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.
• DeJong’s The neurological examination.
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neurology.2010;1:149-54.
• Ditunno JF. Spinal shock revisited: a four-phase model. Spinal Cord (2004) 42,
383–395.
• Robert A. Davidoff, MD. Skeletal muscle tone. Neurology 1992;42:951-963.
• Victor G. Postural Muscle Tone in the Body Axis of Healthy Humans. J
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