Raymond F. Reynolds

Visual guidance of the human foot during a step

When the intended foot placement changes during a step, either due to an obstacle appearing in our path or the sudden shift of a target, visual input can rapidly alter foot trajectory. However, previous studies suggest that when intended foot placement does not change, the path of the foot is fixed after it leaves the floor and vision has no further influence. Here we ask whether visual feedback can be used to improve the accuracy of foot placement during a normal, unperturbed step. To investigate this we measured foot trajectory when subjects made accurate steps, at fast and slow speeds, to stationary floor‐mounted targets. Vision was randomly occluded in 50% of trials at the point of foot‐off. This caused an increase in foot placement error, reflecting lower accuracy and higher variability. This effect was greatest for slow steps. Trajectory heading analysis revealed that visually guided corrections occurred as the foot neared the target (on average 64 mm away). They occurred closer to the target for the faster movements thus allowing less time and space to execute corrections. However, allowing for a fixed reaction time of 120 ms, movement errors were detected when the foot was approximately halfway to the target. These results suggest that visual information can be used to adjust foot trajectory during the swing phase of a step when stepping onto a stationary target, even for fast movements. Such fine control would be advantageous when environmental constraints place limitations on foot placement, for example when hiking over rough terrain.

Fast visuomotor processing made faster by sound

Reaction time to a visual event can be dramatically reduced if the visual stimulus is accompanied by a startling sound. The mechanism may involve a motor programme being stored and triggered early by the sound. However, in a choice reaction task the required response is not known in advance, and so cannot be stored. In this case startling sound does not usually speed up the reaction and may even be detrimental to performance. Here we show that the reaction time of a special type of visually evoked movement can be substantially reduced by startling sound, even though the movement requires choice. The task involved stepping onto an illuminated target that sometimes moved mid‐step left or right, requiring a foot trajectory adjustment. These adjustments occur at much shorter latency than conventional visuomotor reaction tasks and are thought to involve subcortical brain areas. The presence of the sound, which carried no information, shortened the already fast mean response time of 134 ms by ∼20 ms. We attribute this to auditory–visual interaction since sound alone had no effect. Although we observed startle responses, the quickening effect was not contingent upon their presence. Given minimum motor and sensory conduction time, we estimate that the loud sound reduced the central visuomotor processing time by at least 30%.

The resonant component of human physiological hand tremor is altered by slow voluntary movements

Key points  •  Postural physiological hand tremor has a prominent component at ∼8 Hz unlike the associated EMG. Consequently, the gain between EMG and tremor is sharply peaked at ∼8 Hz. •  Deduction and a simple model using pre‐recorded EMG or random noise as an input show that the ∼8 Hz peak is a consequence of resonance. •  During voluntary movement the gain peak enlarges and shifts to a lower frequency but the EMG spectrum shows no corresponding changes. This reflects muscle thixotropy. Adjustment of the muscle properties of the model reproduces the effect. •  These findings suggest that the rhythm of hand tremor in posture and movement is related to muscle and limb mechanics rather than a neural oscillator. •  The discovery that the gain relating EMG to acceleration is very different when static and moving has implications for the control of movement in health and disease.

How a neuropsychiatric brain bank should be run: a consensus paper of Brainnet Europe II

Summary.The development of new molecular and neurobiological methods, computer-assisted quantification techniques and neurobiological investigation methods which can be applied to the human brain, all have evoked an increased demand for post-mortem tissue in research. Psychiatric disorders are considered to be of neurobiological origin. Thus far, however, the etiology and pathophysiology of schizophrenia, depression and dementias are not well understood at the cellular and molecular level. The following will outline the consensus of the working group for neuropsychiatric brain banking organized in the Brainnet Europe II, on ethical guidelines for brain banking, clinical diagnostic criteria, the minimal clinical data set of retrospectively analyzed cases as well as neuropathological standard investigations to perform stageing for neurodegenerative disorders in brain tissue. We will list regions of interest for assessments in psychiatric disorder, propose a dissection scheme and describe preservation and storage conditions of tissue. These guidelines may be of value for future implementations of additional neuropsychiatric brain banks world-wide.

Brain-metabolite transverse relaxation times in magnetic resonance spectroscopy increase as adenosine triphosphate depletes during secondary energy failure following acute hypoxia-ischaemia in the newborn piglet.

The adenosine triphosphate (ATP)-dependent sodium/potassium pump extrudes intracellular sodium in exchange for extracellular potassium. Low ATP causes pump dysfunction increasing both intracellular sodium and water thereby enhancing metabolite mobility. This should be detectable by proton magnetic resonance spectroscopy (MRS) as increased metabolite transverse relaxation times (T2s). During secondary cerebral energy failure in the newborn piglet, proton and phosphorus MRS showed large increases in the T2s of choline, creatine, N-acetylaspartate, and lactate that correlated with ATP depletion. These results provide insight into factors affecting metabolite T2s and show that T2s may be useful for studying cellular oedema.

The effect of trial number on the emergence of the ‘broken escalator’ locomotor aftereffect

Walking onto a stationary platform, which had been previously experienced as moving generates a locomotor aftereffect (LAE), which resembles the ‘broken escalator’ phenomenon. Experimentally, this is achieved by having subjects walk initially onto a stationary sled (BEFORE condition), then onto a moving sled (MOVING condition, or adaptation trials) and then again onto the stationary sled (AFTER condition). Subjects are always appropriately warned of the change in conditions. In this paper, we ask how many adaptation trials are needed to produce such a LAE. Thus, in two experiments, the number of MOVING trials was varied between 20 and 5 (Experiment 1) and between 8 and 1 (Experiment 2). Gait velocity, trunk position, foot contact timing and EMG of the ankle flexor-extensors muscles were measured. In comparison with BEFORE trials all groups in the AFTER trials walked inappropriately fast, experienced a large overshoot of the trunk and showed increased leg EMG, indicating that all groups showed a LAE. In each experiment, and for all variables, no significant difference between the groups (i.e. 20 down to one MOVING trials) was found. The study shows that this LAE, in contrast to other motor aftereffects reported in the literature, can be generated with only one or two adaptation trials and without requiring unexpected ‘catch’ trials. The fast aftereffect generation observed is likely to depend on two types of mechanisms: (1) the nature of the sensorimotor adaptation process, involving multiple sensory feedbacks (visual, vestibular and proprioceptive), anticipatory control and large initial task errors and (2) the involvement of two phylogenetically old neural mechanisms, namely locomotion and fear. Fear-relevant mechanisms, which are notably resistant to cognitive control, may be recruited during the adaptation trials and contribute to the release of this LAE.

The ability to voluntarily control sway reflects the difficulty of the standing task

Standing sway can be reduced simply by conscious effort but the extent to which this ability changes with stance conditions is unknown. Here, the influence of stance width and vision upon the ability to voluntarily reduce sway was investigated. 14 subjects were asked to stand either relaxed or still. Three stance conditions (wide/narrow/tandem) were compared, with eyes open or closed. When standing still, subjects successfully reduced body sway by up to 24% (root mean square of lateral trunk velocity), primarily by attenuating their peak sway frequency (0.2-0.4 Hz). Standing still was associated with a mean increase in ankle muscle co-contraction, but the extent of this increase did not correlate with the ability to reduce sway for individual subjects. Within each stance condition, subjects who swayed more when relaxed also displayed the greatest scope for sway reduction when asked to stand still. However, the opposite trend was observed across conditions: as relaxed sway increased, the capacity for sway reduction was reduced. Hence, voluntary control was lowest during tandem stance and greatest with feet apart, an effect augmented by eye closure. The results show that the degree to which sway can be voluntarily modified is not fixed, but reflects the difficulty of the standing task.

What the “Broken Escalator” Phenomenon Teaches Us about Balance

Gait adaptation is crucial for coping with varying terrain and biological needs. It is also important that any acquired adaptation is expressed only in the appropriate context. Here we review a recent series of experiments that demonstrate inappropriate expression of gait adaptation. We show that a brief period of walking onto a platform previously experienced as moving results in a large forward sway aftereffect, despite full awareness of the changing context. The adaptation mechanisms involved in this paradigm are extremely fast, just 1–2 discrete exposures to the moving platform result in the motor aftereffect. This aftereffect occurs even if subjects deliberately attempt to suppress it. However, it disappears when the location or method of gait is altered, indicating that aftereffect expression is context dependent. Conversely, making gait self‐initiated increases sway during the aftereffect. This aftereffect demonstrates a profound dissociation between knowledge and action. The absence of generalization suggests a relatively simple form of motor learning, albeit involving high‐level processing by cortical and cerebellar structures.

Deficits Underlying Impaired Visually Triggered Step Adjustments in Mildly Affected Stroke Patients

Background. The ability to make step adjustments while walking is often impaired following a stroke, but the basic sensorimotor control deficits responsible have not been established. Objective. To identify these deficits in Patients who have recovered from stroke leaving only mild lower limb impairment. Methods. Ten stroke and 10 age-matched control patients stepped onto an illuminated rectangle. In 40% of trials it jumped 140 mm either medially or laterally when the stepping foot left the ground, thus provoking a mid-step adjustment. In a separate block, patients performed the same task but with the body supported by a frame to eliminate balance responses. Results. Irrespective of support condition stroke patients produced short-latency foot trajectory adjustments compatible with a fast-acting, possibly subcortical, visuomotor process. However, the latency was slightly but significantly longer for the contralesional leg (148 ms) than the ipsilesional leg (141 ms) and longer than for controls (129 ms). Stroke patients’ foot adjustments were executed slower and undershot the target more than controls. These deficits were most pronounced in the medial direction when the body was unsupported. The pattern of undershooting was the same for ipsilesional and contralesional legs. Conclusions. Mildly impaired stroke patients have deficits in initiating and executing visually triggered step adjustments but more profound difficulties with balance control during the adjustment, which caused them to suppress mid-step adjustments of foot placement in the medial direction where balance demands were greatest. Paradoxically, such suppression outside the laboratory may also threaten balance if it leads to unsafe foot placement or obstacle collision.

Postmovement Changes in the Frequency and Amplitude of Physiological Tremor Despite Unchanged Neural Output

Active or passive movement causes a temporary reduction in muscle stiffness that gradually returns to baseline levels when the muscle remains still. This effect, termed muscle thixotropy, alters the mechanical properties of the joint around which the muscle acts, reducing its resonant frequency. Because physiological tremor is affected by joint mechanics, this suggests that prior movement may alter tremor independently of neural output. To address this possibility, vertical acceleration of the outstretched prone hand was recorded in eight healthy subjects, along with EMG activity of the extensor digitorum communis muscle. A series of voluntary wrist flexion/extension movements was performed every 20 s, interspersed by periods during which hand position was maintained. Time-dependent changes in the amplitude and frequency of acceleration and EMG were analyzed using a continuous wavelet transform. Immediately following movement, acceleration displayed a significant increase in wavelet power accompanied by a reduction in peak frequency. During the postmovement period, power declined by 63%, and frequency increased from 7.2 to 8.0 Hz. These changes occurred with an exponential time constant of 2-4 s, consistent with a thixotropic mechanism. In contrast to acceleration, EMG activity showed no significant changes despite being strongly related to acceleration during the movement itself. These results show that prior movement transiently increases the amplitude and reduces the frequency of physiological tremor, despite unchanging neural output. This effect is best explained by a reduction in joint stiffness caused by muscle thixotropy, highlighting the importance of mechanical factors in the genesis of physiological tremor.