11 research outputs found

    Imaging findings of intraventricular and ependymal lesions.

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    National audienceIntraventricular and ependymal lesions comprise a wide spectrum of tumoral, cystic, vascular, infectious and inflammatory disorders. With respect to tumoral and cystic diseases, the location, age and CT and MRI patterns are the main factors for diagnosis. The MRI findings of infectious diseases are supported by the clinical history, immune status and laboratory findings. Intracranial associated lesions may be very helpful for the diagnosis of Sturge-Weber, subependymal giant cell astrocytoma and systemic diseases, such as sarcoidosis and histiocytosis. Intraventricular vascular lesions are rare but present typical features on neuroimaging. The aim of this review is to provide a detailed description of these disorders with an emphasis on the key imaging findings and to generate a narrow differential diagnosis. We present a diagnostic approach based on the solid or cystic aspect of the intraventricular focal mass, its origin from the ventricular wall or choroid plexus and its location within the ventricular system. We also propose a differential diagnosis for ependymal dissemination: the ependymal enhancement may be due to ventriculitis from adjacent parenchymal lesions, the ependymal spread of tumors or infectious or inflammatory/systemic diseases

    Diffusion-weighted MRI in acute stroke within the first 6 hours: 1.5 or 3.0 Tesla?

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    International audienceOBJECTIVES: To compare the sensitivity and specificity of 1.5-T and 3.0-T diffusion-weighted MRI (DWI) to detect hyperacute ischemic stroke lesions. METHODS: We blindly reviewed the DWI of 135 acute stroke patients and 34 controls performed at 1.5 T (n = 108) or 3.0 T (n = 61). The stroke patients all had subsequently proved carotid territory ischemic stroke and were imaged within the first 6 hours after stroke onset. Four readers (2 neuroradiologists and 2 stroke neurologists) blinded to clinical data and magnetic field strength recorded the presence of ischemic lesions on DWI and apparent diffusion coefficient (ADC) maps if necessary. Sensitivity, specificity, and false-negative rates were computed. Signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR), and DWI contrasts were calculated at both field strengths. RESULTS: The accuracy of DWI in stroke diagnosis was superior at 1.5 T (98.8%) than at 3.0 T (90.9%, p = 0.03). The sensitivity decreased from 99.1% at 1.5 T to 92.5% at 3.0 T (p = 0.06) and the specificity from 97.8% to 84.1% (p = 0.002). ADC map readings did not improve accuracy, sensitivity, or specificity. The false-negative rate was 0.6% at 1.5 T and 6.1% at 3.0 T. Type of readers, stroke severity, and type of the coil did not affect diagnosis value. SNR and CNR were significantly higher at 3 T (p < 0.0001) but DWI contrast was lower (p = 0.04). CONCLUSIONS: Blind reading by 4 experts of a large series of images shows that 1.5-T diffusion-weighted MRI (DWI) is better than 3.0-T DWI for the imaging of hyperacute stroke during the therapeutic window of thrombolysis

    Manifestations neurologiques de la maladie de Behçet [Neurological manifestations of Behçet's disease]

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    National audienceNeurological manifestations of Behçet's disease (BD) occur in 5.3 to more than 50% of patients. They are divided into two major forms: "parenchymal" lesions, which include mainly meningoencephalitis as opposed to "extra-parenchymal" lesions (i.e. cerebral venous thrombosis and arterial aneurysms). Myelitis or peripheral neuropathy is exceptional. The neuro-Behçet syndrome (NBS) should be considered in the setting of neurological manifestations, particularly headache and pyramidal signs, in a young man diagnosed with BD. However, its recognition may be difficult when neurological manifestations are the presenting features of BD (one third of cases), and requires a thorough knowledge of clinical manifestations and morphological lesions. Thus, parenchymal NB lesions classically exhibit inflammatory characteristics on MRI and are located at the meso-diencephalic junction and in the brainstem, rarely with a supratentorial extension. Meningitis is not systematically associated, and may be absent in about 30% of cases. The pathogenesis of these lesions is incompletely understood, but inflammatory infiltrates include mainly neutrophils and activated T cells (mainly Th17). Differential diagnoses include infectious diseases (herpes, listeria, tuberculosis), and inflammatory diseases (i.e. multiple sclerosis and sarcoidosis). A prompt recognition of NBS should lead to initiate adequate therapies in order to limit the risk of sequelae, relapses or death.Les manifestations neurologiques de la maladie de Behçet (MB) sont retrouvées chez 5,3 à plus de 50 % des patients selon les séries. Elles sont séparées en deux grands types d'atteintes : les formes " parenchymateuses ", regroupant les atteintes intracérébrales (méningo-encéphalites), par opposition aux formes " extra-parenchymateuses ", incluant les thromboses veineuses cérébrales et les anévrismes artériels. Les atteintes médullaires et les atteintes périphériques sont exceptionnelles. Un syndrome de neuro-Behçet (NB) doit être évoqué devant la survenue de troubles neurologiques, en particulier des céphalées et une atteinte pyramidale, chez un homme jeune suivi pour une MB. Néanmoins, sa reconnaissance est difficile lors des formes inaugurales (un tiers des cas), et nécessite une connaissance des lésions morphologiques. Ainsi, les lésions de NB parenchymateux sont classiquement inflammatoires en IRM et situées à la jonction méso-diencéphalique, ainsi que dans le tronc cérébral, avec rarement une extension sus-tentorielle. Une méningite associée n'est pas systématique, absente dans environ 30 % des cas. La physiopathologie de ces lésions est imparfaitement connue, mais l'infiltrat inflammatoire est majoritairement constitué de polynucléaires neutrophiles et de lymphocytes T activés (notamment de type Th17). Les principaux diagnostics différentiels concernent les pathologies infectieuses (herpès, listériose, tuberculose), et inflammatoires (sclérose en plaques, sarcoïdose) qui doivent être systématiquement évoquées. Le traitement du NB doit être initié dès son diagnostic afin d'en limiter le risque de séquelles, de rechute ou de décès

    Is radiological evaluation as good as computer-based volumetry to assess hippocampal atrophy in Alzheimer's disease?

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    International audienceINTRODUCTION: Hippocampus volumetry is a useful surrogate marker for the diagnosis of Alzheimer's disease (AD). Our purpose was to compare visual assessment of medial temporal lobe atrophy made by radiologists with automatic hippocampal volume and to compare their performances for the classification of AD, mild cognitive impairment (MCI) and cognitively normal (CN). METHODS: We studied 30 CN, 30 MCI and 30 AD subjects. Six radiologists with two levels of expertise performed two readings of medial temporal lobe atrophy. Medial temporal lobe atrophy was evaluated on coronal three-dimensional T1-weighted images using Scheltens scale and compared with hippocampal volume obtained using a fully automatic segmentation method (Spearman's rank coefficient). RESULTS: Visual assessment of medial temporal lobe atrophy was correlated with hippocampal volume (p < 0.01). Classification performances between MCI converter and CN was better using volumetry than visual assessment of non-expert readers whereas classification of AD and CN did not differ between visual assessment and volumetry except for the first reading of one non-expert (p = 0.03). CONCLUSIONS: Visual assessment of medial temporal lobe atrophy by radiologists was well correlated with hippocampal volume. Radiological assessment is as good as computer-based volumetry for the classification of AD, MCI non-converter and CN and less good for the classification of MCI converter versus CN. Use of Scheltens scale for assessing hippocampal atrophy in AD seems thus justified in clinical routine

    Extensive basal ganglia edema caused by a traumatic carotid-cavernous fistula: a rare presentation related to a basal vein of Rosenthal anatomical variation

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    International audienceThe authors report a very rare presentation of traumatic carotid-cavernous fistula (CCF) with extensive edema of the basal ganglia and brainstem because of an anatomical variation of the basal vein of Rosenthal (BVR). A 45-year-old woman was admitted to the authors' institution for left hemiparesis, dysarthria, and a comatose state caused by right orbital trauma from a thin metal rod. Brain MRI showed a right CCF and vasogenic edema of the right side of the brainstem, right temporal lobe, and basal ganglia. Digital subtraction angiography confirmed a high-flow direct CCF and revealed a hypoplastic second segment of the BVR responsible for the hypertension in inferior striate veins and venous congestion. Endovascular treatment was performed on an emergency basis. One month after treatment, the patient's symptoms and MRI signal abnormalities almost totally disappeared. Basal ganglia and brainstem venous congestion may occur in traumatic CCF in cases of a hypoplastic or agenetic second segment of the BVR and may provoke emergency treatment

    MRI features of intra-axial histiocytic brain mass lesions

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    International audienceTo describe MRI features, including diffusion-weighted imaging (DWI), magnetic resonance spectroscopy (MRS), and perfusion-weighted imaging (PWI), of intra-axial tumour-like presentations of four different subtypes of histiocytosis

    Long-term white matter changes after severe traumatic brain injury: a 5-year prospective cohort.

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    International audienceBACKGROUND AND PURPOSE: Extensive white matter damage has been documented in patients with severe traumatic brain injury, yet how this damage evolves in the long term is not well understood. We used DTI to study white matter changes at 5 years after traumatic brain injury. MATERIALS AND METHODS: There were 8 healthy control participants and 13 patients with severe traumatic brain injury who were enrolled in a prospective observational study, which included clinical assessment and brain MR imaging in the acute setting (< 6 weeks) and 2 years and 5 years after injury. Only subjects with mild to moderate disability or no disability at 1 year were included in this analysis. DTI parameters were measured in 20 different brain regions and were normalized to values obtained in an age-matched control group. RESULTS: In the acute setting, fractional anisotropy was significantly lower in the genu and body of the corpus callosum and in the bilateral corona radiata in patients compared with control participants, whereas radial diffusivity was significantly (P < .05) higher in these tracts. At 2 years, fractional anisotropy in these tracts had further decreased and radial diffusivity had increased. No significant changes were detected between 2 and 5 years after injury. The baseline radial diffusivity and fractional anisotropy values in the anterior aspect of the brain stem, genu and body of the corpus callosum, and the right and left corona radiata were significantly (P < .05) associated with neurocognitive sequelae (including amnesia, aphasia, and dyspraxia) at year 5. CONCLUSIONS: DTI changes in major white matter tracts persist up to 5 years after severe traumatic brain injury and are most pronounced in the corpus callosum and corona radiata. Limited structural change is noted in the interval between 2 and 5 years
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