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Biomedical subjects

Y Samson

Publications and source records attributed to Y Samson.

At least 109 records · Page 6Linked to original sources
PubMed1988

Regional specific binding of [11C]RO 15 1788 to central type benzodiazepine receptors in human brain: quantitative evaluation by PET.

The central type benzodiazepine receptors were studied in 17 healthy human subjects with 11C-RO 15 1788 and positron emission tomography (PET). The brain regional distribution of the tracer in eight control studies performed after injection of trace doses of 11C-RO 15 1788 was consistent with that of benzodiazepine receptors. Saturation studies with co-injected cold RO 15 1788 in the remaining subjects showed a dose-dependent decrease of brain radiotracer until full inhibition of specific binding was achieved with doses above 0.1 mg/kg (four studies). Based on the results, a simple method to estimate the specifically bound 11C-RO 15 1788 regionally in a single PET study is proposed, using the data from the full-saturation studies as a stable estimate of the nondisplaceable radioligand concentration. Using this method, it was found that quasiequilibrium between the estimated specifically bound and nondisplaceable components was achieved at times equal to or longer than 20 min after tracer administration. The validity of this method was partly supported by further results, showing a good agreement between the regional specific binding so calculated and postmortem data of receptor density.

Adult↗
PubMed1988

[Dysarthria-clumsy hand syndrome caused by cerebellar infarction].

A 80 year old woman suddenly complained of dysarthria and clumsiness of the right hand. CT scan showed an infarct in the territory of the lateral branch of the right superior cerebellar artery. This dysarthria-clumsy hand syndrome in a patient with paroxysmal atrial fibrillation suggests that the likely cause was an embolus from the heart.

Aged↗
PubMed1987

Utilization of luteinizing hormone-releasing hormone agonist in pulmonary leiomyomatosis.

A patient presenting a recurrent episode of pulmonary leiomyomatosis has been treated with the LH-RH agonist buserelin at a dosage of 200 micrograms tid SC for 7 days, then 500 micrograms SC daily for a total period of 6 months. Basal serum E2 was suppressed during treatment and varied between 62 and 180 pmol/ml (mean, 129.4 +/- 14.5). Pulmonary symptoms completely disappeared during treatment, but no objective regression of the pulmonary lesions was observed. Because of the uncertainty of response of benign metastasizing leiomyomas to castration and because of the reversibility of the medical treatment, LH-RH agonist may be preferred to surgical castration in this pathology.

Adenoma↗
PubMed1987

Cortical hypometabolism and its recovery following nucleus basalis lesions in baboons: a PET study.

The cerebral metabolic rate for glucose was measured serially with positron emission tomography and [18F]fluorodeoxyglucose in five baboons with stereotactic electrocoagulation of the left nucleus basalis of Meynert (NbM). Four days after lesion, a significant metabolic depression was present in the ipsilateral cerebral cortex, most marked in the frontotemporal region, and which recovered progressively within 6-13 weeks. These data demonstrate that adaptive mechanisms efficiently compensate for the cortical metabolic effects of NbM-lesion-induced cholinergic deafferentation. Moreover, unilateral NbM lesions also induced a transient reduction in contralateral cortical metabolic rate, the mechanisms of which are discussed. Explanation of these effects of cholinergic deafferentation in the primate could further our understanding of the metabolic deficits observed in dementia of the Alzheimer's type.

Animals↗
PubMed1986

Crossed cerebellar diaschisis. Further studies.

To investigate further the topographical, clinical and temporal correlates of crossed cerebellar diaschisis (CCD) after supratentorial stroke, 55 patients suffering from a single unilateral ischaemic stroke in the carotid artery territory were studied with the quantitative oxygen-15 steady-state technique and positron tomography. Fourteen patients had one or more follow-up studies, contributing a total of 72 studies. The phenomenon of CCD, defined by depressed oxygen consumption in the contralateral cerebellum, was statistically significant in 58% of the studies. It was more prominent when the supratentorial infarct involved the internal capsule or the cortical mantle extensively, consistent with the hypothesis that it results from destruction of the corticopontocerebellar fibres. Although CCD was associated with the presence of hemiparesis, it also occurred in patients without hemiparesis and was not seen in all those with hemiparesis, suggesting that destruction of the pyramidal tract is neither necessary nor sufficient to induce CCD. Finally, CCD tended to persist over long periods of time after a stroke, pointing towards a transneuronal degeneration possibly akin to crossed cerebellar atrophy as a likely explanation for CCD. Nevertheless, CCD could be seen within hours of a stroke and sometimes disappeared within a few days, suggesting a temporal continuum between early, potentially reversible functional hypometabolism (diaschisis) and irreversible degeneration.

Adult↗
PubMed1986

Effects of thalamic stroke on energy metabolism of the cerebral cortex. A positron tomography study in man.

Positron emission tomography was used to study the effects of unilateral vascular thalamic lesions on cortical oxygen and glucose utilization in 10 patients. There was significant ipsilateral cortex hypometabolism in 9 of the 10 patients, affecting the whole cortical mantle diffusely. The only patient spared was free of neuropsychological deficit at the time of positron emission tomography. In 4 patients, the magnitude of ipsilateral cortical hypometabolism was significantly less at a follow-up PET study, when neuropsychological function had improved. When taken together, the 14 studies showed a significant tendency for the hypometabolism to improve with time after clinical onset. These data suggest that the ipsilateral cortical hypometabolism results from damage to the thalamocortical connections and reflect either loss of nonspecific activating afferences or a degenerative deafferentation-deafferentation process, or both. Its links with the concept of diaschisis are suggested by its tendency to recover. A causal relationship between cortical hypometabolism and neuropsychological deficit, however, although strongly suggested, cannot be firmly established from the present data.

Adult↗
PubMed1986

Local cerebral glucose utilisation in chronic alcoholics: a positron tomographic study.

Using positron tomography, a study of regional cerebral glucose utilisation was performed prospectively in a highly selected group of six neurologically unaffected primary chronic alcoholics. In this group, neuropsychological, behavioural and CT scan anomalies were comparable with those previously reported in more extensive studies. With respect to age-matched control values, cerebral metabolic rate was not significantly modified in the selected cortical, subcortical and cerebellar regions of interest. However, the metabolic regional distribution index, which reflects the distribution pattern of glucose utilisation, was selectively and significantly decreased in the medio-frontal area, pointing to a limbic metabolic dysfunction apparently linked to chronic alcoholism.

Adult↗
PubMed1986

[Cortical hypometabolism after a thalamic lesion in man: positron tomography study].

We used positron emission tomography to study the effects of unilateral vascular thalamic lesions on cortical oxygen or glucose utilisation in 10 patients. There was a significant ipsilateral cortex hypometabolism in 9 of the 10 patients, affecting diffusely the whole cortical mantle. The only patient spared was free of neuropsychological deficit at time of PET study. In 4 patients, the magnitude of ipsilateral cortical hypometabolism was significantly less at follow-up PET study, together with improved neuropsychological function. When plotted altogether, the 14 studies showed a significant tendency for the hypometabolism to improve with time elapsed since clinical onset. On the whole, these data suggest that the ipsilateral cortical hypometabolism reflects an essentially functional alteration an not only a degenerating process. This most likely indicates a cortical deafferentation due to loss of non-specific thalamo-cortical connections, i.e. a phenomenon akin to "diaschisis". However, a causal relationship between cortical hypometabolism and neuropsychological deficit cannot be firmly established from the present data.

Adult↗
PubMed1986

[Isolated sensory deficit of 1 side of the body as a result of a hematoma of the pons].

In a patient with a history of sudden onset of an isolated sensory syndrome of the right side of the body the sensory deficit was exclusively related to lemniscal sensitivity. NMR imaging showed a small hemorrhage in the left paramedian portion of the pontine tegmentum, corresponding precisely to the location of the median lemniscus.

Afferent Pathways↗
PubMed1985

Kinetics and displacement of [11C]RO 15-1788, a benzodiazepine antagonist, studied in human brain in vivo by positron tomography.

The brain regional distribution and kinetics of RO 15-1788, a benzodiazepine (BZD) antagonist labeled with 11C was studied by time-of-flight positron tomography after intravenous injection in four normal human volunteers. In two control studies, there was a high uptake of [11C]RO 15-1788 in gray matter structures initially (brain/blood ratio approximately 3), and subsequent retention that was highest in cerebral cortex, a structure known to have a high density of BZD receptors in vitro. Variation in tissue kinetics of [11C]RO among different gray matter structures may, however, suggest regional differences in binding characteristics or environment of BZD receptors. In two displacement studies, unlabeled RO 15-1788 was injected ten minutes after the radioligand: there was an immediate and marked washout of [11C]brain radioactivity that reached 70% in the occipital cortex with a 0.05 mg/kg dose (indicating a high specific to non-specific binding ratio) but was less prominent with a 0.01 mg/kg dose. These data suggest that [11C]RO 15-1788 may be useful for in vivo mapping of human brain BZD receptors using positron tomography.

Adult↗
PubMed1985

The 15O continuous-inhalation method: correction for intravascular signal using C15O.

Cerebral oxygen metabolism (CMRO2) and fractional extraction (OEF) regional values obtained using the 15O steady-state method and positron-emission tomography (PET) were corrected for the activity remaining in blood vessels (a source of overestimation of the OEF neglected in the simple steady-state model) using an additional scan during continuous inhalation of nontoxic amounts of carbon monoxide labeled with 15O (C15O). The method was applied to ten serial PET studies. In normal tissue, OEF overestimation was 11% +/- 2.6% and 9% +/- 2.0% in gray and white matter, respectively. In pathological tissue, the OEF overestimation was, on average, higher than in normal tissue (28% +/- 17% in the core of lesions), but more variable. In both normal and abnormal tissue, however, it was found that (1) the lower the real OEF, the larger the correction applied, and (2) the correction appears to be particularly necessary in situations of abnormally low OEF. The use of C15O continuous inhalation is a simple, direct, and accurate method for blood-activity correction when the 15O steady-state technique is employed to study pathophysiology.

Aged↗
PubMed1985

Tomographic mapping of brain intracellular pH and extracellular water space in stroke patients.

Functional images of regional intracellular pH (pHi) and of fractional volume of extracellular water (FVECW) were obtained in 10 patients with recent hemispheric infarction (between 10 and 19 days after onset of symptoms) using positron emission tomography (PET). The volume of extracellular water relative to that of total water was evaluated in each pixel of the PET scan 7-8 h after injection of 76Br. The pHi image was calculated from the data obtained after injection of [11C]5,5-dimethyl-2,4-oxazolidinedione and from the FVECW image. Regional CBF, oxygen extraction, and oxygen metabolism were also measured in the same patients. In normal hemisphere, mean +/- SD values for FVECW and pHi were 0.12 +/- 0.01 and 6.86 +/- 0.11, respectively. FVECW was increased in the infarcted area in most patients. pHi was increased in the infarct in seven patients and unchanged in three. The increase in pHi was not correlated with changes in FVECW, CBF, or CMRO2, but there was a significant correlation with the decrease in oxygen extraction fraction in the same region. Thus, the decreased H+ content in the infarcted area was correlated with the occurrence of perfusion in excess of metabolic demand. An alkaline shift in pHi enhances the glycolysis rate and could explain why the glucose metabolism is less affected than the oxygen metabolism in recent cerebral infarction. The pHi measured in the infarct could represent mainly the pHi of phagocytic cells that use aerobic glycolysis to synthesize hydrogen peroxide.

Adult↗
PubMed1985

Subcortical dementia. Frontal cortex hypometabolism detected by positron tomography in patients with progressive supranuclear palsy.

The dementia associated with progressive supranuclear palsy (PSP) is considered to be subcortical because the cerebral cortex, unlike the subcortical structures, is usually free from major neuropathological lesions; the characteristic symptoms point to a dysfunction of the prefrontal lobe. The regional cerebral metabolic rate of glucose (rCMR Glu) was studied by positron emission tomography and 18F-fluoro-2-deoxyglucose18FDG in 6 patients presumed to have PSP and was compared with values found in 8 control subjects of similar age. The results obtained showed a highly significant rCMR Glu decrease in the prefrontal cortex of our patients. The loss of several subcortical afferents to prefrontal cortex may be responsible for the frontal cortical hypometabolism present in PSP.

Aged↗
PubMed1985

[In vivo study of central serotoninergic receptors in man using positron tomography].

In an attempt to characterize in vivo the central serotonergic (5-HT2) receptors in humans with positron emission tomography (PET), we have used 11C-labeled-ketanserin, a seratonergic antagonist that has high affinity and selectivity for the 5-HT2 receptors in vitro. Earlier in vivo studies in rats had demonstrated a preferential accumulation of 3H-ketanserin in the frontal cortex relative to cerebellum, in accordance with known differences in density of 5-HT2 receptor in these two brain structures (5-HT2 receptors are dense in frontal cortex and sparse or absent in cerebellum). In rats, tracer accumulation in frontal cortex represented specific binding of 3H-ketanserin to 5-HT2 receptors in vivo as demonstrated by inhibition, saturation, and displacement studies. In 5 control subjects, we found a statistically significant retention of 11C-ketanserin in frontal cortex relative to cerebellum after intravenous injection of a tracer dose of the radioligand, suggesting specific in vivo binding of 11C-ketanserin to frontal cortex. To substantiate this hypothesis, we studied 4 subjects administered unlabeled chlorpromazine (CPZ) intramuscularly in therapeutic amounts (75 mg) two hours before the PET study. Pretreatment with CPZ decreased significantly the retention of 11C-ketanserin by the frontal cortex, indicating that almost total occupation of the ketanserin receptors by CPZ had been achieved prior to the injection of the radioligand. Despite these positive results, both the duration and the magnitude of tracer retention by frontal cortex in control subjects were much smaller than was reported in rats, presumably indicating lower specific binding, higher nonspecific binding, and faster drug metabolism in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain↗
PubMed1985

[Regional hemodynamic and metabolic consequences of temporo-sylvian anastomosis. Study of 15 patients by positron emission tomography].

Cerebral Blood Flow (CBF), Oxygen Extraction Fraction, and Oxygen utilization (CMRO2) have been studied in 15 patients before and After Extra-Intracranial Arterial bypass (EIAB), using PET and 150 steady-State Inhalation technique. Fourteen patients had carotid artery obstructive lesions and the last one a middle cerebral artery occlusion. In the whole group of patients, both CBF and CMRO2 increased significantly on both cerebral hemispheres after the EIAB. This effect was more marked in patients with extensive occlusive disease of neck vessels. This metabolic improvement afforded by EIAB in our patients suggests that long-standing hemodynamic failure may induce a metabolic depression that's still potentially reversible by surgical revascularization. On the other hand, improvement of focal CBF abnormalities depends, in our patients, upon the preoperative coupling of CBF-CMRO2 (mainly misery perfusion syndrome) as reported earlier.

Adult↗
PubMed1985

[Severe stenoses and persistent occlusions of the middle cerebral artery: hemodynamic and metabolic consequences studied by positron tomography].

Using positron emission tomography and the 15O continuous inhalation technique, we have measured the regional cerebral blood flow (rCBF) oxygen extraction fraction (rOEF) and oxygen consumption (rCMRO2) of non-infarcted tissue in six patients with either tight stenosis (N = 3) or occlusion (N = 3) of the trunk of the middle cerebral artery (MCA); these arterial lesions were shown to be persistent on late and/or repeated angiograms. The patients were studied 1 to 6 months after their last cerebral ischemic event. The data were analyzed in 4 cm2 regions of interest (fig. 1) and were compared to age-matched control values. Regional right/left ratios were tested for significance individually by comparison to 95 p. 100 confidence limits found in control subjects. We found a significant reduction in mean rCBF in the affected MCA territory; concomitantly, there was a lesser decrease in rCMRO2 significant only in the peri-sylvian area; this was associated with a moderate but significant increase in rOEF in the same areas (Table II, fig. 2 and 3). Individually, the reduction in rCBF and the increased rOEF were significant in 5/6 and 2/6 patients, respectively (Table III). These data indicate that rCBF is decreased distal to persistent hemodynamic MCA obstruction in most patients. This hypoperfusion appears due in part to a mild degree of cerebral ischemia (as demonstrated by the occurrence of "misery perfusion"), indicating inadequate perfusion pressure distal to the MCA obstruction. This was associated with a metabolic depression of the cortex possibly resulting from either neuronal loss, or deactivation (diaschisis), or long-standing hemodynamic local failure or any combination of the three.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗