Brief report: attention performance in autism and regional brain metabolic rate assessed by positron emission tomography.
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Publications and source records attributed to N Sicotte.
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Positron emission tomography (PET) measurements of cerebral glucose use were made in 18 patients with generalized anxiety disorder (GAD) during a passive viewing task off medication, and an active vigilance viewing task before and after medication or placebo treatment. In the passive viewing task, patients with GAD were compared with 15 normal controls. A significant difference in pattern of absolute brain metabolism was found. Patients showed lower absolute metabolic rates in basal ganglia and white matter. Relative metabolism was increased in the left inferior area 17 in the occipital lobe, right posterior temporal lobe, and the right precentral frontal gyrus. Significant left-right asymmetry of the parahippocampal gyri was not found in patients with GAD. An active vigilance task resulted in activation of relative basal ganglia metabolism in patients. Benzodiazepine therapy resulted in decreases in absolute metabolic rates for cortical surface, limbic system, and basal ganglia and was not associated with normalization of patterns of glucose metabolism. Change in anxiety scores was significantly correlated with change in limbic system and basal ganglia for the placebo group. The normal-anxious difference in the basal ganglia and the change seen in this region after benzodiazepine treatment are suggestive of a role in anxiety for this structure.
Positron emission tomography with fludeoxyglucose F 18 was used to assess cortical metabolic rate during an olfactory memory task in six patients with dementia of the Alzheimer type. Metabolic activity was compared with that of both age-matched controls performing the olfactory task and controls resting with their eyes closed. Patients had lower metabolic rates in the anterior portion of the medial-temporal cortex than did controls, and the difference was greatest between patients and the controls performing the memory task. This region is known to receive a large olfactory input and has been implicated in the encoding of human memory. Normal controls resting with their eyes closed had significantly lower metabolic rates in this area when compared with normal controls performing the task. Our results are consistent with those of earlier reports of temporal lobe decreases in metabolic rate and extend them through the examination of areas salient to the behavioral loss.
This study is the first report on the effects of total sleep deprivation (about 32 h) on regional cerebral glucose metabolism during wakefulness in man, using positron emission tomography (PET) with F-18 deoxyglucose (FDG). Sleep deprivation leads to a significant reorganization of regional cerebral metabolic activity, with relative decreases in the temporal lobes and increases in visual cortex. Absolute glucose metabolic measurements indicate a decrease in thalamus, basal ganglia, white matter, and cerebellum. No overall decrease in whole brain metabolism was noted after sleep deprivation. As expected, sleep deprivation significantly reduced visual vigilance as assessed by the continuous performance test and this decrease was correlated significantly with reduced metabolic rate in thalamic, basal ganglia, and limbic regions.
Eight women with bulimia and eight age- and sex-matched normal control subjects were studied with positron emission tomography using [18F]-fluorodeoxyglucose (FDG) as a tracer of brain metabolic rate. Subjects performed a visual vigilance task during FDG uptake. In control subjects, the metabolic rate was higher in the right hemisphere than in the left, but patients with bulimia did not have this normal asymmetry. Lower metabolic rates in the basal ganglia, found in studies of depressed subjects, and higher rates in the basal ganglia, reported in a study of anorexia nervosa, were not found. This is consistent with the suggestion that bulimia is a diagnostic grouping distinct from these disorders.
Local cerebral uptake of glucose labelled with fluorine-18 was measured by positron emission tomography in 13 patients with schizophrenia and 37 right-handed volunteers. Patients received no medication for a minimum of 31 days and a mean of 30 weeks. The subjects were administered the labelled deoxyglucose just after the beginning of a 32-minute sequence of blurred numbers as visual stimuli for the Continuous Performance Test. In normal controls, task performance was associated with increases in glucose metabolic rate in the right frontal and right temporoparietal regions; occipital rates were unchanged. Patients with schizophrenia showed both absolutely and relatively reduced metabolic rates in the frontal cortex and in the temporoparietal regions compared with normal controls.
EEG topography was compared in patients with senile dementia of the Alzheimer's type (SDAT), aged normal controls, and young normal controls to assess regional differences. The square root of absolute power was determined for each frequency using a Fast Fourier Transform (FFT). The normal elderly group showed a reduction in all 4 frequency bands, delta, theta, alpha and beta, at each of 32 leads when compared to the young controls. Z-transformation of the data revealed differences in topography. Older normals showed significantly greater mid-parietal and left mid-temporal delta than the younger controls. A similar pattern was seen for theta activity. Elderly controls showed relatively less occipital alpha and greater mid-parietal alpha. Beta activity demonstrated these same significant topographic differences. The elderly/SDAT comparison was significant for delta only. SDAT patients were characterized by a marked delta asymmetry in temporal regions which was not seen in the elderly normals.
The cerebral metabolic rate of glucose was measured during nighttime sleep in 36 normal volunteers using positron emission tomography and fluorine-18-labeled 2-deoxyglucose (FDG). In comparison to waking controls, subjects given FDG during non-rapid eye movement (NREM) sleep (primarily stages 2 and 3) showed about a 23% reduction in metabolic rate across the entire brain. This decrease was greater for the frontal than temporal or occipital lobes, and greater for basal ganglia and thalamus than cortex. Subjects in rapid eye movement (REM) sleep tended to have higher cortical metabolic rates than waking subjects. The cingulate gyrus was the only cortical structure to show a significant increase in glucose metabolic rate in REM sleep in comparison to waking. The basal ganglia were relatively more active on the right in REM sleep and symmetrical in NREM sleep.
This paper reports the preliminary results of a combined twin and family study of anorexia nervosa. Fifty-six per cent of the 25 female monozygotic (MZ) twin pairs and 5% of the 20 female dizygotic (DZ) twin pairs were concordant for anorexia nervosa. Nearly 5% of other female first degree relatives also had a history of anorexia nervosa. Analysis of data from the Eating Disorders Questionnaire (EDI) given to the twins and data as to weight loss, length of amenorrhoea and other characteristics of anorexia nervosa, together with the twin and family data, supports the hypothesis that genetic factors are very significant in the aetiology of anorexia nervosa. Analysis of this data using established techniques of psychiatric genetics suggested that up to 80% of the variance in liability to anorexia nervosa may be accounted for by genetic factors. The problems of this type of analysis are discussed as is the background to the genetics of weight and appetite control. A genetic/environmental model accounting for the features of anorexia nervosa is proposed.
The regional cerebral effects of an anxiolytic (clorazepate) in 20 patients with generalized anxiety disorder were assessed using 16-channel electroencephalogram (EEG) power spectral estimate maps of the left hemisphere. Patients were studied with double-blind random assignment to placebo or drug and were assessed at baseline, day 7, and day 14 with EEG and Hamilton Anxiety Ratings. Ten age- and sex-matched normal controls were also tested. Hamilton Anxiety Ratings were decreased significantly more in the drug group than in the placebo group. Topographic maps of EEG activity revealed decreases in occipital alpha and parietal delta, together with increases in posterior frontal (central EEG leads) and parietal beta. Decreases in delta are consistent with a lack of sedation; the reciprocal beta increases in parietal cortex are similarly consistent. This pattern of regional EEG changes in the direction of alert attentiveness, together with individual differences, observed in frontal/parietal and occipital alpha activity, suggests the importance of at least these two cortical regions for anxiolytic action. Differences between patients with generalized anxiety disorder and normals were restricted to the occipital and temporal regions. These results suggest the importance of multilead recording in assessing EEG correlates of drug action.