Low back pain (LBP) is a global health problem representing
one of the most frequent illness of the human population. It is leading cause
of disability worldwide. In INDIA the occurrence of low back pain is
disturbing. 60% of Indian population have developed low back pain once in their
life time. Prevalence of low back pain in Indian population was found to be
6.2% to 92%. The global prevalence of low back pain due to which activity is
limited for more than one day was found to be 11.1 ± 2.0% and the one month
prevalence was 23.2 ± 2.9%. The one year
prevalence in western countries like the USA was reported to be 10-56% and
point prevalence of LBP is 15%. In countries like CHINA, TURKEY, TIBET
prevalence is more or less similar as compared to western countries ranging
between 36% to 64%.
Prevalence of LBP increases with age. LBP is most prevalent
in age group 40-80 years. LBP is more common in females as compared to males.
Lack of proper education, low socioeconomic status, lifestyle, obesity,
addictions, occupation, poor posture, psychosocial factors like anxiety,
depression, job dissatisfaction, mental stress have been found to be associated
with low back pain.
According to the duration of symptomology, i.e. how long the
pain lasts, low back pain is divided into three categories- acute, subacute and
ACUTE – pain
lasting upto 6 weeks
SUBACUTE – pain lasting 6-12 weeks
CHRONIC –pain lasting more than 12 weeks (3 months)
In a population with 84% people affected with LBP, 23% of
population can develop chronic low back pain (CLBP). Chronic low back pain is
most common cause of disability in persons below 45 years and third common
cause in persons between 45-65 years.
Low back pain can occur due to enormous number of reasons:
Traumatic- vertebral fractures, sprains,
Infective- due to tuberculosis or bacterial
Discogenic- due to lesions in intervertebral
Degenerative –degenerative disc disease,
osteoarthritis, articular degeneration.
Metabolic- osteoporosis, osteomalacia.
Structural deformities- spina bifida,
sacralisation, scoliosis, spondylosis, etc.
Functional deficits- limb length deformities,
contractures of hip, knee.
Referred low back pain from visceral lesions
Abdomen- duodenal ulcer, aortic aneurysm.
Gastrointestinal- renal calculi, peptic ulcer,
colon/rectal disorders, pancreatitis.
Gynaecological diseases and genitourinary
Non-specific low back pain.
Non-specific low back pain is defined as low back pain not
attributable to a recognizable, known specific pathology (e.g. infection,
tumour, osteoporosis, fracture, structural deformity, inflammatory disorder,
radicular syndrome or cauda equine syndrome.) After 3 weeks of non-specific low
back pain patients can have low recovery expectations that can cause them to
have poor functional outcomes upto 6 months or even later. In subsets of
patients having chronic LBP only 40% recovered after 12 months. Thus the main
issue with chronic low back pain (CLBP) is it’s “RECURRENCE”. Patients with
CLBP limit their activities. Amongst patients with CLBP 98% suffer from
depression followed with anxiety disorders or substance abuse.
Pain according to International Association on the study of
Pain (IASP) is defined as “an unpleasant sensory and emotional experience which
follows actual or potential tissue damage”. However a recent definition of pain
by Moseley (2003) defines pain as “a multiple system output that is activated
by an individual’s specific neural signature. This neural signature is
activated whenever person perceives a threat.” In CLBP, persistent pain is not
due to damage to anatomical body structures, rather it is due to abnormal
central pain processing. Patients with CLBP have increased perception of pain
in the absence of actual tissue damage. Hyperexitibilty/ central sensitization
is present in patients CLBP which is defined as “An amplification of neural
signalling in the central nervous system that elicits pain hypersensitivity. In
short, central sensitization leads to allodynia, hyperalgesia and/or referred
pain. Also there is change in somatosensory system. Representation of lower
back in primary somatosensory cortex (S1) is shifted medially and expanded,
invading the area of the leg. The degree of invasion is associated with
chronicity. Wind up phenomenon or temporal summation refers to mechanism in
which repetitive noxious stimulus results in slow temporal summation. I.e.
experience of pain increases. Although exact cause of central sensitization is
not known, studies suggest that alteration in ascending and descending central
modulatory mechanisms for the perception of pain called “neuronal plasticity”
may be responsible for central sensitization.
From this we can conclude that patients with CLBP have both
changes in brain structure and function along with peripheral dysfunctions.
Thus treatment options for CLBP should focus on both.
There are many treatment options for LBP like manual
therapy, specific muscle training, cognitive behavioural therapy, McKenzie,
multidisciplinary pain management programmes all of which target distinct
effects. For e.g. – manual therapy reduces pain; specific muscle training which
restores normal function of trunk muscle reduces disability and increases
performance in mildly disabled persons. But muscle stretching and strengthening
exercises were best type of exercises to improve pain and function. Although
these approaches produce significant benefits across outcome domains they do
not specifically address psychological aspects of pain. Thus multidisciplinary
pain management programmes which focus on cognitive and behavioural aspects
which reduce pain, disability and improve quality of life should be used.
Education to patients in CLBP have been used since a long
time. Many models to address pain use anatomical and biomechanical models,
which has limited efficiency and moreover increase the fear of patients related
to their pain. An approach called Cognitive behaviour therapy (CBT) reassures
patients, reduces their fear related to movement pathology and function. But
studies have found that non- CBT education for LBP had similar results like CBT
education thus denoting its inefficiency. A newer advance in educating the
patient is Pain Neuroscience Education (PNE).
PNE is known to reduce pain and disability in patients with
CLBP. PNE also reduces fear associated with pain i.e. changes the ideas,
attitudes and beliefs of patients towards their pain and thus reduces pain
catastrophization. But it differs from CBT by not focussing on structural
anatomical or biomechanical aspects of pain but rather keeping its focus on
representation or neurophysiology of pain. PNE aims to explain patients about
their own ability to increase or decrease pain i.e. neuroplasticity which will
indeed help the patients to cope up with their persistent LBP.
Numerous studies have been done to find out the
effectiveness of PNE in patients with CLBP. These studies also pair PNE with
other physiotherapy treatment modalities like manual therapy, mobilization, dry
needling, soft tissue massage, manipulation, relaxation exercises, general
exercise programme, neural mobilization techniques etc. But there is lack of
evidence showing use of PNE with specific exercise protocol of only stretching
and strengthening programme in patients with CLBP. Also comparison between PNE
and stretching and strengthening (specific exercise protocol) is not known.
Studies in majority focus on the use of PNE in only CLBP or after lumbar
surgeries. Also the actual effectiveness of PNE cannot be judged due to absence
of control group in these studies. Use of PNE in chronic ‘nonspecific’ LBP is
not known. The effectiveness of treating CLBP with the use of PNE in Indian
population is yet to be explored. Thus, a very strong need arises to find out
the effectiveness of using Pain Neuroscience Education with specific exercise
protocol in comparison with exercise alone along with a control group on pain,
quality of life and movement in Indian patients suffering from chronic
nonspecific low back pain.