General understanding of tone

1. MUSCLE
TONE

2. 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).

3. 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.

4. Neurophysiology of Muscle Tone
Control of Muscle tone
Spinal
control
Supra spinal
control

5. 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.

6. Muscle spindle
• Muscle spindle is a
fusiform structure
laying between and
parallel to the muscle
fibres and sharing their
tendinous attachement.

7. 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

8. 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

9. 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.

10. 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 hornto
synapse with α-motoneurons
• II from muscle spindle synapse with interneurons
• Ib from golgi tendon organ ends in nucleusdorsalis
and synapse with interneurons.

11. 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.

12. Supra-spinal control
The efferent fibres to the muscle spindle, γ-
motoneurones, receive input form higher
centres via :
• Facilitatory fibres and
• Inhibitory fibres

13. Supra-spinal control
In human spastic paretic syndrome, the three important pathways are –
corticospinal, reticulospinal, and vestibulospinal.

14. 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.

15. Inhibitory Supraspinal Pathways
1. Corticospinal pathway –
 Isolated pyramidal lesions have not produced spasticity in conditionssuch
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.

16. 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).

17. 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.

18. Inhibitory
excitatory

19. 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)

20. 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.

21. 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.

22. Disorders of muscle tone
• Abnormalities of the tone :
Hypertonia –
Pyramidal hypertonia (Spasticity)
Extrapyramidal hypertonia (Rigidity)
Hypotonia

23. 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.

24. 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.

25. 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.

26. 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.

27. 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

28. 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.

29. 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).

30. 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

31. 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.

32. 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.

33. 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 return
Denervation supersensitivity
NMDA receptorupregulation
3 1-4w Hyperreflexia (initial) Axon-supported synapse growth
4 1-12m
Hyperreflexia,
Spasticity
Soma-supported synapse growth

34. 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.

35. 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).

36. 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.

37. 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.

38. 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 forrigidity.
2. Segmental and supraspinal influences
 α- motoneurons and possibly cortical excitability is enhanced in rigidity.
 Recurrent Renshaw cell inhibition is normal.

39. 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.

40. 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.

41. 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

42. Hypotonia - causes
Congenital
Genetic
Developmental
Acquired
Genetic
Infectious
Neuromuscular Jn

43. 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

44. Methods
• Inspection : Attitude of the limb atrest.
• Palpation : Feel of the muscle – normal, firm orflabby.
• Range of movement at the joints.
• Passive movement - first slowly and through complete range ofmotion
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 comparefor
differences in tone on the two sides of the body.

45. 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)

46. 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.

47. Specific Maneuvers
3. Pendulousness of the Legs
 The patient sits on the edge of a table, relaxed with legs hangingfreely.
 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 bea
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 beyondthe
normal.

48. 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.

49. Source
• Handbook of clinical neurology. Vinken and Bruyn.
• Ganong’s textbook of physiology.
• DeJong’s The neurological examination.
• Mukherjee A. Spasticity mechanisms – for the clinician.Frontiers in
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
Neurophysiol 96: 2678–2687, 2006