Publications by authors named "Aurélien Benoilid"

7 Publications

  • Page 1 of 1

First Case of Human Cerebral Taenia martis Cysticercosis.

J Clin Microbiol 2015 Aug 27;53(8):2756-9. Epub 2015 May 27.

Laboratoire de Parasitologie et de Mycologie Médicale, Plateau Technique de Microbiologie, Hôpitaux Universitaires de Strasbourg, Strasbourg, France Institut de Parasitologie et Pathologie Tropicale, Fédération de Médecine Translationelle, Université de Strasbourg, Strasbourg, France.

Taenia martis is a tapeworm affecting mustelids, with rodents serving as intermediate hosts. The larval stage (cysticercus) has been found before only rarely in humans or primates. We hereby describe a case of cerebral T. martis cysticercosis in a French immunocompetent patient, confirmed by DNA analyses of biopsy material.
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http://dx.doi.org/10.1128/JCM.01033-15DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4508436PMC
August 2015

Relapsing optic neuritis: a multicentre study of 62 patients.

Mult Scler 2014 06 31;20(7):848-53. Epub 2013 Oct 31.

University Hospital, France Clinical Investigation Centre, INSERM 10002, France.

Background: Optic neuritis (ON) may be the first symptom of a central nervous system demyelinating, systemic or infectious disease but few patients experience recurrent episodes and have a negative workup.

Objective: This disorder, named relapsing optic neuritis (RON), is poorly described in the literature and still presents a particular challenge in diagnosis and management.

Methods: We describe the clinical, laboratory, magnetic resonance imaging (MRI) and disability course of RON in a French cohort of 62 patients, based on a multicentre, retrospective, observational study.

Results: In our cohort, we identified two distinct groups of RON patients. The first is characterised by relapsing inflammatory optic neuritis (RION, 68%), which is non-progressive, whereas the second presented as a chronic relapsing inflammatory optic neuritis (CRION, 32%), which is progressive. We have noted more cases with steroid dependence in the CRION group than the RION group (42% vs 10%). The long-term visual prognosis was more severe in CRION patients and neuromyelitis optica-immunoglobulin G (NMO-IgG)-positive patients.

Conclusion: RON is likely a separate entity corresponding to an autoimmune disease that differs from multiple sclerosis (MS), NMO and vasculitis. We provide a new classification system based on a better understanding of RON which could allow an improved management by early treatment of poor prognosis forms.
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http://dx.doi.org/10.1177/1352458513510223DOI Listing
June 2014

Misleading features of neuroimaging and electroencephalography: insulinoma misdiagnosed as temporal lobe epilepsy.

Epileptic Disord 2013 Mar;15(1):93-7

Département de Neurologie, Hôpital Universitaire de Strasbourg, Strasbourg, France.

Epilepsy is a common disorder but diagnosis remains largely clinical. Although MRI and EEG significantly aid the diagnosis of epilepsy, these techniques may also be misleading and indicate abnormalities not related to phenomenology. Consequences of erroneous diagnosis of epilepsy may lead to aggressive and escalating pharmacotherapy with potentially serious side effects. Metabolic disorders, which may mimic epilepsy, should always be considered as they are potentially curable and may be fatal if untreated. We report a case of an insulinoma, misdiagnosed as temporal lobe epilepsy. We highlight the risks associated with misinterpretation of neuroimaging and EEG and outline an approach to differentiate between symptoms of insulinoma or neuroglycopenia and temporal epileptic seizures.
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http://dx.doi.org/10.1684/epd.2013.0556DOI Listing
March 2013

Heroin inhalation-induced unilateral complete hippocampal stroke.

Neurocase 2013 Aug 25;19(4):313-5. Epub 2012 May 25.

Department of Neurology, Strasbourg University Hospital, Strasbourg, France.

A 33-year-old man presented to our clinic with amnesia 48 hours after his first heroin inhalation. Examination showed lateral tongue biting and anterograde amnesia demonstrated by impaired performance on verbal and visual Wechsler Memory Scale-Revised tests carried out 10 days after onset, suggesting hippocampal involvement. Magnetic resonance imaging (MRI) of the brain was performed 48 hours after heroin snorting and evoked cortical laminar necrosis (CLN) of the left hippocampus without vascular abnormality. This is the first description of complete hippocampal CLN as a complication subsequent to acute intranasal heroine abuse. While the pathogenic mechanism remains uncertain, our case provides a very specific MRI lesion pattern and highlights the risk of intranasal heroin uptake-induced neurological complication.
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http://dx.doi.org/10.1080/13554794.2012.667125DOI Listing
August 2013

Mitochondrial myopathy caused by arsenic trioxide therapy.

Blood 2012 May 16;119(18):4272-4. Epub 2012 Mar 16.

Département de Neurologie, Hôpitaux Universitaires de Strasbourg, Hôpital de Hautepierre,1 Avenue Molière, Strasbourg Cedex, France.

Arsenic trioxide (ATO) has been successfully used as a treatment for acute promyelocytic leukemia (APL) for more than a decade. Here we report a patient with APL who developed a mitochondrial myopathy after treatment with ATO. Three months after ATO therapy withdrawal, the patient was unable to walk without assistance and skeletal muscle studies showed a myopathy with abundant cytoplasmic lipid droplets, decreased activities of the mitochondrial respiratory chain complexes, multiple mitochondrial DNA (mtDNA) deletions, and increased muscle arsenic content. Six months after ATO treatment was interrupted, the patient recovered normal strength, lipid droplets had decreased in size and number, respiratory chain complex activities were partially restored, but multiple mtDNA deletions and increased muscle arsenic content persisted. ATO therapy may provoke a delayed, severe, and partially reversible mitochondrial myopathy, and a long-term careful surveillance for muscle disease should be instituted when ATO is used in patients with APL.
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http://dx.doi.org/10.1182/blood-2011-10-385138DOI Listing
May 2012

TDP43-positive intraneuronal inclusions in a patient with motor neuron disease and Parkinson's disease.

Neurodegener Dis 2010 27;7(4):260-4. Epub 2010 Feb 27.

Department of Neurology, Strasbourg University Hospital, Strasbourg, France.

Background: The role of the 43-kDa transactivation-responsive DNA-binding protein (TDP43) in neurodegenerative diseases is not yet clearly established.

Objective: To assess for the first time the presence of TDP43 in a patient with motor neuron disease (MND) and Parkinson's disease (PD).

Methods: A 78-year-old woman developed poorly dopa-responsive parkinsonism without cognitive alteration. Three years later, MND appeared and led to death in less than a year. Neuropathologic examination was performed.

Results: We observed the presence of PD and MND lesions with TDP43-positive cytoplasmic inclusions in the spinal cord and bulbar nuclei but not in the dentate gyrus and neocortex. The MND was characterized by a severe degeneration of bulbar and cervical lower motor neurons. Numerous senile plaques and topographically limited neurofibrillary tangles were also observed.

Conclusion: The mechanisms underlying the rare co-occurrence of PD and MND are still unclear. The assessment of an abnormal reactivity for TDP43 in our case might gain more insight into the pathophysiology of this association of two diseases. Further studies are needed to confirm these findings and to understand the role of TDP43 in neurodegenerative diseases.
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http://dx.doi.org/10.1159/000273591DOI Listing
January 2011