F-dopa). In patients with PD PET with FDG did not show any significant change in regional cerebral metabolic rates for glucose (rCMR(Glu)). In PDAT glucose metabolism was generally reduced, the most severe decrease was found in parietal cortex. The metabolic pattern was similar to that typically found in patients with Alzheimer's disease (AD). In the patient with strictly unilateral PD rCMR(Glu) was normal, F-dopa PET, however, revealed a distinct reduction of dopa uptake in the contralateral putamen. In PSP glucose metabolism was significantly decreased in subcortical regions (caudatum, putamen and brainstem) and in frontal cortex. Thus PET demonstrated a clear difference of metabolic pattern between PDAT and PSP.     

Normal striatal glucose consumption in two patients with benign hereditary chorea as measured by positron emission tomography

Summary Positron emission tomography (PET) with [¹⁸F]-2-fluoro-2-deoxy-D-glucose (FDG) was used to investigate the regional cerebral metabolic rate of glucose consumption (rCMRGlc) in two patients with benign hereditary chorea (BHC) and 21 normal subjects. Relative and absolute values of cerebellar, striatal, thalamic, and cortical rCMRGlc were within normal limits for both patients with BHC, indicating that the choreic movement disorder encountered in these two patients was not caused by a decrease of energy metabolism in the striatum such as that found regularly in most patients with other forms of chorea (e.g. Huntington's and Wilson's disease).     

Fluorodopa uptake and glucose metabolism in early stages of corticobasal degeneration

Fluorodopa (FDOPA) and fluorodeoxyglucose (FDG) PET was performed in six patients in early stages of corticobasal degeneration (CBD) and compared to Parkinson’s disease (PD) patients with a similar degree of bradykinesia and rigidity and to healthy controls. Statistical parametric mapping analysis comparing CBD to controls showed metabolic decrease in premotor, primary motor, supplementary motor, primary sensory, prefrontal, and parietal associative cortices, and in caudate and thalamus contralateral to the side of clinical signs. Except for the prefrontal regions a similar metabolic pattern was observed when CBD was compared to PD. Putamen FDOPA uptake was decreased in both CBD and PD. Caudate FDOPA uptake in CBD patients was decreased contralateral to clinical signs when compared to controls, but was higher than in PD. In early stages of CBD, FDOPA and FDG PET patterns differed from those observed in PD. In CBD the asymmetry in FDOPA uptake was less pronounced than that of clinical signs or metabolic impairment. Received: 19 January 1999 Received in revised form: 2 July 1999 Accepted: 14 July 1999     

Is FDG‐PET a useful tool in clinical practice for diagnosing corticobasal ganglionic degeneration?

Seven consecutive patients were suspected to suffer from corticobasal ganglionic degeneration (CBGD) and were studied with ([18])F-fluorodeoxyglucose (FDG) PET imaging of the brain. At the time of their FDG-PET scan, 4 of 7 patients fulfilled the clinical criteria of CBGD as proposed by Lang and associates [In Calne DB, 1994; Neurodegenerative disease. Philadelphia: Saunders]. For 2 of these 4 patients, however, an alternative clinical diagnosis was also considered. Three of the seven patients underwent an FDG-PET scan when their clinical features were not yet developed sufficiently to confirm a clinical diagnosis of CBGD. Simple visual analysis of the FDG-PET scans was carried out. All 7 patients showed an asymmetrical pattern of glucose metabolism that was demonstrated in previous studies to be characteristic in patients who had a clinical diagnosis of CBGD. The PET results helped to confirm the clinical suspicion of CBGD in 2 patients and to rule out other diagnoses in 2 other patients. For 3 patients with no sufficient symptoms to diagnose CBGD, the pattern of glucose metabolism was characteristically asymmetrical. A probable diagnosis of CBGD was made in these patients. Our results suggest that routine visual inspection of a cerebral FDG-PET scan is a useful tool to confirm suspicion of the clinical diagnosis of probable CBGD, to differentiate from other hypokinetic-rigid syndromes, and to support a diagnosis CBGD in patients who do not (yet) sufficiently fulfill the clinical criteria.     

Changes in Glucose Metabolism in Cerebral Cortex and Cerebellum Correlate With Tremor and Rigidity Control by Subthalamic Nucleus Stimulation in Parkinson's Disease: A Positron Emission Tomography Study

Objective. Employing [¹⁸F]fluorodeoxyglucose (FDG) positron emission tomography (PET) to assess the correlation between the effect of deep brain stimulation (DBS) on the subthalamic nucleus (STN) and the regional cerebral metabolic rate of glucose (rCMRGlc) in advanced Parkinson's disease patients (N = 8). Materials and Methods. On the basis of patients’ diary records, we performed FDG‐PET during the off‐period of motor activity with on‐ or off‐stimulation by STN‐DBS on separate days and analyzed the correlation between changes in motor symptoms and alterations in the rCMRGlc. Result. When FDG‐PET was performed, the motor score on the unified Parkinson's disease rating scale (UPDRS) was 64% lower with on‐stimulation than with off‐stimulation (p < 0.001, Wilcoxon single‐rank test). STN‐DBS increased the rCMRGlc in the posterior part of the right middle frontal gyrus, which corresponded to the premotor area, and the right anterior lobe of the cerebellum (p < 0.005, paired t‐test). No region exhibited a decrease in rCMRGlc. Among the items of the UPDRS motor score, the changes in resting tremor and rigidity of the left extremities showed a significant correlation with the changes in rCMRGlc observed in the right premotor area (p < 0.02 and p < 0.05, respectively, Spearman's rank correlation). Conclusions. STN‐DBS either activates the premotor area or normalizes the deactivation of the premotor area. These FDG‐PET findings obtained are consistent with the idea that STN‐DBS modifies the activities of neural circuits involved in motor control.     

Lowered cerebral glucose utilization in amyotrophic lateral sclerosis

Regional cerebral metabolic rates for glucose (rCMRGlc) were analyzed in 19 studies of 12 patients with amyotrophic lateral sclerosis (ALS) by positron emission tomography (PET) with [18F]2-fluoro-2-deoxy-D-glucose. In the 8 ALS patients with upper motor neuron signs, the mean cortical rCMRGlc was significantly lower than in 11 age-matched control subjects (p less than 0.01). The degree of hypometabolism correlated with the duration of the clinical signs and extended throughout the cortex and basal ganglia, but not to the cerebellum. Of the 4 such patients who had repeat PET scans, 3 demonstrated significant subsequent reduction in the rCMRGlc, corresponding to the worsening of the clinical picture. In contrast, 4 ALS patients with disease confined to lower motor neurons and 3 patients with lower motor neuron disease from old paralytic poliomyelitis had normal or near-normal rCMRGlc throughout the brain. Because histological evidence shows no generalized neuronal cell loss in the cortex of ALS patients, including in some cases the primary motor regions, the demonstration of severe generalized hypometabolism in structurally normal cortex indicates that some cortical neurons exist in a state of neuronal nonfunction, rather than cell death, and that anatomoclinical correlations may be more complex. The data also indicate that ALS with upper motor neuron involvement extends beyond the corticospinal tracts and differs in cortical function from the ALS confined to lower motor neurons or the other lower motor neuron disorders.     

Positron emission tomography studies of cerebral glucose metabolism in chronic partial epilepsy

Positron emission tomography (PET) performed with [18F]-2-fluoro-2-deoxy-D-glucose ([18F]FDG) was used to measure local cerebral metabolic rate for glucose (lCMRGlc) interictally in 31 patients with chronic partial epilepsy and 16 age-matched normal subjects. Hypometabolic zones were visualized in 25 patients (81%). Cortical lCMRGlc in hypometabolic zones was within 2 standard deviations of the mean for normal temporal cortex in all but 8 patients. However, in 24 patients asymmetry between the hypometabolic cortex and homologous contralateral cortex was more than 2 standard deviations above the mean cortical asymmetry for normals. There was good correlation between hypometabolic zones and electroencephalogram (EEG) foci in patients with unilateral well-defined EEG foci. Diffuse or shifting EEG abnormalities were often associated with normal PET scans. Of 28 patients who underwent magnetic resonance imaging, 10 showed focal temporal lobe abnormalities corresponding to focal hypometabolism. While the [18F]FDG PET scan cannot currently localize an epileptogenic zone independently, the absence of focal hypometabolism or its presence contralateral to a presumed EEG focus suggests the need for additional electrophysiological data.     

PET和TCD对阿耳茨海默病早期诊断的研究

目的 利用正电子发射计算机断层扫描（ｐｏｓｉｔｒｏｎ ｅｍｉｓｓｉｏｎ ｔｏｍｏｇｒａｐｈｙ,ＰＥＴ）和经颅多普勒超声（ｔｒａｎｓｃｒａｎｉａｌ ｄｏｐｐｌｅｒ,ＴＣＤ）相结合的方法探讨阿耳茨海默病（Ａｌｚｈｅｉｍｅｒ’ｓ ｄｉｓｅａｓｅ,ＡＤ）的早期诊断,以及ＡＤ与脑血液供应之间的关系。方法 ２０例可疑ＡＤ患者和２０例正常对照行ＰＥＴ、ＴＣＤ以及临床神经心理量表检查,对局部脑区葡萄糖代谢率（ｒｅ     

Differences in cerebral blood flow and glucose utilization in vegetative versus locked-in patients

Positron emission tomographic studies of regional cerebral metabolic rate for glucose (rCMRGlc) and cerebral blood flow were performed in 7 vegetative and 3 locked-in patients to determine objectively the level of brain function underlying these clinical states. Cortical gray rCMRGlc in the vegetative patients was 2.73 +/- 0.13 (mean +/- SEM) mg/100 gm/min, less than half the normal value of 6.82 +/- 0.23 (p less than 0.001). Cerebral blood flow exhibited similar but more variable reductions. By contrast, cortical rCMRGlc in the locked-in patients was 5.08 +/- 0.69, a 25% reduction (p less than 0.02) from normal. The massive reduction in vegetative rCMRGlc involved not only the cerebral cortex but also the basal nuclei and cerebellum. Such metabolic hypoactivity has precedent only in deep anesthesia and supports clinical evidence that cerebral cognitive function is lost in the vegetative state, leaving a body that can no longer think or experience pain.     

Decreased cortical glucose metabolism correlates with hippocampal atrophy in Alzheimer''s disease as shown by MRI and PET.

OBJECTIVE: To investigate the relation between atrophy of the hippocampus and parahippocampal gyrus (the % hippocampal area) and cerebral metabolic rate for glucose (CMRGlc) in Alzheimer's disease. METHODS: 13 patients with probable Alzheimer's disease by NINCDS-ADRDA criteria (six men; seven women, mean age 71 years, mini mental state 13.8 (SD 4.6)) and age matched controls were studied. T1 weighted MRI (0.5T) images were used for evaluation of the hippocampal area. With a digitiser system, a percentage of the hippocampal area to the brain (the % hippocampal area) was calculated. Eight patients received another T1 weighted MRI (1.5T) for further evaluation of the minimum thickness of the hippocampus. Regional CMRGlc (rCMRGlc) was measured using PET and the FDG technique. RESULTS: The hippocampal area in patients with Alzheimer's disease was significantly lower than that of controls (P < 0.01). All the cortical rCMRGlc values in patients with Alzheimer's disease were lower than those of controls (P < 0.01). A significant correlation (P < 0.05) was found between the % hippocampal area and rCMRGlc in the temporal lobe, temporoparieto-occipital (TPO) region, and frontal lobe in Alzheimer's disease. There was a significant correlation between minimal hippocampal thickness and ipsilateral TPO metabolism on both sides. CONCLUSION: The ipsilateral correlation between hippocampal atrophy and decreased TPO metabolism in Alzheimer's disease suggests a functional relation and the asymmetries show that Alzheimer's disease is an asymmetric disease in its early stages.     

Changed pattern of regional glucose metabolism during yoga meditative relaxation

Using positron emission tomography (PET), measurements of the regional cerebral metabolic rate of glucose (rCMRGlc) are able to delineate cerebral metabolic responses to external or mental stimulation. In order to examine possible changes of brain metabolism due to Yoga meditation PET scans were performed in 8 members of a Yoga meditation group during the normal control state (C) and Yoga meditative relaxation (YMR). Whereas there were intraindividual changes of the total CMRGlc, the alterations were not significant for intergroup comparison; specific focal changes or changes in the interhemispheric differences in metabolism were also not seen; however the ratios of frontal vs. occipital rCMRGlc were significantly elevated (p less than 0.05) during YMR. These altered ratios were caused by a slight increase of frontal rCMRGlc and a more pronounced reduction in primary and secondary visual centers. These data indicate a holistic behavior of the brain metabolism during the time of altered state of consciousness during YMR.     

Motor correlates of occipital glucose hypometabolism in Parkinson's disease without dementia

OBJECTIVE: To determine whether occipital reduction in regional cerebral glucose metabolism in PD reflects retinal versus nigrostriatal dopaminergic degeneration. We hypothesized that occipital glucose metabolic reduction should be symmetric if parkinsonian retinopathy is responsible for the reduction. METHODS: PD patients without dementia (n = 29; age 63 +/- 10 years) and normal controls (n = 27; age 60 +/- 12 years) underwent [18F]fluorodeoxyglucose PET imaging. Regional cerebral glucose metabolic rates were assessed quantitatively. RESULTS: When compared with normal controls, PD patients showed most severe glucose metabolic reduction in the primary visual cortex (mean -15%, p < 0.001). Occipital glucose metabolic reduction was greater in the hemisphere contralateral to the side of the body affected initially or more severely in PD. There was an inverse correlation between side-to-side asymmetries in finger-tapping performance and occipital glucose metabolic reduction (r = -0.45, p < 0.05; n = 28). The correlation was strongest in patients with a relatively early stage of PD with more unilateral motor impairment (Hoehn and Yahr stage I, r = -0.74, p < 0.01; n = 10). CONCLUSION: The results indicate a pathophysiologic association between nigrostriatal dysfunction and occipital glucose metabolic reduction in PD.     

A perfusion-metabolic mismatch in Sturge-Weber syndrome: a multimodality imaging study

Objective: We combined perfusion weighted imaging (PWI) with 2-deoxy-2[¹⁸F]fluoro-D-glucose (FDG) positron emission tomography (PET) to study the relationship between regional metabolic and perfusion abnormalities and their clinical correlates in children with Sturge-Weber syndrome (SWS). Methods: Fifteen children (age: 0.9–10 years) with unilateral SWS underwent high-resolution PWI and FDG PET prospectively. Regional (lobar) asymmetry indices (AIs) of subcortical white matter (WM) cerebral blood flow (CBF) were correlated with corresponding cortical FDG uptake asymmetries, extent of leptomeningeal vascular malformation and clinical seizure variables. Results: Abnormal cortical glucose metabolism and/or subcortical WM CBF were seen in all lobes affected by vascular malformation and extended to lobes not affected by abnormal pial vessels in 6 patients. Lower CBF was associated with lower cortical glucose metabolism in the temporal, parietal and occipital lobes (p ? 0.02). While decreased perfusion was associated with hypometabolism in most cases, increased regional CBF (found in 6 patients) was commonly associated with relatively mild or no hypometabolism. Ten of 24 cerebral lobes with normal glucose metabolism in the affected hemisphere showed abnormal perfusion. High seizure frequency was associated with severe parieto-occipital hypoperfusion (p ? 0.03), while long duration of epilepsy was related to frontal lobe hypometabolism (p = 0.015). Conclusions: Regional perfusion and cortical metabolic abnormalities can extend beyond lobes affected by leptomeningeal vascular malformations and are related to epilepsy in SWS. Despite a general correlation between perfusion and metabolism, increased WM perfusion with preserved cortical metabolism in overlying cortex is a common pattern of a perfusion/metabolic mismatch. This may represent a disease stage where cortical function is preserved while increased WM perfusion provides collateral drainage of cortex via the deep vein system.     

Metabolic correlates of cognitive function in children with unilateral Sturge–Weber syndrome: Evidence for regional functional reorganization and crowding

To evaluate metabolic changes in the ipsi‐ and contralateral hemisphere in children showing a cognitive profile consistent with early reorganization of cognitive function, we evaluated the regional glucose uptake, interhemispheric metabolic connectivity, and cognitive function in children with unilateral SWS. Interictal 2‐deoxy‐2[¹⁸F]fluoro‐D‐glucose (FDG)‐PET scans of 27 children with unilateral SWS and mild epilepsy and 27 age‐matched control (non‐SWS children with epilepsy and normal FDG‐PET) were compared using statistical parametric mapping (SPM). Regional FDG‐PET abnormalities calculated as SPM(t) scores in the SWS group were correlated with cognitive function (IQ) in left‐ and right‐hemispheric subgroups. Interhemispheric metabolic connectivity between homotopic cortical regions was also calculated. Verbal IQ was substantially (≥10 points difference) higher than non‐verbal IQ in 61% of the right‐ and 71% of the left‐hemispheric SWS group. FDG SPM(t) scores in the affected hemisphere showed strong positive correlations with IQ in the left‐hemispheric, but not in right‐hemispheric SWS group in several frontal, parietal, and temporal cortical regions. Significant positive interhemispheric metabolic connectivity, present in controls, was diminished in the SWS group. In addition, the left‐hemispheric SWS group showed inverse metabolic interhemispheric correlations in specific parietal, temporal, and occipital regions. FDG SPM(t) scores in the same regions of the right (unaffected) hemisphere showed inverse correlations with IQ. These findings suggest that left‐hemispheric lesions in SWS often result in early reorganization of verbal functions while interfering with (“crowding”) their non‐verbal cognitive abilities. These cognitive changes are associated with specific metabolic abnormalities in the contralateral hemisphere not directly affected by SWS.     

Compensatory mechanisms in patients with asymptomatic carotid artery occlusion

Twelve patients with asymptomatic occlusion of one (n = 8) or both (n = 4) internal carotid arteries were examined by positron emission tomography (PET) and transcranial Doppler ultrasound. PET measurements included the determination of the regional cerebral blood flow (rCBF), oxygen extraction ratio (rOER), cerebral metabolic rate of oxygen (rCMRO2), and cerebral metabolic rate of glucose consumption (rCMRGlc). Transcranial Doppler ultrasound (TCD) was used to determine the pathways and efficacy of collateralization via the circle of Willis and included spectrum analysis of flow velocities within the middle and anterior cerebral arteries as well as vasoreactivity tests. In correspondence with ultrasound evidence of a haemodynamically effective intracranial collateral circulation no significant differences between patients and controls were observed for rOER, rCMRO2 and rCMRGlc, but rCBF was globally reduced. Furthermore, in all patients with unilateral carotid occlusion PET excluded side asymmetries of any parameter studied. In contrast, flow velocity parameters measured by TCD were significantly reduced ipsilateral and significantly increased contralateral to the carotid obstruction. Vasodilative capacities, however, remained preserved even in the territory of the occluded carotid system. These data indicate that patients with asymptomatic carotid occlusion compensate by haemodynamic and not by metabolic mechanisms in contrast to symptomatic patients.