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Dear subscribers,
I'd like to thank all the respondents to my questions regarding spasticity in CP. In the light of the responses I think I will reformulate the original questions as follows:
1) Does the static cerebral lesion produce distinct neurological phenomena in biarticular and monoarticular muscles?
I think it is fair to say that we had no conclusive answer to this part, although Dr Pandyan did point out work from Burke and from Sheean suggesting that the activity patterns of lower limb biarticular muscles in spastic subjects may be mediated by the vestibular system so that in standing subjects turn on these muscles. Maria Lebiedowska did point out that the hamstrings display a position dependent activity in these subjects and that this may affect our assessment of contracture in the clinical examination as well as be responsible for many inefficient movement patterns. I think the answer that these muscles may have a differential neural input was most eloquently summarised by Garry Allison:
the 2 joint muscles may have some differential CNS drive in the
control setting - it is reasonable that this may be altered or
exaggerated in CNS injury e.g. heads of biceps Brachii & Rectus
Femoris vs Vasti, different proportions of the multifidus muscles and
the diaphragm
In other words, in normally-developing individuals the organisation of the neural output to biarticular muscles may be different in nature to monoarticular muscles. In a CNS lesion, the motor organisation of biarticular muscles may be affected more/is more susceptible than monoarticular muscles. I suppose we could ask the further question "Does the original lesion sometimes occur in the area of the brain that this biarticular organisation takes place?"
2) Given that a muscle has a spastic input (whether mono- or bi- articular) are there structural factors that predispose certain muscles to deformity?
As well as the fibre-transformation and aponeurois length argument that I put forward in an earlier posting, we received some interesting further commentary.
Garry Allison suggested that spastic muscles show altered passive properties that are velocity dependent. He speculated that biarticular muscles may show a greater change in passive properties because they have relatively greater amounts of passive material. I quote:
the relative length ratios of the mm fibres and the connective tissue
(aponeurosis) may vary for the longer most superficial muscles (i.e 2
jt) - indeed some would suggest that the passive elements (i.e not
the muscle fibres) contribute more to the lengthen of the muscle
under stretch. This may account for differentials between the single
and 2 jt muscles
Along with Andrew McAleavy, Garry suggested that biarticular muscles are cut by the surgeon because they are superficial and therefore easy to get to! (You'd never catch me speaking such heresy, but then I do have to work with an orthopod!)
Finally, I'd like to thank Arnel Aguinaldo whose commentary reminded me of a line from Marlowe's Faustus "there is more in heaven and earth than is known in our philosophy". Arnel wrote:
Last week at our weekly chalk talk, Dr. Rick Lieber presented some of his
group's recent findings from biomechanical studies done on spastic muscles
at the sarcomere level. Using a laser diffraction device that can measure
the mechanical properties of a single muscle fiber, they found that fiber
segments from spastic muscles have shorter sarcomere lengths and higher
elastic moduli (ie, they're stiffer) than those taken from normal fibers,
suggesting that the intra- and extra- cellular structures are altered with
an UMN lesion. The specific sources of elasticity range from structural
protein to extracellular collagen but this idea is up for debate.
Regardless, spastic muscle cells that exhibit passive tensions at sarcomere
lengths shorter than normal may have serious clinical implications on how
affected muscle(s) are treated (ie, released or lengthened). Perhaps, future
biomechanical studies, particularly at the lower levels of muscle hierarchy,
may shed some light on this issue but it's definitely food for thought.
Adam
PS Of course, there is always a danger in wanting to know all the answers. Again from Faustus:
"If I had as many souls as there be stars, I'd give them all for Mephistopholes"
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I'd like to thank all the respondents to my questions regarding spasticity in CP. In the light of the responses I think I will reformulate the original questions as follows:
1) Does the static cerebral lesion produce distinct neurological phenomena in biarticular and monoarticular muscles?
I think it is fair to say that we had no conclusive answer to this part, although Dr Pandyan did point out work from Burke and from Sheean suggesting that the activity patterns of lower limb biarticular muscles in spastic subjects may be mediated by the vestibular system so that in standing subjects turn on these muscles. Maria Lebiedowska did point out that the hamstrings display a position dependent activity in these subjects and that this may affect our assessment of contracture in the clinical examination as well as be responsible for many inefficient movement patterns. I think the answer that these muscles may have a differential neural input was most eloquently summarised by Garry Allison:
the 2 joint muscles may have some differential CNS drive in the
control setting - it is reasonable that this may be altered or
exaggerated in CNS injury e.g. heads of biceps Brachii & Rectus
Femoris vs Vasti, different proportions of the multifidus muscles and
the diaphragm
In other words, in normally-developing individuals the organisation of the neural output to biarticular muscles may be different in nature to monoarticular muscles. In a CNS lesion, the motor organisation of biarticular muscles may be affected more/is more susceptible than monoarticular muscles. I suppose we could ask the further question "Does the original lesion sometimes occur in the area of the brain that this biarticular organisation takes place?"
2) Given that a muscle has a spastic input (whether mono- or bi- articular) are there structural factors that predispose certain muscles to deformity?
As well as the fibre-transformation and aponeurois length argument that I put forward in an earlier posting, we received some interesting further commentary.
Garry Allison suggested that spastic muscles show altered passive properties that are velocity dependent. He speculated that biarticular muscles may show a greater change in passive properties because they have relatively greater amounts of passive material. I quote:
the relative length ratios of the mm fibres and the connective tissue
(aponeurosis) may vary for the longer most superficial muscles (i.e 2
jt) - indeed some would suggest that the passive elements (i.e not
the muscle fibres) contribute more to the lengthen of the muscle
under stretch. This may account for differentials between the single
and 2 jt muscles
Along with Andrew McAleavy, Garry suggested that biarticular muscles are cut by the surgeon because they are superficial and therefore easy to get to! (You'd never catch me speaking such heresy, but then I do have to work with an orthopod!)
Finally, I'd like to thank Arnel Aguinaldo whose commentary reminded me of a line from Marlowe's Faustus "there is more in heaven and earth than is known in our philosophy". Arnel wrote:
Last week at our weekly chalk talk, Dr. Rick Lieber presented some of his
group's recent findings from biomechanical studies done on spastic muscles
at the sarcomere level. Using a laser diffraction device that can measure
the mechanical properties of a single muscle fiber, they found that fiber
segments from spastic muscles have shorter sarcomere lengths and higher
elastic moduli (ie, they're stiffer) than those taken from normal fibers,
suggesting that the intra- and extra- cellular structures are altered with
an UMN lesion. The specific sources of elasticity range from structural
protein to extracellular collagen but this idea is up for debate.
Regardless, spastic muscle cells that exhibit passive tensions at sarcomere
lengths shorter than normal may have serious clinical implications on how
affected muscle(s) are treated (ie, released or lengthened). Perhaps, future
biomechanical studies, particularly at the lower levels of muscle hierarchy,
may shed some light on this issue but it's definitely food for thought.
Adam
PS Of course, there is always a danger in wanting to know all the answers. Again from Faustus:
"If I had as many souls as there be stars, I'd give them all for Mephistopholes"
---------------------------------------------------------------
To unsubscribe send SIGNOFF BIOMCH-L to LISTSERV@nic.surfnet.nl
For information and archives: http://isb.ri.ccf.org/biomch-l
---------------------------------------------------------------