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Re: Spasticity of biarticulate muscles in cerebral palsy

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  • Re: Spasticity of biarticulate muscles in cerebral palsy

    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.

    Garry T Allison Associate Professor of Physiotherapy
    The Centre for Musculoskeletal Studies
    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

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