Motor Compensation Research Articles

Internalizing Agency of Self-Action: Perception of One's Own Hand Movements Depends on an Adaptable Prediction About the Sensory Action Outcome

Extensive work on learning in reaching and pointing tasks has demonstrated high degrees of plasticity in our ability to optimize goal-directed motor behavior. However, studies focusing on the perceptual awareness of our own actions during motor adaptation are still rare. Here we present the first simultaneous investigation of sensorimotor adaptation on both levels, i.e., action and action perception. We hypothesized that self-action perception relies on internal predictions about the sensory action outcome that are updated in a way similar to that of motor control. Twenty human subjects performed out-and-back pointing movements that were fed back visually. Feedback was initially presented in spatiotemporal correspondence with respect to the actual finger position, but later rotated by a constant angle. When distorted feedback was applied repetitively, subjects' perceived pointing direction shifted in the direction of the trajectory rotation. A comparable perceptual reinterpretation was observed in control trials without visual feedback, indicating that subjects learned to predict the new visual outcome of their actions based on nonvisual, internal information. The perception of the world, however, remained unchanged. The changes in perception of one's own movements were accompanied by adaptive changes in motor performance of the same amount, i.e., a secondary motor compensation opposite to the direction of the imposed visual rotation. Our results show that the perception of one's own actions depends on adaptable internal predictions about the sensory action outcome, allowing us to attribute new sensory consequences of our actions to our own agency. Furthermore, they indicate that the updated sensory prediction can be used to optimize motor control.

Ipsilateral premotor activity in ALS

Sirs: We would like to thank the authors for their comments in which they point out that in their experiment they adjusted the motor task to the patient’s impaired abilities. Further, they criticize the fact that we only increased the difficulty of the task in the controls group but not in the ALS group thus preventing statistical separation of the factor “difficulty”. Finally, they believe their approach to adjust the force and the subjective effort in patients and controls to be advantageous compared with ours, in which we adjusted the error rates of the control group to match the patient group. Indeed, the way we quoted the work of Konrad et al. [2] is misleading since their task was adapted in that patients and controls performed at 10 % of their individual maximal force. Having equated the subjective effort feeling and having controlled for the pace of the motor task the authors compared the activations of patients and controls. In this way they found that motor activity in ALS was associated with additional recruitment of ipsilateral sensorimotor areas and increased cluster sizes. These findings were interpreted as a general pattern of reorganization in ALS in which enhanced recruitment of functionally related motor areas involved in initiation and planning occurs. Given the elevated age of the patients, the brisk ongoing neurodegenerative changes and the limited options with respect to the therapy, the question whether the cortex of ALS patients is subject to reorganization has a great importance for the development of treatment strategies. The experimental approaches to this question are related to a series of problems that have not yet been solved. Chief among those is that groups of patients with impaired motor abilities have to be compared with healthy controls. As mentioned above Konrad et al. [2] addressed this problem by having patients and controls performing at 10 % of their maximal force in a simple motor task. Our study [3] employed a different experimental strategy. In a first experiment we compared the hemodynamic activation patterns of patients and controls during exactly the same motor task. This revealed similar results to those reported by Konrad et al. [2] in which premotor areas were activated more in patients than in controls. Importantly, ipsilateral recruitment of premotor areas could only be observed in patients during this experiment. The behavioral data indicated that the motor task was much more difficult for patients than for controls at both difficulty levels of the experiment. In their comment the authors suggest that the patient data of our experiment can be interpreted as showing higher brain activation in premotor and cerebellar regions irrespective of the task difficulty. We disagree with this view. We rather believe that in patients the recruitment of brain areas was already involved close to ceiling during the easy difficulty level of the task. Therefore instead of reducing the difficulty in order to make it easier for the patients we have chosen to perform a second experiment in which controls performed in a modified version of the task, where the difficulty was increased. This involved their motor system in a comparable way to the patients resulting in nearly equal error rates. In this experiment the controls exhibited an activation pattern in which premotor ipsilateral and contralateral areas were recruited just as observed in the patient group in the previous experiment. Based on these findings we have suggested that functional motor compensation in ALS patients relies on existing mechanisms that are also used by controls depending on task difficulty. We agree with Konrad et al. on the importance of controlling variables such as the force of the executed movement and the subjective effort. Nevertheless, these variables can not explain the recruitment of ipsilateral areas as found in our experiments since it has been demonstrated that different levels of force do not change the degree of contralateral vs. ipsilateral sensorimotor cortex activation [1]. Therefore we are confident that the recruitment of ipsilateral premotor areas reflects a difficultydependent compensation mechanism that is not primarily developed following the lesion. At present we are far from understanding the neural correlates underlying reorganization and/or compensation processes during neurodegenerative diseases such as ALS. The rapidly advancing disease in a patient population of mid to elevated age with only very limited treatment options remains a big challenge for research and daily clinical work. It is to hope that LETTER TO THE EDITORS

Functional motor compensation in amyotrophic lateral sclerosis

The present study investigated the fMRI correlates of functional compensation/neural reorganization of the motor system in patients with amyotrophic lateral sclerosis (ALS). The hypothesis was that ALS patients would recruit additional brain regions compared with controls in a motor task and that activity in these regions would vary as a function of task difficulty. Patients and controls executed a motor task with two sequences (a simple and a more difficult one) of consecutive button presses. Patients and controls both activated brain regions known to be involved in motor execution and control. Activity in ipsilateral motor areas as well as difficulty-related activity in the left cerebellum could only be observed in patients. The behavioral data indicated that the motor task was much more difficult for patients than for controls. At nearly equal difficulty the observed patterns of hemodynamic activity in controls were very similar to those observed in ALS. The findings suggest that functional compensation in ALS relies on existing resources and mechanisms that are not primarily developed as a consequence of the lesion.

Perceptual bias following visual target selection

Attending to a relevant item in a visual display is thought to require not only selective attention to this item, but also active inhibition of surrounding distractor items. As a consequence of this spatial inhibition, selection of a relevant item in a previous distractor location is slowed (i.e., the spatial inhibition effect). The goal of this study is to identify brain regions that are involved in this spatial inhibition effect using functional magnetic resonance imaging (fMRI). Subjects had to select a target from a display which also included a distractor, while that target was presented in either a new location (control) or in a location previously occupied by a distractor (spatial inhibition). A region of interest analysis revealed decreased activation in the superior parietal lobe (SPL), but increased activation in the motor areas (supplementary motor area, putamen) when the target was presented in a previously inhibited compared to a new location. We take these results to suggest that presenting a target in a previously inhibited location negatively biases the selection of that target in favor of an accompanying distractor. This may result in an initially more efficient selection process, resulting in lower activation in the SPL. Counteracting this perceptual bias possibly requires additional motor activation. This study provides evidence for the notion that to make selection more efficient, prior information concerning an item is used. When this prior information conflicts with the current stimulus demands, compensatory motor actions are taken to correct this perceptual bias.

New Approaches to Enhance Motor Function of the Upper Limb in Patients with Hemiparesis

Abstract A common finding in patients with hemiparesis due to stroke is that they may use altered movement strategies to perform functional arm and hand movements. Altered movement strategies may be considered compensatory if they substitute the movements that are impaired at the behavioural level and yet lead to the accomplishment of the task at the functional level. Motor compensation may be maladaptive in that it may limit recovery of pre-morbid movement patterns. Studies in patients with stroke suggest that, given optimal training strategies and environments, behavioural recovery (re-appearance of pre-morbid movement patterns) may occur even in patients with chronic hemiparesis. On the other hand, it has also been shown that non-guided therapy may lead to the reinforcement of compensatory movements. The challenge facing rehabilitation professionals is to create optimal training environments based on current notions of plasticity and re-organisation in the central nervous system to maximise behavioural and functional recovery.

Summation of visual and mechanosensory feedback inDrosophilaflight control

The fruit fly Drosophila melanogaster relies on feedback from multiple sensory modalities to control flight maneuvers. Two sensory organs, the compound eyes and mechanosensory hindwings called halteres, are capable of encoding angular velocity of the body during flight. Although motor reflexes driven by the two modalities have been studied individually, little is known about how the two sensory feedback channels are integrated during flight. Using a specialized flight simulator we presented tethered flies with simultaneous visual and mechanosensory oscillations while measuring compensatory changes in stroke kinematics. By varying the relative amplitude, phase and axis of rotation of the visual and mechanical stimuli, we were able to determine the contribution of each sensory modality to the compensatory motor reflex. Our results show that over a wide range of experimental conditions sensory inputs from halteres and the visual system are combined in a weighted sum. Furthermore, the weighting structure places greater influence on feedback from the halteres than from the visual system.

Motor enrichment and the induction of plasticity before or after brain injury.

Voluntary exercise, treadmill activity, skills training, and forced limb use have been utilized in animal studies to promote brain plasticity and functional change. Motor enrichment may prime the brain to respond more adaptively to injury, in part by upregulating trophic factors such as GDNF, FGF-2, or BDNF. Discontinuation of exercise in advance of brain injury may cause levels of trophic factor expression to plummet below baseline, which may leave the brain more vulnerable to degeneration. Underfeeding and motor enrichment induce remarkably similar molecular and cellular changes that could underlie their beneficial effects in the aged or injured brain. Exercise begun before focal ischemic injury increases BDNF and other defenses against cell death and can maintain or expand motor representations defined by cortical microstimulation. Interfering with BDNF synthesis causes the motor representations to recede or disappear. Injury to the brain, even in sedentary rats, causes a small, gradual increase in astrocytic expression of neurotrophic factors in both local and remote brain regions. The neurotrophic factors may inoculate those areas against further damage and enable brain repair and use-dependent synaptogenesis associated with recovery of function or compensatory motor learning. Plasticity mechanisms are particularly active during time-windows early after focal cortical damage or exposure to dopamine neurotoxins. Motor and cognitive impairments may contribute to self-imposed behavioral impoverishment, leading to a reduced plasticity. For slow degenerative models, early forced forelimb use or exercise has been shown to halt cell loss, whereas delayed rehabilitation training is ineffective and disuse is prodegenerative. However, it is possible that, in the chronic stages after brain injury, a regimen of exercise would reactivate mechanisms of plasticity and thus enhance rehabilitation targeting residual functional deficits.

Coordinated turn-and-reach movements. I. Anticipatory compensation for self-generated coriolis and interaction torques.

When reaching movements involve simultaneous trunk rotation, additional interaction torques are generated on the arm that are absent when the trunk is stable. To explore whether the CNS compensates for such self-generated interaction torques, we recorded hand trajectories in reaching tasks involving various amplitudes and velocities of arm extension and trunk rotation. Subjects pointed to three targets on a surface slightly above waist level. Two of the target locations were chosen so that a similar arm configuration relative to the trunk would be required for reaching to them, one of these targets requiring substantial trunk rotation, the other very little. Significant trunk rotation was necessary to reach the third target, but the arm's radial distance to the body remained virtually unchanged. Subjects reached at two speeds-a natural pace (slow) and rapidly (fast)-under normal lighting and in total darkness. Trunk angular velocity and finger velocity relative to the trunk were higher in the fast conditions but were not affected by the presence or absence of vision. Peak trunk velocity increased with increasing trunk rotation up to a maximum of 200 degrees /s. In slow movements, peak finger velocity relative to the trunk was smaller when trunk rotation was necessary to reach the targets. In fast movements, peak finger velocity was approximately 1.7 m/s for all targets. Finger trajectories were more curved when reaching movements involved substantial trunk rotation; however, the terminal errors and the maximal deviation of the trajectory from a straight line were comparable in slow and fast movements. This pattern indicates that the larger Coriolis, centripetal, and inertial interaction torques generated during rapid reaches were compensated by additional joint torques. Trajectory characteristics did not vary with the presence or absence of vision, indicating that visual feedback was unnecessary for anticipatory compensations. In all reaches involving trunk rotation, the finger movement generally occurred entirely during the trunk movement, indicating that the CNS did not minimize Coriolis forces incumbent on trunk rotation by sequencing the arm and trunk motions into a turn followed by a reach. A simplified model of the arm/trunk system revealed that additional interaction torques generated on the arm during voluntary turning and reaching were equivalent to < or =1.8 g (1 g = 9.81 m/s(2)) of external force at the elbow but did not degrade performance. In slow-rotation room studies involving reaching movements during passive rotation, Coriolis forces as small as 0.2 g greatly deflect movement trajectories and endpoints. We conclude that compensatory motor innervations are engaged in a predictive fashion to counteract impending self-generated interaction torques during voluntary reaching movements.

Effects of subthalamic nucleus stimulation on actual and imagined movement in Parkinson's disease : a PET study

PET studies in moderately affected Parkinson's disease (PD) patients reveal abnormal cerebral activation during motor execution and imagery, but the effects of subthalamic nucleus (STN) stimulation are not well established. to assess the effect of STN stimulation on cerebral activation during actual and imagined movement in patients with advanced PD. seven severely affected PD patients treated with bilateral STN stimulation were studied with PET and H(2)(15)O. The following conditions were investigated: (1). rest; (2). motor execution of a sequential predefined joystick movement with the right hand and (3). motor imagery of the same task. Patients were studied with and without left STN stimulation while right stimulator remained off. Without STN stimulation, the primary motor cortex was activated only during motor execution whereas the dorsolateral prefrontal cortex (DLPFC) was activated only during motor imagery. An activation of the supplementary motor area (SMA) was seen during both motor execution and motor imagery. Left STN stimulation during motor execution increased the regional cerebral blood flow (rCBF) bilaterally in the prefrontal cortex including DLPFC, in the left thalamus and putamen. In addition, a reduction of rCBF was noted in the right primary motor cortex, inferior parietal lobe and SMA. Under left STN stimulation, during motor imagery, rCBF increased bilaterally in the DLPFC and in the left thalamus and putamen and decreased in the left SMA and primary motor cortex. STN stimulation during both motor execution and imagery tends to improve the functioning of the frontal-striatal-thalamic pathway and to reduce the recruitment of compensatory motor circuits notably in motor, premotor and parietal cortical areas.

最新の脳卒中画像診断 ｆＭＲＩと光トポグラフィーによる脳卒中後の機能画像診断

The mechanism of poststroke motor functional recovery remains to be elucidated. We used functional MRI (fMRI) and near-infrared spectroscopic topography (NIRS) to evaluate the compensatory motor activation of cortical regions during a hand movement task in patients who recovered from poststroke hemiparesis. 1) We evaluated 9 patients with various types of stroke with mild-moderate hemiparesis using fMRI within 1 month of stroke onset and after 2-3 months. At the first examination, the activation of the contralateral hemisphere (primary sensorimotor cortex and supplementary motor area) was markedly reduced during the paretic hand movement. At the second examination, the contralateral activation had recovered in 8 of 9 patients. It addition, activation of ipsilateral motor cortex was seen during the paretic hand movement in 4 of 9 patients. 2) We evaluated 6 patients with massive cerebral infarction in the territory of middle cerebral artery without severe residual hemiparesis using both fMRI and NIRS. Both techniques showed that the activation of ipsilateral primary motor cortex was activated during the paretic hand movement in addition to activation of extended motor areas of the contralateral hemisphere. These observations suggest that motor cortical reorganization, including the ipsilateral hemisphere, contributes to the recovery from poststroke hemiparesis.

Induction of ependymal, glial, and neuronal transactivation by intraventricular administration of the SGLT1 Na+-D-glucose cotransporter inhibitor phlorizin.

Reports that food intake is stimulated by intracerebroventricular (i.c.v.) administration of the SGLT1 Na+-D-glucose cotransport inhibitor, phlorizin, suggest that decreased central glucose uptake is a stimulus for compensatory motor activity underlying restoration of energy imbalance. In order to identify central cell populations that are functionally responsive to decreased SGLT1 function in the brain, the present study utilized immunocytochemical techniques to demonstrate cellular expression of the inducible activator protein-1 transcription factor, Fos, following i.c.v. delivery of phlorizin. Groups of adult male rats were treated with phlorizin at a dose of 10, 50, or 250 microg/animal, then sacrificed 2 hr later by transcardial perfusion. Ependymal expression of Fos-immunoreactivity (-ir) was observed throughout most of the cerebroventricular system, except the medullary fourth ventricle, at each dose examined. Higher doses of the transport inhibitor elicited immunostaining of periventricular glia, characterized by cytoplasmic glial fibrillary acidic protein-ir, underlying the lateral, third, and rostral fourth ventricles and cerebral aqueduct. These doses also resulted in the transcriptional activation of neurons in discrete brain sites, including the rostral medial preoptic area, median preoptic n., preoptic and hypothalamic periventricular n., subfornical organ, thalamic medial habenular and paraventricular n., hypothalamic paraventricular, ventromedial, and arcuate n., and n. of the solitary tract. These results show that nonexcitable cells located throughout much of the central neuroaxis and discrete populations of neurons in the brain are genomically responsive to pharmacological inhibition of central SGLT1 function. Evidence for the functional responsiveness of these cell types to manipulation of energy-dependent glucose transport suggests that cellular uptake of this metabolic fuel may serve as an indicator of central energy substrate availability, and that alterations in glucose uptake via this specific mechanism may be the source of regulatory signals involved in the maintenance of energy homeostasis.

Variations in the relative speeds of orofacial structures with stuttering severity.

Stuttering can be characterized in part as a disorder in the coordination of different muscle systems. In light of basic aspects of orofacial physiology and development, the speeds of the lips and tongue relative to the jaw may be an important dimension for evaluating motor coordination among persons who stutter (PWS). To test this idea, an electromagnetic system was used to obtain measures of lip, tongue, and jaw speed in 38 adults (29 PWS and 9 normally fluent speakers, NFS) as they repeated a simple speech utterance at a normal rate. Using categorical ratings of stuttering severity, ratios of tongue speed to jaw speed were significantly greater in PWS rated as severe, compared to NFS and other PWS. Significant increases in lower lip-to-jaw and tongue-to-jaw speed ratios with stuttering severity were also reflected in correlation analyses relating speed ratios to a continuous measure of stuttering severity. These trends in speed ratio were related to increases in lower lip and tongue speed and decreases in jaw speed with stuttering severity. Sources of the speed differences are discussed in relation to underlying muscle activity, motor compensation processes in adults, and the development of orofacial motor control in children who stutter.

Roles of glutamate receptor subtypes in the development of vestibular compensation after unilateral labyrinthectomy in the guinea pig

We investigated the roles of ionotropic glutamate receptor subtypes in the development and recovery of spontaneous nystagmus (SN) after unilateral labyrinthectomy (UL) in guinea pigs. When administered at 3 h after UL, N-methyl- d-aspartate (NMDA) and kainate (KA), which are NMDA and non-NMDA receptor agonists, respectively, increased the frequency of SN. The effect of KA was more potent than that of NMDA. In contrast to these agonists, MK-801 and CNQX decreased the frequency of SN. Although the administration of KA at 48 h after UL increased the frequency of SN, it did not exhibit any effects at 72 h after UL. MK-801 caused a recurrence of SN following administration at 48 and 72 h after UL. Neither NMDA nor CNQX exhibited any effects after administration at 48 or 72 h after UL. A newly synthesized compound, NC-1200, which has inhibitory action on the glutamate response, decreased the frequency of SN in a dose-dependent manner following administration at 3 h after UL, but did not exhibit any effects when administered at 48 and 72 h after UL. From these results, it was found that NMDA and non-NMDA receptors play important roles in the development of SN after UL, and that the NMDA receptor contributes to the development of ocular motor compensation.

Electropalatographic and acoustic measures of adaptation to palatal perturbation

The present investigation examined adaptation to a palatal perturbation in [s] production, as reflected in both electropalatographic (EPG) and acoustic measures. The goal was to explore the development of compensatory motor programs during the production of individual fricative segments, as well as over a 1-h period of focused practice. Thirty repetitions of the syllable [sa] were produced at each of five time intervals (times 0, 15, 30, 45, and 60 min) by a speaker wearing a specially designed pseudopalate with a 6 mm buildup of acrylic at the alveolar ridge. At times 0 and 60, baseline measures of [sa] production with a thin pseudopalate and with no palate in place were also recorded to characterize unperturbed articulation. Acoustic analyses focused on centroid frequencies for the [s] productions, while a wide range of EPG analyses were conducted including measures of groove length and width, location and duration of maximum constriction, and variability in tongue-palate contact patterns throughout the fricative production. Preliminary analyses indicate a high degree of variability throughout the practice period. Results are discussed in relation to the development of adaptive articulatory programs in speech motor control and the articulatory configurations necessary for adequate [s] production. [Work supported by NSERC.]

Sudden infant death syndrome: a failure of compensatory cerebellar mechanisms?

The mechanisms underlying failure in sudden infant death syndrome may involve inadequate compensatory motor responses to a hypotensive challenge; the insult may result from a shock-like sequence, or from a ventilatory challenge that leads to a hypotensive event. Structures ordinarily not considered in mediating breathing or cardiovascular control, especially cerebellar-related structures, may play a critical role in compensatory responses, and underlie the position-dependent risk for SIDS. Dysfunction in affected brain areas appears to arise prenatally from a compromised fetal environment, with a nicotinic component contributing to the deficient mechanism. Physiologic characteristics of infants who later succumb to SIDS, and cardiovascular events associated with the fatal scenario suggest a failure of interaction between somatomotor and autonomic control mechanisms in infants at risk for the syndrome. A failure of compensatory motor actions to overcome a profound hypotension, perhaps mediated by cerebellar mechanisms that regulate blood pressure, may underlie-the fatal event.

Site-Specific Induction of Fos Immunoreactivity in Preoptic and Hypothalamic NADPH-Positive Neurons during Glucoprivation

Neuronal nitric oxide synthase, e.g. NADPH diaphorase (NADPH-d), catalyzes formation of the free radical, nitric oxide (NO), and occurs within brain structures that have functional significance for energy fuel homeostasis. The following studies examined whether populations of NADPH-d-positive neurons in the hypothalamus and nearby preoptic area express immunoreactivity for the nuclear transcription factor, Fos, in response to glucose substrate imbalance. Eight days after bilateral ovariectomy (OVX) and subcutaneous implantation of silastic capsules containing 30 µg estradiol benzoate/ml, female rats were injected i.p. with the glucose antimetabolite, 2-deoxy-D-glucose (2DG; 400 mg/kg), or the vehicle, saline. The animals were sacrificed by transcardial perfusion 2 h after these treatments. Sections at 150-µm intervals throughout preoptic area and anterior and tuberal regions of the hypothalamus were processed for dual cytoplasmic NADPH-d enzyme activity and nuclear Fos-immunoreactivity (-ir). The glucose antimetabolite elicited expression of nuclear Fos-ir by NADPH-d-positive neurons in several neural structures, including the medial preoptic area, median preoptic nucleus, anterior commissural, periventricular magnocellular supraoptic nucleus, paraventricular nucleus, and medial part of the bed nucleus of the stria terminalis. In contrast, the extensive populations of NADPH-d-positive neurons in the ventromedial hypothalamic nucleus and lateral hypothalamic area showed very little immunolabeling for Fos in response to glucoprivation. This demonstration of nuclear immunoreactivity for Fos suggests that cellular glucopenia elicits the transcriptional activation, via AP-1 regulatory sites, of multiple populations of hypothalamic neurons characterized by the functional capacity to generate NO, and thus that this gaseous neurotransmitter may fulfill a role(s) in central neural mechanisms governing regulation of compensatory motor responses to metabolic imbalance.

Maintenance of adaptive strategies to oral-articulatory perturbations

The present investigation examined whether speakers would adapt to a palatal perturbation in [s] production subsequent to focused practice, and whether the compensatory motor programs developed would be immediately available after a short period of rest. The fricative [s] was produced in three vowel contexts [si sa su] with and without a specially designed artificial palate in place at three time intervals: at the onset of the experiment, after a one-hour period of [s]-intensive practice with the palate in place, one hour later after a period of rest without the palate in place. Recordings of [š] under normal speaking conditions were also made at each time interval to examine any potential carryover effects. Preliminary analyses revealed that centroid frequencies of the [s] productions were significantly lower in the perturbed condition relative to normal upon first insertion of the palate. After the practice period, centroids in the two conditions more nearly approximated one another. However, after a rest period, speakers’ fricative productions were again impaired by the presence of the artificial palate. Results are discussed in relation to the development and retention of adaptive articulatory programs in speech motor control. [Work supported by NSERC.]

Overactivity of cervical premotor neurons in Parkinson’s disease

OBJECTIVESCortical command to upper limb motor neurons is transmitted, in humans, not only through the monosynaptic corticomotor neuronal pathway, but also through cervical premotor neurons. Whether activity in this non-monosynaptic...

The Opioid Receptor Antagonist, Naloxone, Enhances Ocular Motor Compensation in Guinea Pig Following Peripheral Vestibular Deafferentation

The opioid receptor antagonist, naloxone, has been demonstrated to enhance recovery from spinal cord injury and fluid percussion brain injury. The present study investigated, for the first time, the effects of naloxone on behavioral recovery following unilateral peripheral vestibular deafferentation (unilateral labyrinthectomy, UL) in guinea pig. An ip injection of 5 mg/kg naloxone 30 min pre-UL and 5 h post-UL was found to significantly reduce the frequency of spontaneous nystagmus relative to the vehicle control group (P<0.005). However, a lower dose (2.5 mg/kg) had no effect. At either dose, the effects on the postural symptoms, yaw head tilt and roll head tilt, were small by comparison and in most cases nonsignificant. These results suggest that naloxone can reduce the ocular motor effects of UL in a dose-dependent fashion.

Hot topics in speech communication

In speech perception, the issues emphasized are related to long-term representation of speech units, language-specific differences in speech perception by infants and adults, and some new results from cochlear implant and other hearing research relating to the auditory coding of speech cues. New results on the question of prototypes for speech units and how speaker and contextual variability affect listeners’ behavior are reviewed. Next, there is a survey of recent findings on the effect of language background on infants’ and adults’ perception of speech. Finally, results from perceptual studies of cochlear implant patients involving systematically designed stimulus sets are summarized. In speech production, focus is on the applications of instrumentation, on numerical simulation, and on sensory feedback. There is discussion of measuring instruments that are beginning to provide data on motor compensation and coproduction, and sophisticated numerical simulations that are being developed to answer questions about vibratory mechanisms, air flow, and their relation to sound output. Finally, there is a discussion on the roles of receptor and auditory feedback on articulatory coordination and timing. In speech processing, stress is placed on the progress made in auditory representations, in computational models of language, and in statistical methods for text-to-speech synthesis. In auditory-based representations, 100- to 200-ms speech segments may serve as a basis for distance measures for speech coding that reflect perceptual acceptability of acoustic distortions, and as speech-recognition features that capture dynamic aspects of speech production. In spoken-language processing, the gap between stochastic models of speech (e.g., HMM’s and more traditional models of language structure (syntax) and content (semantics) is being bridged. Finally, text-to-speech synthesis is moving, albeit slowly, from hand-tuned to automatically trained systems.