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