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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.
MUSCLE TONE
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 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)
Definitions of Spasticity
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
Neural Mechanisms

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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
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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
Compensation
Hypertonus
Associated Reaction
Without Specific
Lesion
Can develope
to Fixation
Established
Spastic Pattern
Caused through
a Lesion in CNS
Stereotype
Dynamic
Spasticity
Biomechanical
Changes
Ryerson Composite Model for
Intervention
CNS Lesion
Generalized reflex release - spasticity
Altered Sensation
Central Loss of
Force production
Muscle Activation Deficit
Pain
Trunk-Limb linkages
Edema
Intralimb – Arm
Movement linkages
Intralimb – Leg
Movement linkages
Muscle shortening
Muscle shifting
Joint alignment
Altered Postural Control
Clinical Hypertonicity
Initiation
Timing
Cocontraction
Sequencing
Cessation
Loss of Refined Movement
Susan Ryerson 2003
UMN LESION
Non-neural
Flaccidity
Mal-alignment
Length changes
Biomechanical changes
Mass patterns
Hypertonia
Poor voluntary activity
with poor specificity
Neural
Neuralshock
Diaschisis
Plasticity
Loss of pre-synaptic control
Loss of recurrent inhibition
Loss of reciprocal inhibition
Novel connections (sp cord)
Peripheral input gains control of SCC
Inc Hyper-reflexia and AR`s
Loss of Golgi activity
during voluntary movement
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
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Basic trunk-limb (girdle) movement patterns
Spasticity is different from clinical hypertonicity

Intralimb movement sequences
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Muscle activation deficits result in disruption of voluntary
movement

Prevent persistent posturing
Ryerson, 2003
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
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
hypertonicity
Ryerson 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
Definitions of Spasticity
“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
“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
Definitions of Spasticity
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
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