Muscle tone
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Transcript of Muscle tone
MUSCLE TONE
Dr PS Deb MD, DM
Director Neurology GNRC Hospital
Assam, India
“Tonus is status of contraction of resting muscle”
• Muller 1833
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 Types Type A Type B Type C
Size of M.Unit Large Small Intermediate
Diameter of muscle fiber Small Intermediate
Small
Capillary Small Intermediate
Large
Mitochondrial ATPase Low Medium High
Glycogen content High Medium Low
Contraction Speed Fast Slow Intermediate
Maximum Tetanic tension High Low Intermediate
Fatigability Low Very high High
Post tetanic potentiation of twitch contraction
Poor Good Good
Post tetanic repetitive activity Absent Present Absent
Electric stimulation of peripheral nerve, motor cortex
Fascilitation
Inhibition
Distribution Flexor Extensor, Antigravity
MUSCLE SPINDLE
MUSCLE SPINDLE: STRETCH RECEPTOR
THE INFLUENCE OF AFFERENT ACTIVITY ON MOTOR BEHAVIOR
STATIC AND DYNAMIC RESPONSE OF MUSCLE SPINDLE AFFRENTS
Static response is the discharge at any constant length of the muscle. The greater the muscle length greater is the stretch in the spindle and the higher is the static response of the spindle affrents. Both the primary (Iα) and secondary II spindle affrents gives static or length sensitive responses.
The dynamic response of a spindle affrents refer to the discharge during stretch of the muscle. If the spindle affrents gives greater response during a fast stretch than it dose during a slow stretch (velocity different but distance of stretch same) it is said to poses a dynamic response component. Only the primary spindle affrents gives a dynamic or velocity sensitive response.
STATIC AND DYNAMIC FUSIMOTOR NEURONS Dynamic fusimotor fiber increase the dynamic response
of the primary spindle affrents (Iα) and have little or no effect on secondary.
Static fusimotor fibers increases the static response of both the primary and secondary spindle affrents. However the effect of static fusimotor fiber on primary spindle affrents is less marked than their effect on the secondary.
Static fusimotor fiber terminate as trail endings (mostly present in nuclear chain fibers).
Experiment using depletion of muscle glycogen as an index of muscle fiber activity have shown that repetitive stimulation of the static fusimotor fiber result primarily in chain fiber glycogen depletion.
Dynamic fusimotor stimulation produces mostly bag fiber glycogen depletion.
STRETCH REFLEX
POLYSYNAPTIC REFLEX
ALPHA AND GAMMA MOTOR NEURONS ARE COACTIVATED DURING VOLUNTARY MOVEMENTS
WITHDRAWAL REFLEX
POLYSYNAPTIC WITHDRAWAL REFLEX
WITHDRAWAL AND CROSSED EXTENSOR REFLEX
GROUP II FIBER REFLEX (MASS REFLEX)
In spinal animal group II fiber from muscle spindle causes polysynaptic generalized facilitation of flexor muscle and inhibition of extensor muscle
Sometime it radiate to the contralateral limbs
FUSIMOTOR FUNCTION IN MOTOR CONTROL
The fusimotor reflexes are characteristically polysynaptic
It receive only weak reflex effect from muscle proprioceptors
Cutaneous afferent fibers are very effective in provoking fusimotor excitation
It has lower threshold for reflex activity In tonic muscle (soleus) the fusimotor neuron
have higher tonic discharge rate than the skeletomotor neuron
Among phasic muscles where many skeletomotor neuron are silent the fusimotor neuron may sometime show level of activity
COMPENSATORY MECHANISM FOR FUSIMOTOR
During extrafusal muscle contraction they keep the muscle spindle receptors in tune, sending proprioceptive information centrally and thereby allowing CNS to judge. Whether or not the degree of muscle contraction is appropriate for the motor task.
They permit the Ia afferent to continue their support of the skeletomoter neuron discharge during contraction by contraction by monosynaptic facilitation.
GOLGI TENDON ORGAN
GOLGI TENDON ORGAN
CEREBELLAR AWARENESS OF MUSCLE TONE
After MS stimulation (stretch) APs are conducted along the afferent fiber (Ia)
It enters into the spinal cord and divides into several collaterals.
Some of these collaterals synapse on the cell bodies of neurons which ascend to the cerebellum (anterior and posterior spinocerebellar tracts).
Thus, at all times the cerebellum is aware of the state of stretch in muscles, in other words the TONE of muscles.
CEREBELLAR CONTROL OF MUSCLE TONE
Golgi tendon organs detects tension in the tendon.
Afferent neurons conduct action potentials to the spinal cord.
Afferent neurons synapse with inhibitory (inter) association neurons (secretes GABA) which in turn synapse with alpha motor neurons.
Inhibition of the alpha motor neurons causes muscle relaxation, relieving the tension in the muscle.
CLASP KNIFE REFLEX
Seen in decerebrate rigidity On stretching the muscle beyond a point
causes Ib affrent inhibitory discharge from GTO which reflexly inhibits homonymous stretched muscle
EXTRAPYRAMIDAL PATHWAY
Vestibulospinal tract Reticulospinal tract Rubrospinal tract Tectospinal tract
VESTIBULOSPINAL TRACT
Origen: Lateral vestibular nucleus
Course: Un-corssed Termination: Periphery of the
ant white column of spinal cord
Affrent: Neck proprioceptive affrent, Labrynth
Effect: Fasilitation of α γ motor neuron and stretch reflex.
Produces decerebrate rigidity, abolished by damage to lateral vestibular nucleus
RETICULOSPINAL TRACT (INHIBITORY)
A. Noradrinergic RST arise at Locus Ceruleus
B. Serotonergic RST arise near median raphe
Pathway ? Function: Replal short latency
flexor affrent, transient excitation of flexor and inhibition of extensor by asynchronus activity in flexon lasting 200-300 μ sec. accompanied by compansatory prolonged inhibition of extensors
Helps in locomotion
DORSAL RETICULOSPINAL SYSTEM
Arises from pontomedulary reticular formation and traverses the dorsolateral funiculus of spinal cord
Suppress Ib disynaptic inhibition and first interneuron of FRA pathway
Lesion of this tract in decerebrate cat produce spasticity and transform the reflex effect of group II affrent fibers from one of potentiating to one of inhibiting the stretch reflex of extensor muscle as the muscle is progressively lengthened
Release of FRA -> flexor spam in paraplegia
INHIBITORY RETICULOSPINAL TRACT
Origin: Ventromedian medulla Course: Crossed and Uncrossed ant to lateral
corticospinal tract in man Driven by motor cortex by descending tract
to medulla Inhibits transmission of Ia affrent fiber
(suppressing stretch reflex) as well as other terminal synapsing on motor neuron
Break reflex standing to walking Lesion: Hypereflexia and Hypertonia
FASCILITATORY RETICULOSPINAL TRACT
Origin: Pontine and medullary reticuar formation
Course: Near sulcomarginal region near vestibulospinal tract
Facilitate flexion of upper limb and extension of lower limb -> Reflex standing
OTHER TRACT
Rubrospinal Tract: Facilitatory like pyramidal not seen in man
Tectospinal tract: Like vestibulospinal system help rotatory movement of head and trunk in response to visual stimuli
Pyramidal tract: Promote extension of upper limb and flexion of lower limb through α + γ motor neuron
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
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 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 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
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
THANKS