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We have found that passive velocity dependence [increase in
resistance to movement at increased velocities - without any
discernible EMG activation] in normals and individuals with CNS
damage. The fact that the control group had an order of magnitude
less than the pathology is of interest. Rather than describing the
phenomena as 'present' and 'absent' suggesting a dichotomy of
physiological response I would suggest that we see two ends of a
continuum (granted bimodal). In terms of 2 joint muscles - I do not
know of any specific models to test the adaptation / differential
mechanisms but if there is one then they would have to control for
aspects as evidenced by;
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
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
children's muscle adapt to lengthening differently - so findings in
Cerebral Palsy may be fundamentally different to findings in other
human models (e.g Head injury)
in terms of motor control adaptation - if the response of the CNS to
injury is to decrease the df of the control strategies [utilising
spasticity and synergies] then one could argue that the 2 Jt muscles
would also contribute to the linking of multiple segments. Therefore
there could be a functional advantage of having increased spasticity
/ increased stiffness in these muscles.
Synergist patterns for the initiation of movement also impact on
resting posture - it is well known that a muscle will adapt to
changes in length by altering the number of sarcomeres. We have
shown that the better predictor of ankle contracture in individuals
with Head Injury within an intensive specialist hospital setting was
predicted by the presence of dystonia rather than spasticity.
My 2C worth.
GTA.
--
________________________________________________
Garry T Allison Associate Professor of Physiotherapy
The Centre for Musculoskeletal Studies http://www.cms.uwa.edu.au/
School of Surgery and Pathology, The University of Western Australia.
Level 2 Medical Research Foundation Building
Rear 50 Murray Street
Perth Western Australia 6000.
email
ph: (618) 9224 0219
Fax (618) 9224 0204
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resistance to movement at increased velocities - without any
discernible EMG activation] in normals and individuals with CNS
damage. The fact that the control group had an order of magnitude
less than the pathology is of interest. Rather than describing the
phenomena as 'present' and 'absent' suggesting a dichotomy of
physiological response I would suggest that we see two ends of a
continuum (granted bimodal). In terms of 2 joint muscles - I do not
know of any specific models to test the adaptation / differential
mechanisms but if there is one then they would have to control for
aspects as evidenced by;
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
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
children's muscle adapt to lengthening differently - so findings in
Cerebral Palsy may be fundamentally different to findings in other
human models (e.g Head injury)
in terms of motor control adaptation - if the response of the CNS to
injury is to decrease the df of the control strategies [utilising
spasticity and synergies] then one could argue that the 2 Jt muscles
would also contribute to the linking of multiple segments. Therefore
there could be a functional advantage of having increased spasticity
/ increased stiffness in these muscles.
Synergist patterns for the initiation of movement also impact on
resting posture - it is well known that a muscle will adapt to
changes in length by altering the number of sarcomeres. We have
shown that the better predictor of ankle contracture in individuals
with Head Injury within an intensive specialist hospital setting was
predicted by the presence of dystonia rather than spasticity.
My 2C worth.
GTA.
--
________________________________________________
Garry T Allison Associate Professor of Physiotherapy
The Centre for Musculoskeletal Studies http://www.cms.uwa.edu.au/
School of Surgery and Pathology, The University of Western Australia.
Level 2 Medical Research Foundation Building
Rear 50 Murray Street
Perth Western Australia 6000.
ph: (618) 9224 0219
Fax (618) 9224 0204
---------------------------------------------------------------
To unsubscribe send SIGNOFF BIOMCH-L to LISTSERV@nic.surfnet.nl
For information and archives: http://isb.ri.ccf.org/biomch-l
---------------------------------------------------------------