MUSCLE TONE AND SPASTICITY

Irfan

Motor Unit

Basic unit of contraction in skeletal muscle

Composed of one or more muscle fibers and the motor neuron that controls them

AP in motor neuron results in contraction

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.

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.

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.

MUSCLE TONE

Negative feedback regulation of muscle tension by Golgi tendon organs

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)

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

Neural Mechanisms Weakness and decreased skills (Astereognosia) Changes in anticipatory contrast Cutane hyperreflexia Hyperexitability of motorneurons Muscle hypertonicity (hyporeflexia of tendon)

Non-neural Mechanisms Biomechanical changes in muscles Tixotrophia (stiffness of myosin cross links)

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

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

Sensory Deficits

Deficits in awareness, processing and interpretation and kinesthetic memory Fewer attempts at spontaneous movements Altered sence of „weight“ of a limb Altered sence of timing and speed Difficulty replaying movements in their imagination

and recognizing them in facilitation Contributes to development of pain

Ryerson, 2003

Spasticity

CompensationHypertonus

Can develope to Fixation

StereotypeDynamic

BiomechanicalChanges

Associated ReactionEstablished

Spastic Pattern

Without SpecificLesion Caused through

a Lesion in CNS

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

linkagesMuscle 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

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

NeuralNon-neural

UMN LESION

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

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

Process of plastic adaptation in the neuro-muscular systems

Process of plastic adaptation in the neuro-muscular systems

Primary DenervationFlaccid / Low tone

Associated ReactionsRecovery / New

EtablishmentFunctional use

Secondary ProblemsBio-mechanical Changes of muscles

Contractures Deformity

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.

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

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

Spasticity

Spastic movements disorders Dietz 2003

Clinical hypertonicityRyerson 2003

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

“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

Definitions of Spasticity

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

Volker Dietz

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

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

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

Sekian