This document provides an overview of spasticity including: - Definitions of spasticity and tone as the continuous partial contraction of muscles at rest. - Pathophysiology involving an imbalance between excitatory and inhibitory signals to motor neurons due to lack of descending inhibition. - Characteristics including increased resistance to passive movement and hyperactive stretch reflexes. - Factors that can aggravate spasticity like pain, stress, and infection. - A spectrum of care including oral drugs, rehabilitation, intrathecal baclofen, and neurosurgery to manage spasticity based on individual needs.

1. MAHATMA GANDHI MEDICAL
COLLEGE AND HOSPITAL
DR SURBHI CHATURVEDI
NEUROLOGY DEPARTMENT
ACADEMICS
Spasticity

2. Tone
 It is the continuous and passive partial
contraction of the muscles, or the
muscle's resistance to passive stretch
during resting state.

4. Spasticity
Spastikos - “to draw or tug”
 Motor disorder
 Velocity-dependent increased resistance
to passive stretch
 Exaggerated tendon jerks
 Hyperexcitability of the stretch reflex
- James Lance (1980)

5. Pathophysiology of Spasticity
Theory
 Imbalance between excitatory and
inhibitory impulses to the alpha motor
neuron
 Due to a lack of descending inhibitory
input to the alpha motor neuron
Descending
Inhibition
Sensory
Excitation

6. Stretch Reflex
 Skeletal muscle contain specialized
proprioceptors called muscle spindles.
 These receptors sense a change in
length for extrafusal skeletal fibers.
 Leaving the muscle spindles are Ia sensory
axons.
 Ia enter the spinal cord, via dorsal
horn, branch repeatedly and form
excitatory synapses on interneurons
and alpha lower motor neurons.

7.  Ia input is very powerful
 When the muscle spindles sense a
change in length (such as during a
pull) the Ia fibers are activated, and
send excitatory stimulus to the alpha
lower motor neuron.

8.  While eliciting reflex we stretch muscle
spindles which further activates the
stretch reflex.

9. Pathophysiology of
Cerebral Origin Spasticity
Inhibitory signals
modulate reflex
signals–tone
remains normal
Lack of neural
inhibition leads to
spasticity
Normal brain
delivers inhibitory
neural signals to
the spinal cord
Damaged brain
fails to generate or
sends inadequate
inhibitory signals

10. Pathophysiology of
Spinal Origin Spasticity
Inhibitory signals
modulate reflex
signals–tone
remains normal
Lack of neural
inhibition leads to
spasticity
Inhibitory neural
signals sent to the
alpha motor
neuron
Damaged spinal
cord fails to relay
adequate inhibitory
signals
Normal Damaged

11. Inhibitory Supraspinal Pathways
 Corticospinal pathway - Pyramidal tract lesion alone is more
responsible for weakness and loss of superficial reflexes such as
abdominal reflexes rather than spasticity, hyper-reflexia and Babinski's
sign.
 Spasticity however may be caused in lesions of area 4 if the lesions
include the premotor and supplementary motor areas.
 Fibers responsible for spasticity run with the pyramidal tract to end in
the bulbar reticular formation (corticoreticular pathway).
 Lesions (vascular) 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.
 Large middle cerebral artery territory infarcts involving corticospinal
and corticoreticular pathways produce spasticity

12.  Corticoreticular pathways and dorsal 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 premotor area (frontal cortex) or
internal capsule reduces control over medullary center
to produce hypertonicity.
 Dorsal RST situated in the ventral part of the lateral
funiculus of the spinal cord carries the inhibitory
influence from the medullary center.

13.  Dorsal RST inhibits FRA(Flexor arc reflex) as well as
stretch reflex arc. “Flexor spams” are release
phenomenon of flexor reflexes due to damage to dorsal
reticulospinal pathway. Clasp-knife phenomenon is also
a release phenomenon due to loss of inhibitory effects
on FRA.

14. Excitatory supraspinal pathways
 Vestibulospinal tract - Vestibulospinal tract (VST) is a
descending motor tract originating from lateral
vestibular (Deiter's) nucleus and is virtually uncrossed.
The tract ends mostly on interneurons but also excites
motor neurons monosynaptically. This excitatory
pathway helps to maintain posture and to support
against gravity and so control extensors rather than
flexors.

15.  Medial (ventral) RST – Through this tract
reticular formation exerts facilitatory influence
on spasticity. The tract has a diffuse origin being
mainly from pontine tegmentum. Unlike dorsal
RST, it is not affected by stimulation of motor
cortex or internal capsule and not inhibitory to
FRA. This pathway is more important than
vestibulospinal system in maintaining spastic
extensor tone

16.  Muscle tone is maintained by a controlled
balance on stretch reflex arc by inhibitory
influence of CST and dorsal RST and
facilitatory influence (on extensor tone)
by medial RST and to a lesser extent in
humans by VST.

18. Clinical Correlations in Lesions of
Descending Pathways
1. 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 dorsal RST originating from this
center, facilitatory action of medial RST becomes
unopposed. This results in spastic hemiplegia with
antigravity posturing, but flexor spams are unusual.

19. 2. Spinal lesions –
(a) Incomplete (partial) myelopathy involving lateral
funiculus (e.g., early multiple sclerosis) may affect CST only
to produce paresis, hypotonia, hyporeflexia, and loss of
cutaneous reflexes. If dorsal RST is involved in addition,
unopposed medial RST activity then results in hyper-reflexia
and spasticity (similar to cortical or capsular lesions), the
latter being marked in antigravity muscles to produce
paraplegia in extension. Extensor and flexor spasms may
occur, the former being commoner.

20. (b) 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
medial RST and VST. The latter factor is also responsible for lack of
extensor hypertonia and in presence of release of flexor reflexes by
dorsal RST lesion, helps to produce paraplegia in flexion. Paraplegia in
flexion is also possible in partial myelopathy if FRA get stimulated by
factors like pressure sores.
(c) Isolated dorsal RST involvement with CST sparing may explain
marked spasticity and spasms but little weakness in many cases of
spastic paraparesis. Only hyper-reflexia with normal tone is again a
possibility in isolated anterior cord lesion.

21. UMN lesion but still have LMN
signs
 This initial period of “hypotonia” after upper
motor neuron injury is called spinal shock, and
reflects the decreased activity of spinal circuits
suddenly deprived of input from the motor
cortex and brainstem.
 After several days, however, the spinal cord
circuits regain much of their function for
reasons that are not fully understood.

22.  It suggests that this is not just simply a question of switching off
supraspinal inhibition, or altering the balance. It implies that there
must be some sort of rearrangement, a kind of neuronal plasticity,
occurring within the spinal cord, and most probably at the cerebral
level as well. One possibility is sprouting of afferent axons. Afferent
fibers might sprout, attach to previously inhibitory synapses, and
convert them to excitatory synapses. Alternatively there could be
development of denervation hypersensitivity due to upregulation of
receptors

24. Factors aggravate spasticity
Age and Ageing 2013; 42: 435–41.

26. Causes
BMJ 2014;349:g4737 doi: 10.1136/bmj.g4737 (Published 5 August 2014)

27. Characteristics of Spasticity
 Hyperactive stretch reflex
 Increased resistance to passive movement
 Posturing of extremities
 Stereotypical movement synergies
Spasticity of arm showing excessive flexion of
elbow, wrist, and fingers
BMJ 2014;349:g4737 doi: 10.1136/bmj.g4737 (Published 5 August 2014)

28.  One more important thing is that an
Arm flexor synergy: Shoulder flexion,
adduction, internal rotation; elbow
flexion; wrist flexion; finger flexion, is
more common in the UE and a Leg
extensor synergy: Hip, knee extension;
ankle plantar flexion is more common
in the LE.

29. Clinical features of spasticity
 Clonus
 Involuntary rhythmic contractions triggered by stretch; these can
interfere with walking, transfers, sitting, and care
 Spasms
 Sudden involuntary movements that often involve multiple muscle
groups and joints in response to somatic or visceral stimuli
 Spastic dystonia
 Tonic muscle overactivity without any triggers owing to the inability of
motor units to cease firing after a voluntary or reflex activity; results in
characteristic limb postures and contractures
 Spastic co-contraction
 Inappropriate activation of antagonistic muscles during voluntary
activity due to lack of reciprocal inhibition causing a loss of dexterity
and slowness in movements
BMJ 2014;349:g4737 doi: 10.1136/bmj.g4737 (Published 5 August 2014)

30. Consequences of Spasticity
 May interfere with mobility, exercise,
joint range of motion
 May interfere with activities of daily living
 May cause pain and sleep disturbance
 Can make patient care more difficult

31. Measuring Spasticity
 Ashworth and Modified Ashworth scales
 Spasm and reflex scales
 Passive quantitative tests
 Active tests of movement

33. Differential diagnosis
 Contractures
 Rigidity
 Catatonia

34. AIMS OF SPASTICITY
MANAGEMENT
The aims of treatment should be the following:
 Improve function - mobility, dexterity
 Symptom relief
- Ease pain-muscle shortening, tendon pain, postural effects
-Decrease spasms - Orthotic wearing
 Postural - body image
 Decrease care burden - care and hygiene, positioning,
dressing
 Optimize service responses - to avoid unnecessary
treatments, facilitate other therapy, delay/prevent surgery.

35. Spectrum of Care for
Management of Spasticity
Injection
Therapy
Neurosurgery
Orthopedic
Treatments
Rehabilitation
Therapy
Prevent
Nociception
Intrathecal
Baclofen
(ITB™)
Therapy
Oral
Drugs
Patient

36. Traditional Step-Ladder Approach
to Management of Spasticity
Neurosurgical
Orthopedic
Neurolysis
Oral medications
Rehabilitation Therapy
Remove noxious stimuli

37. Rehabilitation Therapy
 Stretching
 Weight bearing
 Inhibitory casting
 Vibration of the
antagonist
 Pool therapy
 EMG biofeedback
 Electrical stimulation
 Positioning and
rotary movements

38. Correct positioning in side lying
Age and Ageing 2013; 42: 435–41.

39. Correct Wheelchair Positioning
Age and Ageing 2013; 42: 435–41.

40. Pharmacological Intervention
Oral Medications
 Centrally acting drugs
a) Baclofen
b) Alpha 2 agonist
c) Anticonvulsants
 Peripherally acting drugs
a) Dantrolene Sodium

41. Baclofen
 first-line treatment
 works pre- and postsynaptically as a gamma
aminobutylic acid (GABA) B agonist at the spinal
level and binds to its receptors, leading to
membrane hyperpolarization.
 This restricts calcium influx, which subsequently
(1) restricts endogenous excitatory
neurotransmitters from being released and (2)
inhibits mono- and polysynaptic spinal reflexes

42.  Adverse effects - systemic muscle relaxation, sedation,
fatigue, hepatotoxicity(need to monitor liver function
with baclofen use)
 Furthermore, caution should be taken when treating
patients in the recovery phase of brain injury because
there has been some evidence of deleterious effects on
brain plasticity.4 Withdrawing baclofen treatment has
been associated with hyperthermia, seizures, and
altered mental status,19 but these symptoms can be
avoided by tapering off the drug gradually.

43. Alpha-2 Agonists
 Clonidine is an alpha-2 agonist that
inhibits excessive afferent sensory
transmission below the level of injury,
decreasing spasticity
 However, nowadays it is rarely used as a
single agent in the treatment of spasticity
because of adverse effects such as
hypotension, bradycardia, and
drowsiness.

44.  Tizanidine often has been used in conjunction
with other oral drugs, such as baclofen, for
additive effects. It is an imidazoline alpha-2
agonist that decreases tone through an increase
in the presynaptic inhibition of motor neurons.
This action decreases the release of excitatory
amino acids from spinal interneurons.
 Common side effects are sedation, hypotension,
xerostomia, muscle weakness, and
hallucinations

45. Anticonvulsants
 Benzodiazepines - Diazepam, a benzodiazepine, works
postsynaptically on GABAA receptors, depressing the action of the
CNS.
 Along with clonazepam, another benzodiazepine, diazepam induces
significant sedation.
 Because of this sedation, a potential benefit is the reduction of
spasticity at night, permitting uninterrupted sleep.
 Diazepam has a tendency to act primarily on flexor refexes, but it
can work on extensors in higher doses.
 Because spinal spasticity has a propensity toward flexor reflexes,
diazepam is better suited for spinal spasticity than for cerebral
spasticity.

46.  Gabapentin - It has a structure similar to that of GABA
but does not bind to those receptors.
 The exact mechanism of the drug is relatively unknown,
but it is thought to act at the alpha-2δ1 subunit of
voltage-dependent calcium channels, thus inhibiting
calcium currents.
 Gabapentin is often prescribed when patients describe
symptoms that are consistent with neuropathic pain
along with spasticity

47. Dantrolene Sodium
 only oral antispasticity medication approved by the US
Food and Drug Administration that works peripherally.
 It acts on the muscles themselves, uncoupling excitation
and contraction by inhibiting calcium release at the
sarcoplasmic reticulum
 Adverse effects – liver toxicity, general muscle weakness
 can be considered an adjunct in spasticity refractory to
other treatments

48. Pharmacological Intervention
Oral agents…
BMJ 2014;349:g4737 doi: 10.1136/bmj.g4737 (Published 5 August 2014)

49. Pharmacological Intervention
 [Ward (2002)]
 Generalized spasticity
 Oral agents
 Regional spasticity
 Intrathecal baclofen phenol
nerve block
 Focal Spasticity
 Botulinum toxin phenol block

50. Pharmacological Intervention
Regional Spasticity
 Intrathecal Drug Therapy -
administered directly into subarachnoid space of
CNS with a programmable pump
 Intrathecal Baclofen, Morphine
Sulphate (Infumorph), Fentanyl.
 Improvement in walking speed,
functional mobility without impairing
uninvolved extremity.
 Fewer systemic side effects because
not circulating in blood stream.
 Infection, impaired wound healing,
pump malfunction, and catheter
dislocation in 20-25% of cases.

51. Intrathecal Baclofen
 The most common centrally acting intervention is the
use of intrathecal baclofen (ITB), which uses the same
mechanism of action as oral baclofen, but the
medication is delivered in the CNS at the spinal level.
 This allows a higher CNS concentration of the drug at
the spinal cord level at lower doses while avoiding the
vast systemic side effects that oral baclofen induces.
This intervention is most effective for lower limb
spasticity because the drug concentration is believed to
be highest at lower spinal level.

52.  Main advantages of this intervention is the ability to vary
intrathecal infusion.Varying drug titration depending on the
patient's activities allows more flexibility in self-care throughout
the day, and it helps patients more effectively control night time
spasms.
 The disadvantages of any mechanical implantable device are
device failure and complications associated with device
placement. Pump failure can lead to either overdose, resulting in
respiratory depression and coma, or withdrawal, resulting in
hyperthermia, rhabdomyolysis, and disseminated intravascular
coagulation. Issues with the operative or perioperative
management of the pump placement can lead to infection at the
site of implantation and cerebrospinal fluid leak, leading to
headaches

53. Botulinum Toxin Injection
 Botox – trade name
 Currently the most widely used treatment for focal
spasticityand avoids the generalized weakness and
sedation accompanying oral medications.
 Works by inhibiting the release of vesicular
acetylcholine from presynaptic nerve terminals at the
neuromuscular junction.
 Major side effect - possible dissemination to other
areas of the body, which can lead to dysphagia if it is
being used in the upper limbs or neck muscles, the
development of immunoresistance to the toxin, as with
all injections, this procedure is to be used with caution
in patients receiving anticoagulation therapy.

54. Phenol/Alcohol Injection
 Phenol concentrations ranging from 3–7% or alcohol
concentrations ranging from 50–100% are used to
reduce spasticity by chemical neurolysis. These high
concentrations are essentially injected perineurally to
irreversibly destroy the nerve causing spasticity.
 causes chemical (Wallerian) denervation.
 Dose dependent, hit proximal muscles first.
 Works at alpha motorneurons directly.
 Pain at administered site, causalgia w/ sensory
nerve injury.

55. Pharmacological Intervention
Oral Drugs
Diazepam Brainstem reticular formation
and spinal polysynaptic
pathways
Fatigue; reduced motor coordination, intellect,
attention, memory
Dantrolene Sodium Skeletal muscle calcium stores Hepatotoxicity, generalized muscle weakness
Oral Baclofen GABA-b receptors Drowsiness, confusion, headache, lethargy
Tizanidine Hydrochloride a2-adrenergic receptors Dizziness, sedation, dry mouth
Intrathecal Drugs
Intrathecal Baclofen Gaba-b receptors Pump malfunction/ dislocation
Focal Drugs
Phenol Injection Neuromuscular junction Causalgia with sensory nerve injury, pain at
injection site, hematoma
Botulinum Toxin Nerve Injection site pain, muscle weakness in injected
muscle, hematoma, muscle necrosis, phlebitis
•[Gallichio, (2004)]
Drug Site of Action Adverse Effects

56. Spasticity in Children
 A widely used therapy for children is botulinum neurotoxin injections.
 The American Academy of Neurology and the Practice Committee of
the Child Neurology Society concluded that in localized spasticity,
botulinum toxin A “should be offered as an effective and generally safe
treatment.
 Botox is not yet approved by the Food and Drug Administration for the
treatment of spasticity in children
 Selective dorsal rhizotomy (SDR) is a procedure that interrupts motor
nerve signal transduction to reduce spasms and pain
 Some studies show that oral baclofen is well-tolerated in children.

57. Neurosurgery
Surgical Treatments
Neurodestructive Procedures
 Selective Dorsal Rhizotomy (SDR)
 Rhizotomy
 Neurectomy
 Myelotomy
 Cordectomy

58. SDR: The Basics
 SDR involves cutting sensory nerve roots
that when stimulated, trigger exaggerated
motor responses as measured by EMG
intraoperatively

59. SDR: Procedure
 Multilevel laminectomy vs. minimally
invasive approaches
 L1 – S1 sensory roots are identified and
divided into 3-5 rootlets
 Each rootlet is stimulated and responses
are measured via EMG
 Rootlets with the most abnormal signal
are cut
 Surgery takes about 4 hours

60. SDR: Potential Complications
 Paralysis of legs
 Neurogenic bladder
 Sensory loss or dysethesias
 Wound infection
 CSF leak

61. SDR: Outcomes of Metanalysis
 Children with diplegic CP (GMFCS II-III)
received SDR + PT, or PT w/o SDR.
 Concluded that SDR + PT is efficacious in
reducing spasticity and has a small effect
on gross motor function
McLaughlin J et al. Dev Med Child Neuro 2002, 44: 17-25.

62. SDR versus ITB
 1-year outcomes of 71 children who underwent SDR before
1997 versus 71 children with ITB, matched by GMFCS and age
 Both interventions significantly decreased Ashworth scores,
increased PROM, improved function and resulted in high
parental satisfaction
 Compared with ITB
 SDR provided greater improvements in muscle tone,
PROM, and gross motor function
 Fewer patients in the SDR group required subsequent
orthopedic procedures
 No difference between the degree of parents’ satisfaction
Kan P et al. Childs Nerv Syst. 2007 Sep 5.

63. SDR: Outcomes
Short and long term outcomes demonstrate:
 Decreased spasticity
 Improved or unchanged strength
 Improved gait pattern
 Decreased oxygen cost
 Improved overall function including
decreased use of walking aids

64. Nerve block
 Peripheral nerve blockade using neurolytic agents is one of the
therapeutic possibilities in the treatment of spasticity.
 Nerve block refers to the application of chemical agents to a nerve
to impair, either temporarily or permanently, the conduction along
that nerve.
 The agents most frequently used are phenol, alcohol, and local
anesthetics. This can be done with the help of fluoroscopy or nerve
stimulation
 The obturator nerve is the commonest and most accessible nerve
blocked for adductor spasticity. The posterior tibial nerve is the
second common nerve blocked for calf muscle spasticity. The main
indication is debilitating or painful spasticity.

65. Conclusion
 Spasticity is a frequent and debilitating feature of
common neurological conditions such as stroke,
multiple sclerosis, and traumatic brain and spinal cord
injuries
 The disorder is often associated with pain and
discomfort and increased care needs
 Spasticity is difficult to manage and requires a
collaborative approach involving multiple disciplines
 The evidence for both drug and non-drug treatments
of spasticity is limited
 More research is required to determine the
effectiveness of various treatments of spasticity