MUSCLE TONE AND SPASTICITY - PowerPoint Presentation

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MUSCLE TONE AND SPASTICITY

Irfan

Slide2

Motor Unit

Basic

unit of contraction in skeletal muscle

Composed of one or more muscle fibers and the motor neuron that controls themAP in motor neuron results in contraction

Slide3

Comparison of the function of muscle spindles and Golgi tendon organs.

Golgi tendon organs are arranged in series with extrafusal muscle fibers because of their location at the junction of muscle and tendon.

Slide4

The motor unit. (A) Diagram showing a motor neuron in the spinal cord and the course of its own axon to the muscle. (B) Each alpha motor neuron synapses with multiple muscle fibers. The motor neuron and the fibers it contacts defines the motor unit. Cross section through the muscle shows the distribution of muscle fibers (red dots) contacted by the motor unit.

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A state of partial contraction that is characteristic of normal muscle, is maintained at least in part by a continuous bombardment of motor impulses originating reflexively, and serves to maintain body posture.

MUSCLE TONE

Muscle tone refers to the amount of tension or resistance to passive movement in a muscle.

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MUSCLE TONE

Slide7

Negative feedback regulation of muscle tension by Golgi tendon organs

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SPASTICITY

Traditional concept

Muscle hypertonia: velocity dependent resistance to stretch

Exaggerated reflexes (Ashworth‘s Scale)

New concept

Loss of longer latency reflexes (spinal)

Decrease of muscle activity during function

Change in non-neural factors as a result of the decrease of supraspinal control

Biomechanical changes in both passive and active muscles (Dietz 2003)

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The increase of stretch reflexes is not the only reason for etablished spasticity.

Factors which can lead to a mechanical resistant in movement are the reduced elasticity of the tendons and the biomechanical changes of musclefibres.

Dietz 1992

Definitions of Spasticity

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Neural MechanismsWeakness and decreased skills (Astereognosia)Changes in anticipatory contrast

Cutane hyperreflexia

Hyperexitability of motorneurons

Muscle hypertonicity (hyporeflexia of tendon)Non-neural MechanismsBiomechanical changes in muscles

Tixotrophia (stiffness of myosin cross links)

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Central Loss of Force Production

Loss of central command to generate and sustain force

No loss of contractile capacity: not the same as peripheral weakness,

Myopathy or general weakness Sahrmann 2002

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Muscle Activation Deficits

Delayed initiation and termination of muscle contraction

Chae 2002

Altered sequence of muscle firing Dewald 2001

Excessive activation/cocontraction: too many muscles with inappropriate force

Sarmann 1977

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Sensory Deficits

Deficits in awareness, processing and interpretation and kinesthetic memory

Fewer attempts at spontaneous movements

Altered sence of „weight“ of a limbAltered sence of timing and speedDifficulty replaying movements in their imagination and recognizing them in facilitationContributes to development of pain

Ryerson, 2003

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Spasticity

Compensation

Hypertonus

Can develope

to Fixation

Stereotype

Dynamic

Biomechanical

Changes

Associated Reaction

Established

Spastic Pattern

Without Specific

Lesion

Caused through

a Lesion in CNS

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Ryerson Composite

Model for

Intervention

CNS Lesion

Altered Sensation

Pain

Edema

Central Loss of Force production

Muscle Activation Deficit

Trunk-Limb linkages

Intralimb – Arm Movement linkages

Intralimb – Leg Movement linkages

Muscle shortening Muscle shifting Joint alignment

Initiation Timing Cocontraction Sequencing Cessation

Altered Postural Control

Clinical Hypertonicity

Loss of Refined Movement

Generalized reflex release - spasticity

Susan Ryerson 2003

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Flaccidity Mal-alignment Length changes

Neuralshock Diaschisis Plasticity

Biomechanical changes

Loss of pre-synaptic control Loss of recurrent inhibition Loss of reciprocal inhibition Novel connections (sp cord)

Mass patterns

Peripheral input gains control of SCC

Inc Hyper-reflexia and AR`s

Poor voluntary activity with poor

specificity

Hypertonia

Loss of Golgi activity during voluntary movement

Neural

Non-neural

UMN LESION

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CLINICAL IMPLICATIONS

Non-neural components can be

as

significant in hypotonicity as hypertonicity

The non-neural effects can also add to the neural mechanism

Limiation of range prevents movement and the static state further interferes with modulation of tonus

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Clinical Hypertonicity:

Muscle Activation Deficits

Clinical Significance:

Do not treat the hypertonicity, treat the underlying cause

Central loss of force production is unique

Basic trunk-limb (girdle) movement patterns

Spasticity is different from clinical hypertonicity

Intralimb movement sequences

Muscle activation deficits result in disruption of voluntary

movement

Prevent persistent posturing

Ryerson, 2003

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Process of plastic adaptation in the

neuro-muscular systems

Primary Denervation

Flaccid / Low tone

Associated Reactions

Recovery / New

Etablishment

Functional use

Secondary Problems

Bio-mechanical Changes of muscles

Contractures

Deformity

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Anticipatory maintenance of body posture.

At

the onset of a tone, the subject pulls on a handle, contracting the biceps muscle. Contraction of the gastronemius muscle precedes that of the biceps to ensure postural stability.

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Has Spasticity a definition?

„

Nowadays, the expression „spasticity“ is found so often in medical literature and is such an elementary neurological term that no one really expects a definition.“ Thilmann A.F. 1993

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The importance of spasticity has changed:There is no relationship between spasticity and functional performance

when

Spasticity is defined as a stretch reflex No consistant relationship between the amount of spasticiy and the performance for relearning skills and functions

The different definitions are contradictory and are describing different clinical symptoms

Slide23

Spasticity

S

pastic

movements disorders Dietz 2003

C

linical

hypertonicity

Ryerson 2003

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Definitions of Spasticity

Classic Definition:

Increased resistance of a limb to externally imposed passive joint movement

Resistance increases with increasing amplitude and velocity

Often accompanied by increased tendon jerks and clonus

Lance

1980

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“Spasticity is a slowly developing movement disorder following a complete or partial loss of supraspinal control on the

function

of the spinal cord.

Spasticity can be recognized through altered activity of the motor units as an answer to sensory or central command, which leads to abnormale cocontraction, masspatterns of movement and abnormale Postural control.“ Wiesendanger

1991

Definitions of Spasticity

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Definitions of Spasticity

“

the loss of sarcomers leads very soon to changes of the mechanical properties in muscles and therefore to hypertonicity.”

Volker Dietz

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Definitions of Spasticity

“

Intrinsic mechanical stiffness of

muscles can be responsible for spastic

hypertonissity.

This stiffness can come about through

structural changes of the

mechanical properties or through

changes of the state in the muscle tissue

itself.”

Katz und Rymer 1989

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It

could

be demonstrated that the tissue which surrounds

the

slow

twitch

muscle fibres are more sensitive to immobilisation as the

ones

which are surrounding the

fast twitch fibres. Given et al 1995

Definitions of Spasticity

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The neurological deficit

Primary Impairments

Neurological weakness

Muscle activation deficit

Spasticity

Changes in tone

Secondary Impairments

Altered alignment

Changes in muscle length and position

edema

pain

Composite Impairments

Clinical hypertonicity (spastic movement disorder)

Altered postural control

Loss of selective movement

Slide30

Sekian