University of Sulaimani

College of nursing

Effect of Transcutaneous Electrical Nerve Stimulation (TENS) on Knee osteoarthritis

Graduation Research: Submitted to the School of Nursing/University of Sulaimani as part

of requirements for Bachelor Degree in Nursing Science.

Prepared by:

Muhammad Abdwlkareem Hamaali Shaho Ako Sdiq

Shwana Muhammad Jawad Sallahadin Saeed Mala Qadr

Supervised by:

AL/ Khanda Mustafa Ahmed

2016-2017
Acknowledgements

First of all, great thanks to God. The most gracias and most merciful, who has given
us the opportunity to accomplish this task.

We would like to take this opportunity to thanks our supervisor Assistant Lecturer

(Khanda Mustafa Ahmed) for her support throughout the study.

Our sincere thanks to our family for their support and encouragement throughout the
course of this year.
 Introduction

Osteoarthritis (OA) is the most common type of joint disease, affecting more than 20 million
individual in United States alone. It is the leading cause of chronic disability in those older than 70 years,
costing the United State greater than $100 billion annually. (Jeffries MA 2014).

OA is a degenerative joint disease that, over time, causes inflammation and loss of cartilage in the
joints. Often referred to as “the wear and tear disease,” OA causes inflexibility and pain and stiffness, and
is primarily felt in weight-bearing joints such as the knees, hips and spine. It can, however, occur in any
joint. Unlike systemic, autoimmune forms of arthritis (Lupus, Rheumatoid Arthritis), Osteoarthritis
doesn’t affect organs in the body. (Felson 2000).

OA is considered a multifactorial disease, the main cause of work disability in individuals over 50
years of age. The available epidemiological studies indicate that OA affects 10-15% of the world
population, with an incidence of 60% in men and 70% in women over 65 years of age. (Shen JM – 2014)

The most commonly affected peripheral joints are the knees, hips and small joints of the hands with an
estimated overall prevalence in the general adult population of 11% for hip OA and 24% for knee OA,
respectively. (Annals of Rheumatic Disease - April 2013; NICE Clinical Guideline 2014).

Since incidence and prevalence increase with age, longer life expectancy will result in an increase of OA
in the future. (Bull World Health Organ 2003; Rheum Dis Clin North Am 2007 ).

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Definition of osteoarthritis (OA)

OA is the most common type of arthritis and is seen especially among older people. Sometimes it is
called degenerative joint disease. OA mostly affects cartilage, the hard but slippery tissue that covers the
ends of bones where they meet to form a joint. Healthy cartilage allows bones to glide over one another. It
also absorbs energy from the shock of physical movement. In OA, the surface layer of cartilage breaks
and wears away. This allows bones under the cartilage to rub together, causing pain, swelling, and loss of
motion of the joint. Over time, the joint may lose its normal shape. Also, small deposits of bone—called
osteophytes or bone spurs—may grow on the edges of the joint. Bits of bone or cartilage can break off
and float inside the joint space. This causes more pain and damage. (NIH: National Institutes of Health -
2016).

OA, sometimes called degenerative joint disease or degenerative arthritis, is a clinical syndrome of
joint pain accompanied by varying degrees of functional limitation and reduced quality of life. It is the
most common form of arthritis and one of the leading causes of pain and disability worldwide. The most
commonly affected peripheral joints are the knees, hips and small joints of the hands .Other joints, such as
shoulders, wrists, elbows, are rarely affected (NICE Clinical Guideline 2014; www.arthritis.org).

Etiology and risk factors of osteoarthritis

The OA can be classified as primary (idiopathic) when its etiology is not well defined and secondary
when there is a specific disease-causing process. (National Clinical Guideline Centre 2014).

The secondary is the result of genetic factors, trauma, more common in men at any age, inflammatory,
neuropathic, metabolic or endocrine diseases result from congenital abnormality of the joint, joint
infection, inflammatory disorders, metabolic arthritis, hemochromatosis repeated, traumatic injuries and
deformities, acquired articular incongruity, joint misalignment or instability of the joint. Therefore, most
of the cases are secondary to OA another condition. (Batt ME- 2014; Kloppenburg M 2013).

2
 The main risk factors for OA are advancing age, genetic predisposition, mechanical stress and a
sedentary lifestyle. However, there are factors that directly interfere in its prevalence, such as gender,
trauma, inflammatory diseases, obesity (which accelerates the degradation process), primary changes in
cartilage, heredity, mechanical, hormonal and metabolic factors, and infections. It is believed that the
etiology of OA is related to a lack of adaptation to the functional demands of the body, i.e., surges, macro
traumas or micro traumas. (National Clinical Guideline Centre 2014).

Symptoms of osteoarthritis

Pain is the first symptom of inflammatory process. This is triggered by degenerative changes (bone
remodeling, subchondral micro fractures, periostitis, and nerve compression by osteophytes) that occur in
conjunction with osteoarthritis. (Evans CH1 2013)

The volume joint can be increased because an amount of synovial fluid or the presence of osteophytes.
A higher sensitivity is observed in articular margins, the capsule insertion points and periarticular
tendons. This increase in joint volume can form bone nodules joint. Distal interphalangeal joints,
Heberden nodes and proximal interphalangeal, Bouchard’s nodes. Often occurs palmar and lateral
deviation of the distal phalanges, due to the presence of Heberden nodes. These are more prevalent in
females and appear to be associated with family conditions. (Doherty M 2005).

A common complaint is rigidity to rise, but is short-lived. This condition helps in the diagnosis. The
stiffness can remain for more than one hour. (Batt ME- 2014; Evans CH1 2013).

Disease progression cause the movement limitation associated with muscle spasm, contraction of the
capsule and osteophytes (mechanical limit) or intra-articular bodies. (Batt ME- 2014; Evans CH1 2013).

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Pathophysiology of knee OA

The knee is the largest synovial joint in the body and one the most complex biomechanical system
known. The purpose of synovial joints, also known as diarthroses, is to allow movement. The knee
supports flexion and rotation, promoting complete stability and control under large variety of conditions
(Gold blatt JP 2003).

The knee is composed by four main bones—the femur or thigh bone, the tibia, the fibula or outer skin
bone and patella or knee cap. The foremost movements of the knee joint occur between the three bones:
femur, patella and tibia. The patella, located at top center, is small and is flat triangular—shaped bone that
moves and rotates with knee .(Flandry F 2011).

The distal end of the femur has a medial and a lateral condyle, the structure of these condyles is
important in the movement of the tibia on the femur. The proximal end of the tibia forms a plateau with
medial and lateral sections. The menisci intensify the shape of plateaus and serve to increase the
conformity of the joint and help the rotation of the knee. (Flandry F 2011).

Therefore, the structure of the femur, tibia, and patella highly contributes to the stability, strength and
flexibility of the knee joint, with static and dynamic restrictions of the ligaments and crossing the joint
(Gold blatt JP 2003).

The knee is composed by tendons and ligaments that are essentially constituted by connective tissues.
The former connect muscle to bones and the latter connect bone to bone. Whether the tendons as
ligaments are made of strands of elastic proteins. Ligaments prevent bones from moving too far and
tendons help in the movement of muscles. The patella is inside a tendon, the patellar tendon which
annexes the quadriceps muscles on the front of thigh and cover the patella. (Gold blatt JP 2003).

The synovial membrane of the knee-joint is the largest in the body. This membrane start at the upper
edge of the patella, on the lower part of the front of the femur that communicates with a bursa interposed
between the tendon and the front of the femur. (Gold blatt JP 2003).

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 The synovial membrane is a specialized mesenchymal tissue covering the spaces of diarthrodial joints,
bursae, and tendon. This membrane has two layers, the inner layer, constituted by macrophages or
synoviocytes, and outer layer, composed of two to three layers of synoviocytes over connective tissue
with fibroblasts, secreting collagen, and other extracellular matrix proteins. The outer layer has few
macro- phages and lymphocytes, blood vessels with contain nutrients to the synovial membrane and the
adjacent avascular cartilage and fat cells .(Anguir DP 2014).

The synovial membrane is surrounding the cavity of joints, taking the space with synovial fluid. It has
an important role in nutrition of the articular cartilage. The synovial fluid lubricates the ends of the bones
making possible them to move often. The inefficiency to keep the level of metabolism starts destructive
process. (Bobick J 2008; Korochina 2016).

Knee OA is a long-term condition characterized by synovitis, cartilage destruction, degradation of

collagen, bone marrow lesions and involves all tissues of the joint and related structures. Synovitis is the
worst condition in OA and has an important role in the structural degeneration of the cartilage, which is
characterized by pain, swelling, warm joint and limited range of motion. When synovitis occurs, there is a
proliferation of lining cells and inflammatory infiltration, which is usually composed of lymphocytes and
monocytes. Also, there is evidence that systematic inflammatory mediators, such as C-reactive protein
(CRP), are significantly increased, especially in women with early knee OA. Synovitis is not localized
and tends to diffuse to areas of chondral defects, causing blood vessel proliferation and increasing
macrophage level infusion to the synovium. (Schaible H 2012; Dray A.2007)

When the articular cartilage wears away the bone underneath, the cartilage becomes stiff and the joint
space becomes narrow which may lead to bony spurs or osteophyte formation. (Schaible H 2012; Dray
A.2007)

As with other chronic pain conditions, pain in OA is a complex combination of affective, cognitive and
sensory processes, which involves both the peripheral and the central level of the nervous system. The
mechanism of OA occurs at the joint level, the dorsal root ganglia (DRG) and the higher center of the
brain that processes the pain. (Schaible H 2012)

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 When inflammation occurs, pro-inflammatory mediators may be released into the damaged joint, such
as prostanoids, nerve growth factor (NGF) and nitric oxide (NO).The inflammatory mediators can act to
activate the peripheral nociceptors, as well as causing localized damage to tissues such as the synovium.
(Sofat N.2011)

The noxious stimulus is transmitted from the first order neurons to the second order neurons into the
dorsal horn of the spinal cord via the DRG, then to the spinothalamic tract ending up in the thalamus for
final processing. (Bourne S.2014)

An alteration of nociceptive function may be a cause for developing persistent pain. The repetitive
activation of primary afferents can lead to increased excitability of the peripheral and central nervous
system, which is called “wind up” or central sensitization. (Bourne S.2014; Poleshuck EL 2006; Change
SH 2009)

It has been believed that the N-Methyl-D-Aspartic acid (NMDA) receptor mediates the activation of
primary afferent neurons. It also seems that the activation of such neurons may be influenced by
biochemical and structural changes, and not only by localized noxious stimuli associated with
inflammation. (Bourne S.2014; Poleshuck EL 2006; Change SH 2009)

The World Health Organization (WHO) has estimated that 25% of people with OA are unable to carry
out their daily activities, while 80% experience some degree of limitations. The major outcomes
associated with OA is the pain, which leads to the development of disability, a decrease in the range of
motion and muscle strength, and patients failing to perform their daily activities satisfactorily, resulting in
more problems with self-care. As the disease progresses and the pain becomes more persistent and severe,
maladaptive thoughts begin to develop, which are associated with avoidance and hyper-vigilance,
resulting in a decrease in overall physical condition, and social and leisure activities.(Anderson BJ
2008;Bertolini A2006).

There is no cure for knee OA. The main objective and resulting strategy are to improve joint mobility,
decrease pain, reduce disability, limit the progression of joint damage, and improve health-related quality
of life and knee function.

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Treatment of knee OA

During the last day there has been rapid development and treatment guidelines in OA and especially
knee OA as a result a number at evidence -based guidelines and recommendation has been developed the
help health care professional. Physician and patients in the management of hip knee OA. There is at the
sometime, however a lack of agreement and recommendations for the management of hip and knee OA.
(Zhany et al 2006).

The three recent clinical practice guidelines. The European League Against Rheumatism (EULAR), the
American college of Rheumatology (ACR) and the (NICE) guidelines. Include updated guidelines for the
management of OA in general and for Knee OA in practitioner. There are some differences in these
guidelines, which may be related to the clinical trial included, their systematic review or the cost
effectiveness of modalities that have been used. (Zhang W 2006; Hochberg MC2012; NICE guidelines
2016)

The most recent of guidelines is the NICE, which was updated on September 2016 and aimed at
providing updated, evidence-based, concise recommended pharmacological and non-pharmacological
treatment in the management of OA. It also addresses problems surrounding the referral of currying,
recommendation for diagnosis and follow-up. (NICE guidelines 2016)

The pharmacological treatment of knee OA includes paracetamol, topical and oral- non steroidal anti-
inflammatory drugs (NSAIDs), plus protein pump inhibitors (PPI) to reduce gastro-intestinal
complications, topical capsaicin and opioids. The non-pharmacological treatment includes exercise, such
as message strengthening aerobic exercise, weight loss, thermo-therapy, electro therapy such as: TENS,
using aid, or appliances like knee bracing to supper joints, manual therapy such as manipulation and
stretching and patient education and intra-articular corticosteroid injection. (NICE guidelines 2016)

Despite the inclusion of pharmacological and non-pharmacological modalities in the treatment of knee
OA in the NICE guidelines, a holistic approach and assessment is required for the patient, which is also
concerned with impact of OA in the person's quality of life, occupation, social relationship, and
psychology. The assessment can be conducted through questionnaire depending on the patient's condition.
(NICE guidelines 2016)

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Definition of Transcutaneous Electrical Nerve Stimulation (TENS)

TENS is a noninvasive self-administered technique that delivers pulsed electrical currents through the
intact surface of the skin to activate peripheral nerves. (Jones I 2009).

Electrophysiological evidence suggests that TENS-induced afferent activity inhibits onward

transmission of nociceptive information in the CNS, and this generates hypoalgesia in healthy humans
exposed to noninjurious experimentally-induced pain and pain relief in pain patients. (DeSantana JM
2008).

Principles of TENS
The use of electricity to relieve pain dates back to 2500 BC when the Ancient Egyptians used electric
fish to treat various ailments. In 1965, the gate-control theory of pain provided a rational mechanism of
action for pain relief by electrically stimulating the skin. Clinical observations confirmed that pain relief
could be obtained by stimulating the skin, the dorsal columns and structures on the descending pain
inhibitory pathways, such as the periaqueductal gray in the midbrain.( Johnson MI etal.2011)

TENS was used to predict the success of spinal cord stimulation implants until it was realized that
TENS could be used successfully as a treatment in its own right .(Shealy CN 1974).

Nowadays, TENS devices can be purchased without prescription from pharmacy stores or over the
internet in many countries and it is prescribed by pain clinicians for symptomatic relief of pain of any
origin. (Chipchase LS 2009).
TENS can be used as a stand-alone treatment or in combination with pain medication to reduce drug
dosage, side effects and costs. (Bjordal JM 2003; Chabal C 1998).

It has also been used successfully for children as young as 4 years of age and in the management of
nonpainful conditions, including alleviating incontinence (Hagstroem S 2009), constipation (Clarke MC
2009), the progression of dementia (Cameron M 2003), postoperative nausea and vomiting.([Ezzo JM
2006), and to facilitate wound healing (Gardner SE 1999), skin-flap survival (Atalay C 2009) and bone
healing when delivered as microampere currents (Goldstein C 2010) .The evidence for success in these
conditions is inconclusive.

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TENS techniques

By strict definition, any technique that delivers electricity across the intact surface of the skin to
activate underlying nerves is TENS, although in healthcare the term is used to describe stimulation using
a ‘standard TENS device’. Standard TENS devices are portable battery-powered machines that produce
biphasic pulsed electrical currents up to 60 mill amperes in amplitude, pulse widths durations of (50–500
µs), pulse rates (frequencies) of 1–250 pulses per second and various pulse patterns (modes), including
continuous (normal), burst (intermittent trains of pulses) and modulated amplitude, modulated frequency
and modulated pulse duration. Lead wires take the currents from the TENS device to reusable self-
adhering electrode pads made of knitted stainless steel attached to the intact surface of the skin.
Commonly, square electrodes 50 × 50 mm are used, although a variety of other shape and sizes of
electrodes are readily available. The cathode activates the axonal membrane, so the cathode electrode
(normally the black lead) is placed proximal to the anode for monophasic waveforms, although nowadays,
most TENS devices use biphasic waveforms with zero net current flow between the electrodes to prevent
skin irritation. There is tentative evidence that smaller electrodes (8 × 8 mm) are more comfortable for
stimulating superficial nerves lying at depths of 1 mm in the skin and larger electrodes (41 × 41 mm) for
stimulating nerves at depths of 11 mm .(Kuhn A 2010).

Glove, sock and belt electrodes are available (Cowan S 2009), and electrode arrays have been developed
to spatially target stimulation more precisely. (Kuhn A 2009).

The proliferation of TENS-like devices over the last few decades appears to have been driven by
developments in technology, rather than proven efficacy or biological rationale. Evidence suggests that a
standard TENS device is most likely to be efficacious in the first instance. (Johnson MI 2001).

The main techniques that are administered using a standard TENS device are conventional TENS (low-
intensity, high-frequency) and acupuncture-like TENS (AL-TENS; high-intensity, low-frequency).
The purpose of conventional TENS is to stimulate low threshold non-noxious afferents (e.g., A-b fibers)
without concurrently activating high-threshold noxious afferents A-d and C fibers. (Charlton J 2005).

9
 Activity in A-b afferents reduces transmission of pain-related information in the spinal cord and
brainstem. A strong, comfortable, non-painful electrical paresthesia beneath the electrodes or in the
painful area is indicative of selective A-b activity and patients titrate current amplitude to achieve this
effect.(Charlton J 2005).

Frequencies of between 10 and 200 pps, with a continuous pulse pattern, are commonly used during
conventional TENS, although patients often experiment with stimulator settings to maintain the most
comfortable stimulation for that moment in time. . ( Charlton J 2005).

The purpose of AL-TENS is to activate A-d afferents from deeper (muscular) structures in order to
release opioid peptides in the CNS. (Eriksson M 1976; Johnson MI 1998).

AL-TENS is a form of ‘hyper stimulation’ and is delivered using high-intensity currents (maximum
tolerable sensation) at a low frequency (either single pulses (~100 pps).( Charlton J 2005).

AL-TENS is delivered at painful sites, on acupuncture points, and over muscles, motor points and
trigger points. There has been debate about whether muscle twitching is a prerequisite for AL-TENS.
(Johnson MI 1998).

Clinical practice is variable and the presence or otherwise of muscle twitching will depend on whether
electrodes are positioned over muscles or motor nerves. It is claimed that AL-TENS is useful for patients
resistant to conventional TENS and for patients with radiating neurogenic pain, pain associated with
altered skin sensitivity and pain arising from deep structures. (Sjölund B 1990).

Other types of TENS include ‘Acu-TENS’ to describe TENS on acupuncture points using a wide
variety of parameters and ‘intense TENS’ to describe high-frequency painful TENS given for short
durations for wound-dressing changes, suture removal and venipuncture. (Brown L 2009).

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Adequate TENS technique

The critical factors in TENS outcome are electrode position and pulse amplitude (intensity), with
evidence suggesting that an adequate TENS technique is achieved when a strong non-painful TENS
sensation is produced within the site of pain. (Bjordal JM 2003; Brown L 2007).

Optimal electrode placement

In clinical practice, TENS electrodes are usually positioned over the site of pain so that the TENS
sensation covers the pain. However, this may not be appropriate for neuropathic pain as TENS may
aggravate tactile allodynia and dysesthesias. Paradoxically, this is not always the case. In addition, it may
be difficult to achieve TENS paresthesia when there is diminished skin sensitivity from nerve damage
(e.g., numbness following peripheral neuropathy). In these circumstances, electrodes are positioned over
nerves that are proximal to the site of pain. Sometimes it is possible to project TENS sensations into distal
body parts, for example, into phantom limbs to relieve phantom limb pain. (Cheing GL 2009).

Optimal dosage of TENS

Evidence suggests that pain relief is rapid in onset and offset, and that maximal benefit occurs during
stimulation, with successful long-term TENS users administering TENS for many hours each day. (Koke
AJ 2004).

Over 50% of chronic pain patients who try TENS gain short-term benefit from TENS, but this declines
in the long-term because effects wear off over time and/or the effort to use TENS regularly is
disproportionate to the amount of pain relief obtained. (Koke AJ 2004).

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Contraindications and precautions of TENS

Active implants such as pacemakers and ventricular assist devices (artificial hearts) are absolute
contraindications for TENS. (Chartered Society of Physiotherapy C 2006).

TENS also produces inadvertent shocks with internal cardiac defibrillators and generates artefacts on
fetal monitoring equipment. (Holmgren C 2008)

In exceptional circumstances, TENS has been used in these situations, using electrode positions that are
distant from the chest following approval from the medical specialist. TENS should not be administered
on the neck or head in individuals with epilepsy, or close to bleeding tissue, malignancy (except in
palliative care), active epiphysis or on the abdomen during pregnancy .(Coldron Y 2007).

Also cannot use TENS over the chest of patients with cardiac disease, over the patient eyes, and over
laryngeal or pharyngeal muscles, head /neck of the patient with a history of a stroke, and over mucosal
membranes, also contraindicate near phrenic nerve gonads, and history of spontaneous abortion in
pregnant women, in pregnant women, near the pelvis, lumbar spine, hips, and abdomen. (Siegelman R
2009).

Contraindications to electrotherapy in general should be observed. Electrotherapy might be used under

some of the circumstances listed below when benefit outweigh the perceived risk. (Michlovitz SL 2012).

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 Care should be taken when TENS is administered for patients with metal implants, stents, percutaneous
central catheters or drainage systems, and close to transdermal drug delivery systems. Adverse events
from TENS appear to be rare and are due to inappropriate technique. (Ford KS 2005).

TENS worsens pain in some individuals, may produce mild erythema and produce a vasovagal
response, leading to nausea, dizziness and even syncope. Skin irritation and redness, hives, welts, broken
skin area, and skin infection are precaution for TENS. (Siegelman R 2009).

Research indicates that there is no risk of infection from reusing electrode pads on the same patient as
long as the clinician follows the manufactures guidelines. (Cattell J 2011).

Numerous studies have examined the efficacy of TENS for knee OA. Gladys et al. In 2003 conducted a
trial to examine the optimal stimulation duration of TENS for relieving pain and patient with knee OA
and the duration (as measured by half- life) of post- stimulation analgesia. 38 subjects were included in
the study.
They received either (TENS20) 20 minutes or (TENS40) 40 minutes or (TENS60) 60 minutes or (TENS
PL) for 60 minutes for 5 days 1 week for 2 weeks duration. Visual analyze Scale (VAS) 10-cm horizontal
line was used and assess patient's pain before and after TENS treatment.

The results suggested that there was statistically significant reduction on VAS scale by day 10 in all
treatment group. There was (83.40, 68.37%) and 54.59%) for (TENS 20, TENS 40, TENS 60) respectively
with p< 0. 001. After repeated daily stimulation for 2 weeks, the drop on visual analyze score was (p<
0.001) for all the 3 active groups.
The half-life. Life post treatment on day 1 the average time (minute) for TENS 40 and TENS 60 was
longer than that of TENS 20 and TENS PL. group. (TENS20= 162, TENS40 =380, TENS60=352, TENS
PL=163. By day 10 the TENS 60 group produced the longest pain relieve period. TENS20 =168, TENS40=
256, TENS60= 258, TENS PL=35). However, by the follow-up session the TENS40 group produced the
longest pain relieve period.

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 A year later Low PP et al. conducted a study evaluate the efficacy of TENS at ( 2HZ , 100HZ) or
alternating 2Hz/100Hz for 40 minutes, 5 times a week for 2 weeks. Thirty-six subject were recruited from
one local care home, the subjects were randomized into 4 equal groups (n=9 each).
The first treatment group (TG1) received TENS at a frequency of (2HZ) .The second treatment group
(TG2) received TENS at a frequency of (100HZ) and the third treatment group (TG3) received TENS
alternating between a frequency of (2HZ) and (100HZ) .The CG received placebo TENS using a machine
identical to the real treatment unit, but with the internal circuit disconnected.
All 4 treatment groups received treatment for 40 minutes, 5 times a week for 2 weeks. The VAS scores
were recorded at (0, 0.2, 0.4, 0.6, 0.8, and 100) minutes during each session and at the 2 weeks follow up
session. The VAS score was recorded as a measurement based on the mark subjects made on a 10cm line,
each VAS score was recorded on a separate sheet so that subjects could not look at the previous VAS
score.

The results showed that there was statistically significant difference in VAS scores within the 3
treatment groups across session, but not within the placebo group. The authors also reported statistically
significant differences between each of the 3 treatment groups to the placebo group at a session 10 and the
2 week follow up, it was ( 5.0 , 4.3 , 3.8 , 1.4 ) for ( TG1 , TG2 , TG3 , and CG ) respectively.
However the study has a number of limitation,: Firstly, there was a study loss of 2 out of 36 subjects,
one was for medical reason and the other was because the subject had moved out of the elderly complex,
this result in a total 6% loss, there was no mention of intention to treat to treat analysis to account for the
study losses, or which groups the withdrawals were from and at what point they dropped out of the study
Secondly, is lack of blinding of therapists. Finally, is the small sample size, with only 9 subjects per
group.

Similar to above studies Grace et al. conducted a trial in 2012 to evaluate the efficacy of high.
Frequency TENS (HF-TENS) and low- frequency TENS, (LF- TENS) on several outcome measures (pain
at rest, movement evoked pain and pain sensitivity in people with knee OA. The study was double-blind
randomized trial, it was a single TENS treatment for 20 minutes. The trail included 75 people with knee
OA who were randomized either to receive HF-TENS. (100 Hz) or LF-TENS (4Hz) or placebo TENS.
There was on assessment before and after for each measures.

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 The study showed that there was significant decrease in pain at rest on p=0.001, p=0.01 and p=0.001 for
HF-TENS, LF-TENS and placebo TENS respectively and on 100mm visual analogue scale (VAS) the
average was 24 and 28mm. However; 15% (11) of the patients were taking opioid and 72% (52) were
taking non-opioid medication.
Pressure pain threshold(PPT) cutaneous mechanical pain threshold(CMPT) was not affected by HF-
TENS,LF-TENS as the pain was increased as compared with pre TENS and it was (P=0.002)and (P=0.5)
in HF-TENS & LF-TENS respectively. Also pain during Timed "up and go" test was significantly
decreased in all the 3 groups.it was (p=0.001, p=0.03, p=0.001) for HF TENS LF-TENS and placebo
TENS.
However ;there was no change in function, and this may be due to the fact that the TUG minimally
increased pain above that at rest did not produce enough pain in the subject to evaluate movement evoked
pain. Therefore TUG may be not appropriate measure for examine movement evoked pain function it
would be better to use a function test that produce greater pain such as stair climbing. Also, the study
limited to one single treatment and the blinding was not appropriate as the subjects know they receiving
TENS and placebo TENS. Furthermore; most of the subjects were female.

Furthermore, the efficacy of TENS was examined by David et al. the pain purpose of the study was to
explore the pain inhibiting effect of burst TENS in OA in knee patient and to explore the prognostic value
of central sensitization on the pain inhibiting effect of Tens. 120 subjects were involved to the trial for
period of 6-12 weeks. They randomly allocated to either TENS or from TENS group. They received
internal frequency of Tens 100HZ or burst TENS 3Hz for 40minute 1 day over two week.
There was follow-up self-reported knee pain difficulty with physical function measured using the
Western Ontario and McMaster universities (WOMAC). The result shows that there was significant
difference in the reduction of pain by 4.7 points on VAS on TENS group as compared to sham TENS
group. However, there was no enough data in the study. In addition the follow-up was done through a
weekly phone calls and fill out the dairy which may affect the result of the study.

In general, from above studies it could be suggested that TENS was effective in reducing pain but did
not improve physical functions for individuals with knee OA. However, in one study that used a high and
low frequency of TENS the results was not significant and another study used fixed and an alternating
stimulation of TENS the results was not very significant between groups.

15
 In order to support further the effect and safety of TENS, a systematic review included 36 randomized
placebo-controlled trails with 2434 patient were 1391 patient received active treatment.
The findings suggest that TENS was effective in reliving short-term pain for patient with OA knee than
placebo. The data presented in this review comes from good quality studied and for duration 1-12 week
follow up after this treatment. Limitations must be noted that heterogeneity existed in methodological
design. Outcome measure and using different tools to assess patient condition.

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Conclusion

Osteoarthritis (OA), sometimes called degenerative joint disease or degenerative arthritis, it is a

clinical syndrome of joint pain accompanied by varying degrees of functional limitation and reduced
quality of life. (NICE Clinical Guideline 2016).

The OA can be classified as primary (idiopathic) when its etiology is not well defined and secondary
when there is a specific disease-causing process. (National Clinical Guideline Centre 2014).

The secondary is the result of genetic factors, trauma, more common in men at any age, inflammatory,
neuropathic, metabolic or endocrine diseases result from congenital abnormality of the joint, joint
infection, inflammatory disorders, metabolic arthritis, hemochromatosis repeated, traumatic injuries and
deformities, acquired articular incongruity, joint misalignment or instability of the joint. (Batt ME 2014;
Kloppenburg M 2013).

The clinical features of OA are severe pain, joint stiffness, instability of movement, swallowing of
affected joint. (Evans CH1 2013; Doherty M – 2005).

Although there is no cure for knee OA include, the main objective of treatment is to reduce pain,
improve mobility and minimize disability. The pharmacological options include paracetamol, topical and
oral non NSAIDs, plus PPI to reduce gastro-intestinal complications, topical capsaicin and opioids. The
non-pharmacological treatment includes exercise, such as message, strengthening aerobic exercise, weight
loss, thermo-therapy, electro therapy such as TENS. (NICE guidelines 2016)

It could be concluded that using TENS alone was effective in reducing pain. However, in one study that
used fixed and an alternating stimulation of TENS the results were similar in each group. Also in another
study that aimed to show the difference between high and low frequency of TENS the result was not
significant between groups. In conclusion; however, with the short coming with these trials and some
failed to determine the positive outcome about TENS. It could be concluded that these literatures
reviewed support the recommendation of NICE guidelines that the non-pharmacological option of TENS
was effective in treating knee OA symptoms.

17
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