Dors ret
Cort Sp Rubrospinal SP syst
Joint
NA ret. Sp Cut
Excitatory
Inhibitory
Figure 1.45 Convergent inputs to the lb inhibitory interneurone to the motoneurone. Afferent inputs from lb golgi tendon organs, cutaneous (Cut.) and descending inputs from
Electrical stimuli delivered at a strength which is perceived to be non-noxious is believed to stimulate the low threshold mechanoreceptors including Merkel discs, Meissners corpuscles, Paccinian corpuscles and Ruffini endings. These receptors are innervated by
The im portance o f the descending systems (corticospinal and rubrospinal) is that they normally provide tonic facilitation o f the Ib inhibitory intem eurones which receive cutaneous afferent input and golgi tendon organ afferent input, and which mediate reflex inhibition o f the m otoneurones from these sources. In addition to spinal reflex circuitry which produces inhibition o f m otoneurones in response to cutaneous afferent input, there are also spinal pathways which produce excitation o f m otoneurones via excitatory intemeurones. These are provided by the same cutaneous afferents which in addition to synapsing with Ib intem eurones also branch to (i) synapse with excitatory intemeurones and (ii) ascend in the dorsal column tracts. The normal balance o f spinal reflex effects in m otoneurones in response to cutaneous stimulation can be deduced from studies o f CMRs
recorded from ID I for patients with KaUmann’s syndrome (Mayston et al. 1997). In their
study, 3 patients showed evidence o f strong ipsilateral control o f distal hand muscles as TMS o f the m otor cortex produced larger ipsilateral responses recorded from ID I compared with contralateral responses, suggesting an abnormally developed a n d /o r novel ipsilateral projection o f corticospinal axons. CMRs showed that only a spinal response, E l, was recorded in ID I ipsilateral to digital nerve stimulation but simultaneously only II and E2 com ponents were recorded contralaterally. Given that the net effect o f cutaneous stimulation was a short latency facilitation o f EM G which was o f a spinal latency, in the absence o f II and E2 com ponents we could suppose that the net effect o f afferent inputs from such a network onto the m otoneurone is usually weighted in favour o f excitation. This discussion has necessarily centred around the “Ib” inhibitory pathway because the convergence o f afferent inputs to these intem eurones have been extensively studied. There may o f course be additional chains o f intem eurones involved in mediating reflex effects from cutaneous afferents.
O n this basis, a loss o f descending facihtatory drive to the Ib inhibitory intem eurones due to corticospinal damage following stroke would therefore be expected to result in a loss or reduction o f the power o f the Ib cutaneous afferent inhibitory pathway normally mediated by these intemeurones. Therefore, the overall reflex effect o f cutaneous stimulation is altered such that there is unopposed excitation o f the m otoneurones (via the excitatory
Changes in E 1 components during normal development
In new-born babies and infants, electrical stimulation o f the digital nerves o f the finger produces a monophasic reflex response where only a marked E l spinal com ponent is present (Issler & Stephens 1983), and a similar response is observed in muscles o f the lower leg following stimulation o f the second toe (Crum & Stephens 1982). Subsequently, in ID I, towards the end o f the first year o f life, there is a gradual reduction in the size o f the E l com ponent and the appearance o f the II com ponent and this is followed by the emergence o f the E2 com ponent during the second year o f life (Issler & Stephens 1983). It is possible that changes in this reflex configuration are due to the a gradual increase in descending facilitation o f transmission along inhibitory Ib spinal pathways. It could be suggested that these putative changes in descending inputs during development are the converse o f changes after stroke described above where the loss o f facilitation o f Ib inhibitory intem eurones may occur.
Changes in the la reciprocal inhibitory pathway have been shown during development. In human neonates, there is a homonymous projection o f la afferent inputs from biceps brachii muscles but also there are heteronymous projections to the antagonistic triceps
muscles which becom e restricted and focussed during the first 4 years o f life (O’Sullivan et
ai 1991). This maturation is dependent on the corticospinal tract inputs and disruption to the corticospinal inputs may result in abnormal persistence o f these heteronymous
projections and exaggerated responses to muscle afferent input (O ’Sullivan et al. 1998).
Therefore descending inputs have been shown to be significant in the refining o f reflex responses to afferent input in the la pathway.
In conclusion, therefore, the exaggerated com ponents observed in EM G recorded from ID I following stroke for patients with poor m otor recovery may be due to the loss o f balance between activity in excitatory and inhibitory pathways projecting to m otoneurones in response to cutaneous afferent stimuli due to the loss o f tonic facilitation o f inhibitory intem eurones following interm ption o f descending (including corticospinal) input. A similar mechanism may also operate to produce larger (but not exaggerated) E l com ponents on the stroke side compared with the non-stroke side for patients with m oderate/good recovery. However, for these patients, this effect on the E l com ponent may be less marked because there is less dismption o f the corticospinal input.
Could the exaggerated E 1 components on the stroke side be due to the delivery of a stronger stimulus strength"^
3 /5 patients with poor recovery showed exaggerated E l com ponents on the stroke side b u t did n ot show a raised threshold for perception o f electrical stimuli (on the stroke side). Therefore, for these 3 patients, the exaggerated E l com ponents cannot be accounted for by delivering an increased stimulus strength to the stroke side. However, for SK6, threshold for perception o f electrical stimuli was increased and the strength o f stimulus delivered to the stroke side was m uch higher than the non-stroke side, representing between 3-4.5 times the threshold o f the non-stroke side. Therefore, it may be suggested that for this patient the exaggerated E l com ponents on the stroke side could be due to increased stimulus strength relative to the non-stroke side. Findings from CMRs recorded from a healthy subject do no t support this view because the sizes o f the E l com ponents were no t shown to significantly increase above stimulus strengths o f 2T up to 3.5T, with the latter stimulus strength being the highest level which was n ot noxious. Therefore, it is unlikely that stimulus strengths o f greater than 3.5T (which were n ot noxious to the patient on the stroke side) would produce the exaggerated E l com ponents for this patient.
To summarise, differences in threshold for perception are unlikely to be responsible for producing either exaggerated E l com ponents on the stroke side a n d /o r asymmetry in the sizes o f these spinal com ponents compared to the non-stroke side.
Consideration of individual subjects
Subject SK9
1 /5 patients with poor recovery o f m otor function, SK9, did n ot show E l com ponents which were exaggerated in size. This contrasts with findings from the remaining 4 /5 patients in this recovery group. For SK9, during the early time period, E2 com ponents were initially absent on the stroke side, but at the late time period, E2 com ponents were often present and the mean E2 com ponent size was slightly larger than the non-stroke side.
preserved. This is a possible mechanism which may prevent the imbalance o f excitatory and inhibitory inputs to m otoneurones via intem eurones and thus prevent exaggeration o f the E l com ponents. The origin o f putative spared descending inputs could be either from the contralateral corticospinal tract o f the damaged hemisphere or, they could originate from the uncrossed portion o f the corticospinal tract (anterior) from the intact cortex. Some support for the latter comes from TMS studies which have dem onstrated that activity in ipsilateral corticospinal pathways originating from the intact cortex may be present following stroke but only in patients w ho eventually showed a poor functional
recovery (Turton 1996; N et2 et al. \991).