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Biomedical subjects

C Pierrot-Deseilligny

Publications and source records attributed to C Pierrot-Deseilligny.

At least 19 recordsLinked to original sources
PubMed2006

Reproduction of self-rotation duration.

The vestibular system detects the velocity of the head even in complete darkness, and thus contributes to spatial orientation. However, during vestibular estimation of linear passive self-motion distance in darkness, healthy human subjects mainly rely on time, and they replicate also stimulus duration when required to reproduce previous self-rotation. We then made the hypothesis that the perception of vestibular-sensed motion duration is embedded within encoding of motion kinetics. The ability to estimate time during passive self-motion in darkness was examined with a self-rotation reproduction paradigm. Subjects were required to replicate through self-driven transport the plateau velocity (30, 60 and 90 degrees /s) and duration (2, 3 and 4s) of the previously imposed whole-body rotation (trapezoid velocity profile) in complete darkness; the rotating chair position was recorded (500 Hz) during the whole trials. The results showed that the peak velocity, but not duration, of the plateau phase of the imposed rotation was accurately reproduced. Suspecting that the velocity instruction had impaired the duration reproduction, we added a control experiment requiring subjects to reproduce two successive identical rotations separated by a momentary motion interruption (MMI). The MMI was of identical duration to the previous plateau phase. MMI duration was fidelitously reproduced whereas that of the plateau phase was hypometric (i.e. lesser reproduced duration than plateau) suggesting that subjective time is shorter during vestibular stimulation. Furthermore, the accurate reproduction of the whole motion duration, that was not required, indicates an automatic process and confirms that vestibular duration perception is embedded within motion kinetics.

Adult↗
PubMed2005

Upbeat nystagmus due to a small pontine lesion: evidence for the existence of a crossing ventral tegmental tract.

We report a patient with an isolated large upbeat nystagmus (UBN) in the primary position of gaze. Eye movements were filmed and recorded using electro-oculography. The upward vestibulo-ocular reflex gain, evaluated by pitching the head forward, was markedly reduced compared to when pitching the head back. The lesion was a probable lacunar infarction located in the paramedian and posterior part of the basis pontis, at the upper pons level. This UBN case, with one of the smallest brainstem lesions reported so far, supports the existence in humans of the crossing ventral tegmental tract, described in the cat and transmitting excitatory upward vestibular signals to the third nerve nucleus. It is also suggested that the decussation of this tract lies at the same upper pons level as in the cat but in a slightly more ventral location, i.e. in the posterior basis pontis.

Brain Injuries↗
PubMed2005

Vertical nystagmus: clinical facts and hypotheses.

The pathophysiology of spontaneous upbeat (UBN) and downbeat (DBN) nystagmus is reviewed in the light of several instructive clinical findings and experimental data. UBN due to pontine lesions could result from damage to the ventral tegmental tract (VTT), originating in the superior vestibular nucleus (SVN), coursing through the ventral pons and transmitting excitatory upward vestibular signals to the third nerve nucleus. A VTT lesion probably leads to relative hypoactivity of the drive to the motoneurons of the elevator muscles with, consequently, an imbalance between the downward and upward systems, resulting in a downward slow phase. The results observed in internuclear ophthalmoplegia suggest that the medial longitudinal fasciculus (MLF) is involved in the transmission of both upward and downward vestibular signals. Since no clinical cases of DBN due to focal brainstem damage have been reported, it may be assumed that the transmission of downward vestibular signals depends only upon the MLF, whereas that of upward vestibular signals involves both the MLF and the VTT. The main focal lesions resulting in DBN affect the cerebellar flocculus and/or paraflocculus. Apparently, this structure tonically inhibits the SVN and its excitatory efferent tract (i.e. the VTT) but not the downward vestibular system. Therefore, a floccular lesion could result in a disinhibition of the SVN-VTT pathway with, consequently, relative hyperactivity of the drive to the motoneurons of the elevator muscles, resulting in an upward slow phase. UBN also results from lesions affecting the caudal medulla. An area in this region could form part of a feedback loop involved in upward gaze-holding, originating in a collateral branch of the VTT and comprising the caudal medulla, the flocculus and the SVN, successively. Therefore, it is suggested that the main types of spontaneous vertical nystagmus due to focal central lesions result from a primary dysfunction of the SVN-VTT pathway, which becomes hypoactive after pontine or caudal medullary lesions, thereby eliciting UBN, and hyperactive after floccular lesions, thereby eliciting DBN. Lastly, since gravity influences UBN and DBN and may facilitate the downward vestibular system and restrain the upward vestibular system, it is hypothesized that the excitatory SVN-VTT pathway, along with its specific floccular inhibition, has developed to counteract the gravity pull. This anatomical hyperdevelopment is apparently associated with a physiological upward velocity bias, since the gain of all upward slow eye movements is greater than that of downward slow eye movements in normal human subjects and in monkeys.

Brain Diseases↗
PubMed2005

[Contribution of proton magnetic resonance spectroscopy to the diagnosis of Balo's concentric sclerosis].

INTRODUCTION: Balo's concentric sclerosis is a neuropathological type of multiple sclerosis characterized by alternating rings of spared myelin and demyelination. Diagnosis is based on MRI, but very few data are available concerning the lesion features using serial proton magnetic resonance spectroscopy (1H-MRS). METHODS: We report 1H-MRS initial findings and disease course in one case of Balo's concentric sclerosis. RESULTS: The first 1H-MRS study of 2 concentric ring-enhanced lesions showed a decreased N-acetyl-aspartate (NAA) peak, an increased choline peak, 2 broad lactate peaks and the presence of a lipid peak at 0.9 ppm. Six months later, 1H-MRS showed a decrease of choline peak, whereas the lactate peak had disappeared. The NAA peak was still at a low level. CONCLUSION: These findings are similar to those reported in demyelinating disorders, such as multiple sclerosis. Thus, in Balo's concentric sclerosis, 1H-MRS may provide neurochemical arguments for inflammation and demyelination, and indicate the severity of axonal damage and recovery.

Adult↗
PubMed2005

[From the abducens nucleus to spatial memory: an ocular motor journey].

Advances in our knowledge on eye movements over the last 25 years are reviewed, focusing on the author's experience. First, the advantages of binocular frontal vision, which is a common characteristic of all predator mammals, are compared to those of lateral vision, characterizing their preys. Binocular frontal vision implies a perfect parallelism of both eyes, which is ensured in the pons by means of the abducens nucleus, controlling abduction as well as adduction. The pathological example of the "one-and-a-half" syndrome, in which the abducens nucleus and the adjacent medial longitudinal fasciculus are simultaneously impaired, is described. The main brainstem syndromes involving vertical eye movements are also reviewed: in particular, the third nerve nucleus syndrome, in which both ipsilateral third nerve paralysis and contralateral superior rectus paralysis (with hypotropia) result from a unilateral third nerve nucleus lesion. A case of upbeat nystagmus (in the primary position of gaze) due to a small upper pontine lesion, probably affecting the ventral tegmental tract (VTT) is also reported. This is an opportunity to emphasize that, although a number of cases of upbeat nystagmus due to focal brainstem lesions affecting the upward vestibular pathway (UVP)--either at the upper pontine (VTT) or caudal medullary level--exist in the literature, no convincing cases with downbeat nystagmus (in the primary position of gaze) due to a focal brainstem lesion have been reported. Downbeat nystagmus could result from a UVP hyperactivity (secondary to a floccular lesion) and the notion that this pathway is physiologically predominant compared to the downward pathway, maybe due to gravity, is developed. A new hypothesis about the role of the caudal medulla in UVP is also proposed. Next, the cortical control of saccadic eye movements is reviewed, with a reminder that reflexive saccades are mainly triggered by the parietal eye field whereas intentional saccades depend upon the frontal eye field. The inhibition of reflexive saccades is mainly controlled by the dorsolateral frontal cortex (DLPFC), i.e. area 46 of Brodmann. A few examples of the use of saccades as a research tool and model in cognitive neurosciences are given. The use of memory-guided saccades allowed us to study spatial memory and led us to propose a relatively original conception of the cortical control of spatial memory in which the DLPFC, the parahippocampal cortex and the hippocampal formation could be involved successively according to specific periods of time. An experiment using functional magnetic resonance imaging in a paradigm studying decision is described, again with the involvement of the DLPFC in the decisional process. Lastly, the usefulness of eye movements in clinical neuro-ophthalmology at the bedside as well as in neurophysiological or even neuropsychological research in the laboratory is emphasized.

Abducens Nerve↗
PubMed2005

[Convergence nystagmus and vertical gaze palsy of vascular origin].

A case of convergence-retraction nystagmus with upward vertical gaze paralysis and skew deviation (right hypotropia), without any other neurological signs, is reported. The probably vascular lesion was located at the mesodiencephalic junction, lying between the right border of the posterior commissure, the right interstitial nucleus of Cajal and the periaqueductal grey matter, accounting for the three ocular motor signs. The particular interest of this case is due to the relative smallness of the lesion.

Coiled Bodies↗
PubMed2003

Antisaccade deficit after anterior cingulate cortex resection.

Suppression of unwanted reflexive saccades is a crucial process allowing to sustain voluntary fixation, when required. This inhibition process, which is mainly controlled by the dorsolateral prefrontal cortex, may also involve other cortical and subcortical structures. We prospectively studied the effect of frontal cortical resections involving adjacent regions to the anterior cingulate cortex on the ability to inhibit reflexive saccades. This lesion study included six patients undergoing resection of frontal low grade gliomas, studied prior and after surgery with electro-oculography, using the antisaccade paradigm. Lesions were normalized and mapped in Talairach space allowing to detail the structures whose lesions were associated with antisaccade deficits. In three of the six patients significant early post-operative antisaccade errors were associated with resection of a common critical region, mainly involving the posterior part of the anterior cingulate cortex. This same region was spared in the three remaining patients with no antisaccade deficit, suggesting that the anterior cingulate cortex, known as the cingulate eye field, could play a role in suppression of unwanted saccades.

Adult↗
PubMed2003

Cortical control of ocular saccades in humans: a model for motricity.

Our knowledge of the cortical control of saccadic eye movements (saccades) in humans has recently progressed mainly thanks to lesion and transcranial magnetic stimulation (TMS) studies, but also to functional imaging. It is now well-known that the frontal eye field is involved in the triggering of intentional saccades, the parietal eye field in that of reflexive saccades, the supplementary eye field (SEF) in the initiation of motor programs comprising saccades, the pre-SEF in learning of these programs, and the dorsolateral prefrontal cortex (DLPFC) in saccade inhibition, prediction and spatial working memory. Saccades may also be used as a convenient model of motricity to study general cognitive processes preparing movements, such as attention, spatial memory and motivation. Visuo-spatial attention appears to be controlled by a bilateral parieto-frontal network comprising different parts of the posterior parietal cortex and the frontal areas involved in saccade control, suggesting that visual attentional shifts and saccades are closely linked. Recently, our understanding of the cortical control of spatial memory has noticeably progressed by using the simple visuo-oculomotor model represented by the memory-guided saccade paradigm, in which a single saccade is made to the remembered position of a unique visual item presented a while before. TMS studies have determined that, after a brief stage of spatial integration in the posterior parietal cortex (inferior to 300 ms), short-term spatial memory (i.e. up to 15-20 s) is controlled by the DLPFC. Behavioral and lesion studies have shown that medium-term spatial memory (between 15-20 s and a few minutes) is specifically controlled by the parahippocampal cortex, before long-term memorization (i.e. after a few minutes) in the hippocampal formation. Lastly, it has been shown that the posterior part of the anterior cingulate cortex, called the cingulate eye field, is involved in motivation and the preparation of all intentional saccades, but not in reflexive saccades. These different but complementary study methods used in humans have thus contributed to a better understanding of both eye movement physiology and general cognitive processes preparing motricity as whole.

Cerebral Cortex↗
PubMed2003

Decisional role of the dorsolateral prefrontal cortex in ocular motor behaviour.

Three patients with a unilateral cortical lesion affecting the dorsolateral prefrontal cortex (DLPFC), i.e. Brodmann area 46, were tested using different paradigms of reflexive saccades (gap and overlap tasks), intentional saccades (antisaccades, memory-guided and predictive saccades) and smooth pursuit movements. Visually guided saccades with gap and overlap, latency of correct antisaccades and memory-guided saccades and the gain of smooth pursuit were normal, compared with controls. These results confirm our anatomical data showing that the adjacent frontal eye field (FEF) was unimpaired in these patients. The specific pattern of abnormalities after a unilateral DLPFC lesion, compared with that of the FEF lesions previously reported, consists mainly of: (i) a bilateral increase in the percentage of errors in the antisaccade task (misdirected reflexive saccades); (ii) a bilateral increase in the variable error in amplitude, without significant decrease in the gain, in the memory-guided saccade task; and (iii) a bilateral decrease in the percentage of anticipatory saccades in the predictive task. Taken together, these results suggest that the DLPFC plays a crucial role in the decisional processes, preparing saccades by inhibiting unwanted reflexive saccades (inhibition), maintaining memorized information for ongoing intentional saccades (short-term spatial memory) or facilitating anticipatory saccades (prediction), depending upon current external environmental and internal circumstances.

Adult↗
PubMed2002

[Acute orthostatic intracranial hypotension].

The case of a young female with an acute idiopathic low cerebrospinal fluid pressure is presented. Clinical-imaging manifestations were typical and two consecutive blood patches resulted in a complete and durable resolution of the symptomatology. We present a review of the various investigation and therapeutic techniques.

Adult↗
PubMed2002

[Recurrent idiopathic stupor in a patient: responsibility of exogenous or endogenous benzodiazepines?].

Recurrent transitory consciousness loss represents a neurological diagnostic difficulty. A 56 year old man was hospitalised for recurrent stupor episodes. Explorations allowed to exclude hepatic, renal or respiratory failures, epilepsy or sleep disorder. During a stuporous state, since the patient was clearly awakened by flumazenil administration, the retained diagnosis was idiopathic recurrent stupor, a rare and not well-known disease. The authors discuss the possible effect of a treatment with zolpidem, though its pharmacokinetic characteristics did not correspond to the patient manifestations, and the possible responsibility of endogenous benzodiazepines in the genesis of this trouble.

Benzodiazepines↗