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F Viader

Publications and source records attributed to F Viader.

At least 19 recordsLinked to original sources
PubMed2005

Using voxel-based morphometry to map the structural changes associated with rapid conversion in MCI: a longitudinal MRI study.

Capturing the dynamics of gray matter (GM) atrophy in relation to the conversion from mild cognitive impairment (MCI) to clinically probable Alzheimer's disease (AD) would be of considerable interest. In this prospective study we have used a novel longitudinal voxel-based method to map the progression of GM loss in MCI patients over time and compared converters to non-converters. Eighteen amnestic MCI patients were followed-up for a predefined fixed period of 18 months and conversion was judged according to NINCDS-ADRDA criteria for probable AD. Each patient underwent a high-resolution T1-weighted volume MRI scan both at entry in the study and 18 months later. We used an optimal VBM protocol to compare baseline imaging data of converters to those of non-converters. Moreover, to map GM loss from baseline to follow-up assessment, we used a modified voxel-based morphometry (VBM) procedure specially designed for longitudinal studies. At the end of the follow-up period, seven patients had converted to probable AD. Areas of lower baseline GM value in converters mainly included the hippocampus, parahippocampal cortex, and lingual and fusiform gyri. Regions of significant GM loss over the 18-month follow-up period common to both converters and non-converters included the temporal neocortex, parahippocampal cortex, orbitofrontal and inferior parietal areas, and the left thalamus. However, there was significantly greater GM loss in converters relative to non-converters in the hippocampal area, inferior and middle temporal gyrus, posterior cingulate, and precuneus. This accelerated atrophy may result from both neurofibrillary tangles accumulation and parallel pathological processes such as functional alteration in the posterior cingulate. The ability to longitudinally assess GM changes in MCI offers new perspectives to better understand the pathological processes underlying AD and to monitor the effects of treatment on brain structure.

Aged↗
PubMed2005

[Quantitative relationships between ADC and perfusion changes in acute ischemic stroke using combined diffusion-weighted imaging and perfusion MR (DWI/PMR)].

UNLABELLED: MR-based diffusion- and perfusion-weighted imaging (DWI/PWI) has become the standard imaging technique to assess the individual brain pathophysiological status in acute ischemic stroke. The finding of a "mismatch" with larger PWI than DWI abnormality is thought to reflect the presence of tissue at-risk of infarction, i.e., penumbra. However, there has been no detailed study of the quantitative relationships between perfusion and diffusion changes in stroke patients. According to the experimental concept of penumbra, the ADC would be expected to remain unchanged despite decreasing perfusion until a critical threshold is reached. We have tested this hypothesis directly in man. METHODS: DWI/PWI was performed in 7 patients with MCA territory stroke within 4-10 hrs from onset. Mismatch was defined on diffusion and rMTT maps, and circular ROIs were positioned within the ADC lesion (D), the mismatch area (M), and the normal appearing cortex (N); mirror ROIs were also obtained, and affected/unaffected ratios for ADC and rCBF were computed for each ROI. RESULTS: The mean (+/-1 SD) ADC ratios were 0.60 +/- 0.09, 0.95 +/- 0.10 and 1.02 +/- 0.04 in L, M and N, respectively; the corresponding rCBF ratios were 0.32 +/- 0.12, 0.75 +/- 0.14 and 0.97 +/- 0.09, respectively. The relationship was non-linear, with the rCBF but not the ADC ratio for M being significantly lower (p < 0.01) than that for N. A threshold for decline in ADC was apparent around 0.50 rCBF ratio. COMMENT: These results directly document in man that the ADC declines only after hypoperfusion has reached a certain degree (about 50%), consistent with the concept of the ischaemic penumbra.

Acute Disease↗
PubMed2004

[At the boundary between normal aging and Alzheimer disease].

Accurately predicting the development of probable Alzheimer's disease (AD) early in the course of the disease would have major implications. Hence, the pre-dementia stage of AD has become a major topic of current research. Amnestic 'mild cognitive impairment' (MCI) has recently emerged as the most convenient avenue to address this Issue, since most of MCI patients will progress to AD, at a rate of 10% to 15% per Year, suggesting that MCI represents the clinical manifestation of incipient AD (Petersen et al., 2001). However, all MCI patients would probably not convert to AD, at least in the near future, so that the Issue of prospective longitudinal studies is to detect specific indices of rapid conversion. In this paper, we focus on longitudinal studies using either neuropsychology, or morphological or functional neuroimaging to find predictive markers allowing to distinguish those MCI patients that rapidly convert to AD from those that do not develop the disease during the follow-up period. Whereas functional neuroimaging, and more specifically FDG-PET, seems particularly accurate to predict AD, the combination of multiple approaches is likely to be a promising avenue.

Aging↗
PubMed2003

Mild cognitive impairment: Can FDG-PET predict who is to rapidly convert to Alzheimer's disease?

Patients with mild cognitive impairment (MCI) were assessed, and a metabolic profile associated with conversion to AD at 18-month follow-up was sought. As compared with nonconverters (n = 10), converters (n = 7) had lower fluorodeoxyglucose uptake in the right temporoparietal cortex (p = 0.02, corrected for cluster size), without individual overlap. Awaiting replication in an independent sample, these findings suggest that among patients with MCI, fluorodeoxyglucose PET may accurately identify rapid converters.

Alzheimer Disease↗
PubMed2001

Semantic acquisition without memories: evidence from transient global amnesia.

Transient global amnesia (TGA), characterised by a profound anterograde amnesia, is a model of interest to study the acquisition of novel meanings independent of episodic functioning. Three patients were tested during a TGA attack, two in the early recovery phase and the third during the acute phase of TGA, with a semantic priming task involving a restructuring process of conceptual knowledge. During TGA, all patients demonstrated priming effects. Results obtained the day after the episode with the same task showed that these effects persisted at least one day. Episodic memory seems not to be critical for the formation of novel connections among unrelated semantic representations, in accordance with Tulving's model of memory, i.e. episodic memory is not necessary for the acquisition of semantic information.

Acute Disease↗
PubMed2001

Voxel-based mapping of brain hypometabolism in permanent amnesia with PET.

In this study, we used voxel-based mapping methods to compare the resting cerebral metabolic rate of glucose (CMRglc) measured with PET in five patients with permanent amnesia (three with chronic Wernicke-Korsakoff and two with postanoxia syndrome) to that of nine healthy age-matched subjects. We assessed (i) a group pattern of relative hypometabolism; and (ii) the consistency of this group pattern, if any, in individual subjects, according to etiology. The results from the group analysis documented that permanent amnesia is associated with hypometabolism in the thalamus, posterior cingulate cortex, and mesial prefrontal cortex (near the anterior cingulate gyrus), bilaterally, as well as in the left supramarginal and middle temporal gyri. The individual analysis showed that this group pattern was found in essentially each patient, regardless of the cause of amnesia. Thus, permanent amnesia is subtended by dysfunction in structures belonging to Papez/limbic circuits as well as in left-hemisphere areas typically concerned with verbal functions, probably through a mechanism of thalamo-cortical disconnection and possibly involved in retrograde amnesia. The use of a voxel-based method allowed us to map a common network of synaptic dysfunction in a neuropsychological syndrome regardless of etiology. Our results indicate that this should be a powerful method in functional neuropsychology.

Adult↗
PubMed2001

Aluminium increases xanthine oxidase activity and disturbs antioxidant status in the rat.

The mechanisms responsible for the neurotoxic effects of Al remain poorly understood. In order to determine whether Al promotes oxidative stress in vivo, we measured the enzymatic activity of xanthine oxidase (XO), superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione-S-transferase (GST) and glutathione reductase (GR) in four groups of rats after eight days of intraperitoneal administration of variable concentrations of Al (0, 5, 10, and 15 mg/kg body weight, respectively). XO activity was measured in both plasma and liver samples, and the activities of the remaining enzymes were further determined in the brain and red blood cells (RBC). The most significant changes were observed in XO and GPX activities, that were enhanced and depressed, respectively. In both instances, the enzyme activities were correlated with Al concentrations, either positively (XO) or negatively (GPX). Enhancement of XO and inhibition of GPX activity may lead to the accumulation of intermediate toxic compounds such as hydrogen peroxide and hydroxyl radicals, since SOD activity is increased as well. The latter finding must be taken with some caution because previous studies have shown contradictory results in this field. Our data suggest that Al toxicity could be mediated by its action on both pro- and anti-oxidant enzymes. The biological significance of these findings remains to be established.

Aluminum↗
PubMed2001

Disorders in intentional gestural organization in Alzheimer's disease: combined or selective impairment of the conceptual and production systems?

This study examines disorders which affect the intentional gestural organization in Alzheimer's disease. An original and prospective protocol which assessed both the conceptual and production systems (with reference to the Roy and Square model 1985) was presented to 16 patients with Alzheimer's disease (mild to moderate dementia) and 40 healthy elderly subjects. Our study showed impairment of both systems in the Alzheimer's patients group. Two patients presented reverse performance profiles, which were characterized in one case by preservation of the conceptual system and impairment of the production system and in the other by the reverse dissociation. The findings demonstrated that disorders in the intentional gestural organization in Alzheimer's disease usually affect both the conceptual and production systems. The hypothesis concerning the existence of two functionally distinct systems underlying the organization of intentional body movement was corroborated (1) by a lack of significant correlation between the scores obtained in the assessment of the two systems and (2) by the demonstration of the double dissociation.

Aged↗
PubMed2001

[Contribution of positron emission tomography to functional neuroimaging in Alzheimer's disease].

When combined with cognitive investigations, functional neuroimaging methods such as positron emission tomography allow to depict the neural substrates that underlie the neuropsychological alterations in Alzheimer's disease. Capitalising on the variance in both cognitive performances and resting cerebral metabolic rate of glucose (CMRGlc) in Alzheimer's disease, it is possible to correlate these two quantitative variables on a pixel-by-pixel basis and to generate maps showing the significant correlations in stereotaxic space. Some examples using this approach in the domain of memory disorders are presented in this brief review. We notably show that the localisation of the significant correlations differs from one memory system to another, as evaluated by clinical memory tasks. This approach also unravels the compensatory mechanisms that take place with evolution of the disease. Over and above its interest in clinical neuropsychology, this method constitutes a new source of inferences complementary to the classic activation paradigm in normal subjects, as the latter identifies the cerebral structures that are involved with, but not necessarily indispensable for, the normal execution of the task. This approach highlights the interest of combining functional neuroimaging and neuropsychology to better understand the neural substrates of cognitive deficits in both patients with memory disorders and elderly normal subjects.

Alzheimer Disease↗
PubMed2000

Nitrous oxide anesthesia-associated myelopathy.

BACKGROUND: The role of nitrous oxide exposure in neurologic complications of subclinical cobalamin deficiency has been reported, but few cases are well documented. OBSERVATION: Two weeks after surgery for prosthetic adenoma, a 69-year-old man developed ascending paresthesia of the limbs, severe ataxia of gait, tactile sensory loss on the 4 limbs and trunk, and absent tendon reflexes. After a second surgical intervention, the patient became confused. Four months after onset, the patient had paraplegia, severe weakness of the upper limbs, cutaneous anesthesia sparing the head, and confusion. Moderate macrocytosis, low serum B12 levels, and a positive Schilling test result led to the diagnosis of pernicious anemia. Results of electrophysiologic examinations showed a diffuse demyelinating neuropathy. Magnetic resonance imaging of the spinal cord disclosed hyperintensities of the dorsal columns on T2-weighted images. CONCLUSIONS: Pernicious anemia can result in severe neurologic symptoms with only mild hematologic changes. The role of nitrous oxide anesthesia in revealing subclinical B12 deficiency must be emphazised. Magnetic resonance imaging of the spinal cord might be helpful in making the diagnosis.

Adenoma↗
PubMed2000

Atrophy of the corpus callosum correlates with white matter lesions in patients with cerebral ischaemia.

Many studies of white matter high signal (WMHS) on T2-weighted MRI have disclosed that it is related to cerebral ischaemia and to brain atrophy. Atrophy of the corpus callosum (CC) has also been studied in relation to ischaemia. Our objective was to test the hypothesis that CC atrophy could be due to ischaemia. We therefore assessed CC, WMHS and brain atrophy in patients with risk factors without strokes (the risk factor group) and in those with infarcts (the infarct group), to investigate the relationships between these factors. We studied 30 patients in the infarct group, 14 in the risk factor group, and 29 normal subjects. Using axial T1-weighted MRI, cortical atrophy and ventricular enlargement (brain atrophy) were visually rated. Using axial T2-weighted MRI, WMHS was assessed in three categories: periventricular symmetrical, periventricular asymmetrical and subcortical. Using the mid-sagittal T1-weighted image, the CC was measured in its anterior, posterior, mid-anterior and mid-posterior portions. In the normal group, no correlations were noted between parameters. In the infarct group, there were significant correlations between CC and brain atrophy, and between CC atrophy and WMHS. After removing the effects of age, gender and brain atrophy, significant correlations were noted between some CC measures and subcortical WMHS. In the risk factor group, there were significant correlations between CC and brain atrophy and between CC atrophy and WMHS. After allowance for age, gender and brain atrophy, significant correlations between some CC measures and periventricular WMHS remained. The hypothesis that CC atrophy could be due to cerebral ischaemia was supported by other analyses. Namely, for correlations between the extent of infarcts and partial CC atrophy in patients with anterior middle cerebral artery (MCA) and with posterior MCA infarcts, there were significant correlations between the extent of infarct and mid-anterior CC atrophy in the former, and posterior CC atrophy in the latter. Our findings could indicate that CC atrophy is associated with cerebral ischaemia.

Adult↗
PubMed1999

Relationships between striatal dopamine denervation and frontal executive tests in Parkinson's disease.

Indirect evidence from human and monkey investigations supports the idea that impaired frontal tasks in Parkinson's disease (PD) may result from striato-frontal disruption caused by dopamine (DA) denervation of the caudate nucleus. To directly investigate this hypothesis, we used PET with 11C-S-Nomifensine (11C-S-NMF), a sensitive marker of striatal DA denervation, in 10 non-demented PD patients in whom two frontal executive tests, the object alternation (OA) and the conditional associative learning (CAL) tasks, thought to reflect mainly set-shifting/inhibition and planning, respectively, were given. In addition, the central executive function of verbal working memory was assessed with the Brown Peterson paradigm (BPP). We found a highly significant correlation between right caudate 11C-S-NMF specific binding and OA performance, less significant and reverse-direction correlations between CAL performance and putamen 11C-S-NMF binding, and no significant correlation with BPP performance. Thus, caudate DA denervation may subtend poor set-shifting/inhibition process in PD. Our results also point to distinct and complex relationships between striatal DA and specific frontal tasks.

Adult↗
PubMed1999

Voxel-based mapping of irreversible ischaemic damage with PET in acute stroke.

Objective mapping of irreversible tissue damage in the acute stage of ischaemic stroke would be useful for prognosis and in assessing the efficacy of therapeutic manoeuvres in impeding extension of infarction. From our database of 30 patients studied with 15O-PET within 5-18 h after onset of first-ever middle cerebral artery territory stroke, we extracted a subgroup of 19 survivors (age 74.6 +/- 8.5 years) in whom late CT coregistered with PET was available to determine final infarct topography. By means of a voxel-based analysis of the PET data, we determined putative thresholds for irreversible tissue damage as the lower limit of the 95% confidence interval calculated from all voxels within the ultimately non-infarcted brain parenchyma ipsilateral to the insult. The following values were found: 8.43 ml/100 ml/min, 0.87 ml/100 ml/min, 1.64 ml/100 ml, 0.27 and 2.21/min, for cerebral blood flow (CBF), oxygen consumption (CMRO2), blood volume (CBV), oxygen extraction fraction and the ratio CBF : CBV, respectively. Voxels below these thresholds occurred significantly more frequently in the final infarct region than in the non-infarcted parenchyma for CBF and CMRO2 (P = 0.016 and P = 0.0045, respectively, Wilcoxon test), but not for the other PET variables. Furthermore, with both CBF and CMRO2, the percentage of irreversible tissue damage voxels in the affected hemisphere relative to the opposite hemisphere was significantly positively correlated to both the volume of final infarct and the neurological outcome at 2 months (all P < 0.005, Spearman ranked test). These findings validate our voxel-based CBF and CMRO2 thresholds for probabilistic mapping of irreversible tissue damage within the 5-18 h interval after stroke onset; however, whether they would be applicable to earlier intervals remains to be determined. Transfer of our procedure for determination of irreversible tissue damage thresholds to other imaging modalities such as single proton emission computed tomography and diffusion-weighted MRI should be straightforward.

Aged↗
PubMed1999

Episodic memory in transient global amnesia: encoding, storage, or retrieval deficit?

OBJECTIVES: To assess episodic memory (especially anterograde amnesia) during the acute phase of transient global amnesia to differentiate an encoding, a storage, or a retrieval deficit. METHODS: In three patients, whose amnestic episode fulfilled all current criteria for transient global amnesia, a neuropsychological protocol was administered which included a word learning task derived from the Grober and Buschke's procedure. RESULTS: In one patient, the results suggested an encoding deficit, and in two others, a storage deficit. CONCLUSIONS: The encoding/storage impairment concerning anterograde amnesia documented in our patients stands in clear contrast with the impairment in retrieval which must underly the retrograde amnesia that also characterises transient global amnesia. This dissociation in turn favours the idea of a functional independence among the cognitive mechanisms that subserve episodic memory.

Aged↗
PubMed1998

[Ataxic hemiparesis with cerebellar dysarthria due to an opercular lesion].

A 63 year-old-man, with an opercular infarct had a motor deficit with ataxic hemiparesis and cerebellar dysarthria. The motor deficit disappeared, but the cerebellar signs remained after three months. A voice instrumental analysis confirmed the cerebellar pattern of the dysarthria. CT and MRI showed the opercular lesion and the normality of the cerebellum and the pons. A volumic MRI analysis precised the localisation and the volume of the lesion. The oxygen consumption (CMRO2) was measured with PET and showed no cerebellar diaschisis. We propose that, in this case, the cerebellar dysarthria is the orofacial ataxic component of the hemiparesis. We suggest that it is related to disruption of the cortico-cerebellar tract, connecting the right orofacial frontal area of the primary motor cortex with the paravermal segment of the left cerebellar hemisphere.

Ataxia↗
PubMed1997

Plasma superoxide dismutase and glutathione peroxidase activity in sporadic amyotrophic lateral sclerosis.

To determine the possible role of oxydative stress in the pathology of amyotrophic lateral sclerosis (SALS), we measured the plasma activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX), together with GPX and malone dialdehyde (MDA, a marker of lipoperoxydation) plasma concentrations in a sample of 21 SALS patients and 7 normal control (NC) subjects. MDA concentration and SOD activity were significantly higher, whereas GPX activity was significantly lower in SALS patients than in NC. Increased MDA concentration provides indirect confirmation of excess lipoperoxydation. Increased plasma SOD activity might reflect the involvement of extra-cellular SOD (SOD3), a hitherto unreported finding in SALS. Impaired GPX activity, which has already been found in red blood cells and brain tissue of SALS patients, might play a part in the pathogenesis of this disease.

Adult↗