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European Journal of Neurology 12/2012; 19(12):e144-5. · 3.69 Impact Factor
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ABSTRACT: Voluntary or reactive saccades predominate in rapid eye movements. Their goal is to preserve an active and optimal visual perception of the environment. Saccades cannot be guided once launched. Oculomotor plasticity, or saccadic adaptation, is still partially unknown, in particular the role played by the basal ganglia. New neuro-ophthalmological rehabilitation techniques require understanding the neurophysiological basis and demonstrating the neuronal structures involved in this plasticity.
This study assessed the reactive saccade adaptation in patients with idiopathic Parkinson disease, as a model of basal ganglia dysfunction. We predicted that saccadic adaptation would be preserved in this pathology.
Five patients with mild idiopathic hemi-Parkinson disease were included, as well as four age-matched controls. Reactive saccade adaptation was studied using the double-step target paradigm, in patients with OFF-Dopa treatment and in controls.
Group analysis demonstrated that patients had a lower level of adaptation than the controls (p<0.05). Individually, two patients did not adapt for bilateral saccades and one for ipsilateral (compared to Parkinson motor clinical syndrome) saccades. Two additional patients adapted on both sides but with a deficit in contralateral saccades when compared to the control group.
These preliminary results suggest basal ganglia involvement in reactive saccadic adaptation, which remains to be clarified.
Journal francais d'ophtalmologie 10/2011; 35(4):242-50. · 0.51 Impact Factor
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ABSTRACT: Abnormal eye movements in multiple sclerosis (MS) are often persistent and known to be associated with general disability. However, there is no precise knowledge concerning their incidence and resulting visual handicap. The aim of our study was to describe the persistent ocular motor manifestations in MS and relate them to visual functions tested with visual acuity and with a vision-related questionnaire. We selected 24 MS patients complaining of persistent visual disability associated with ocular motor manifestations without any anterior visual pathway deficit. Internuclear ophthalmoplegia was the most frequently observed symptom, followed by gaze-evoked nystagmus, saccadic hypermetria, and then pendular nystagmus. Pendular nystagmus, saccadic hypermetria, and the association of internuclear ophthalmoplegia and gaze-evoked nystagmus were associated with decreased visual acuity and visual functional scores. There was a correlation between the number of abnormal eye movements and visual functions. This study demonstrates that ocular motor dysfunction in MS induces specific visual dysfunction and handicap.
Annals of the New York Academy of Sciences 09/2011; 1233:327-34. · 3.15 Impact Factor
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ABSTRACT: To propose a method of diagnosis of mild papilloedema (PO) using peripapillary total retinal (PTR) thickness measurement by spectral domain optical coherence tomography (OCT).
24 eyes in 24 patients with PO caused by increased intracranial pressure and 22 eyes in 22 normal subjects were studied. OCT high-quality fundus images were analysed and graded by three masked observers using the Modified Frisén Scale. Eyes with PO were divided into two subgroups: those with mild PO (n=18) and those with moderate-severe PO (n=6). Two methods of measurements were evaluated and compared: retinal nerve fibre layer (RNFL) thickness measurements using standard optic disc cube 200 × 200 acquisition protocol and PTR thickness measurements using the 'macular' cube 512 × 128 acquisition protocol centred on the optic disc. Thickness values were calculated globally and for each quadrant (temporal, superior, nasal, inferior) and compared among the three groups (control, mild PO, moderate-severe PO). The main outcome measures were RNFL and PTR thickness.
Average RNFL and PTR thickness in the moderate-severe PO, mild PO and control groups were 299.3 ± 10.9, 112.4 ± 6.3, 96 ± 5.7 and 804.5 ± 17, 463.1 ± 9.8 and 332.4 ± 8.9 μm, respectively. Moderate-severe PO differed from mild PO and control groups using both RNLF thicknesses and PTR thicknesses measurements. Mild PO did not differ from controls using RNLF thickness measurement (p=0.17), but was statistically different using PTR thickness measurement (p<0.001).
PTR thickness measurement increases the sensitivity of detection of mild PO compared with conventional RNFL measurement. This new way of using OCT may be useful for clinicians to detect mild PO.
The British journal of ophthalmology 06/2011; 96(3):375-9. · 2.92 Impact Factor
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J Seguin,
M Formaglio,
A Perret-Liaudet,
I Quadrio,
Y Tholance,
O Rouaud,
C Thomas-Anterion,
B Croisile,
H Mollion,
O Moreaud,
M Salzmann,
A Dorey,
M Bataillard,
M-H Coste, A Vighetto,
P Krolak-Salmon
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ABSTRACT: To describe CSF biomarker profiles in posterior cortical atrophy (PCA), which induces high-order visual deficits often associated with Alzheimer disease (AD) pathology, and relate these findings to clinical and neuropsychological assessment.
This prospective observational study included 22 patients with PCA who underwent CSF biomarker analysis of total tau (t-tau), phosphorylated tau on amino acid 181 (p-tau181), and amyloid β (Aβ(42)). At group level, the CSF profiles of patients with PCA were compared to those of patients with typical AD and patients with other dementia (OD). Individually, the clinical presentation of patients with PCA was correlated to their CSF profile to assess the predictability of clinical features for diagnosis of underlying AD pathology.
At group level, the PCA biomarker profile was not different from that of the AD group, but very different from that of the OD group (p < 0.001). More than 90% of patients with PCA had CSF profiles consistent with AD. All patients with PCA with either isolated higher-order visual deficit (n = 8) or visual deficit associated with memory impairment (n = 11) had CSF profiles consistent with AD. Only one of the 3 patients with PCA with asymmetric motor signs fulfilled biological CSF criteria for AD.
PCA syndrome is usually associated with CSF biomarkers suggestive of AD, as shown by previous neuropathologic studies. This does not apply in case of motor signs suggesting associated corticobasal syndrome. CSF biomarkers help to discriminate AD from non-AD processes associated with this condition.
Neurology 05/2011; 76(21):1782-8. · 8.31 Impact Factor
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ABSTRACT: Acquired pendular nystagmus occurs mainly in multiple sclerosis (MS) and focal brainstem lesions. In the later case, it is part of the syndrome of oculopalatal tremor. Even though pathophysiology of acquired pendular nystagmus has been clearly characterized experimentally in both etiologies, there is a persisting ambiguity in clinical literature, which leads one to consider both clinical conditions as a common entity. The objective of our work was to compare in a prospective study clinical features, eye movement recording, and functional consequences of acquired pendular nystagmus in 14 patients with oculopalatal tremor and 20 patients with MS.
Besides complete neurologic evaluation, evaluation of visual function, 3-dimensional eye movement recording, and functional scores of the Visual Function Questionnaire were recorded.
One patient with oculopalatal tremor and 15 patients with MS disclosed signs of optic neuropathy. The nystagmus in the oculopalatal group showed significant larger mean amplitude (8 deg vs 1 deg), higher mean peak velocity (16 deg/s vs 6 deg/s), lower mean frequency (1-3 Hz vs 4-6 Hz), and larger asymmetry and irregularity of ocular oscillations compared to the MS group. The vision-specific health-related quality of life was more deteriorated in the oculopalatal tremor group than in the MS group.
This study emphasizes the need to consider acquired pendular nystagmus in MS and oculopalatal tremor as 2 different clinical entities. This is of particular importance regarding the future evaluation of potential specific effects of pharmacologic agents.
Neurology 05/2011; 76(19):1650-7. · 8.31 Impact Factor
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ABSTRACT: Idiopathic vasospastic angiopathy of the internal carotid arteries is a rare and largely unknown cause of ischemic stroke.
We report the case of a 39-year-old man with migraine treated by beta-blockers, who had been suffering from progressive right visual impairment and headache for one week. He then experienced a seizure and left hemiparesis. Ophthalmological examination revealed right retinal ischemia and partial left homonymous hemianopia. MRI revealed a long stenosis of both carotid arteries and a recent ischemic stroke in the territory of the right middle cerebral artery. The diagnosis of vasospastic angiopathy of the internal carotid arteries was made based on a second MRI and colored duplex sonography which showed a decrease in the stenosis and no intraparietal hematoma confirming the vasospasm mechanism for stenosis. The clinical course was favorable with calcium channel blockers and aspirin. Use of vasoconstrictor treatments was contraindicated.
Idiopathic vasospastic angiopathy of the internal carotid arteries has been rarely documented. Association with migraine has been mentioned but remains unclear in the literature. This etiology for stroke is probably under-diagnosed due to lack of rapid and repeated examinations of the cervical arteries (angio-MR and colored duplex sonography) to confirm the vasospasm mechanism. Recurrences have been reported justifying a specific secondary preventive treatment to induce vasodilatation. Vasoconstrictor treatments should be contraindicated.
Revue Neurologique 04/2011; 167(8-9):626-31. · 0.49 Impact Factor
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European Neurology 03/2011; 65(3):160-3. · 1.81 Impact Factor
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ABSTRACT: Malignant optic tract gliomas are very aggressive and extremely rare tumors progressing to blindness and death in a few months. We report here the case of a 73-year-old patient who presented a sudden decrease in visual acuity in his left eye associated with papilledema and headache: it revealed an optochiasmatic anaplastic glioma. A few months later, the glioma had grown, with infiltration of the right optic nerve and right peripapillary intraocular invasion. Through this case, we discuss the importance of achieving imaging for atypical optic neuropathies and stress the exceptional nature of intraocular invasion by a glioma.
Journal francais d'ophtalmologie 10/2010; 33(8):564-7. · 0.51 Impact Factor
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ABSTRACT: It is rarer for a patient to present with transient binocular visual loss than transient monocular visual loss. This symptom usually results from a cerebral dysfunction. When transient binocular visual loss results from papilledema, ophthalmological examination is critical for an accurate diagnosis. In other cases, examination may be normal and a thorough history is of paramount importance for making a diagnosis and deciding whether or not imaging is necessary. The three main cerebral causes for transient binocular visual loss are migraine with visual aura, partial seizures occurring in the occipital lobe, and vertebrobasilar ischemia.
Journal francais d'ophtalmologie 11/2009; 32(10):770-4. · 0.51 Impact Factor
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ABSTRACT: Cerebral venous and sinus thrombosis (CVT) is a rare but potentially alarming condition, which remains a diagnostic and therapeutic challenge. Endovascular procedure may be a therapeutic option when evolution is unfavourable despite medical treatment, but the use of stenting is rarely reported in CVT treatment. We report the case of a man who presented a jugular vein thrombosis responsible for severe intracranial hypertension. Because of clinical worsening despite intravenous heparin and symptomatic treatment, endovascular procedure including the placement of five venous stents, thrombolysis and balloon angioplasty, was performed and led to venous recanalization with successful clinical outcome. The patient is still asymptomatic 3 years later. Our report shows that venous stenting could represent an efficient alternative in the management of decoagulation refractory CVT.
Journal of Neuroradiology 09/2009; 37(3):182-4. · 1.21 Impact Factor
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ABSTRACT: A patient with remittent multiple sclerosis presented subacutely macular visual dysfunction and superior altitudinal hemianopia documented with static and kinetic perimetry. MRI showed extensive demyelination in both temporo-occipital optic radiations. This is the first reported case of altitudinal hemianopia due to multiple sclerosis.
07/2009; 11(1):25-27.
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ABSTRACT: In this chapter we describe a variety of rare but clinically identifiable ocular motor syndromes, including ocular neuromyotonia, superior oblique myokymia, ocular motor synkinesis, third nerve palsy with cyclic spasms, and paroxysmal manifestations of multiple sclerosis. These syndromes share many characteristics. They result from neurogenic hyperactivity, causing episodic spasms of one or several extraocular muscles. The pathophysiology is not fully understood, but it usually includes both a focal and partial lesion of one of the ocular motor nerves and a central rearrangement of neuronal activity in the ocular motor nuclei. Treatment with membrane-stabilizing agents, such as carbamazepine, is usually effective to reduce the symptoms. The above-mentioned syndromes result from a number of different diseases. A proportion of apparently idiopathic cases may be related to a neurovascular compression syndrome.
Neurochirurgie 04/2009; 55(2):272-8. · 0.34 Impact Factor
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ABSTRACT: Vertigo is an illusion of rotatory or linear movement that demonstrates a functional or lesional disturbance of the vestibular system, from periphery to central connections. According to the ANAES report (1997), benign paroxysmal positional vertical vertigo, vestibular neuronitis and Ménière's disease account for 40-50% of all mixed vertigo etiologies. Central etiologies may account for 20-40% of causes and 10-40% remain more difficult to classify, and are usually classified under the term of "peripheral vestibulopathy." These include vertigo due to neurovascular compression syndrome of the VIIIth nerve. Clinical manifestations, differential diagnosis, and treatment of the main etiologies of vertigo will be developed in this chapter. A specific section will discuss the subject of neurovascular compression syndrome of the VIIIth nerve. Even though some publications should be challenged, it appears that neurovascular compression syndrome of the VIIIth nerve might explain some cases of vertigo or chronic instability, with or without cochlear signs. The diagnosis is difficult and must be established on multiple clinical, electrophysiological and radiological arguments. A therapeutic test with antiepileptic drugs is helpful. The treatment includes these drugs as a first option but may require a neurosurgical approach if medical treatment fails.
Neurochirurgie 04/2009; 55(2):259-67. · 0.34 Impact Factor
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ABSTRACT: Clinical and functional assessment of the vestibular nerve is fundamental in demonstrating vestibular signs and searching for associated otological and neurological signs. This may help orient topographic diagnosis toward central or peripheral syndrome and etiologic diagnosis.
Neurochirurgie 04/2009; 55(2):158-61. · 0.34 Impact Factor
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ABSTRACT: The vestibular system detects head movements such as angular rotation, translation, and head position relative to gravity. It acts to stabilize the eyes and posture through subcortical reflexes. Its signals are also integrated at the cortical level to participate in the elaboration of a body scheme, used for different functions such as spatial orientation and motor control. The vestibular nerve shows a resting discharge rate that is modulated up or down according to head motion or position. Central functioning depends on the detection of an asymmetry between signals coming from a pair of peripheral sensors, one on either side. In pathological cases, unilateral peripheral dysfunction is interpreted by the central system as an asymmetry resulting from a change in head position leading to nystagmus, postural disturbances, and vertigo. The dysfunction can be either a deficit, such as observed in vestibular neuronitis, or hyperactivity such as observed in neurovascular compression syndrome of the VIIIth nerve. Anatomically, the VIIIth nerve has a long Root Entry Zone (REZ) that extends over 10mm before entering the brainstem. The VIIIth nerve is also physiologically close to numerous vessels at the pontocerebellar angle and internal auditory meatus. Therefore, vestibular syndrome resulting from neurovascular compression syndrome of the VIIIth nerve may exist, but it is very difficult to prove using radiological imagery.
Neurochirurgie 04/2009; 55(2):127-31. · 0.34 Impact Factor
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ABSTRACT: Posterior cortical atrophy (PCA) is a clinically and radiologically defined syndrome, in which predominant symptoms focus on higher visual dysfunction with progressive course and association with cortical atrophy or hypometabolism that predominates in the posterior part of the hemispheres. Homonymous hemianopia (HH) has rarely been described in this syndrome.
We report on six patients (four females, two males, aged 63 to 80) referred for visual disorder which led to demonstration of HH using perimetry testing. These patients were followed for 1 to 5 years after discovery of HH. Brain imaging with MRI or CT scan was obtained in the six cases and a SPECT scan was performed in four cases.
HH was left-sided in four cases and right-sided in two cases. Associated symptoms related to higher visual dysfunction were simultagnosia, alone or as part of a full Balint's syndrome, alexia, constructional apraxia, dressing apraxia, visual form agnosia, prosopagnosia and hemispatial neglect. These symptoms were mild at onset but invariably worsened with disease progression. Dementia eventually developed in all cases. The clinical diagnosis was probable Alzheimer's disease in five cases and corticobasal degeneration in one case. Radiology showed posterior cortex atrophy in all cases as well as reduced cerebral blood flow in the same region, with an asymmetrical pattern compatible with the side of HH.
Elementary cortical lesions in PCA can develop mainly in the associative visual areas and even in the primary visual area, resulting in HH. HH has rarely been documented in PCA, but its prevalence would probably be higher if systematic search was conducted. Apparently isolated HH of insidious onset should suggest PCA and lead to neuropsychological testing and search for discrete atrophic changes of the posterior cortex on MRI as well as for metabolic alterations with SPECT or PET.
Revue Neurologique 02/2009; 165(3):256-62. · 0.49 Impact Factor
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ABSTRACT: Neurosarcoidosis is a rare disease that can involve all the nervous system with variable clinical onset and prognosis. The initial therapeutic approach is mainly based on corticosteroids and immunosuppressive agents. Treatment of refractory forms of neurosarcoidosis is not well established and emerging immunomodulating drugs like infliximab have been recently tested. The clinical report of a new case of neurosarcoidosis responding to infliximab is followed by a review of the new therapeutic agents available for the treatment of refractory neurosarcoidosis.
Revue Neurologique 02/2009; 165(2):197-200. · 0.49 Impact Factor
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ABSTRACT: PURPOSE: To review the current concepts in the biological diagnosis of Alzheimer's disease (AD) and related disorders. CURRENT KNOWLEDGE AND KEY POINTS: As new therapeutics specific of AD may be available soon, early diagnosis of AD in the context of mild cognitive impairment (MCI) or dementia appears to be challenging. The high amount of atypical clinical forms of AD leads to develop new tools allowing in vivo diagnosis. New CerebroSpinal Fluid (CSF) biomarkers seem to reflect specific aspects of deep neuropathological changes observed in AD, i.e. amyloid deposits and neurofibrillary tangles. Amyloid beta-peptide 1-42 (Abeta(1-42)) and hyperphosphorylated tubulin associated unit (tau) isoforms appear to be the most sensitive and specific CSF biomarkers, the combination of these biomarkers depicting the best diagnosis value for AD. These molecules are also efficient in the prediction of the conversion from the MCI state to the dementia state of AD. Combined to clinical and neuro-imaging information, CSF biomarkers appear thus to be highly relevant in improving the early etiological diagnosis of dementia. FUTURE PROSPECTS AND PROJECTS: The current research focalises on the development of new molecules coming from Abeta and tau protein families, in the CSF and in the serum, as well as molecules reflecting other pathological metabolism changes, as alpha-synuclein in Lewy Body Disease. The diagnosis value of CSF biological markers is so promising that they have been recently included in the research diagnosis criteria of AD.
La Revue de Médecine Interne 07/2008; 29(10):785-93. · 0.61 Impact Factor
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ABSTRACT: To date, two positron emission tomography (PET) studies have explored 5-HT(1A) receptor density in the hippocampus of Alzheimer's disease (AD) patients. They showed early changes of 5-HT(1A) receptors in this brain region, known to have a dense serotonergic innervation. These studies only reported measurements in hippocampus. In the present PET study, we used an antagonist of 5-HT(1A) receptors, the [(18)F]MPPF (1) to explore 5-HT(1A) receptor density in the whole brain of AD patients at a mild stage of dementia and amnestic mild cognitive impairment (aMCI) patients compared to a control population; (2) to explore more precisely the 5-HT(1A) receptor density in the limbic brain regions of AD patients and aMCI patients compared to controls. Voxel-based analyses were performed to assess differences in the [(18)F]MPPF binding potential (BP) between AD patients and aMCI patients compared to controls. Analyses of whole-brain [(18)F]MPPF BP showed a global decrease in AD brains in contrast with a global increase in aMCI brains. In AD brains, a significant decrease of BP was detected in hippocampus and parahippocampal gyrus, whereas a significant increase of BP was observed in the inferior occipital gyrus in aMCI brains. These whole brain results are in accordance to hippocampal data reported in a previous study, showing an increase of [(18)F]MPPF binding in the aMCI group contrasting with a decrease in the AD group. Altogether, these results suggest the implication of a compensatory mechanism illustrated by an up regulation of serotonergic metabolism at the aMCI stage before a breakdown of this mechanism at the AD stage. This difference of serotonergic receptor labeling allows to distinguish the groups of aMCI patients from mild AD patients with specific [(18)F]MPPF PET profiles for each patient group.
NeuroImage 05/2008; 40(3):1251-6. · 5.89 Impact Factor
