MUSCLE TONEMunish Kumar

Muscle Tone

• The word TONUS was first used to designate the state of contraction of resting muscle by Muller in 1838.

• Vulpian defined Tone as a state of permanent muscular tension.

• Muscle tone is usually described as the resistance of a limb to passive movement (Foster 1892).

Neurophysiology of Muscle Tone

• In a normally relaxed individual , the only

resistance felt on moving the limb at a joint is

that due to the mechanical properties of the

limb ,its joints , ligaments and muscles.

Neurophysiology of Muscle Tone

Control of Muscle tone

Spinal control Supra spinal control

Spinal control of muscle tone

• Stretch reflex of Sherrington is the basic

mechanism of tonic activity.

• Muscle spindle and alpha and gamma

motoneurons are mainly implicated.

Muscle spindle

• Muscle spindle is a

fusiform structure

laying between and

parallel to the muscle

fibres and sharing their

tendinous attachement.

Muscle spindle

• It consisting of about 4 to 12 intrafusal fibres, which have a smaller diameter than the extrafusal fibres.

• Intrafusal fibres are of two types :

Nuclear bag fibres and Nuclear chain fibres.

• Serve to monitor both the length of the muscle and the velocity of its contraction

Nuclear bag fibers

• These bulge out at the middle,

where they are the most elastic .

• A large diameter myelinated

sensory nerve fibre (Ia) ends at

nuclear bag.

• Motor fibres ( γ efferents) which

subserve contraction of of its

striated portion.

• This is the dynamic component of

the stretch reflex

Golgi Tendon Organ

• Net like collection of knobby nerve endings among the fascicles of a tendon.

• Stimulated by passive stretch & active contraction of muscle.

• Signals the tension and provides negative feedback control of muscle contraction and regulates muscle force rather than length.

Afferent and efferent pathways

Efferent pathway

• α-motoneurons runs from cell body in ant. horn to extrafusal muscle fibre.

• γ- motoneurons runs from cell body in ant. horn to intrafusal muscle spindle.

Afferent pathway

• Ia from nuclear bag fibre passes via dorsal horn to synapse with α-motoneurons

• II from muscle spindle synapse with interneurons• Ib from golgi tendon organ ends in nucleus dorsalis

and synapse with interneurons.

Tone - Mechanism

• γ- motoneurons activity causes

the intrafusal fibre to contract

this streches the

primary sensory ending, thus

increasing afferent discharge

causing depolarisation of

α-motoneurons supplying the

extrafusal muscle, thereby

increasing muscle tone.

Supra-spinal control

The efferent fibres to the muscle spindle, γ-

motoneurones, receive input form higher

centres via :

• Facilitatory fibres and

• Inhibitory fibres

Supra-spinal controlIn human spastic paretic syndrome, the three important pathways are –

corticospinal, reticulospinal, and vestibulospinal.

Medial and lateral descending brain stem pathways involved in motor control

Medial pathways (reticulospinal,

vestibulospinal, and tectospinal) terminate in

ventromedial area of spinal gray matter and

control axial and proximal muscles

Lateral pathway (rubrospinal) terminates in

dorsolateral area of spinal gray matter and

controls distal muscles.

Inhibitory Supraspinal Pathways

1. Corticospinal pathway –

Isolated pyramidal lesions have not produced spasticity in conditions such as

destruction of motor cortex (area 4), unilateral lesion in cerebral peduncle,

lesions in basis pontis and medullary pyramid (Bucy et al., 1964; Brooks,

1986). Instead of spasticity these lesions produced weakness, hypotonia, and

hyporeflexia.

Spasticity however may be caused if the lesions include the premotor and

supplementary motor areas.

Lesions in the anterior limb of internal capsule and not in the posterior limb

produce spasticity as fibers from supplementary motor area pass through

anterior limb.

Inhibitory Supraspinal Pathways

2. Corticoreticular pathways and dorsal (lateral) reticulospinal tract –

Medullary reticular formation is active as a powerful inhibitory center

to regulate muscle tone (stretch reflex) and the cortical motor areas

control tone through this center.

Lesions of supplementory motor area or internal capsule reduces

control over medullary center to produce hypertonicity.

Flexor spams and Clasp-knife phenomenon are due to damage to

dorsal reticulospinal pathway (Fisher and Curry 1965).

Excitatory Supraspinal pathways

1. Medial (ventral) Reticulospinal Tract –

Through this tract reticular formation exerts facilitatory influence on spasticity.

Origin mainly from pontine tegmentum.

More important than vestibulospinal system in maintaining spastic extensor tone.

2. Vestibulospinal pathway:

Vestibulospinal tract (VST) is a descending motor tract originating from lateral vestibular

(Deiter’s) nucleus and is virtually uncrossed.

This excitatory pathway helps to maintain posture and to support against gravity and so

control extensors rather than flexors. This pathway is important in maintaining decerebrate

rigidity but has lesser role in human spasticity (Fries et al., 1993).

The cerebellum through its connections with the vestibular nuclei and reticular formation

may indirectly modulate muscle stretch reflexes and tone.

Inhibitory

excitatory

Decerebration

• A complete transection of the

brain stem between the superior

and inferior colliculi permits the

brain stem pathways to function

independent of their input from

higher brain structures. This is

called a midcollicular

decerebration. (A)

Decerebration

• This lesion interrupts all input from the

cortex (corticospinal and corticobulbar

tracts) and red nucleus (rubrospinal tract),

primarily to distal muscles of the

extremities.

• The excitatory and inhibitory

reticulospinal pathways (primarily to

postural extensor muscles) remain intact.

• The excitatory reticulospinal pathway

leads to hyperactivity in extensor muscles

in all four extremities which is called

decerebrate rigidity.

Decortication

• Removal of the cerebral cortex

(D) produces decorticate

rigidity.

• The flexion can be explained

by rubrospinal excitation of

flexor muscles in the upper

extremities.

• The hyperextension of lower

extremities is due to the same

changes that occur after

midcollicular decerebration.

Disorders of muscle tone

• Abnormalities of the tone :

Hypertonia –

Pyramidal hypertonia (Spasticity)

Extrapyramidal hypertonia (Rigidity)

Hypotonia

Pyramidal hypertonia (Spasticity)

• Spasticity – a motor disorder characterized by

velocity- dependent increase in muscle tone with

exaggerated tendon jerks, resulting from

hyperexcitability of the stretch reflex.

• Pyramidal hypertonia is most pronounced in the

muscle groups most used in voluntary movements.

Spasticity

• Physiologic evidence suggests that interruption of

reticulospinal projections is important in the genesis of

spasticity.

•  In spinal cord lesions, bilateral damage to the pyramidal

and reticulospinal pathways can produce severe

spasticity and flexor spasms, reflecting increased tone in

flexor muscle groups and weakness of extensor muscles.

Spasticity - EDX

• There will be increased H reflexes, identified with an

increase of maximum amplitude H reflex compared

to the M wave – H/M ratio.

• Increased F wave amplitude.

Spasticity – The Mechanism

1. α- motoneuron excitability-

enhanced H:M ratio and F-wave

amplitude suggest enhanced

excitability of α- motoneuron.

2. γ- motoneuron excitability –

causes increased spindle

sensitivity to stretch, augmenting

the Ia afferent response to stretch,

and exaggerates the stretch reflex.

Spasticity – the mechanism

3. Recurrent inhibition –recurrent collateral

axons from motoneurons activate

Renshaw cell, which inhibit α-

motoneurons. Changes in recurrent

inhibition plays a role in the

pathophysiology of spasticity.

4. Reciprocal inhibition-During active

contraction, it is necessary to inhibit MNs

supplying the antagonist muscle(s),at the

same rate ( Sherrington’s law of

reciprocal innervation).

This is to prevent their reflex contraction

in response to stretch.

5. Presynaptic inhibition

Clinical correlation

In cortical and internal capsular lesions, the

controlling drive on the inhibitory center in

the medullary brain stem is lost and so in

absence of inhibitory influence of lateral

RST originating from this center, facilitatory

action of ventral RST becomes unopposed.

This results in spastic hemiplegia with

antigravity posturing, but flexor spams are

unusual.

Clinical correlation - Spinal lesions

1. Incomplete (partial) myelopathy

involving lateral funiculus may affect CST

only to produce paresis, hypotonia,

hyporeflexia, and loss of reflexes.

(Peterson et al., 1975)

If lateral RST is involved in addition,

unopposed ventral RST activity then

results in hyper-reflexia and spasticity

(similar to cortical or capsular lesions).

Clinical correlation - Spinal lesions

2. Severe myelopathy with involvement of all the

four descending pathways produces less marked

spasticity compared to isolated lateral cord lesion

because of lack of unopposed excitatory

influences of ventral RST.

Neuroplasticity of the spinal cord in the form of

receptor supersensitivity of neurons to a loss of

synaptic input and sprouting of axon terminals

are also responsible for hypertonicity in complete

myelopathy with delayed reorganization after a

variable period of spinal shock

Clonus • Clonus is the phenomenon of involuntary rhythmic contractions

in response to sudden sustained stretch.

• A sudden stretch activates muscle spindles, resulting in the

stretch reflex.

• Tension produced by the muscle contraction activates the Golgi

tendon organs, which in turn activate an ‘inverse stretch reflex’,

relaxing the muscle.

• If the stretch is sustained, the muscle spindles are again

activated, causing a cycle of alternating contractions and

relaxations.

Spinal shock

• In 1750, Whytt first described the

phenomenon of spinal shock as a loss of

sensation accompanied by motor paralysis

with gradual recovery of reflexes.

• There are four phases of spinal shock.

Proposed mechanisms for the four phases of spinal shock (Ditunno et al.)

Phase Time Physical exam finding Possible neuronal mechanisms

1 0-1d Areflexia/Hyporeflexia

Lost norml supraspinal excitation

Increased spinal inhibition

Reduced neuronal metabolism

2 1-3d Initial reflex returnDenervation supersensitivity

NMDA receptor upregulation

3 1-4w Hyperreflexia (initial) Axon-supported synapse growth

4 1-12mHyperreflexia,

SpasticitySoma-supported synapse growth

Cerebellum and muscle tone

• The cerebellum does not seem to have a direct effect on

muscle tone determining spinal reflex pathways as

there is no direct descending cerebellospinal tract.

• The cerebellum mainly influences muscle tone through

its connections with the vestibular and brain stem

reticular nuclei.

• Pure cerebellar lesions classically produce hypotonia.

Cerebellum and muscle tone

• Gamma motor neurons selectively depressed

• Alpha motor neurons can respond to inflow from

spindles to produce tendon jerk.

• Associated corticospinal tract involvement produces

varying degrees of spasticity as seen in spino-

cerebellar ataxia (SCA).

Extrapyramidal hypertonia (Rigidity)

• Rigidity is characterized by an increase in muscle tone

causing resistance to externally imposed joint movements.

• It does not depend on imposed speed and can be elicited at

very low speeds of passive movement.

• It is felt in both agonist and antagonist muscles and in

movements in both directions.

Extrapyramidal hypertonia (Rigidity)

• 'Cogwheel' rigidity and 'leadpipe' rigidity are two types.

• 'Leadpipe' rigidity results when an increase in muscle tone causes a

sustained resistance to passive movement throughout the whole

range of motion, with no fluctuations.

• 'Cogwheel' rigidity occus in association with tremor which presents

as a jerky resistance to passive movement as muscles tense and

relax.

• Basal ganglia structures are clearly implicated in pathophysiology

of rigidity.

Extrapyramidal hypertonia (Rigidity)Nurophysiology

1. Reflex origin of rigidity

Enhanced tonic reflex activity ( a stimulus produces a prolonged

discharge of motor neurons causing sustained muscle contraction).

The phasic stretch reflex (monosynaptic) is not responsible for rigidity.

2. Segmental and supraspinal influences

α- motoneurons and possibly cortical excitability is enhanced in rigidity.

Recurrent Renshaw cell inhibition is normal.

Extrapyramidal hypertonia (Rigidity)

It has been suggested that the distribution of higher facilitatory

influence between flexor and extensor motoneurons may be

unequal in pyramidal and approximately equal in

extrapyramidal type.

3. Inadequate voluntary relaxation.

Dystonia

• Characterized by abnormal muscle spasm producing

distorted motor control and undesired postures.

• A principle finding is the loss of cortical inhibition.

• Failure of “surround inhibition”. Brain activates a

specific movement and simultaneously inhibits

unwanted movements.

Hypotonia

• Hypotonia may affect a muscle’s resistance to passive

movement and/or its extensibility.

• Aetiological types of hypotonia :

1. Nerve trunk and root lesion

2. A lesion of anterior horn

3. Cerebellar lesions

4. Cerebral lesions

Hypotonia - causes

Congenital

Genetic

Developmental

Acquired

Genetic

Infectious

Neuromuscular Jn

Clinical Examination

Tone is difficult to assess.

The determination of tone is subjective and prone to interexaminer

variability.

The most important part of the examination of tone is determination

of the resistance of relaxed muscles to passive manipulation as well

as the extensibility, flexibility, and range of motion.

The examination of tone needs a relaxed & cooperative patient

Methods

• Inspection : Attitude of the limb at rest.

• Palpation : Feel of the muscle – normal, firm or flabby.

• Range of movement at the joints.

• Passive movement - first slowly and through complete range of motion

and then at varying speeds.

• Shake the distal part of the limb.

• Brace a limb and suddenly remove support.

• Bilateral examination of homologous parts helps compare for differences

in tone on the two sides of the body.

Specific Maneuvers

• The Babinski Tonus Test

• The Head Dropping Test

• Wartenberg’s Pendulum Test

• The Shoulder Shaking Test

• The Arm Dropping Test ( Bechterew’s Sign in

spasticity)

Specific Maneuvers

1. The Babinski Tonus Test

The arms are abducted at the shoulders, and the forearms are passively flexed at

the elbows.

With hypotonicity there is increased flexibility and mobility, and the elbows can be

bent to an angle more acute than normal.

With hypertonicity there is reduced flexibility and passive flexion cannot be

carried out beyond an obtuse angle.

2. The Head-Dropping Test

The patient lies supine without a pillow, completely relaxed, eyes closed and

attention diverted.

The examiner places one hand under the patient's occiput and with the other hand

briskly raises the head, and then allows it to drop. Normally the head drops rapidly

into the examiner's protecting hand, but in patients with extrapyramidal rigidity

there is delayed, slow, gentle dropping of the head because of rigidity.

Specific Maneuvers

3. Pendulousness of the Legs

The patient sits on the edge of a table, relaxed with legs hanging freely.

The examiner either extends both legs to the same horizontal level and then

releases them (Wartenberg's pendulum test), or gives both legs a brisk, equal

backward push.

If the patient is completely relaxed and cooperative, there will normally be a

swinging of the legs that progressively diminishes in range and usually

disappears after six or seven oscillations.

In spasticity, there may be little or no decrease in swing time, but the

movements are jerky and irregular, the forward movement may be greater and

more brisk than the backward, and the movement may assume a zigzag pattern.

In hypotonia, the response is increased in range and prolonged beyond the

normal.

Specific Maneuvers

4. The Shoulder-Shaking Test

The examiner places her hands on the patient's shoulders and shakes them briskly

back and forth, observing the reciprocal motion of the arms.

With extrapyramidal disease, there will be a decreased range of arm swing on the

affected side.

With hypotonia, especially that associated with cerebellar disease, the excursions of

the arm swing will be greater than normal

5. The Arm-Dropping Test

The patient's arms are briskly raised to shoulder level, and then dropped. In

spasticity, there is a delay in the downward movement of the affected arm, causing

it to hang up briefly on the affected side (Bechterew's or Bekhterew's sign).

With hypotonicity the dropping is more abrupt than normal.

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• Ganong’s textbook of physiology.

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neurology.2010;1:149-54.

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383–395.

• Robert A. Davidoff, MD. Skeletal muscle tone. Neurology 1992;42:951-963.

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