Download Module 3 The integration of postural control and selective movement

Module 3 The integration of postural control and selective movement for functional
activities, Part B (Formerly Part B ‘management of the patient with established
movement dysfunction’)
This module will further develop movement analysis and therapeutic handling skills to
enhance selective movement for locomotion, and functional reach.
The aims of the module are:
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To discuss the upper motor neurone syndrome and its consequences for the patient
with established movement dysfunction
Practical sessions with an emphasis on distal key points
Patient assessment and treatment
To link evidence base and clinical practice
The pathophysiology of the upper motor neurone (UMN) syndrome is complex (Sheean
2001) and our understanding of the underlying mechanisms, the interaction of neural and
biomechanical changes and the significance of the sequalae continues to evolve.
Gracies (2005) describes how paresis and/or muscle weakness that occurs as the initial
consequence of neurological insult imposes a level of immobility on the individual.
Neuroplastic adaptation follows leading to the development of the positive features of the
UMN syndrome. The biomechanical consequences of initial immobility may be
exacerbated by muscle overactivity which in turn increases the development of
contracture.
Muscle tone is the sensation of resistance that is encountered as a joint is passively
moved through a range of movement. When an individual is at rest the resistance felt is
due to a combination of the physical inertia of the limb and the viscoelastic properties of
the muscles and connective tissues. Tension within the muscle due to reflex contraction
(tonic stretch reflexes) contributes to the resistance only during movement in the
neurologically intact adult. (Morris 2002).
To understand the features of the UMN syndrome a review of spinal reflex circuitry is
necessary. There are two types of spinal segmental reflexes: afferent disinhibited spinal
segmental reflexes – proprioceptive, cutaneous and nociceptive information from the
periphery; efferent – tonic supraspinal drive (related to cortical / brainstem regions of
CNS).
The muscle spindle located within the belly of the muscle has its own efferent supply via
the gamma system to maintain tension in spindle fibres as the extrafusal muscle fibres
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contract. The muscle spindle signals change in length of the muscle. The action potential
generated is transferred along the large 1a afferent via the dorsal route ganglion to the
alpha motor neuron within the spinal cord where it: mediates a stretch reflex through local
spinal circuitry; ascends to mediate transcortical reflex like activity.
Within the spinal cord 1a fibres from the muscle spindle make monosynaptic excitatory
connections to alpha motor neurons of the same muscle and that of its synergists. A
further connection to the 1a inhibitory interneurone inhibits activity in the antagonist. This
forms the basis of reciprocal inhibition, i.e. excitation of agonist/inhibition of antagonist.
As the 1a inhibitory interneurone receives both excitatory and inhibitory inputs from the
descending pathways, lack of supraspinal control can decrease the level of reciprocal
inhibition leading to more co-contraction. This combination of influences is described as
reciprocal innervation. Reciprocal innervation is important not only during reflex activity but
also during voluntary movement. The degree of stiffness around a joint can therefore be
modified according to task requirements.
A collateral from the motor neurone axon excites the Renshaw cell, another inhibitory
interneurone, it then inhibits its own motor neurone and other neighboring populations of
motor neurons. This creates a negative feedback system, which helps to stabilize the firing
rate of the motor neurone.
The motor neurones and inhibitory interneurons receive multiple inputs from the
descending supraspinal pathways, from afferent input from the periphery and within the
body allowing further modulation of output.
The afferent from another sensory receptor must also be considered. The golgi tendon
organ (GTO) located at the musculotendinous junction responds to changes in tension
within the muscle. As the muscle contracts tension increases compressing the GTO. The
action potential travels along the 1b afferent via the dorsal root ganglion to the 1b inhibitory
interneurone, which then inhibits the activity of the alpha motor neurone also known as
autogenic inhibition. As described above convergent input from within the body, the
periphery and via descending pathways from supraspinal areas acting upon the !b
inhibitory interneurone modulates output. A further consideration of the 1b system is that
state dependent reflex reversal means that during locomotion or in a loaded posture the 1b
system results in excitation rather than inhibition.
Most reflex pathways are disynaptic or polysynaptic, with one or more interneurons
between sensory and motor neurons. Supraspinal centres are able to co-ordinate muscle
activity around a joint.
Positive features of the UMN may be considered as an aberrant sensorimotor behaviour
due to either the primary disruption of descending control or the resultant functional and
structural reorganisation within the nervous system.
Movement disorders as part of the UMN syndrome vary in different conditions e.g. stroke,
MS, SCI. Lesion location determines the presentation of features of the UMN syndrome.
An understanding of the descending control is therefore essential to appreciate the
significance of lesion location.
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A balance of modulation between the excitatory medial reticulospinal and vestibulospinal
and inhibitory lateral reticulospinal systems determines the overall motor behaviour at a
movement level. This can then be influenced and further modulated by inputs from other
descending systems. Disruption to the descending systems and / or pathways therefore
results in alterations to the levels of excitation and inhibition and resultant negative and
positive features seen within the individuals presentation following brain or spinal cord
injury or disease.
Following a cortical lesion e.g. stroke the descending influence from the cortex on to the
brainstem and spinal cord is interrupted reducing the (inhibitory) influence to the alpha
motoneurone. A discrete lesion interrupting the lateral corticospinal pathway will result in
distal weakness.
A lesion within the brain stem influencing the ventromedial reticular formation will result in
a further loss of inhibitory influences and the balance of modulation is tipped towards
excitation. The resulting presentation is characterised by more positive features of the
UMN syndrome.
A lesion interrupting the dorsal (lateral) reticulospinal pathway within the spinal cord results
in a similar loss of inhibition.
A complete lesion of the brainstem/spinal cord interrupting ALL of the descending systems
results in a loss of all inhibitory and excitatory influences. Motor behaviour is therefore at
the behest of the peripheral input on the spinal reflex circuitry. Voluntary movement control
is no longer a possibility following this type of lesion.
The initial presentation following an UMN lesion is a result of the disruption of descending
spinal control and includes: weakness, disinhibition and hyperexcitation. The clinical
presentation (positive and negative features develops over time following structural and
functional reorganisation of the nervous system as a result of processes such as:
denervation super-sensitivity, collateral sprouting and unmasking of latent synapses.
Clinical features of the UMN syndrome are described as either negative (loss of features)
or positive (new features). Positive features are characterised by muscle over-activity
and/or co-contraction.
Negative features
Weakness
Loss of dexterity
Fatiguability
Acute hypotonia
Loss of postural responses
Positive features
Spasticity
Hyperreflexia
Positive Babinski response
Dysynergic patterns of co
contraction
Spasms
Positive feature can further be described as those occurring at rest or during movement.
Spasticity is only one feature of the UMN syndrome, but is a term that is frequently used to
describe some or all positive features of the UMN syndrome. There is no universal
definition of spasticity nor agreement about how it should be measured (Malhotra et al
2009). The definition of spasticity from Lance (1980) is perhaps the most widely used and
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states that spasticity is a motor disorder characterised by a velocity – dependent increase
in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks (phasic stretch
reflex), resulting from hyper excitability of the stretch reflex, as one component of the
upper motor neurone syndrome. This definition was considered by many to be narrow and
outdated. Three areas were identified as requiring modification within any definition of
spastcity:
1. Velocity dependent changes in limb stiffness during passive movement are not
solely due to neural changes but are contributed to by the normal viscoelastic
properties of soft tissues
2. In addition to hyperexcitable stretch reflexes, activity in other pathways (afferent,
supraspinal and changes in alpha motoneurone) is also important in the
development of spasticity
3. Spasticity cannot be exclusively considered a ‘motor disorder’ as afferent activity
(cutaneous and proprioceptive) is also involved
The European Assembly for Spasticity Measurement (EU SPASM) in 2005 published a
new definition of spasticity as: “disordered sensory-motor control, resulting from an upper
motor neuron lesion, presenting as intermittent or sustained involuntary activation of
muscles”. This new definition is considered to be broad enough to include all the positive
features of the UMN syndrome and yet still exclude secondary biomechanical changes
which although they contribute to stiffness and resistance to movement are not a primary
feature of the UMN syndrome. There is evidence to suggest that hyper-reflexia results
from a failure to modulate tonic stretch reflexes, rather than only hyper-excitability of the
reflex. Singer et al 2001 describe spasticity as “a motor disorder in which failure to actively
inhibit velocity sensitive stretch reflexes can lead to exaggerated muscle resistance to both
externally and self-imposed muscle stretch and consequently, to impaired voluntary
movement.”
The physiological mechanisms underlying changes in the excitability of the reflex circuitry
include:
• Increased fusimotor drive
• Alpha motoneurone hyperexcitability
• An increase in the gain of the spinal reflex circuitry
• A lowering of the threshold of the spinal circuitry
It is important to remember that the spastic movement disorder and presenting features
are not only different in different conditions e.g. stroke and SCI but also vary over time
(Bennett 2008).
In the clinical setting muscle tone is assessed by moving the limb and feeling the
resistance as the limb is moved passively. The resistance that is felt when limb is moved
at rest is a combination of the physical inertia of the extremity and the inherent viscoelastic
properties of the muscle and connective tissue.
The tension set up in the muscle by reflex contraction caused by muscle stretch
contributes to the resistance only during movement.
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Following an upper motoneurone lesion patients’ will try to function within their
environment as best they can. For the majority of patients this will involve coping with
postural instability and displacement, against a background of abnormal postural
alignment and low tone / weakness
In some patients this may result in an associated reaction. Associated reactions frequently
occur in response to a loss of anticipatory postural adjustments during perturbations.
Perturbations may occur as a result of activities such as sneezing, laughing, or effortful
movement. Should the associated reaction be repeated frequently biomechanical changes
to muscle and soft tissue length may occur.
The limited or altered movement that occurs as a result of the neural consequences of the
UMN syndrome also results in changes to both the myogenic and arthrogenic structures
within the body. Changes within the muscles include a loss of sarcomeres in muscles held
in a shortened position, altered protein synthesis with a proportional increase in the
amount of collagen within muscle. Muscle fibre type has been shown to alter in response
to the changed demand and cross bridge formation and release has also been implicated
in changes to muscle compliance. Changes in the collagenous structures around and
within joints include reductions in lubrication and alignment of collagen fibres and results in
intra-articular adhesions (Singer et al 2001).
The relative contribution of the neural and non-neural changes varies between individuals
and over time. The contribution of non-neural changes to altered alignment of soft tissues,
joints and limbs and the contribution to the movement disorders seen post UMN damage
can be significant.
In the assessment of a patient it is essential to consider
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Alignment
Muscle length
Postural control / balance
Activity
Compensation
Function
Proprioceptive input
Consideration should be given to the environment in which the patient is functioning, the
postures the patient adopts over the 24 hours, the assistance that the patient receives. It is
also essential to be aware of any pharmacological management of increased tone as well
as any strategies such as splinting being used to manage biomechanical changes.
In the treatment of the patient careful emphasis on optimal alignment of both muscles and
joints within the limbs and trunk will ensure optimal potential for recovery of postural
control, selective movement and function.
Reading
Ada L, O’Dwyer N, O’Neill E. (2006) Relation between spasticity, weakness and
contracture of the elbow flexors and upper limb activity after stroke: an observational study
Disability and Rehabilitation 28: 891-897.
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Adams MM, Hicks AL. (2005) Spasticity after spinal cord injury. Spinal Cord 43: 577-586.
Azari N, Seitz R. (2000) ‘Brain plasticity and recovery from stroke’. American Scientist
88:426-31
Bakheit AMO, Maynard VA, Curnow J, Hudson N, Kodapala S. (2003) The relation
between Ashworth scale scores and the excitability of the α motor neurones in patients
with post stroke spasticity. Journal of Neurology, Neurosurgery and Psychiatry 74: 646-64.
Bruton A. (2002) Muscle plasticity: response to training and detraining. Physiotherapy
88(7):398-408.
Fraser C et al (2002) Driving plasticity in human adult motor cortex is associated with
improved motor function after brain injury. Neuron 34:831-40
Gracies JM (2006) Pathophysiology of spastic paresis: Paresis and soft tissue changes.
Muscle Nerve 31: 535-551.
Gracies JM. (2005) Pathophysiology of spastic paresis ll: emergence of muscle
overactivity Muscle and Nerve 31:522-71.
Lance J(1980) Symposium synopsis. In Feldman R, Young R, Koella W (eds) Spasticity:
Disordered Motor Control. Year Book, Chicago.
Jörg Wissel J, Manack A, Brainin M. (2013) Toward an epidemiology of post stroke
spasticity Neurology 80: (S2) S13-S19 DOI 10.1212/WNL.0b013e3182762448.
Lundstrom E, Smits A, Terent A, Borg J. (2010) Time course and determinants of
spasticity during the first six months following first ever stroke Journal of Rehabilitation
medicine 42: 296-301.
Malhotra S, Pandyan AD, DayCR, Jones PW, Hermens H. (2009) Spasticity, an
impairment that is poorly defined and poorly measured Clinical Rehabilitation 23: 651-658.
Malhotra S, Cousins E, ward A, Day C, Jones P, Hoffe C, Pandyan A. (2008) An
investigation into the agreement between clinical, biomechanical and neurophysiological
measures of spasticity. Clinical rehabilitation 22:1105-1115.
Nielsen JB, Crone C, Hultborn H. (2007) The spinal pathophysiology of spasticity – from a
basic science point of view 189: 171-180.
Nozaki D, Kawashima N, Aramaki Y, Akai M, Nakazawa K, Nakajima Y, Yano H. (2003)
Sustained muscle contractions maintained by autonomous neuronal activity within the
spinal cord. Journal of Neurophysiology 90: 2090-2097.
Pandyan AD, Gregoric M, Barnes MP, Wood D et al (2005) Spasticity: clinical perceptions,
neurological realities and meaningful measurement. Disability and Rehabilitation
27(1&2):2-6.
Patrick T, Ada L. (2006) The Tardieu Scale differentiates contracture from spasticity
whereas the Ashworth Scale is confounded by it. Clinical Rehabilitation 20: 173-182
Patten C, Lexell J, Brown HE. (2004) ‘Weakness and strength training in persons with post
stroke hemiplegia: rationale, method and efficacy. J Rehabil Res Dev 41(3A):293-312.
Satkunam LE. (2003) Rehabilitaion medicine: 3. Management of adult spasticity Canadian
Medical Association Journal 169: 1173- 1179.
Sheean G. (2002) The pathophysiology of spasticity. European Journal of Neurology
9(s1):3-9.
Singer B, Dunne J, Allison G. (2001) Reflex and non-reflex elements of hypertonia in
triceps surae muscles following acquired brain injury: implications for rehabilitation.
Disability and Rehabilitation 23(17):749-75.
Sommerfeld DK, Eek E, Svensson AK, Holmquist LW, von Arbin MH. (2004) Spasticity
after stroke: Its occurrence and association with motor impairments and activity limitations
35: 134-139.
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