Publications by authors named "Chedru F"

Introduction: Crossed anarthria cases are uncommon and rather old.

Observation: We report the case of a right-handed 55-year-old man who presented crossed pure anarthria due to a hemorrhage in the premotor cortex (feet of F1 and F2) and in the high part of Pierre-Marie's quadrangle.

Conclusion: The study of different tasks (articulation, verbal fluency, direct object word-generation from a verb) showed a dissociated lateralisation of his language.

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Background And Purpose: The usual onset of intramedullary spinal cord metastases at an advanced stage of cancer disease explains that surgical removal of such lesions is rarely performed. We tried to define the place for surgery in the management of such lesions.

Methods: We report the observation of a 52-year-old male patient presenting with a metastasis of the conus medullaris revealing a lung cancer.

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Four patients with a stroke developed micrographia. In two patients, the condition was pure and in the two other patients it was associated with signs of writer's cramp. We conclude that infarct of the left lenticular nucleus could either mimic pure micrographia similar to that of Parkinson's disease or micrographia associated with dystonia.

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BACKGROUND-The use of intima-media thickness (IMT) as an outcome measure in observational studies and intervention trials relies on the view that it reflects early stages of atherosclerosis and cardiovascular risk. There is little knowledge concerning the relation between IMT and brain infarction (BI). METHODS AND RESULTS-We investigated the relation of IMT with BI and its subtypes in 470 cases and 463 controls.

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Background And Purpose: Nitric oxide (NO) synthesized by endothelial constitutive NO synthase (ecNOS) plays a key role in vascular regulation and atherosclerosis. Little is known concerning the role of the ecNOS gene (NOS3) as a risk factor for brain infarction (BI). Our aim was to investigate the relation between the Glu298Asp polymorphism in exon 7 of NOS3 with BI and its subtypes.

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A diabetic 66 year old man who presented with pilomotor seizures in his right hemibody is described. The seizures recurred with an increasing frequency, leading to a status-like condition associated with Korsakoff's syndrome. An EEG was performed and several electroclinical seizures were recorded.

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Factor XIII catalyzes the formation of covalent bounds between fibrin monomers, thus stabilizing the fibrin clot and increasing its resistance to fibrinolysis. The frequency of a frequent Val34Leu polymorphism in the FXIII A-subunit gene has been shown to be lower in patients with myocardial infarction or venous thrombosis than in controls, whereas it was higher in patients with hemorrhagic stroke than in controls. Our aim was to study the relation between brain infarction (BI) and the FXIII Val34Leu polymorphism in 456 patients consecutively recruited with a BI confirmed by MRI, and 456 matched controls.

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We report five cases of superficial siderosis of the central nervous system. All patients developed progressive deafness and cerebellar ataxia associated with pyramidal tract signs or mental deterioration. The cerebrospinal fluid examinations usually revealed an elevated protein level, without other abnormalities.

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Objective: To evaluate the clinicopathologic features and prognostic factors of 100 patients with chronic inflammatory demyelinating polyneuropathy (CIDP).

Methods: Comparison of clinical and biopsy findings with functional score evaluated an average of 6 years after referral.

Results: CIDP followed a relapsing course in 14% of the patients and a progressive course in 45%.

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Familial hemiplegic migraine (HM) is an autosomal dominant migraine with aura. In 20% of HM families, HM is associated with a mild permanent cerebellar ataxia (PCA). The CACNA1A gene encoding the alpha1A subunit of P/Q-type voltage-gated calcium channels is involved in 50% of unselected HM families and in all families with HM/PCA.

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Background And Purpose: Cerebral venous thrombosis (CVT) is an infrequent condition with a large variety of causes. However, in 20% to 35% of cases, no cause is found. We studied coagulation parameters, including activated protein C resistance associated with factor V gene mutation (factor V Leiden) and anticardiolipin antibodies, in a large series of patients with CVT with or without identified cause or risk factor.

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Objective: To determine whether migraine is a risk factor for ischaemic stroke in young women.

Design: A case-control study.

Setting: Five hospitals in Paris and suburbs.

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Subependymomas are uncommon, benign, slowly growing lesions usually located in the fourth ventricle. Their morphology is characteristic, but their histogenesis remains controversial. Seven cases observed in our laboratory over a period of 7 years are reported.

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Background And Purpose: An association between atrial septal aneurysm and embolic events has been suggested. Atrial septal aneurysm has been shown to be associated with patent foramen ovale and, in some reports, with mitral valve prolapse. These two latter cardiac disorders have been identified as potential risk factors for ischemic stroke.

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In two patients with Waldenström's macroglobulinaemia complicated with peripheral neuropathy, purified monoclonal immunoglobulin M showed antibody activity specifically directed against vimentin, a major polypeptide of mesenchymal cell cytoskeleton and therefore in Schwann's cell. The neuropathy was of the sensory-motor type. It was improved in one case by plasma exchanges combined with chemotherapy.

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Twelve patients with transient global amnesia (TGA) had prior migraines (six classical and six common). In three patients, classic migrainous phenomena accompanied TGA, and in nine patients severe headache accompanied the amnestic attack. Migrainous vascular dysfunction in the dominant posterior cerebral artery territory could explain TGA: (1) The pathophysiology and transient nature of TGA have led many to postulate posterior circulation vascular disease; migraine is a vascular disorder with a posterior circulation bias.

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A case of neuromyopathy due to chronic chloroquine intoxication is reported. The neuromyopathy developped 9 months after malaria suppression therapy with chloroquine was started. The clinical picture was that of a peripherical neuropathy in the lower limbs and of a generalized myasthenic syndrome.

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