muscle tone and spasticity irfan motor unit basic unit of contraction in skeletal muscle basic unit...
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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.
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