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Thomas TOURDIAS




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Cursus:
MD: Radiology, Bordeaux (2008)
PhD: Neurosciences, Bordeaux (2011)
Post doc: Stanford University, CA, USA (2013)
Professeur des Universités - Praticien Hospitalier; PU PH (2016)






80 publication(s) depuis Décembre 2006:


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2012 | Cerebrovasc Dis   IF 2.7
Atraumatic nonaneurysmal sulcal subarachnoid hemorrhages: a diagnostic workup based on a case series.
Renou P , Tourdias T , Fleury O , Debruxelles S , Rouanet F , Sibon I

Abstract:
INTRODUCTION: Atraumatic and nonaneurysmal sulcal subarachnoid hemorrhage (sSAH) is a rare type of cerebrovascular disease with various etiologies previously reported in small case reports. In this study, we propose to analyze clinical presentations, imaging patterns and etiologies in a large case series of such patients in order to propose a diagnostic workup. METHODS: We retrospectively analyzed clinical and radiological data of consecutive patients with a diagnosis of atraumatic and nonaneurysmal sSAH, admitted to our institution between 2008 and 2011. All patients had both computed tomography (CT) and magnetic resonance imaging (MRI) as a part of their initial evaluation. RESULTS: 30 patients (18 women and 12 men, mean age: 60 years) were identified. The main clinical symptoms at presentation were focal and transient neurological deficit (n = 22) and thunderclap headache (n = 10). Four patients had progressive headache and 4 other had partial or generalized epileptic seizures. MRI abnormalities associated with sSAH were prior hemorrhages, microbleeds, severe leukoencephalopathy and hemosiderosis suggesting cerebral amyloid angiopathy (CAA; n = 9), vasogenic edema in parieto-occipital areas compatible with a posterior reversible encephalopathy syndrome (PRES; n = 3), cortical venous thrombosis (n = 2) and concomitant acute cortical stroke (n = 3). Other underlying causes of sSAH, not diagnosed on MRI, were reversible cerebral vasoconstriction syndrome (RCVS) based on clinical criteria and conventional angiography (n = 4), angiitis diagnosed by skin biopsy (n = 1), vascular malformation diagnosed on CT and digital subtraction angiographies (n = 3), and overanticoagulation (n = 1). Four cases remained unresolved. CONCLUSION: This study confirmed that sSAH is a rare condition related to a wide spectrum of etiologies. Combination of brain MRI and magnetic resonance angiography and eventually digital subtraction angiography allowed the identification of an underlying etiology for 87% of patients. CAA, RCVS and PRES represented more than 50% of the etiological mechanisms. Among older patients, sSAH was mainly related to CAA while in younger patients, RCVS represented the most frequent etiology.




12/2011 | Neuro Oncol   IF 10.1
Descriptive epidemiology of CNS tumors in France: results from the Gironde Registry for the period 2000-2007.
Baldi I , Gruber A , Alioum A , Berteaud E , Lebailly P , Huchet A , Tourdias T , Kantor G , Maire JP , Vital A , Loiseau H

Abstract:
An increase in the incidence of CNS tumors has been observed in many countries in the last decades. The reality of this trend has been much debated, as it has happened during a period when computer-assisted tomography and MRI have dramatically improved the detection of these tumors. The Gironde CNS Tumor Registry provides here the first data on CNS tumor incidence and trends in France for all histological types, including benign and malignant tumors, for the period 2000-2007. Incidence rates were calculated globally and for each histological subtype. For trends, a piecewise log-linear model was used. The overall annual incidence rate was found to be 17.6/100 000. Of this rate, 7.9/100 000 were neuroepithelial tumors and 6.0/100 000 were meningiomas. An overall increase in CNS tumor incidence was observed from 2000 to 2007, with an annual percent change (APC) of +2.33%, which was explained mainly by an increase in the incidence of meningiomas over the 8-year period (APC = +5.4%), and also more recently by an increase in neuroepithelial tumors (APC = +7.45% from 2003). The overall increase was more pronounced in women and in the elderly, with an APC peaking at +24.65% in subjects 85 and over. The increase in the incidence rates we observed may have several explanations: not only improvements in registration, diagnosis, and clinical practice, but also changes in potential risk factors.




11/2011 | Lancet Neurol   IF 28.8
DWI-FLAIR mismatch for the identification of patients with acute ischaemic stroke within 4.5 h of symptom onset (PRE-FLAIR): a multicentre observational study.
Thomalla G , Cheng B , Ebinger M , Hao Q , Tourdias T , Wu O , Kim JS , Breuer L , Singer OC , Warach S , Christensen S , Treszl A , Forkert ND , Galinovic I , Rosenkranz M , Engelhorn T , Kohrmann M , Endres M , Kang DW , Dousset V , Sorensen AG , Liebeskind DS , Fiebach JB , Fiehler J , Gerloff C

Abstract:
BACKGROUND: Many patients with stroke are precluded from thrombolysis treatment because the time from onset of their symptoms is unknown. We aimed to test whether a mismatch in visibility of an acute ischaemic lesion between diffusion-weighted MRI (DWI) and fluid-attenuated inversion recovery (FLAIR) MRI (DWI-FLAIR mismatch) can be used to detect patients within the recommended time window for thrombolysis. METHODS: In this multicentre observational study, we analysed clinical and MRI data from patients presenting between Jan 1, 2001, and May 31, 2009, with acute stroke for whom DWI and FLAIR were done within 12 h of observed symptom onset. Two neurologists masked to clinical data judged the visibility of acute ischaemic lesions on DWI and FLAIR imaging, and DWI-FLAIR mismatch was diagnosed by consensus. We calculated predictive values of DWI-FLAIR mismatch for the identification of patients with symptom onset within 4.5 h and within 6 h and did multivariate regression analysis to identify potential confounding covariates. This study is registered with ClinicalTrials.gov, number NCT01021319. FINDINGS: The final analysis included 543 patients. Mean age was 66.0 years (95% CI 64.7-67.3) and median National Institutes of Health Stroke Scale score was 8 (IQR 4-15). Acute ischaemic lesions were identified on DWI in 516 patients (95%) and on FLAIR in 271 patients (50%). Interobserver agreement for acute ischaemic lesion visibility on FLAIR imaging was moderate (kappa=0.569, 95% CI 0.504-0.634). DWI-FLAIR mismatch identified patients within 4.5 h of symptom onset with 62% (95% CI 57-67) sensitivity, 78% (72-84) specificity, 83% (79-88) positive predictive value, and 54% (48-60) negative predictive value. Multivariate regression analysis identified a longer time to MRI (p<0.0001), a lower age (p=0.0009), and a larger DWI lesion volume (p=0.0226) as independent predictors of lesion visibility on FLAIR imaging. INTERPRETATION: Patients with an acute ischaemic lesion detected with DWI but not with FLAIR imaging are likely to be within a time window for which thrombolysis is safe and effective. These findings lend support to the use of DWI-FLAIR mismatch for selection of patients in a future randomised trial of thrombolysis in patients with unknown time of symptom onset. FUNDING: Else Kroner-Fresenius-Stiftung, National Institutes of Health.




11/2011 | AJNR Am J Neuroradiol   IF 3.3
Perianeurysmal brain inflammation after flow-diversion treatment.
Berge J , Tourdias T , Moreau JF , Barreau X , Dousset V

Abstract:
BACKGROUND AND PURPOSE: Flow-diverter stents are an alternative treatment for challenging and recurrent aneurysms. Thrombosis of the sac is thought to induce perianeurysmal brain inflammation, but such phenomena have never been studied in flow-diverter devices. We developed imaging data to explain the clinical exacerbation of symptoms after flow-diversion treatment. MATERIALS AND METHODS: Seventeen patients with unruptured aneurysms were treated by using a flow-diverter device. Clinical symptoms and angiographic and MR imaging features were recorded before and after treatment, during both the acute and chronic phases, to look for inflammatory reaction. RESULTS: Seven of the 17 patients (41%) showed a delayed clinical aggravation of symptoms posttreatment consisting of a headache (n = 7) with aggravation of pre-existing compressive symptoms (n = 4) and the appearance of compressive symptoms (n = 1). This clinical deterioration was transient; it was observed between 3 and 15 days posttreatment and resolved by day 30. MR imaging revealed signs highly suggestive of perianeurysmal inflammation with vasogenic edema and blood-brain barrier breakdown. The association between MR imaging inflammatory features and clinical aggravation was statistically significant. Large aneurysmal size and its proximity to surrounding brain tissue were predictive of this inflammatory reaction after flow diversion. CONCLUSIONS: The main finding of the series is that MR imaging-defined perianeurysmal inflammation is observed with a high frequency after treatment of unruptured aneurysms with flow diverters and is, in most cases, associated with a transient clinical deterioration.




10/2011 | j Neuroradiol   IF 3.3
[Grading of adults primitive glial neoplasms using arterial spin-labeled perfusion MR imaging].
Canale S, Rodrigo S , Tourdias T , Mellerio C , Perrin M , Souillard R , Oppenheim C , Meder JF

Abstract:
PURPOSE: We investigated the relationship between tumor blood-flow measurement based on perfusion-imaging by arterial spin-labeling (ASL) and histopathologic findings in adults' primitive glial tumours. PATIENTS AND METHODS: Thus, 40 primitive brain tumors (8 low-grade and 32 high-grade gliomas according to the Sainte-Anne classification) were imaged using pulsed (n=19) or continuous (n=21) ASL. Relative cerebral blood flow (rCBF=tumoral blood flow/normal cerebral blood flow) between high- and low-grade gliomas were compared. RESULTS: Using pulsed ASL, differences in mean rCBF were observed in high- and low-grade gliomas although no significant (respectively 1.95 and 1.5). Using continuous ASL, mean rCBF were significantly higher for high-grade than for low-grade gliomas (P<0.05). High-grade gliomas could be discriminated using a CBF threshold of 1.18, with a sensitivity of 88%, specificity of 60%, predictive positive value of 88%, and predictive negative value of 60%. CONCLUSION: ASL-based perfusion provides a quantitative, non-invasive alternative to dynamic susceptibility contrast perfusion MR methods for evaluating CBF. ASL is a suitable method for gliomas initial staging and could be useful to identify intermediate tumoral evolution.




08/2011 | Exp Neurol   IF 4.6
Adapted focal experimental autoimmune encephalomyelitis to allow MRI exploration of multiple sclerosis features.
Tourdias T , Hiba B , Raffard G , Biran M , Nishiguchi T , Aussudre J , Franconi JM , Brochet B , Petry KG , Dousset V

Abstract:
We aimed to determine an optimal protocol for inducing a focal inflammatory lesion within the rat brain that could be large enough for an easier MRI monitoring while still relevant as a multiple sclerosis (MS) like lesion. We adapted a two-hit model based on pre-sensitization of the Lewis rat with myelin oligodendrocyte protein (MOG) followed by stereotaxic injection of pro-inflammatory cytokines (TNFalpha+IFNgamma) within the internal capsule. We compared the following two strategies to increase focal lesion development for an easier MR translation: (1) a higher sensitization step (MOG50) or (2) a higher cytokine step with lower sensitization (MOG25). Control animals were administered only cytokines without MOG pre-sensitization. Animals were followed with T2, diffusion and T1 post gadolinium weighted images at 1, 3 and 7days following cytokine injection. Immunostaining was performed at the same time points for macrophages (ED1), myelin (MBP and Luxol Fast Blue) and blood brain barrier integrity (IgG). At day 1, the focal lesions depicted with T2-weighted images were very similar among groups and related to vasogenic edema (high apparent diffusion coefficient (ADC), gadolinium enhancement and IgG extravasation) induced by cytokines irrespective of the pre-sensitization step. Then, at day 3, MOG50 rats developed statistically larger T2 lesions than MOG25 and control rats that were correlated with inflammatory cell accumulation. At day 7, MOG50 rats also showed larger T2 lesions than MOG25 and control rats, together with loss of anisotropy that were correlated with demyelination. In contrast, MOG25 and control rats developed similar MR lesions decreasing over time and almost undetectable at day 7. We conclude that with a high pre-sensitization step, the focal lesion can be monitored by MRI whose signal reflects some features of a MS-like lesion, i.e. edema, inflammatory cell accumulation and later demyelination.




24/05/2011 | Neurology   IF 8.7
Fenestration of the internal carotid artery mimicking floating thrombus on CT and MR angiography.
Tourdias T , Berge J , Menegon P , Sibon I

Abstract:





02/2011 | AJNR Am J Neuroradiol   IF 3.3
Final cerebral infarct volume is predictable by MR imaging at 1 week.
Tourdias T , Renou P , Sibon I , Asselineau J , Bracoud L , Dumoulin M , Rouanet F , Orgogozo JM , Dousset V

Abstract:
BACKGROUND AND PURPOSE: Stroke volume, an increasingly used end point in phase II trials, is considered stationary at least 30 days after the ictus. We investigated whether information conveyed by MR imaging measurements of the 'final' infarct volume could be assessed as early as the subacute stage (days 3-6), rather than waiting for the chronic stage (days 30-45). MATERIALS AND METHODS: Ninety-five patients with middle cerebral artery stroke prospectively included in a multicenter study underwent MR imaging during the first 12 hours (MR imaging-1), between days 3 and 6 (MR imaging-2), and between days 30 and 45 (MR imaging-3). We first investigated the relationship between subacute (FLAIR-2) and chronic volumes (FLAIR-3), by using a linear regression model. We then tested the relationship between FLAIR volumes (either FLAIR-2 or FLAIR-3) and functional disability, measured by the mRS at the time of MR imaging-3, by using logistic regression. The performances of the models were assessed by using the AUC in ROC. RESULTS: A linear association between log FLAIR-2 and log FLAIR-3 volumes was observed. The proportion of FLAIR-3 variation, explained by FLAIR-2, was high (R(2) = 81%), without a covariate that improved this percentage. Both FLAIR-2 and FLAIR-3 were independent predictors of mRS (OR, 0.79 and 0.73; 95% CI, 0.64-0.97 and 0.56-0.96; P = .026 and .023). The performances of the models for the association between either FLAIR volume and mRS did not differ (AUC = 0.897 for FLAIR-2 and 0.888 for FLAIR-3). CONCLUSIONS: Stroke damage may be assessed by a subacute volume because subacute volume predicts the 'true' final volume and provides the same clinical prognosis.




2011 | J Neuroinflamm   IF 5.7
Differential aquaporin 4 expression during edema build-up and resolution phases of brain inflammation.
Tourdias T , Mori N , Dragonu I , Cassagno N , Boiziau C , Aussudre J , Brochet B , Moonen C , Petry KG , Dousset V

Abstract:
BACKGROUND: Vasogenic edema dynamically accumulates in many brain disorders associated with brain inflammation, with the critical step of edema exacerbation feared in patient care. Water entrance through blood-brain barrier (BBB) opening is thought to have a role in edema formation. Nevertheless, the mechanisms of edema resolution remain poorly understood. Because the water channel aquaporin 4 (AQP4) provides an important route for vasogenic edema resolution, we studied the time course of AQP4 expression to better understand its potential effect in countering the exacerbation of vasogenic edema. METHODS: Focal inflammation was induced in the rat brain by a lysolecithin injection and was evaluated at 1, 3, 7, 14 and 20 days using a combination of in vivo MRI with apparent diffusion coefficient (ADC) measurements used as a marker of water content, and molecular and histological approaches for the quantification of AQP4 expression. Markers of active inflammation (macrophages, BBB permeability, and interleukin-1beta) and markers of scarring (gliosis) were also quantified. RESULTS: This animal model of brain inflammation demonstrated two phases of edema development: an initial edema build-up phase during active inflammation that peaked after 3 days (ADC increase) was followed by an edema resolution phase that lasted from 7 to 20 days post injection (ADC decrease) and was accompanied by glial scar formation. A moderate upregulation in AQP4 was observed during the build-up phase, but a much stronger transcriptional and translational level of AQP4 expression was observed during the secondary edema resolution phase. CONCLUSIONS: We conclude that a time lag in AQP4 expression occurs such that the more significant upregulation was achieved only after a delay period. This change in AQP4 expression appears to act as an important determinant in the exacerbation of edema, considering that AQP4 expression is insufficient to counter the water influx during the build-up phase, while the second more pronounced but delayed upregulation is involved in the resolution phase. A better pathophysiological understanding of edema exacerbation, which is observed in many clinical situations, is crucial in pursuing new therapeutic strategies.




2010 | Cerebrovasc Dis   IF 2.7
Reliability of the ECASS radiological classification of postthrombolysis brain haemorrhage: a comparison of CT and three MRI sequences.
Renou P , Sibon I , Tourdias T , Rouanet F , Rosso C , Galanaud D , Drier A , Coudert M , Deltour S , Crozier S , Dormont D , Samson Y

Abstract:
BACKGROUND: Postthrombolysis brain haemorrhagic transformations (HT) are often categorized with the CT-based classification of the European Cooperative Acute Stroke Study (ECASS). However, little is known about the reliability of this classification and its extension to MRI. Our objective was to compare the inter- and intraobserver reliability of this classification on CT and 3 MRI sequences. METHODS: Forty-three patients with postthrombolysis HT on CT or at least 1 of the 3 MRI sequences: fluid-attenuation inversion recovery (FLAIR), diffusion-weighted imaging (DWI), and T2* gradient recalled echo (T2*GRE) were selected. Twelve control patients without any bleeding were added to avoid a bias based on a pure HT-positive cohort. Each series of images were independently classified with the ECASS method by 6 blinded observers. Inter- and intraobserver reproducibility was categorized from poor to excellent depending on kappa values. RESULTS: The inter- and intraobserver overall concordance of the classification was good for T2*GRE, DWI and CT (kappa > 0.6) and moderate for FLAIR (kappa < 0.6). The interobserver concordance for parenchymal haematomas was excellent for T2*GRE (kappa > 0.8) and moderate for CT, FLAIR and DWI. CONCLUSION: The T2*GRE sequence is the most reproducible method to categorize postthrombolysis HT and has an excellent reliability for the severe parenchymal haematoma category, suggesting that this sequence should be used to assess HT in thrombolytic therapy trials.