Quadrupedal coordination of bipedal gait: implications for movement disorders

During recent years, evidence has come up that bipedal locomotion is based on a quadrupedal limb coordination. A task-dependent neuronal coupling of upper and lower limbs allows one to involve the arms during gait but to uncouple this connection during voluntarily guided arm/hand movements. Hence, despite the evolution of a strong cortico-spinal control of hand/arm movements in humans, a quadrupedal limb coordination persists during locomotion. This has consequences for the limb coordination in movement disorders such as in Parkinson's disease (PD) and after stroke. In patients suffering PD, the quadrupedal coordination of gait is basically preserved. The activation of upper limb muscles during locomotion is strong, similar as in age-matched healthy subjects although arm swing is reduced. This suggests a contribution of biomechanical constraints to immobility. In post-stroke subjects a close interactions between unaffected and affected sides with an impaired processing of afferent input takes place. An afferent volley applied to a leg nerve of the unaffected leg leads to a normal reflex activation of proximal arm muscles of both sides. In contrast, when the nerve of the affected leg was stimulated, neither on the affected nor in the unaffected arm muscles EMG responses appear. Muscle activation on the affected arm becomes normalized by influences of the unaffected side during locomotion. These observations have consequences for the rehabilitation of patients suffering movement disorder

Recent advances in spinal cord neurology

This short review summarizes developments and achievements made during the last few years in spinal neurology and includes all relevant papers published in the Journal of Neurology during this time. A focus of the review concerns the debate about the significance of translational medicine in spinal cord injury with the introduction of new drugs directed to achieve some spinal cord repair

Degradation of neuronal function following a spinal cord injury: mechanisms and countermeasures

The aim of this study was to evaluate the course of spinal neuronal activity following spinal cord injury (SCI). In patients with a complete SCI, the leg muscle EMG activity early and up to 33 years after an SCI was analysed during locomotor movements induced and assisted by a driven gait orthosis (DGO). Only in chronic SCI patients did a premature exhaustion of neuronal activity occur. This was reflected in a reduced density and fading of leg muscle EMG activity. The early exhaustion of EMG activity was more pronounced in the leg flexor (e.g. biceps femoris) than extensor (e.g. gastrocnemius) muscles. The timing of the leg muscle pattern remained unchanged in the chronic patients. A preserved amplitude of motor action potentials following repetitive peripheral nerve stimulation and during spasms indicated an interneuronal site of impairment. In patients who participated in a locomotor training programme lasting up to 13 weeks, no positive effect on the slope of exhaustion was seen. It is concluded that a degradation of spinal neuronal activity takes place following an SCI. If in the future regeneration of spinal tract fibres becomes feasible in patients with complete SCI, such an approach can only become functionally successful if neuronal activity below the level of the lesion is maintained. This might be achieved by a continuous training approach starting early after injur

Restoration of sensorimotor functions after spinal cord injury

Current efforts to restore function after spinal cord injury are based largely on exploiting neuroplasticity within the sensorimotor system, while preclinical research seeks ways to compensate for loss of descending input after complete cord transection. Dietz and Fouad review both approaches, highlighting key challenges and areas of particular promis

The occurrence of the Babinski sign in complete spinal cord injury

The purpose of the present study was to explore factors that influence the occurrence of the Babinski sign (BS) in complete spinal cord injury patients. At Balgrist University Hospital, Zurich, Switzerland, thirty-five subjects suffering from a complete traumatic spinal cord injury (ASIA A) were examined for the occurrence of the BS, tendon reflex excitability and spastic muscle tone (Modified Ashworth Scale). Five subjects were acute/subacute (1-6months after spinal cord injury (SCI)), 30 were chronic (SCI>1year). In one subject, the measures were examined before and after injection of intrathecal Baclofen. Subjects with a negative BS were investigated electrophysiologically for possible peripheral nerve damage. In 17 subjects (49%), the BS was present, while it was absent in 18 subjects (51%). The occurrence of the BS did not depend on the level of lesion. Most patients with a positive BS also presented a high spastic muscle tone, while those with a negative BS showed low level or absent spastic muscle tone. In 11 SCI subjects, absence of the BS was associated with peripheral nerve damage. In one patient, the BS along with spastic signs disappeared after intrathecal injection of Baclofen. In complete SCI subjects, the occurrence of the BS is connected with spastic muscle tone. The absence of the BS is frequently due to associated peripheral nerve damag

Locomotor activity in spinal man: significance of afferent input from joint and load receptors

The aim of this study was to differentiate the effects of body load and joint movements on the leg muscle activation pattern during assisted locomotion in spinal man. Stepping movements were induced by a driven gait orthosis (DGO) on a treadmill in patients with complete para‐/tetraplegia and, for comparison, in healthy subjects. All subjects were unloaded by 70% of their body weight. EMG of upper and lower leg muscles and joint movements of the DGO of both legs were recorded. In the patients, normal stepping movements and those mainly restricted to the hips (blocked knees) were associated with a pattern of leg muscle EMG activity that corresponded to that of the healthy subjects, but the amplitude was smaller. Locomotor movements restricted to imposed ankle joint movements were followed by no, or only focal EMG responses in the stretched muscles. Unilateral locomotion in the patients was associated with a normal pattern of leg muscle EMG activity restricted to the moving side, while in the healthy subjects a bilateral activation occurred. This indicates that interlimb coordination depends on a supraspinal input. During locomotion with 100% body unloading in healthy subjects and patients, no EMG activity was present. Thus, it can be concluded that afferent input from hip joints, in combination with that from load receptors, plays a crucial role in the generation of locomotor activity in the isolated human spinal cord. This is in line with observations from infant stepping experiments and experiments in cats. Afferent feedback from knee and ankle joints may be involved largely in the control of focal movement

Locomotion in stroke subjects: interactions between unaffected and affected sides

The aim of this study was to evaluate the sensorimotor interactions between unaffected and affected sides of post-stroke subjects during locomotion. In healthy subjects, stimulation of the tibial nerve during the mid-stance phase is followed by electromyography responses not only in the ipsilateral tibialis anterior, but also in the proximal arm muscles of both sides, with larger amplitudes prior to swing over an obstacle compared with normal swing. In post-stroke subjects, the electromyography responses were stronger on both sides when the tibial nerve of the unaffected leg was stimulated compared with stimulation of the affected leg. This difference was more pronounced when stimuli were applied prior to swing over an obstacle than prior to normal swing. This indicates an impaired processing of afferent input from the affected leg resulting in attenuated and little task-modulated reflex responses in the arm muscles on both sides. In contrast, an afferent volley from the unaffected leg resulted in larger electromyography responses, even in the muscles of the affected arm. Arm muscle activations were stronger during swing over an obstacle than during normal swing, with no difference in electromyography amplitudes between the unaffected and affected sides. It is concluded that the deficits of the affected arm are compensated for by influences from the unaffected side. These observations indicate strong mutual influences between unaffected and affected sides during locomotion of post-stroke subjects, which might be used to optimize rehabilitation approache

Impaired modulation of quadriceps tendon jerk reflex during spastic gait: differences between spinal and cerebral lesions

In healthy subjects, functionally appropriate modulation of short latency leg muscle reflexes occurs during gait. This modulation has been ascribed, in part, to changes in presynaptic inhibition of Ia afferents. The changes in modulation of quadriceps tendon jerk reflexes during gait of healthy subjects were compared with those of hemi- or paraparetic spastic patients. The spasticity was due to unilateral cerebral infarction or traumatic spinal cord injury, respectively. The modulation of the quadriceps femoris tendon jerk reflex at 16 phases of the step cycle was studied. The reflex responses obtained during treadmill walking were compared with control values obtained during gait-mimicking standing postures with corresponding levels of voluntary muscle contraction and knee angles. In healthy subjects the size of the reflexes was profoundly modulated and was generally depressed throughout the step cycle. In patients with spinal lesion the reflex depression during gait was almost removed and was associated with weak or no modulation during the step cycle. In patients with cerebral lesion there was less depression of the reflex size associated with a reduced reflex modulation on the affected side compared with healthy subjects. On the 'sunaffected' side of these patients reflex modulation was similar to that of healthy subjects, but the reflex size during gait was not significantly different from standing control values. These observations suggest that the mechanisms responsible for the depression of reflex size and the modulation normally seen during gait in healthy subjects are impaired to different extents in spasticity of spinal or cerebral origin, possibly due to the unilateral preservation of fibre tracts in hemiparesi