Research
The Bobath Centre undertakes research into the nature of cerebral palsy and acquired neurological conditions in children & adults, and investigates ways of mitigating their effects.

Research Papers
Gibbs J, et al.
Does abnormal branching of inputs to motor neurones explain abnormal muscle cocontraction in cerebral palsy?
Dev Med Child Neurol. 1999 Jul;41(7):465-72.
PMID: 10454230; UI: 99382033.

Gibbs J, et al.
Cutaneomuscular reflex responses recorded from the lower limb in children and adolescents with cerebral palsy.
Dev Med Child Neurol. 1999 Jul;41(7):456-64.
PMID: 10454229; UI: 99382032.

Mayston MJ, et al.
A neurophysiological study of mirror movements in adults and children.
Ann Neurol. 1999 May;45(5):583-94.
PMID: 10319880; UI: 99251598.

Krams M, et al.
Mirror movements in X-linked Kallmann's syndrome. II. A PET study.
Brain. 1997 Jul;120 ( Pt 7):1217-28.
PMID: 9236632; UI: 97379833.

Mayston MJ, et al.
Mirror movements in X-linked Kallmann's syndrome. I. A neurophysiological study.
Brain. 1997 Jul;120 ( Pt 7):1199-216.
PMID: 9236631; UI: 97379832.

Davies JM, et al.
Electrical and mechanical output of the knee muscles during isometric and isokinetic activity in stroke and healthy adults.
Disabil Rehabil. 1996 Feb;18(2):83-90.
PMID: 8869510; UI: 97023150.

Carr LJ, et al.
Patterns of central motor reorganization in hemiplegic cerebral palsy.
Brain. 1993 Oct;116 ( Pt 5):1223-47.
PMID: 8221056; UI: 94036081.

Farmer SF, et al.
Plasticity of central motor pathways in children with hemiplegic cerebral palsy.
Neurology. 1991 Sep;41(9):1505-10.
PMID: 1891104; UI: 91367338.

Does abnormal branching of inputs to motor neurones explain abnormal muscle cocontraction in cerebral palsy?

Gibbs J, Harrison LM, Stephens JA, Evans AL
Department of Physiology, University College of London, UK.
Dev Med Child Neurol 1999 Jul;41(7):465-72
PMID: 10454230, UI: 99382033

The common synaptic drive shared between two groups of motor neurones synchronizes the timing of discharges between the motor-neurone groups. Recordings were made of motor-unit discharges during cocontraction of ipsilateral pairs of thumb muscles in eight subjects with cerebral palsy (CP) aged 4 to 13 years and eight neurologically healthy subjects aged 4 to 12 years, and in pairs of lower-limb muscles in 21 subjects with CP and 21 control subjects, both aged 3 to 15 years. Common synaptic drive, likely to be derived at least partly from activity in branched corticospinal-tract neurones, produced motor-unit synchronization between pairs of thumb muscles in control subjects but was absent in all subjects with CP. Motor unit synchronization was not found between lower-limb antagonist muscles that cocontract abnormally in CP, nor was synchronization present in more widely separated muscle pairs. Therefore, abnormal patterns of muscle activation and more widespread muscle reflex responses do not result from an abnormal distribution of common synaptic drive in CP.

Cutaneomuscular reflex responses recorded from the lower limb in children and adolescents with cerebral palsy.

Gibbs J, Harrison LM, Stephens JA, Evans AL
Department of Physiology, University College of London, UK.
Dev Med Child Neurol 1999 Jul;41(7):456-64
PMID: 10454229, UI: 99382032

Cutaneomuscular reflex (CMR) responses were recorded from lower-limb and trunk muscles in 27 subjects with cerebral palsy (CP) (spastic, 21; athetoid, six) and in neurologically healthy (control) subjects, aged 3 to 15 years, while standing. In the 21 subjects with spastic CP, but not in the six subjects with athetoid CP, CMR responses were more widely distributed between ipsilateral lower-limb and trunk muscles compared with age-matched control children. CMR responses in older subjects with CP were similar to younger control subjects, lacking supraspinally mediated, long-latency components. Short-latency, spinally-mediated, excitatory CMR components were seen simultaneously in pairs of distal, antagonistic lower-limb muscles in half of the subjects with spastic CP, but in none of the control children. In subjects with spastic-type CP, the abnormal reflex responses indicate disordered spinal and supraspinal inputs to motor neurones, although there was no convincing correlation between these responses and the severity of spasticity.

A neurophysiological study of mirror movements in adults and children.

Mayston MJ, Harrison LM, Stephens JA
Department of Physiology, University College London, UK.
Ann Neurol 1999 May;45(5):583-94
PMID: 10319880, UI: 99251598

The mechanism underlying mirrored activity/movements in normal individuals is unknown. To investigate this, we studied 11 adults and 39 children who performed sequential finger-thumb opposition or repetitive index finger abduction. Surface electromyographic (EMG) activity recorded from the left and right first dorsal interosseous muscles (1DI) during unilateral sequential finger-thumb opposition (voluntarily activated muscle, 1DIvol) showed mirrored EMG activity (homologous muscle of the opposite hand, 1DImm) that decreased with increasing age. The time of onset of involuntary compared with voluntary EMG activity was variable but could start at the same time. A significant increase in E2 (transcortical component) size of the cutaneomuscular reflex recorded from the 1DImm indicated increased excitability of the motor cortex ipsilateral to the 1DIvol during active index finger abduction compared with the 1DIvol relaxed. Transcranial magnetic stimulation, using the Bistim technique, indicated that the transcallosal inhibitory pathway in children may not operate in the same way as in the adult. Cross-correlation analysis did not detect shared synaptic input to motoneuron pools innervating homologous left and right hand muscles. We conclude that the mirrored movements/activity observed in healthy adults and children are produced by simultaneous activation of crossed corticospinal pathways originating from both left and right motor cortices.

Mirror movements in X-linked Kallmann's syndrome. II. A PET study.

Krams M, Quinton R, Mayston MJ, Harrison LM, Dolan RJ, Bouloux PM, Stephens JA, Frackowiak RS, Passingham RE
Wellcome Department of Cognitive Neurology, Institute of Neurology, London, UK.
Brain 1997 Jul;120 ( Pt 7):1217-28
PMID: 9236632, UI: 97379833

To investigate the mechanism of mirror movements seen in X-linked Kallmann's syndrome, we measured changes of regional cerebral blood flow with H2 15O-PET. We studied six right-handed Kallmann male subjects and six matched, right-handed control subjects during an externally paced finger opposition task. The analyses were done both on a single subject and a group basis. The Kallmann group showed a strong primary motor cortex (M1) activation contralateral to the voluntarily moved hand, but there was also a significant degree of M1 activation ipsilateral to the voluntarily moved hand, i.e. contralateral to the mirroring hand. However, when comparing contralateral to ipsilateral M1 activation, the M1 activation contralateral to the voluntarily moved hand was significantly stronger. In the controls, significant increases in rCBF were seen in the contralateral M1 during voluntary movement of either hand; a small ipsilateral M1 activation was found in two out of six normal subjects when they moved their left hand. In a second experiment it was shown that, in two out of two Kallmann subjects, passive movements of the right hand resulted in left M1 activation that was similar to the activation in the left M1 when subjects made mirror movements with their right hand. This suggests, but does not prove, that the small but significant activation of the ipsilateral M1 in Kallmann's subjects may be due to sensory feedback from the involuntarily mirroring hand.

Mirror movements in X-linked Kallmann's syndrome. I. A neurophysiological study.

Mayston MJ, Harrison LM, Quinton R, Stephens JA, Krams M, Bouloux PM
Department of Physiology, University College London, UK.
Brain 1997 Jul;120 ( Pt 7):1199-216
PMID: 9236631, UI: 97379832

Possible mechanisms underlying the pathological mirror movements that are seen in the majority of patients with X-linked Kallmann's syndrome have been investigated using neurophysiological techniques. An EMG was recorded from the first dorsal interosseous muscle (1DI) during voluntary self-paced abduction of one indexed finger; EMG activity could also be recorded simultaneously from the contralateral 1DI. There was no significant difference between the time of onset of the bursts of voluntary and involuntary mirroring EMG. Focal magnetic stimulation of the hand area of the motor cortex revealed the presence of fast conducting bilateral corticospinal projections from each motor cortex in all subjects. However, both inter- and intra-subject differences exist when considering the ratio of ipsilaterally to contralaterally projecting axons. Cross-correlation analysis of multi-unit EMGs recorded during simultaneous voluntary sustained activation of homologous left and right pairs of distal upper limb muscles was performed. A short duration central peak was seen in the cross-correlograms indicating the presence of a common drive to left and right homologous motor neuron pools. This common drive may result from the synchronous activation of intermingled ipsilaterally and contralaterally projecting corticospinal neurons in the motor cortex. Cutaneomuscular reflexes were recorded from the 1DI following stimulation of the digital nerves of the index finger. Typically each reflex comprises spinal and longer latency trans-cortical components. In these subjects, the long latency components of the reflex response could, in addition, be recorded from the 1DI of the non-stimulated side. We conclude that these subject have a novel ipsilateral at least in part, for the pathological mirroring.

Electrical and mechanical output of the knee muscles during isometric and isokinetic activity in stroke and healthy adults.

Davies JM, Mayston MJ, Newham DJ
Biomedical Sciences Division, Kings College London, UK.
Disabil Rehabil 1996 Feb;18(2):83-90
PMID: 8869510, UI: 97023150

Surface electromyography (EMG) and torque were measured from knee flexors and extensors in 12 control subjects (CS) aged 25-59 years (10 female) and bilaterally in 12 stroke subjects (SS) aged 27-75 years (four female) with hemiparesis and mild clinical spasticity. They performed isometric and isokinetic maximal voluntary contractions (MVC) and also isokinetic passive movements at angular velocities from 30 to 300 degrees/s. The time taken to walk 10 m was documented. Greater torque was recorded during passive extension in the paretic legs when compared with both non-paretic and control limbs (p < 0.01). No EMG activity was measured in any subject. Isometric MVC torque of both muscles in the paretic leg was less (p < 0.01) than both the non-paretic and control limbs. The SS generated relatively less torque bilaterally at the lower velocities than CS. Not all SS reached the higher velocities and none of the paretic limbs achieved 300 degrees/s during flexion. Gait speed correlated with maximal paretic knee extension velocity (p < 0.001). The extent of co-contraction during MVCs was generally low or absent and similar in all three groups. These results suggest a mechanical rather than reflex cause for the restraint detected clinically. Low force generation by the paretic agonists appeared to be the major cause of reduced torque, rather than antagonist opposition.
Comments:
Comment in: Disabil Rehabil 1996 Dec;18(12):638

Patterns of central motor reorganization in hemiplegic cerebral palsy.

Carr LJ, Harrison LM, Evans AL, Stephens JA
Department of Physiology, University College London, UK.
Brain 1993 Oct;116 ( Pt 5):1223-47
PMID: 8221056, UI: 94036081

Central motor reorganization was studied in 33 subjects with hemiplegic cerebral palsy. Corticospinal projections were investigated using focal magnetic stimulation of the motor cortex. Reflex pathways were examined with digital nerve stimulation. Cross-correlation analysis of multi-unit EMG was used to detect activity in branched common stem last order presynaptic inputs to motor neuron pools. The neurophysiological findings were related to the clinical outcome. In 21 of the subjects studied (64%), there was evidence for reorganization of central motor pathways. The clinical and neurophysiological findings revealed two different forms of reorganization. In both forms focal magnetic stimulation demonstrated novel ipsilateral motor pathways from the undamaged motor cortex to the hemiplegic hand. Ipsilateral projections were not demonstrated from the damaged motor cortex. Eleven subjects had intense mirror movements. In these subjects cross-correlation analysis and reflex testing suggested that corticospinal axons had branched abnormally and projected bilaterally to homologous motor neuron pools on both sides of the spinal cord. The remaining 10 subjects did not have intense mirror movements and in these subjects there was no evidence for last order branching of corticospinal axons. It was found that good function of the hemiplegic hand was associated with the presence of EMG responses in that hand following magnetic stimulation of the contralateral motor cortex. When EMG responses were absent, hand function was poor unless the subject had intense mirror movements.

Plasticity of central motor pathways in children with hemiplegic cerebral palsy.

Farmer SF, Harrison LM, Ingram DA, Stephens JA
Department of Physiology, University College London, UK.
Neurology 1991 Sep;41(9):1505-10
PMID: 1891104, UI: 91367338

To obtain neurophysiologic evidence for a reorganization of central motor pathways in children who had suffered a cerebral lesion at birth, we performed cross-correlation analyses of multiunit EMG recordings obtained from children with hemiplegic cerebral palsy and marked mirror movements. We found that the motoneuron pools of homologous left and right hand muscles received common synaptic input from abnormally branched presynaptic axons. The results of electromagnetic brain stimulation, cutaneomuscular, and tendon reflex testing suggested that these common inputs are provided by abnormally branched corticospinal tract fibers whose origin is the undamaged motor cortex.