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Biomedical subjects

B Gaymard

Publications and source records attributed to B Gaymard.

18 recordsLinked to original sources

Influence of lateral gaze on electroencephalographic spectral power.

The effects of maintaining lateral gaze (as opposed to looking straight ahead) on electroencephalographic spectral power were tested in 12 right handed male subjects during eye opening (EO) and eye closure (EC). Our working hypothesis, based on Kinsbourne's paradigm, was that maintaining right lateral gaze activates the left hemisphere while maintaining left lateral gaze activates the right hemisphere, this activation resulting in a reduction in the spectral power over the hemisphere in question. Results showed that the variations in spectral power involved mainly the alpha frequency band. In the EC condition, the results were consistent with our working hypothesis: right lateral gaze produced a marked reduction in left hemispheric spectral power. In the EO condition, alpha power was constantly higher in the right hemisphere whether lateral gaze was maintained to the right or to the left. This can possibly be due to an attentional effect. Results are discussed with regard of the type of alpha rhythm and of the activation of cortical oculomotor centres. They shed light on the controversy concerning the existence of specific EEG correlates of cognitive activity, which preferentially involve each of the cerebral hemispheres.

Adult

Plus-minus lid syndrome.

A patient presented with ipsilateral ptosis and contralateral superior eyelid retraction due to a nuclear third nerve syndrome. The CT brain scan revealed a paramedian mesencephalic lesion contiguous with the oculomotor nucleus, sparing the midbrain tectum and the posterior commissure.

Aged

Smooth pursuit disorders.

Smooth pursuit is a relatively recent eye movement which has developed in frontal-eyed species. The smooth pursuit system is involved during foveal smooth pursuit, the 'rapid' component of OKN slow phase and VOR suppression. The cortical areas controlling smooth pursuit (at the temporo-parieto-occipital junction and in the FEF) send ipsilateral projections onto the pontine nuclei, mainly the DLPN, passing through the anterior part of the midbrain. A midbrain or DLPN lesion results in ipsilateral smooth pursuit impairment (i.e. decreased gain) (Table 1). After the pontine nuclei, all smooth pursuit pathways pass through the cerebellum. They project onto the flocculus, mainly contralaterally (first decussation of the lateral smooth pursuit circuitry), and bilaterally onto the posterior vermis. Eye velocity is encoded in the activity of the floccular Purkinje cells, whereas target velocity is encoded in that of the vermal Purkinje cells. Unilateral floccular lesions and posterior vermal lesions (involving both sides of this structure) result in ipsilateral and bilateral smooth pursuit impairment, respectively. The flocculus sends an ipsilateral inhibitory projection onto the MVN, the y-group nucleus and the SVN, controlling contralateral, upward and perhaps downward smooth pursuit, respectively. Alternatively, the downward smooth pursuit pathway could pass through the dentate nuclei. The MVN sends a contralateral excitatory projection onto the abducens nucleus (second decussation of the lateral smooth pursuit circuitry). These anatomical and physiological characteristics of lateral smooth pursuit pathways, in addition to the results of lesion studies, suggest that, besides the floccular inhibitory Purkinje cell, there is another inhibitory neurone in the circuitry preceding this cell, perhaps within the flocculus itself. The posterior vermis projects onto the fastigial nuclei, which also control smooth pursuit. These nuclei could send efferents to those periabducens cells involved in ipsilateral smooth pursuit. The final part of the pathways involved in vertical smooth pursuit could pass mainly through the BC, originating in the y-group nucleus for upward movement and in the SVN or the dentate nuclei for downward movement. Alternatively, a ventral tegmental tract could transmit upward smooth pursuit signals between the y-group nucleus and the oculomotor nucleus. The MLF also belongs to this vestibulo-oculomotor circuitry, but does not appear to be crucial for vertical smooth pursuit since this eye movement is only partially impaired after MLF lesions. Lastly, parallel to the direct vestibulo-ocular motor nuclei pathways, there are other pathways passing through the brain stem integrators, converting eye velocity signals to eye position signals during all eye movements, including smooth pursuit.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals

Cortical control of memory-guided saccades in man.

Memory-guided saccades were electro-oculographically recorded in 30 patients with limited unilateral cerebral infarction, documented by computerized tomographic scan and/or magnetic resonance imaging. The lesions affected either (1) the posterior parietal cortex (PPC), (2) the dorsolateral frontal cortex (DLFC), involving the frontal eye field (FEF) and/or the prefrontal cortex (PFC) (area 46 of Brodmann), or (3) the supplementary motor area in the dorsomedial frontal cortex (DMFC). Patients were divided into 6 groups according to the location (PPC, DLFC, DMFC) and side of the lesions. Both latency and accuracy (expressed as percentage of error in amplitude) of memory-guided saccades were compared in each group of patients to values obtained from 20 age-matched normal subjects. Latency was significantly increased, for both directions of saccades in the two DLFC groups and in the right PPC group, and for leftward saccades in the left PPC group. The percentage of error in amplitude was also significantly increased for both directions of saccades in the right PPC group and the left DLFC group, and for leftward saccades in the right DLFC group. Results were near the normal values in patients with lesions affecting the DMFC. Thus, both the PPC (essentially on the right side) and the DLFC appear to play a role in the control of memory-guided saccades. It is suggested that the cortical pathway involved in these saccades includes the PPC, the PFC and the FEF, successively. The PPC could have a dual role: visuospatial integration, and early selection and preparation of certain collicular cells by pre-excitation. Both functions could be ensured by two different types of cells, corresponding, in the monkey, to area 7a and to lateral intraparietal area, respectively. The DLFC could also have a dual role: memorization of visuospatial information by the PFC, and triggering of memory-guided saccades by the FEF.

Cerebral Cortex

Cortical control of reflexive visually-guided saccades.

Reflexive visually-guided saccade triggering may be facilitated or inhibited by the cerebral cortex. To study this control, saccades made towards suddenly appearing visual targets (saccade task) or away from them (antisaccade task) were recorded electro-oculographically in 45 patients with limited unilateral cerebral infarction. Lesions affected (1) the superior part of the angular gyrus (area 39 of Brodmann) in the posterior parietal cortex (PPC), (2) the dorsolateral prefrontal cortex (PFC) (area 46 of Brodmann), (3) the frontal eye field (FEF), or (4) the supplementary motor area (SMA). As these 4 types of lesions were located either in the right or the left cerebral hemisphere, patients were divided into 8 groups. Saccade latency, in the saccade task, and the percentage of errors (misdirected saccades made towards the visual target), in the antisaccade task, were compared in each group of patients with the values of 20 control subjects. In the saccade task, saccade latency was significantly increased bilaterally in the right PPC group. In the left PPC group, the increase in latency was less marked, and significant only for saccades made contralaterally to the lesion. In the different frontal groups, latency was unchanged or only slightly increased. These results confirm that the main area facilitating the triggering of reflexive visually-guided saccades is located in the PPC, in or near the superior part of the angular gyrus. The difference between right and left parietal lesions could be due to the predominance of the right hemisphere in the control of these saccades. In the antisaccade task, the percentage of errors was significantly increased bilaterally in both PFC groups compared with the control group and also to the FEF and SMA groups. These results suggest that the PFC is the main area in the cerebral hemisphere inhibiting reflexive visually-guided saccades.

Cerebral Cortex

Saccade deficits after a unilateral lesion affecting the superior colliculus.

A 70 year old patient with a small haematoma largely restricted to the area of the right superior and inferior colliculi is reported. Eye movements were electro-oculographically recorded 17 and 80 days after the onset of the haematoma. At the first examination, latency of lateral reflexive visually-guided saccades was asymmetrical, both in the gap task (central fixation point switched off 200 ms before the onset of the lateral target) and in the overlap task (central fixation point remaining switched on). Furthermore, latency of leftward saccades in the overlap task was increased, and accuracy of these saccades was impaired, at both examinations. In the immobility task (fixation straight ahead while lateral targets suddenly occurred) and in the anti-saccade task (saccade made away from the lateral target), the percentages of errors (saccades made to the target) were high at the first examination, and noticeably lower at the second. These results suggest that the superior colliculus plays an important role both in the triggering and inhibition of reflexive visually-guided saccades.

Aged

Two mesencephalic lacunar infarcts presenting as Claude's syndrome and pure motor hemiparesis.

Two exceptional cases of mesencephalic lacunar infarcts located both in the anterior vascular territory are reported. In patient 1, the infarct selectively involved the red nucleus, thus resulting in a Claude's syndrome. In patient 2, the lesion was limited to the external 2/3 of the cerebral peduncle, and was responsible for a pure motor hemiplegia (PMH). CT scan easily demonstrated the lesion in both cases. Claude's syndrome is very unusual, and PMH has only been reported once before in a mesencephalic infarct. The reasons why these lesions are so uncommon are discussed.

Aged

[Abnormal eye movements].

Abnormal eye movements constitute a pathological entily characterized by the inability to maintain an immobile gaze, gazing being unwillingly disturbed by displacement of the eyes. The semiology of abnormal eye movements is very accurate. It is based on clinical analysis and on eye movements recording. It is important to study abnormal eye movements, since many of them have localizing or pathological value.

Eye Movements

Impairment of sequences of memory-guided saccades after supplementary motor area lesions.

Different paradigms of saccades were recorded electro-oculographically in 2 patients with infarction affecting the left supplementary motor area. Saccades made toward visual targets (visually-guided saccades) or away from them (antisaccades) were normal in both patients. Memory-guided saccades, made to the remembered position of a flash occurring 2 seconds before, were preserved in 1 patient and only slightly impaired in the other. However, sequences of two or three memory-guided saccades were severely impaired in both patients. It has previously been reported that the supplementary motor area plays an important role in programming sequential limb movements. Our data suggest that this area plays a similar role in the control of sequential eye movements.

Adult

Progressive necrosis of the conus medullaris: magnetic resonance imaging and surgical findings.

A 67-year-old man with non-insulin-dependent diabetes mellitus progressively developed, over a 2-year period, lower extremity sensory and motor defects associated with impaired bladder function and perineal and perianal sensation related to a disease of the conus medullaris extending from T12 to S5. The magnetic resonance imaging scan suggested myelomalacia and the diagnosis of progressive necrotic myelopathy was confirmed by surgical intervention.

Aged

Cerebellar hemangioblastoma and primary hyperparathyroidism.

The authors report the case of a 52-year-old woman presenting with cerebellar hemangioblastoma and primary hyperparathyroidism. It is the second reported case involving this new association. The relationship between these two tumors is discussed.

Cerebellar Neoplasms

Chronic subdural hematoma presenting as ataxic hemiparesis.

A 57-year-old man was admitted for a typical left ataxic hemiparesis syndrome. He presented no vascular risk factor, with normal blood pressure. CT scan showed a frontoparietal right subdural hematoma. After surgery, the symptomatology disappeared completely. This observation reveals that subdural hematoma must be considered as a possible etiology of ataxic hemiparesis syndrome. The physiopathology is discussed.

Ataxia

Chronic cervical radiation myelopathy diagnosed by MRI.

We report a case of chronic cervical myelopathy which developed after radiotherapy for differentiated carcinoma of the buccal cavity. The myelopathy was diagnosed by the finding of severe cervical cord atrophy at MRI.

Adult

[The optostatic system and abnormal ocular movements].

The function of the oculomotor system is to assure gaze movements. Its equilibrium is essential to allows the stability of gaze, especially fixation. Therefore, an opto-static system is necessary to complete the kinetic organisation of eye movements. A disorder in this opto-static system produces abnormal eye movements. Their appearance depends on the location nd on the nature of the lesion in the opto-static system.

Cerebral Cortex