Publications by authors named "Genevieve Fourcade"
Background: Cerebral amyloid angiopathy (CAA) can be associated with primary vasculitis of small/medium-sized leptomeningeal and cortical arteries, called CAA-related inflammation (CAA-ri).
Objective: To compare hemorrhagic and diffusion-weighted imaging (DWI) MRI features in CAA and CAA-ri.
Methods: We prospectively scored in a consecutive CAA and CAA-ri cohort: presence/number of chronic intracerebral hemorrhage (ICH), cerebral microbleeds (CMB), and cortical superficial siderosis (CSS) on initial T2*-weighted imaging, and DWI lesions on both initial and follow-up imaging.
Background: Decreased cerebrospinal fluid (CSF) amyloid-β 1-40 (Aβ40) and amyloid-β 1-42 (Aβ42) and increased total and phosphorylated tau (t-tau, p-tau) concentrations have been described in cerebral amyloid angiopathy (CAA).
Objective: Our aim was to analyze these biomarkers in patients with CAA-related inflammation (CAA-I).
Methods: We prospectively recruited nine patients with acute phase CAA-I fulfilling Chung criteria.
Background: FDG-PET in ALS most typically demonstrates a primary (and sometimes also supplementary) motor cortex hypometabolism, often associated with more diffuse cortical hypometabolism involving mostly the dorsolateral prefrontal cortex, the medial and lateral premotor cortices, and the bilateral insular cortex involvement. In ALS-FTD, extensive temporal hypometabolism is seen in addition to severe diffuse frontal hypometabolism.
Methods: This study analyses FDG-PET findings in 6 ALS patients and 4 ALS-FTD patients.
Brain FDG-PET after radiation therapy is classically used to differentiate between tumor recurrence and radiation-related tumor necrosis. Little is known about FDG-PET in patients with radiation-induced leukoencephalopathy without radiological aspect of necrosis. We present a 69-year-old woman who had preventive whole brain radiation after a diagnosis of paraneoplastic Lambert-Eaton syndrome related to small cell lung cancer Five months after radiation therapy, she developed radiation-induced leukoencephalopathy manifested by ataxia.
View Article and Find Full Text PDFBackground And Purpose: Laminopathies arise through mutations in genes encoding Lamin A/C (LMNA) or associated proteins. They cause 4 different groups of disorders with diverse severity and often overlapping features: diseases of striated muscle (leading to muscular or cardiac involvement), peripheral neuropathy, lipodystrophy syndromes, and accelerated aging disorders.
Summary Of Case: We report on a familial case of atypical Werner syndrome (a progeroid syndrome with Werner syndrome phenotype but without typical RECQL2 mutation) presenting with acute ischemic cerebral disease or peripheral artery disease associated with diffuse atherosclerosis, attributable to transmission of a novel LMNA mutation.