Muscle Tone andSpasticity Physical Therapy Department Dong-eui Medical Center
The dying Lioness(an Assyrian relief dating from about 650 B.C and supplied through the courtesy of The Trustees of the British Museum)shows this vividly injury to the spinal cord has paralyzed the otherwise undamaged hind legs.
2004년 4월30일 오전 카자흐스탄 초원에 무사히 착륙한 러시아 소유스 TMA-3의 우주비행사들. 이들은 국제우주정거장(ISS)에서 9일~6개월 근무한뒤 지구로 귀환했다. 왼쪽부터 미국인 마이크 폴, 러시아인 알렉산더 카렐리, 유럽우주국(ESA) 소속 네덜란드인 앙드르 퀴퍼스.
Overall organization of neural structures involved in the control of movement. Four distinct systems make essential and distinct contributions to motor control Motor Cortex Planning, initiating,and Directing voluntary movement Brainstem Centers Basic movements and Postrural control BASAL GANGLIA Gating proper initiation Of movement CEREBELLUM Sensory motor coordination Brain stem tracts Coticospinal tracts Motor neuron pools Lower motor neurons Local circuit neurons Reflex coordination SPINAL CORD AND BRAINSTEM CIRCUITS SKELETAL MUSCLES
The stretch reflex of the calf muscles is differentially gated during locomotion. Presumed action of the short latency stretch reflex during the stance (a)and swing phase (b)of locomotion a. this reflex system is facillitated by supraspinal influences on the pre-and postsynaptic elements during the stance phase for the rapid compensation of ground irregularities b. During the swing phase. The stretch-induced reflex activity in the triceps.avoked by active dorsiflexion of the foot,is inhibited pre and postsynaptically to allow proper placing of the foot.
Comparison of the force and fatigability of the three different types of motor units. In each case. The response reflects stimulation of a single motor neuron. (A) Change in tension in response to single motor neuron action potentials. (B) Tension in response to repetitive stimulation of the motor neurons (C) Response to repeated stimulation at a level that evokes maximum tension. The y axis represents the force generated by each stimulus.
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
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 role of gamma motor neuron activity in regulating the responses of muscle spindles. The gamma motor neurons can regulate the gain of muscle spindles so that they can operate efficiently at any length of the parent muscle.
Summary view of descending pathways, showing multiple projections and different laminar locations of cortical output neurons. Note that superficial laminae(ⅡⅢ) project to other cortical areas, whereas deep cortical laminae(ⅤⅥ)give rise to descending projections, both pyramidal and estrapyramidal. Lamina Ⅳ(granule layer)is poorly developed in most parts of primary and secondary motor cortex
Anticipatory maintenance of body posture. At the onset of a tone, the subject pulls on a handle, contrcting the biceps muscle. Contraction of the gastronemius muscle precedes that of the biceps to ensure postural stability.
Schematic of the mechanisms that contribute to spastic paresis and spastic movement disorder. A central motor lesion leads to changes in the excitability of spinal reflexes and a loss of supraspinal drive. As a consequence, changes in muscle properties occur. The combination of all sequels of the primary lesion leads to the spastic movement disorder. CNS;central nervous system.
SPASTICITY • Traditional conecept - Muscle hypertonia: velocity dependent resistance to stretch -Exaggerated reflexes(Ashworth’s Scale) • New concept - Loss of longer latency reflexes(spinal) - Decrease of nuscle activity during function - Chane 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 established 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 - Weakness and decreased skills (Astereognosia) - Changes in anticipatory contrast - Hyperexitability of motorneurons - Muscle hypertonicity (Hyporeflexia of tendon) • Non-neural Mechanisms - Biomechanical changes in muscle - Thixotrophia (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
Compensation Hypertonus Established Spastic Pattern Associated Reaction Caused through A lesion in CNS Without Specific Lesion Stereotype Dynamic Can develop to Fixation Biomechanical Changes Spasticity
Ryerson Composite model for Intervention CNS Lesion Generalized reflex release - spasticity Altered Sensation Pain Edema Central Loss of Force Production Muscle Activation Deficit Trunk-Limb linkages Initiation Timing Cocontraction Sequencing Cessation Intralimb –Arm Movement linkages Intralimb – Leg Movement linkages Muscle shortening Muscle shifting Joint alignment Altered Postural Control Clinical Hypertonicity Loss of Refinde Movement
UMN LESION Non-neural Neural Flaccidity Mal-alignment Length changes Neuralshock Diaschisis Plasticity Loss of pre-synaptic control Loss of recurrent inhibition Loss of reciprocal inhibition Novel connections(SP cord) Biomechnical changes Mass Patterns Peripheral input gains control of SCC Hypertonia Inc Hyper-reflexia and AR’s Poor voluntary activity With poor specificty Loss of Golgi activity During voluntary movement
CLINICAL IMPLICTIONS • Non-neural components can be as singnificant in hypotonicity as hypertonicity. • The non-neural effects can also add to the neural mechanism • Limitation 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