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Dear all,
There have been a few responses so far across the Biomch-L and cga lists. It is clear that my initial question needs to be broken down a bit!
The first question: are biarticular muscles more affected by the altered neural drive in an upper motor neurone condition such as spastic CP?
Maria Lebiedowska refers to two or more components that are typical of spasticity: velocity-dependent reflexes (actually, the Lance definition of "spasticity"); position-dependent activation dependent on the length of the muscle and background (I believe chronic low-level) activity. The question remains "why biarticulate muscles?" or am I misunderstanding the problem and is it all muscles that are affected equally by the cerebral lesion? Is it just that the manifestation of spasticity is more evident in the multijoint muscles because of their action in gait and other tasks? This question remains unanswered I think, so let's move on to the next!
Is it something to do with the intrinsic structure or fibre composition of muscles that spastic muscles become deformed? Fibre composition was rejected by Scott Stackhouse (Carrie Laughton's mail) but he supposed that the architecture of muscles particularly the biarticular variety might have something to do with it (quoting a number of papers from that illustrious physiologist Richard Lieber). It has long been my proposition that the architecture of muscles is a very important factor but that fibre composition has a role to play (see Shortland et al. Dev Med Child Neurol April 2002). The argument goes like this:
1) the chronic low level activity of these muscles leads to a transformation of fibre type from fast to slow (consistent with the chronic electrical stimulation studies of Salmons, Vrbova, Henriksson, Eisenberg and others) and that this results in generally smaller diameter fibres (also shown by workers in this area). This is consistent with the histological findings of Jessica Rose and co-workers in CP muscle.
2) In muscles with long aponeuroses (internal tendons) and short(ish) fibres, it is the average diameter of the muscle fibres that is the primary determinant of muscle belly length. It follows that those muscles with longer aponeuroses and an altered neural drive (chronically-stimulated) may shorten (deform) more dramatically than their longer-fibred neighbours. This is one explanation of why we observe differential deformity amongst muscles.
If this hypothesis is true then it has some interesting consequences for treatment, particularly surgery. For example, semimembranosus (SM) has a relatively longer aponeurosis than semitendinosus and long head of biceps. According to my proposition, it would be the more affected muscle (assuming equal neural inputs). Perhaps, it would be advisable that surgeons lengthen SM only in the first instance and assess the size of the correction before proceeding to other hamstrings. If the other muscular could be preserved perhaps we would not encounter iatrogenic consequences of hamstring lengthening at the hip. A differential effect in the plantarflexors could also be explained in this way with the largely slow soleus being relatively unaffected compared to its faster twitch neighbour, the gastrocnemius.
Gabor notes that biarticular muscles lengthen or shorten at either end. This could be true only if there were significant connections between the muscle and other muscles (there are in fact some very good examples of these connections within our own experience but this is going to be the subject of my next question to the list!). Rather, I believe that biarticular muscles act over quite a narrow range of lengths, in general, and glide over the underlying musculature due the sympathetic motion of the joints that they cross. Gabor also mentions the excellent work of Scott Delp and his associates that shows that the length of the biarticular hamstring musculotendinous units in crouch gait are equal or greater than those of normally-developing heel-toe walkers. I think that this may be a case of short equals long! It is likely that the forces that the hamstrings need to generate in crouch gait are greater than in normal walking. To accomodate this the hamstring bellies need to act at longer lengths, moving right on the Blix curve, so that they be in the right range (in terms of active and passive fibre properties) to generate the necessary forces.
Finally, Maria seems to believe that muscle shortness is not fixed but dynamic. I would encourage her to accompany an orthopaedic surgeon to the operating room or to inspect some MRI images of these children: the bellies of these muscles are structurally short!
All the best,
Adam
Adam Shortland PhD, MIPEM, SRCS
One Small Step Gait Laboratory,
Guy's Hospital
London
UK
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There have been a few responses so far across the Biomch-L and cga lists. It is clear that my initial question needs to be broken down a bit!
The first question: are biarticular muscles more affected by the altered neural drive in an upper motor neurone condition such as spastic CP?
Maria Lebiedowska refers to two or more components that are typical of spasticity: velocity-dependent reflexes (actually, the Lance definition of "spasticity"); position-dependent activation dependent on the length of the muscle and background (I believe chronic low-level) activity. The question remains "why biarticulate muscles?" or am I misunderstanding the problem and is it all muscles that are affected equally by the cerebral lesion? Is it just that the manifestation of spasticity is more evident in the multijoint muscles because of their action in gait and other tasks? This question remains unanswered I think, so let's move on to the next!
Is it something to do with the intrinsic structure or fibre composition of muscles that spastic muscles become deformed? Fibre composition was rejected by Scott Stackhouse (Carrie Laughton's mail) but he supposed that the architecture of muscles particularly the biarticular variety might have something to do with it (quoting a number of papers from that illustrious physiologist Richard Lieber). It has long been my proposition that the architecture of muscles is a very important factor but that fibre composition has a role to play (see Shortland et al. Dev Med Child Neurol April 2002). The argument goes like this:
1) the chronic low level activity of these muscles leads to a transformation of fibre type from fast to slow (consistent with the chronic electrical stimulation studies of Salmons, Vrbova, Henriksson, Eisenberg and others) and that this results in generally smaller diameter fibres (also shown by workers in this area). This is consistent with the histological findings of Jessica Rose and co-workers in CP muscle.
2) In muscles with long aponeuroses (internal tendons) and short(ish) fibres, it is the average diameter of the muscle fibres that is the primary determinant of muscle belly length. It follows that those muscles with longer aponeuroses and an altered neural drive (chronically-stimulated) may shorten (deform) more dramatically than their longer-fibred neighbours. This is one explanation of why we observe differential deformity amongst muscles.
If this hypothesis is true then it has some interesting consequences for treatment, particularly surgery. For example, semimembranosus (SM) has a relatively longer aponeurosis than semitendinosus and long head of biceps. According to my proposition, it would be the more affected muscle (assuming equal neural inputs). Perhaps, it would be advisable that surgeons lengthen SM only in the first instance and assess the size of the correction before proceeding to other hamstrings. If the other muscular could be preserved perhaps we would not encounter iatrogenic consequences of hamstring lengthening at the hip. A differential effect in the plantarflexors could also be explained in this way with the largely slow soleus being relatively unaffected compared to its faster twitch neighbour, the gastrocnemius.
Gabor notes that biarticular muscles lengthen or shorten at either end. This could be true only if there were significant connections between the muscle and other muscles (there are in fact some very good examples of these connections within our own experience but this is going to be the subject of my next question to the list!). Rather, I believe that biarticular muscles act over quite a narrow range of lengths, in general, and glide over the underlying musculature due the sympathetic motion of the joints that they cross. Gabor also mentions the excellent work of Scott Delp and his associates that shows that the length of the biarticular hamstring musculotendinous units in crouch gait are equal or greater than those of normally-developing heel-toe walkers. I think that this may be a case of short equals long! It is likely that the forces that the hamstrings need to generate in crouch gait are greater than in normal walking. To accomodate this the hamstring bellies need to act at longer lengths, moving right on the Blix curve, so that they be in the right range (in terms of active and passive fibre properties) to generate the necessary forces.
Finally, Maria seems to believe that muscle shortness is not fixed but dynamic. I would encourage her to accompany an orthopaedic surgeon to the operating room or to inspect some MRI images of these children: the bellies of these muscles are structurally short!
All the best,
Adam
Adam Shortland PhD, MIPEM, SRCS
One Small Step Gait Laboratory,
Guy's Hospital
London
UK
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For information and archives: http://isb.ri.ccf.org/biomch-l
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