(1/168) The adolescent decline of NREM delta, an indicator of brain maturation, is linked to age and sex but not to pubertal stage.

Two dramatic phenomena of human adolescence are sexual maturation and a steep decline in the delta EEG of non-rapid eye movement (NREM) sleep. It has long been speculated that these developmental changes are causally related. Here, we present the first longitudinal data on this issue. Cohorts of 9- and 12-year-old children (n = 31, 38) were studied with in-home sleep EEG recordings at 6-mo intervals over 2 years. Pubertal (Tanner) stage, height, and weight were obtained at each time point. NREM delta power density (DPD) did not change significantly over ages 9-11 years, and its level did not differ in boys and girls. DPD declined by 25% between ages 12 and 14 years. This decline was parallel in the two sexes, but levels were lower in girls, suggesting that their DPD decline began earlier. Mixed effect analyses demonstrated that DPD was strongly related to age with Tanner stage, height, weight and body mass index controlled but that none of these measures of physical and sexual development was related to DPD with age controlled. NREM delta is the sleep EEG component homeostatically related to prior waking duration and the intensity of waking brain activity. We hypothesize that the DPD decline is caused by age-programmed synaptic pruning that decreases waking brain metabolic rate. This reduced rate would decrease the "substrate" for delta homeostasis. Whether or not this interpretation proves correct, these longitudinal data demonstrate that the delta decline in adolescence reflects brain processes that are not predicted by physical growth or sexual maturation.  (+info)

(2/168) The sub-clinical see-saw nystagmus embedded in infantile nystagmus.

A transient, decompensated vertical phoria in an individual with infantile nystagmus syndrome (INS) resulted in two images that oscillated vertically-a diplopic oscillopsia. Ocular motor studies during the vertical oscillopsia recreated by vertical prisms, led to the identification of a sub-clinical see-saw nystagmus (SSN), present under the prism-induced diplopic condition. Retrospective analysis of ocular motor recordings made prior to the above episode of vertical diplopia revealed the presence of that same sub-clinical SSN. The SSN had not been detected previously despite extensive observations and recordings of this subject's pendular IN over a period of forty years. Three- dimensional search-coil data from fourteen additional INS subjects (with pendular and jerk waveforms) confirmed the existence of sub-clinical SSN embedded within the clinically detectable horizontal-torsional IN in seven of the fifteen and a sub-clinical, conjugate, vertical component in the remaining eight. Unlike the clinically visible SSN found in achiasma, the cause of this sub-clinical SSN is hypothesized to be due to a failure of the forces of the oblique muscles (responsible for the torsional component of the IN) to balance out the associated forces of the vertical recti; the net result is a small, sub-clinical SSN. Thus, so-called "horizontal" IN is actually a horizontal-torsional oscillation with a secondary, sub-clinical SSN or conjugate vertical component. The suppression of oscillopsia by efference copy in INS appears to be accomplished for each eye individually, even in a binocular individual. However, failure to fuse the two images results in oscillopsia of one of them.  (+info)

(3/168) Accuracy of the bedside head impulse test in detecting vestibular hypofunction.

OBJECTIVE: To determine the accuracy of the bedside head impulse test (bHIT) by direct comparison with results from the quantitative head impulse test (qHIT) in the same subjects, and to investigate whether bHIT sensitivity and specificity changes with neuro-otological training. METHODS: Video clips of horizontal bHIT to both sides were produced in patients with unilateral and bilateral peripheral vestibular deficits (n = 15) and in healthy subjects (n = 9). For qHIT, eye and head movements were recorded with scleral search coils on the right eye and the forehead. Clinicians (neurologists or otolaryngologists) with at least 6 months of neuro-otological training ("experts": n = 12) or without this training ("non-experts": n = 45) assessed video clips for ocular motor signs of vestibular deficits on either side or of normal vestibular function. RESULTS: On average, bHIT sensitivity was significantly (t test: p<0.05) lower for experts than for non-experts (63% vs 72%), while bHIT specificity was significantly higher for experts than non-experts (78% vs 64%). This outcome was a consequence of the experts' tendency to accept bHIT with corresponding borderline qHIT values as still being normal. Fitted curves revealed that at the lower normal limit of qHIT, 20% of bHIT were rated as deficient by the experts and 37% by the non-experts. CONCLUSIONS: When qHIT is used as a reference, bHIT sensitivity is adequate and therefore clinically useful in the hands of both neuro-otological experts and non-experts. We advise performing quantitative head impulse testing with search coils or high speed video methods when bHIT is not conclusive.  (+info)

(4/168) The role of the ventrolateral frontal cortex in inhibitory oculomotor control.

It has been proposed that the inferior/ventrolateral frontal cortex plays a critical role in the inhibitory control of action during cognitive tasks. However, the contribution of this region to the control of eye movements has not been clearly established. Here, we describe the performance of a group of 23 frontal lobe damaged patients in an oculomotor rule switching task for which the association between a centrally presented visual cue and the direction of a saccade could change from trial to trial. A subset of 16 patients also completed the standard antisaccade task. Ventrolateral damage was found to be a significant predictor of errors in both tasks. Analysis of the rate at which patients corrected errors in the rule switching task also revealed an important dissociation between left and right hemisphere damaged patients. Whilst patients with left ventrolateral damage usually corrected response errors with secondary saccades, those with right hemisphere lesions often failed to do so. The results suggest that the inferior frontal cortex forms part of a wider frontal network mediating inhibitory control over stimulus elicited eye movements. The critical role played by the right ventrolateral region in cognitive tasks may arise due to an additional functional specialization for the monitoring and updating of task rules.  (+info)

(5/168) Torsional deviations with voluntary saccades caused by a unilateral midbrain lesion.

Three dimensional eye rotations were measured using the magnetic search coil technique in a patient with a lesion of the right rostral interstitial nucleus of the medial longitudinal fasciculus (RIMLF) and in four control subjects. Up to 10 degree contralesional torsional deviations with each voluntary saccade were revealed, which also could be seen during bedside examination. There was no spontaneous nystagmus. Based on MRI criteria, the lesion involved the RIMLF but spared the interstitial nucleus of Cajal. To date, this deficit has not been described in patients. Our results support the hypothesis that the vertical-torsional saccade generator in humans is organised similarly as in monkeys: each RIMLF encodes torsional saccades in one direction, while both participate in vertical saccades.  (+info)

(6/168) Evidence for cortical visual substitution of chronic bilateral vestibular failure (an fMRI study).

Bilateral vestibular failure (BVF) is a rare disorder of the labyrinth or the eighth cranial nerve which has various aetiologies. BVF patients suffer from unsteadiness of gait combined with blurred vision due to oscillopsia. Functional MRI (fMRI) in healthy subjects has shown that stimulation of the visual system induces an activation of the visual cortex and ocular motor areas bilaterally as well as simultaneous deactivations of multisensory vestibular cortex areas. Our question was whether the chronic absence of bilateral vestibular input (BVF) causes a plastic cortical reorganization of the above-described visual-vestibular interaction. We used fMRI to measure the differential effects of horizontal visual optokinetic stimulation (OKN) on activations and deactivations in 10 patients with BVF and compared their data directly to those of pairwise age- and sex-matched controls. We found that bilateral activation of the primary visual cortex (inferior and middle occipital gyri, Brodmann area BA 17, 18, 19), the motion-sensitive areas V5 in the middle and inferior temporal gyri (BA 37), and the frontal eye field (BA 8), the right paracentral and superior parietal lobule and the right fusiform and parahippocampal gyri was significantly stronger and the activation clusters were larger than that of the age-matched healthy controls. Small areas of BOLD signal decreases (deactivations), located primarily in the right posterior insula containing the parieto-insular vestibular cortex, were similar to those in the healthy controls. No other sensory brain areas showed unexpected activations or deactivations, e.g. the somatosensory or auditory cortex areas. Our finding of enhanced activations within the visual and ocular motor systems of BVF patients suggests that they might be correlated with an upregulation of visual sensitivity during tracking of visual motion patterns. Functionally, these enhanced activations are independent of optokinetic performance, since the mean slow-phase velocity of OKN in the BVF patients did not differ from that in normals. Although psychophysical and neurophysiological tests have provided various examples of how sensory loss in one modality leads to a substitutional increase of functional sensitivity in other modalities, this study presents the first evidence of visual substitution for vestibular loss by functional imaging.  (+info)

(7/168) The eye movements of dyslexic children during reading and visual search: impact of the visual attention span.

The eye movements of 14 French dyslexic children having a VA span reduction and 14 normal readers were compared in two tasks of visual search and text reading. The dyslexic participants made a higher number of rightward fixations in reading only. They simultaneously processed the same low number of letters in both tasks whereas normal readers processed far more letters in reading. Importantly, the children's VA span abilities related to the number of letters simultaneously processed in reading. The atypical eye movements of some dyslexic readers in reading thus appear to reflect difficulties to increase their VA span according to the task request.  (+info)

(8/168) Task and context determine where you look.

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