MOTOR TRAINING ASSOCIATED NEURAL PLASTICITY

IN CHRONIC LOW BACK PAIN

ABSTRACT
TITLE: Motor training associated neural plasticity in chronic low back pain.

Background: Individuals diagnosed with chronic low back pain typically exhibits postural and congenital abnormalities and
disc injuries , problems with spinal muscles, nerves, bones, tendons, ligaments. Which tends to further deteriorate with the
progression of the disease if not rehabilitated well. For this reason, pharmacological therapies are not sufficient to adequately deal
with conditions like herniated disc, sciatica, scoliosis, spinal stenosis, and other musculoskeletal disorder and injuries, so physical
therapy is essential to cope with the deterioration in motor functions. within the physical therapy domain, the efficacy of a therapy
associated with the, Repetative trans cranial direct stimulation, trans cranial magnetic stimulation, peripheral magnetic
neurostimulation of multifidus muscle as well as paravertebral muscles. So motor training and therapy proved to be successful.

Objective : the purpose of this literature review was to determine the effect of motor training in neural plasticity with chronic low
back pain, improving the training of muscles , postural and congenital abnormalities in CLBP patients in general.

Method : An extensive research using relevant medical databases like Google Scholar, Pubmed, Elsevier, Science Direct, Scopus,
Clinical Key, ProQuest, Web of Science was performed.

Conclusion: overall this review suggests that the stimulation and training of muscles is a useful and effective tool in improving
the postural and congenital abnormalities and spinal motor control parameters, kinematics and manual therapy reducing patient
affected with Chronic low back pain, and improves the quality of living in CLBP patients.

Keywords: The keywords used are Motor plasticity OR AND Neuroplasticity and LBP or CLBP and brain plasticity in LBP.
 INTRODUCTION
Chronic low back pain (CLBP) is a prevalent and disabling musculoskeletal condition with few effective
treatments. Although precise mechanisms remain unclear, structural and functional reorganization of the
sensory motor cortex has been identified in CLBP, and is associated with pain severity, pain duration and
movement dysfunction. Cortical re-organization in CLBP is hypothesised to be a marker of Mal adaptive
synaptic plasticity, and this concept provides the foundation for contemporary theories of pain
persistence, Importantly, synaptic plasticity is regulated by homeostatic mechanisms (termed
homeostatic plasticity), that if impaired, could explain aberrant synaptic plasticity and potentially
symptom persistence in CLBP. Despite this, a patho -physiological role for changes in homeostatic
plasticity has been overlooked in musculoskeletal pain or use dependent synaptic plasticity involves the
expression of lasting changes in synaptic efficacy underpinned by long-term potentiation (LTP, synaptic
strengthening) and long-term depression(LTD; synaptic weakening).

However, synaptic plasticity relies on a positive feedback loop that left unchecked would lead to either too
much strengthening and excessive neuronal excitability (LTP), or too much weakening and neuronal
silencing (LTD). In the healthy brain, homeostatic plasticity mechanisms enforce stability and maintain
brain excitability within a normal range by shifting the threshold for LTP and LTD based on the history
of synaptic activity. For example, authors, previous study literature. There are few ,yet there is a derth of
literature investigating. The threshold of a synapse with a history of high excitability will shift to favour
induction of LTD. Homeostatic plasticity can be assessed in humans using non-invasive brain stimulation.
For example, in healthy individuals a homeostatic response is elicited when two blocks of excitatory brain
stimulation are applied at short intervals. Homeostatic plasticity is observed as an increase in cortical
excitability following the first block of excitatory stimuli (synaptic strengthening) that is reversed towards
inhibition (synaptic weakening) when the second block of excitatory stimuli is applied after a few minutes.
In this way, the brain corrects for exposure to excessive levels of excitation and prevents aberrant
synaptic plasticity. Evidence from neurological conditions such as migraine suggests a link between
impaired homeostatic plasticity and symptoms. For example, these individuals exhibit re-organization of
the sensory motor cortex as well as excessive cortical excitability impaired homeostatic plasticity is
hypothesized to contribute to abnormal cortical re-organization and sensory motor symptoms in these
conditions as a results of inappropriate and excessive LTP - like effects resulting from a failure to shift
the threshold towards LTD when excitability is high.

A comparable failure of homeostatic control in CLBP could explain similar observations of maladaptive
cortical re organization and symptoms persistence in this population yet, no study has investigated
homeostatic plasticity in musculoskeletal disorders. Importantly, impaired homeostatic plasticity has
been shown to be generalized throughout the sensory motor system and is not restricted to the cortical
representations of affected muscles. For instance, this study aims to investigate primary motor cortex
since there is derth of literature regarding CLBP and motor plasticity this study aims to identify
accumulate the current evidence regarding a motor plastic changes past training in individuals with
CLBP. Together these findings indicate a global impairment in homeostatic plasticity that has been
suggested to provide evidence for a primary role of impaired homeostatic plasticity in pathophysiology of
these conditions. This study aimed to investigate homeostatic plasticity in the primary motor cortex
representation of individuals with CLBP and pain-free controls.

Neural plasticity” refers to the capacity of the nervous system to modify itself, functionally and
structurally, in response to experience and injury. As the various chapters in this volume show, plasticity
is a key component of neural development and normal functioning of the nervous system, as well as a
response to the changing environment, aging, or pathological insult. This discusses how plasticity is
necessary not only for neural networks to acquire new functional properties, bur also for them to remain
robust and stable. The article also reviews the seminal proposals developed over the years that have
driven experiments and strongly influenced concepts of neural plasticity.

exercises for changing pain, involve learning and practicing new skills and strategies for
Neuroplastic
managing pain. Repeating tools for thinking, acting and being different helps to “dampen” the pain
pathways; changing pain and our brain’s relationship to pain over time.

Chronic low back pain prevalence was 4.2% in individuals aged between 24 and 39 years old and 19.6%
in those aged between 20 and 59. of nine studies with individuals aged 18 and above, six reported chronic
low back pain between 3.9% and 10.2% and three, prevalence between 13.1% and 20.3% the lifetime
prevalence of non-specific LBP is estimates at 60% to 70% in industrialized countries (one-year
prevalence 15% to 45%, adult incidence 5% per year). the prevalence rate of children and adolescents is
low that seen in adults but is rising. The techniques used in the treatment are of trans cranial magnetic
stimulation, repetative peripheral magnetic neuro stimulation, Trans cranial direct stimulation.

Need for the study: low back pain is very common. It can result from a strain (injury) to muscles or
tendons in the back other causes include arthritis, structural problems and disk injuries. Pain gets better
with physical therapy so in order to overcome of pain making ability of brain to change through growth
and reorganization, changes range from individual neuron pathways making new connections, to
systematic adjustments like cortical mapping. Learning and practicing new skills and strategies for
managing pain. Aim of the study is to assess the current knowledge regarding motor plastic changes that
occur post-treatment/ post intervention in individuals with CLBP to better inform future mechanistic and
clinical motor lastic research. Targetting LBP.
 METHODOLOGY
SEARCH STRATEGY:

A Review of literature was undertaken to utilize an electronic search of the following databases: PubMed,

Science Direct, Scopus, Clinical key, Pro Quest, Web of science, and coherence database inception until

2020 using keywords, searched for the last 6 years 2016 to 2021.

Out of these …………………..no. of articles were retrieved …………………………articles were reviewed.

Study selection

The inclusion criteria used in the narrative review were as follows:

1) Studies published in English

2) Included quantification of atleast one neuroplastic outcome measure.

EXCLUSION CRITERIA : in this study were as follows,

1) Studies are not included LBP.

2) Outcome measures not asessing motor neuroplasticity

3) Studies Including : 1) reviews and 3)conference abstracts or presentations.

4) Studies that are not performed individual with LBP.

5) Studies not performed on Human participants.

 SEARCH STRATEGY KEYWORDS NO.OF ARTICLES FOUND NO.OF ARTICLES
USED
Google Scholar Motor plasticity OR AND Neuroplasticity and LBP N=1,11,000 N= 135
OR CLBPVBB

PubMed Motor plasticity OR Neuro plasticity AND LBP OR N=56 N= 4

CLBP

Cochrane Brain plasticity in CLBP N= 17 N= 5

CinHal Neural plasticity associated with chronic LBP N= 0 N=0
Pedro Pain, Brain, Plasticity, education, manual therapy, N=3 N= 2
SLR, remapping

Science Direct Primary motor cortex. Intracortical inhibition and N= 5,325 N=10
facilitation. TMS, Ultrasound imaging, multifidus
motor control. Chronic low back pain.

Scopus Neural plasticity, pain, LBP. N=51,469 N= 0

Literature review:

AUTHOR NAME METHODOLOGY RESULT CONCLUSION

1)Hugo Masse-Alariea,
Louis-David Beaulieua,
Richard preuss b,Cyril
Schneider a,c
For a 3 week daily
practice,24 persons with
CLBP were randomly
assigned to ISOM and
GLOB groups. The onset
of superficial MF ( MF-S)
activation during ballistic
limb movements
ISOM and GLOB both ISOM influenced
helped with pain and brain plasticity
impairment.only ISOM, on better, according to
the other hand, had an effect changes in
on M1 function ( decreased coricospinal
corticospinal excitability excitability and MF-
and enhanced intra cortical S postural
inhibition) MF-S postural adaptations.

2)Hugo Masse-Alarie, Louis-
David Beaulieu, Richar
Preuss, Cyril
Schneider
3)Adriaan Louw, Kevin
Farrell, Merrill Landers,
Martin Barclay, Elise
Goodman, Jordan Gitlund,
Sara McCaffrey & Laura
Timmerman
(bilateral shoulder flexion
in standing; unilateral hip
extension in prone lying),
MF-S corticomotor
control tested by tms of
M1, and pain,
kinesiophobia, and
disability assessed by
standardized
questionnaires were used
to assess pre/post training
after-effects.
Twenty-one participants
with CLBP were
randomly allocated to
[RPMS+training] and
[Sham+training] groups
for three sessions (S1-S3)
over a week where MF
was stimulated before
training (volitional
contraction).
Training was also home-
practiced twice a day.
Changes were tested at S1
and S3 for anticipatory
postural adjustments
(APAs) of MF and semi-
tendinosus (ST), MF
EMG activation, cortical
motor plasticity
(transcranial magnetic
stimulation) and
pain/disability.
Methods: Sixty-two
patients with chronic low
back pain(CLBP) were
recruited for the study.
Following consent,
demographic data were
obtained as well as pain
ratings for low back pain
(LBP) and leg pain
(NUMERIC Pain Rating
Scale), disability
(Oswestry Disability
index), fear-
avoidance(Fear-
Avoidance-Beliefs
Questionnaire), forward
flexion (fingertips-to-
floor), and straight leg
raise (SLR)
(inclinometer).
Patients were then
activation, and
kinesiophobia.
RPMS group showed
immediate decrease of pain
at S1, then improvement of
MF activation, ST APA, M1
facilitation, and
pain/disability at S3.
Changes were larger when
brain excitability was lower
at baseline. Disability index
remained improved one
month later.
Results: Sixty-two patients
(female 35 [56.5%]), with a
mean age of 60.1 years and
mean duration of 9.26 years
of CLBP participated in the
study. There were no
statistically significant
interactions for LBP (p
= .325), leg pain (p = .172),
and trunk flexion (p = .818)
between the groups, but
SLR showed a significant
difference in favor of the
neuroplasticity explanation
(p = .041). Additionally, the
neuroplasticity group were
7.2 times (95% confidence
interval = 1.8-28.6) more
likely to improve beyond the
MDC on the SLR than
participants in the
Future research
should look into
whether our novel
findings are related
to the effects of the
exercises on
lumbopelvic
muscular control
and cognitive
function.
Before prescribing
one of these two
traditional exercises
for pain relief, a
clinical evaluation
of the individual is
still required.
Combining RPMS
with training of MF
in CLBP impacted
motor planning, MF
and lumbopelvic
spine motor control
and pain/diability
one week ager the
onset of protocol.
Brain plasticity
might have
favoured motor
learning and
improved daily
lumbopelvic sine
control without pain
generation
The results of this
study indicate that a
neuroplasticity
explanation,
compared to a
traditional
viomechanical
explanation,
resulted in a
measureable
difference in SLR in
patients with CLBP.
The results also
indicate no
differences between
the groups in
regards to LBP, leg
pain, and forward
flexion. Future
studies should
investigate long-
 randomly allocated to mechanical group. term effects of such
receive one of two education and may
explanations be also from a
(neuroplasticity or combination of
mechanical), a manual therapies including
therapy technique to their neuroscience
lumbar spine, followed by education.
post-intervention
measurements of LBP,
leg pain, forward flexion,
and SLR.
4)Tribikram Thapa examined homeostatic Compared with baseline, These data
Thomas Graven-Nielsen plasticity in fifty MEP amplitudes increased indicate impaired
Lucinda S. Chipchase individuals with chronic at all time points in both homeostatic
Siobhan M. Schabrun low back pain (cLBP) groups following plasticity in the
and the single tDCS protocol primary motor
twenty-five pain-free (P < 0.003). Following the cortex of individ-
controls. A single block double tDCS protocol, uals with cLBP
(7-min) of anodal MEP amplitudes
transcranial direct decreased in
current stimulation pain-free controls at all
(‘single tDCS’), or two time points compared with
subsequent blocks (7- baseline (P < 0.01), and
min and 5-min were unchanged in the
separated by 3-min rest; cLBP group.
‘double tDCS’), were
randomised across two
experimental sessions to
confirm an excitatory
response to tDCS
applied alone,
and evaluate
homeostatic plasticity,
respectively.
Corticomotor
excitability was assessed
in the
corticomotor
representation of the
first dorsal interosseous
muscle by transcranial
magnetic
stimulation-induced
motor evoked potentials
(MEPs) recorded before
and 0, 10, 20, and 30-
min following
each tDCS protocol.
5)F.A. Hazime, A.F. Ninety-two patients with A two points reduction The results
Baptista CLBP were randomized was achieved only by the suggest that tDCS
D.G. de Freitas to receive tDCS + PES + PES and PES
R.L. Monteiro R.L. 12 sessions on (mean reduction [MR] = alone are
Maretto nonconsecutive days of 2.6, CI95% = 4.4 to 0.9) effective in
R.H. Hasue anodal tDCS (primary and PES alone relieving CLBP in
S.M.A. Joao motor (MR = 2.2, CI95% = 3.9 to the short term.
cortex, M1), 100 Hz 0.4) compared with the However, only
sensory PES (lumbar sham group, tDCS + PES
spine), tDCS + PES or but not of tDCS alone (MR induced a long-
sham = 1.7, CI95% = 3.4 to 0.0). lasting analgesic
tDCS + PES. Pain In addition effect. tDCS alone
intensity (11-point to maintaining the showed no clinical
numerical rating scale), analgesic effect for up to meaningful pain
disability three months, tDCS + PES relief.
and global perception had a higher proportion of
were applied before respondents in different
treatment and four cutoff points. Global
weeks, perception was improved
three months and six at four weeks and
months post maintained three months
randomization. after treatment only with
tDCS + PES. None of the
treatments improved
disability and the affective
aspect of pain consistently
with pain
reduction.

FLOW DIAGRAM
IDENTIFICATION

Records identified through Records after duplicate

database searching removed

Google scholar (n=130) (n=126)

SCREENING
 Records excluded (n=35)
Records screened
Non English article (n=5)
(n=126)
-non-free full text article (n=30)

Full-text articles assessed for

ELIGIBILITY

eligibility

(n=91)

Full-text articles excluded

(n=82)

Articles included in qualitative

synthesis (n=9)
INCLUDED

Discussion
The literature review reviewed the “The use of brain plasticity in chronic low back pain patients”. various studies performed by the
rehabilitation professionals showed a positive trend in the quality of life, functional and disability levels, and functional mobility exercises
concerning the practice of motor training brain plasticity. Research has identified that exercise has both positive physical and psycho social
effects for LBP patients. New research developments in the recovery of function following low back pain as well as basic and applied
research relevant to perception and production, seem to point to the suggestion that motor training interventions that directly address the
restoration of function as opposed to developing compensatory mechanisms, in certain circumstances, may now be a more appropriate
treatment approach. Physiotherapists provide physical rehabilitation to maximize the independence of those with compromised functions.

In a randomized controlled trial, relational active motor training brain plasticity approaches were tested in the post acute phase of the
disease. Motor functions and psychological were assessed for post treatments.

According to the certain study - influence of para veretebral muscles traning on brain plasticity and postural control in chronic low back
pain, The original experimental-designed study testing in CLBP the different influence of two exercises on APA and M1 function related to
the control of MF muscle confirmed the working hypothesis. ISOM training influenced brain function and fastened MFAPA but likely only
in an acute manner after the exercise session at S4 for brain function and for GLOB exercise.

Other changes that occurred as a result of the ISOM exercise could have helped to minimize pain. The over activation of the superficial
trunk muscles is linked to discomfort in CLBP, and ISOM training has been found to attenuate this over activation. As a result, it’s
reasonable to believe that the decrease in cortico spinal drive to MF-S. As evidenced by a decrease in MEP amplitude, motor neurons had a
role, to normalize APA and regulate MF-S over activation.
Thus, the effects of exercise could be different in patients with CLBP who have a varied amount of M1 excitability i.e. increased or
decreased M1 excitability. MEP amplitude, which indicates a change in corticomotorneuronal activity, excitability can represent changes in
motor cortical excitability as well as changes in spinal excitability caused by peripheral stimuli. Rate of tonic MF activation between
sessions, which could have an impact on cognitive-behavioural intervention could improve motor control of the paravertebral muscles. And
Kinesiophobia, fear- avoidance, and anxiety could alter several variables of spine motor control. As a result, it’s possible that M1 plasticity
and pain were altered by cognitive mechanisms engaged in physical activity.

The study examined the effects of RPMS combined with MF muscle motor training on M1 function, spine motor control, and pain in CLBP
to the effects of sham stimulation combined with motor training. The data back up the premise that RPMS combined with motor training
improves performance. Should provide more benefits than just motor training (sham combination). In the RPMS, there was an earlier
development of ST muscle after one week of exercise.

MF activation during the bilateral shoulder flexion task, as well as group for the bilateral shoulder flexion task. Forward bending, up-
regulation of corticospianl facilitation M1 circuits, and pain and impairment were reduced , and the effects lasted for a month . potential pain
processing and functional plasticity mechanisms are investigated.

Two studies in the literature found some modifications after one RPMS session in CLBP. Our correct findings revealed a considerable
difference. Pain reduction in the first session after intervention and persistence over one session. Sham on the other hand , had no effect
during the week. These impacts are more powerful than they were previously found that pain was still reduced four days following the
procedure. Stimulation, had returned to a more normal state. As a result, the current situation, pain reduction(VAS score) and function
improvement(ODI & PSFS) were studied. Over the course of a week adds to the evidence that several RPMS treatments are beneficial. ( at
least 3 sessions) in addiction to motor skills tus , how RPMS combination with motor training drove M1 plasticity.

Conclusion:
In conclusion motor training provides beneficial effects for enhancing postural and congenital abnormalities affected by chronic low back
pain, performance and dynamic stability. The present findings can be reliably interpreted, and analyzed. And included studies had a ‘’fair”
overall quality. The respective review strongly suggest the incorporation of motor training enhancing all the low back pain abnormalities
and reducing the risk of pain in the patients by performing the training duration of at least 20-30 minutes daily in a week.