Reducing spasticity and pain after stroke to improve function

1. Aditya Johan Romadhon, SST.Ft, M.Fis

2. Spasticity is a common, but not an inevitable condition, in patients with stroke
Spasticity following stroke is often associated with pain, soft tissue stiffness, and joint contracture,
and may lead to abnormal limb posture
Spasticity was first described by Lance in 1980 as a motor disorder characterized by a velocity-
dependent increase in tonic stretch reflflexes (muscle tone)
The new defifinition from the Support Program for Assembly of a Database for Spasticity
Measurement (SPASM) defines spasticity as “disordered sensory-motor control, resulting from an
upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of

3. Spasticity is common after stroke, with the prevalence ranging from 30% to 80% of
survivors
The incidence of spasticity among paretic patients has been reported to be 27% at 1
month, 28% at 3 months, 23% and 43% at 6 months, and 34% at 18 months after
stroke
The onset of spasticity is highly variable in the post-stroke period, and studies have
showed that spasticity develops and peaks at 1-3 months after stroke
Spasticity is more often found in the flexor muscles of the upper limb (fingers, wrist,
and elbow flexors) and extensor muscles of the lower limb (knee and ankle extensors)

4. Damage of the upper motor neurons disrupts communication between the brain and the spinal cord, resulting in a
of net disinhibition of the spinal reflexes
Spasticity can be divided into two components: spasticity mediated by the neural reflex and spasticity due to muscle
contracture, which is often referred to as non-reflex spasticity
Spasticity is generated due to the local activation of muscle spindles, but the propagation and manifestation of
require involvement of the central nervous system
Any lesion or damage along the pyramidal tract or extrapyramidal tract can cause abnormality in muscle tone.

5. An increase in the viscosity of the
extracellular matrix leading to active
muscle stiffness.
Exacerbation of neurally mediated reflex
mechanisms due to subclinical
contractures affecting the threshold of
muscle spindle activation
Fibrosis due to collagen deposition and
an increase in passive muscle stiffness.
Morphometric and histochemical
investigations show changes in
mechanical muscle fiber properties
Consequently, the Ashworth scale and
modified Ashworth scale remain low-
sensitivity instruments for distinguishing
between soft tissue and neural
contributions to hypertonia
Electromyographic measurements can
quantify the resistance to passive
movement, but cannot determine how
much resistance is produced by the tonic
stretch reflex and how much is produced
by soft tissue stiffness
DOI 10.1007/s40141-014-0052-3

6. › Ultrasound elastosonography can be used to assess tissue stiffness as shown in the image
of a spastic tibialis anterior muscle
› The various colors represent areas of scanned tissue with different elasticities, more elastic
(red) or more stiff (blue)

9. The Reticulospinal tract
is responsible primarily
for locomotion and
postural control.
The Reticulospinal tract
is comprised of the
medial (pontine) tract
and the lateral/dorsal
(medullary) tract
The dorsal RST
dominant inhibitory
effects to spinal reflex
circuits, while medial
RST and VST provide
excitatory inputs.
Therefore, medial and
lateral RSTs provide
balanced excitatory
inhibitory inputs to
spinal motor neuron
network
doi: 10.3389/fneur.2019.00468

10. balanced excitatory and inhibitory
inputs to spinal motor neuron network

11. › In the context of stroke with cortical and internal capsular lesions, damages often occur
to both CST and corticoreticular tracts
› This leaves the facilitatory medial RST and VST unopposed, thus hyperexcitability
doi: 10.3389/fneur.2019.00468

12. Spinal mechanism in spasticity
• Reduce reciprocal inhibition
• Decreased presynaptic inhibition of 1a
• Decreased homosynaptic depression
Changed in the muscle properties
• Muscle fiber athropy
• Deposition of excessive connective tissue
• Increased stiffness of connective tissue
• Increased in spindle 1a responses
• Muscle overactivity and spasticity
• Poor posture/alignment
• pain

14. Lalith E. Satkunam CMAJ 2003;169:1173-1179

15. The extracellular matrix is composed of adipose cells, glycosaminoglycans, and
hyaluronic acid. Hyaluronic acid is however the chief component
Immobilization or paresis decreases the normal turnover of the extracellular matrix,
increasing its concentration within and between the muscular compartments
It is known that hyaluronic acid behaves like a non-Newtonian fluid at high
concentrations and becomes more viscous
The increased viscosity of the loose connective tissue may cause decreased gliding
between the layers of collagen fibers, which may be perceived by patients as
stiffness
the presence of dense connective tissue (fibrosis)

17. Repetitive transcranial
magnetic stimulation
(rTMS) is noninvasive
brain stimulation that can
alter the excitability of the
human cortex for several
minutes
High-frequency rTMS
(more than 5 Hz)
increases cortical
excitability, whereas low-
frequency rTMS (1 Hz or
less) suppresses cortical
excitability
In particular, inhibitory
rTMS over the unaffected
hemisphere decreases
Trans-Callosal Inhibition
(TCI) from the unaffected
to the affected
hemisphere and
the excitability of the
affected hemisphere
This would translate into
improved motor function
of the affected hand

18. http://dx.doi.org/10.1136/jnnp-2017-
317371

19. DOI: 10.1177/1545968311433295

20. › CCFES is a new treatment aimed
at improving recovery of volitional
hand function in patients with
hemiplegic stroke
› CCFES stimulates the paretic
finger and thumb extensors with
intensity in proportional to the
degree of volitional opening of the
contralateral unimpaired hand
› The unimpaired hand wears an
instrumented glove that detects the
degree of hand opening
http://dx.doi.org/10.4172/2329-9096.1000147

21. an electromyography monitored neuromuscular
electrical stimulation
uses three reusable, self-adhering,
round surface electrodes (one
ground over a bony protrusion;
two active electrodes over the
motor point of the targeted
Muscle)
A computer inside the device
evaluates the amount of activity
present in the muscle, and
determines whether the patient’s
muscle activity meets or exceeds a
preset threshold

22. It has been reported that stroke survivors
with lower sensorimotor function have a
decreased potential for recovery than
those who are less severely affected
The sensory components of large afferent
fiber activation, proprioceptive input and
increased cognitive sensory attention are
all weighted in the direction of spasticity
reduction, helpful in the return of
movement and increased function
increased cerebral blood flow in the
sensory-motor cortex area on the injured
side, during EMG-controlled FES session
compared to simple active movement or
simple electrical stimulation

23. DOI: 10.3389/fnint.2013.00032

24. Hemiplegic patients with stage 2-3 spasticity
in the wrist muscles based on the Ashworth
scale were divided into two groups. Both
groups were applied stretching
Neuromuscular electrical stimulation (NMES)
to the wrist extensors, in the form of pulsed
current, 100 Hz, with a pulse duration of 0.1
msec, and a resting duration of 9 seconds, for
15 minutes to provide the maximum muscular
contraction
The results of this study showed that NMES
given together with stretching of the wrist
extensor muscles was more effective than
stretching of the wrist extensor muscles alone
in reducing spasticity
https://www.researchgate.net/publication/51722451_The_efficacy_of_electrical_stimulation_in_reduc
ing_the_post-stroke_spasticity_A_randomized_controlled_study

25. Central Post-Stroke Pain (CPSP) is a term used to describe the symptom of pain arising after a stroke that is secondary to a lesion within the central
system
Among these patients, central post-stroke pain (CPSP) is the most frequent diagnosis
Estimates of the prevalence of Post Stroke Pain (PSP) vary widely, with one recent large study estimating that 10.6% of all patients with ischemic strokes
experience some type of chronic PSP
While pain can create its own disabilities secondary to a decrease in function
Pain after stroke is a common symptom that is poorly understood by many practitioners

26. Results: Of 6506 articles identified, 10
studies with 360 subjects were
included in the review.
Transcutaneous electrical nerve
stimulation alone or as additional
therapy is superior to placebo TENS to
reduce post-stroke spasticity assessed
with Modified Ashworth Scale
Conclusion: Transcutaneous electrical
nerve stimulation can provide
additional reduction in chronic post
stroke spasticity, mainly as additional
therapy to physical interventions
https://doi.org/10.1080/09638288.2018.15037
36

27. Symptoms of CPSP can be
induced or spontaneous
In the case of CPSP, the
lesion includes some
portion of central pain
pathways, and this
creates the sensation of
pain with minimal or no
stimulation of the
peripheral pain receptors
injury to the sensory
pathways would lead to a
compensatory
overactivation within the
thalamus, thus causing
spontaneous pain or
allodynia
The onset of CPSP can be
quite variable as well, most
commonly beginning 1 to
3 months after stroke, with
the majority of affected
patients developing
symptoms by 6 months
In a cross-sectional study
of 40 CPSP patients, 27
(65.5%) were also
diagnosed with myofascial
pain syndrome, a non-
neuropathic painful
disorder characterized by
painful, stiffened muscles
with taut bands and
discernible trigger points
doi:10.1016/j.pmrj.2016.05.015.

30. Complex regional pain syndrome
(CRPS), sometimes referred to as
reflex sympathetic dystrophy
Characterized by burning pain,
increased sensitivity to tactile
stimulation, and vasomotor
changes including edema and
changes in skin temperature and
color
The classic theory holds that CRPS
is the result of local hyperactivity of
the sympathetic nervous system
This is supported by data showing
an alteration in temperature
regulation between the affected
and non-affected limbs in CRPS
patients
Other mechanisms have been
proposed including sensitization of
the somatic sensory pathway,
overactivation of inflammatory
responses, and hypoxia

31. One study from 1994 that followed 36 post-stroke CRPS patients
was able to examine the shoulder capsules of 7 patients on
and found evidence of previous trauma, suggesting that CRPS
be due in part to pre-existing or post-stroke musculoskeletal
initiated a protocol of strict protection of the shoulder
from subluxation, painful positioning, and trauma; this
reduced the incidence of CRPS post-stroke from 27%
before the protective protocol to 8%