Olivier Felician

Publications (47) View all

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  Available from: Olivier Felician

  Article: [Use of CSF biomarkers in the diagnosis of Alzheimer's disease in clinical practice].

  L Koric, O Felician, M Ceccaldi
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  ABSTRACT: INTRODUCTION: The diagnosis of Alzheimer's disease (AD) currently relies on clinical criteria that are primarily based on the presence of an amnestic syndrome of the mesial temporal lobe type. In recent years, new diagnostic tools have been developed, such as the possibility of measuring a set of proteins directly involved in the pathophysiological process of AD. A profile suggestive of AD has been defined, characterized by decreased beta-amyloid peptide, combined with increased Tau protein and phopho-Tau. STATE OF KNOWLEDGE: According to current data available in the medical literature, the potential usefulness of CSF biomarkers in the common forms of AD fulfilling usual clinical criteria remains modest. In contrast however, they could be of significant help in the diagnosis of early-onset AD, in particular in atypical forms with prominent non-memory impairment (involving vision, language or behavior). In addition, due to their close relationship with the pathological process, they bring useful prognosis information upon the aggressiveness of the disease. CONCLUSION AND PERSPECTIVE: Taken together, in the current state of knowledge, use of CSF biomarkers in clinical practice should first be recommended for the assessment of early-onset cognitive disturbances, in particular when initial symptoms are of a non-memory type. Their development, however, offers new avenues in the fields of clinical and pharmacological research.
  Revue Neurologique 03/2011; 167(6-7):474-84. · 0.49 Impact Factor
• Article: Brain anomalies in maternally inherited diabetes and deafness syndrome.

  I Fromont, F Nicoli, R Valéro, O Felician, B Lebail, Y Lefur, J Mancini, V Paquis-Flucklinger, P J Cozzone, Bernard Vialettes
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  ABSTRACT: Maternally inherited diabetes and deafness (MIDD) and myoencephalopathy, lactic acidosis, stroke-like episodes (MELAS) syndromes are characterized by the same A3243G mutation of mitochondrial DNA (mtDNA). Should there be a link between these two clinical entities, one could expect to observe minor signs of MELAS in MIDD patients. To examine this issue, extensive evaluations of brain function and imaging in patients with mitochondrial diabetes and in age-matched type 1 diabetic patients were conducted and compared. MIDD patients (nine A3243G, two T14709G) and nine age-matched type 1 diabetic patients (T1D) were submitted for evaluation of cognitive functions, brain magnetic resonance (MR) imaging, and 1H-MR spectroscopy. Three MIDD patients exhibited cerebellar ataxia. The MIDD group exhibited poorer performances in sustained attention, verbal memory working, and abstract reasoning procedures, in comparison with the T1D group. MR imaging showed cerebellar atrophy in seven out of ten MIDD patients (versus 3 mild/8 in T1D controls) and basal ganglia calcifications in one MIDD patient. No evidence of (sub)acute stroke was detected. White-matter anomalies were observed in both groups (50%). 1H-MR spectroscopy revealed a significant decrease of N-acetyl aspartate only in vermis in the MIDD group, suggesting functional defect and/or neuronal loss. Lactate was detected in cerebrospinal fluid (CSF) in two MIDD and one T1D patient. Typical manifestations of MELAS are rare in MIDD syndrome, suggesting two different clinical entities. However, cerebellum involvement as assessed by imaging and 1H-MR spectroscopy is shared by both phenotypes.
  Journal of Neurology 07/2009; 256(10):1696-704. · 3.47 Impact Factor
• Article: [Pure progressive amnesia: an amnestic syndrome with preserved independence in daily life].

  E Tramoni, M Didic, E J Barbeau, S Joubert, O Felician, M Poncet, M Ceccaldi
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  ABSTRACT: Pure progressive amnesia, a form of progressive focal cortical atrophy is thought to represent the early stages of a rare form of Alzheimer's disease (AD). This syndrome is characterized by the insidious and slowly progressive breakdown of memory, in the absence of a significant impairment in other cognitive domains or in the realm of behavior. The aims of the present study were to contribute to the characterization of this poorly documented type of amnesia, to compare it with other forms of amnestic syndromes resulting from lesions to the medial temporal lobes and to discuss its potential pathophysiological basis. We carried out three single case studies in patients presenting with pure progressive amnesia. They all underwent a neuropsychological evaluation that included an extensive assessment of spatial and recognition memory, along with brain magnetic resonance imaging and a cerebral blood flow study. All three patients had a severe deficit in the storage of context-free information, along with a severe visual recognition memory impairment, as previously reported in a case study on a patient with pure progressive amnesia (Cognitive Neuropsychology 23 (2006) 1230-1247). Yet, spatial memory remained well preserved, and patients maintained totally independent in everyday life. In addition, a significant atrophy of the medial temporal structures was found. This specific pattern of impairment differs from other types of amnestic syndromes after medial temporal damage and raises the question of lesional topography, as well as possible compensatory phenomena. We suggest that pure progressive amnesia results from selective damage to the ventral subhippocampal route into the hippocampal formation leading to impaired context-free memory. Spatial memory may remain intact because the dorsal parahippocampal route into the hippocampus remains functional. Pure progressive amnesia may contribute to a better understanding of the neural systems involved in declarative memory and provide a better understanding into the nature of the memory impairment that characterizes the initial stages of AD.
  Revue Neurologique 02/2009; 165(6-7):549-59. · 0.49 Impact Factor
• Article: [Isolated autobiographical amnesia: a neurological basis?].

  O Felician, E Tramoni, E Barbeau, F Bartolomei, M Guye, M Poncet, M Ceccaldi
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  ABSTRACT: The term "autobiographical memory" (AuM) refers to contextually bound experiences that occurred in a specific time, place, and affective setting. AuM is a component of memory commonly impaired in amnestic disorders. Alteration occurs rarely in isolation but rather in the setting of a larger memory impairment. Isolated AuM deficit is a controversial clinical entity, however, recently reported in the context of temporal lobe epilepsy. This study aims at characterizing this poorly documented clinical syndrome and at discussing its potential pathophysiological basis. We studied a group of three subjects with a history of pharmacosensitive epilepsy and severe AuM complaints. They all were submitted to a neuropsychological evaluation that included an extensive episodic memory assessment, along with wake/sleep electroencephalogram (EEG) and brain magnetic resonance imaging (MRI). We observed the following findings: preserved autonomy and intact global cognitive functioning; normal performance to standardized episodic memory assessment, contrasting with decreased performance to specific AuM evaluation; frontal and/or temporal epileptic activity on EEG; and normal structural brain MRI. We reported on a group of patients exhibiting selective impairment of some components of personal memory, associated with interictal frontal and/or temporal abnormalities on EEG. To account for these findings, we hypothesise that interictal epileptic-related activity is impeding long-term consolidation or storage of autobiographical material.
  Revue Neurologique 02/2009; 165(5):449-59. · 0.49 Impact Factor
• Article: Your body and mine: a neuropsychological perspective.

  O Felician, P Romaiguère
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  ABSTRACT: The concept of "shared representations" suggests the existence of a common representation network between self and other. Strong support for this theory is derived from the discovery in the monkey of a population of neurons, which encode object-directed actions performed by oneself and by others. In the human, the issue of "shared representations" has been raised in brain-damaged studies, in particular in the setting of "pointing to body parts" disorders. According to the dominant view, body part designation engages a shared representation system, which encodes the visuospatial characteristics of both one's own body and the bodies of other individuals. However, the recent observation of two patients, JR and AP, with dissociated performance in pointing to body parts leads to question this model. JR presented a deficit in pointing to his own body parts, while his capacity to point to the body parts of other persons was not altered. AP exhibited the reverse pattern of impairment. Lesion study indicated a putative area of dysfunction setting in the left superior parietal lobule (SPL) in JR, and in the left inferior parietal lobule (IPL) in AP. This double dissociation, along with two subsequent neuroimaging studies, suggests that the left SPL and IPL participate in the building of differential representations between oneself and other individuals.
  Neurophysiologie Clinique/Clinical Neurophysiology 07/2008; 38(3):183-7. · 1.98 Impact Factor