Gate Control Theory Of Pain Health And Social Care Essay

OA knee pain – prevalence, cost to NHS etc. Physio treatment of neck pain→ electro modalities, esp TENS

Pain is something that everyone suffers with at one time or another. Pain can be a huge burden on employers due to absenteeism (White et al, 2005). There are many methods used to relive pain with TENS being one method.

Having completed a review of current literature, it is clear that the application of tens has a significant effect on the pressure pain threshold of a subject, however no study to date has researched the effects the positioning of the TENS being applied has on the pressure pain threshold. Therefore this study has the aim of investigating whether the positioning of the electrodes at the nerve root level will affect the pressure pain threshold of the relevant dermatomal area giving rationale for the use of TENS as a pain reliving modality for injuries to the extremities.

Literature Review 4k

Literature Search

This research is investigating the effect of transcutaneous electrical nerve stimulation at a nerve root has on the pressure pain threshold at the periphery in relation to osteoarthritis of the knee. A review of the current literature was conducted using the following databases: PubMed, ScienceDirect, MetaLib (Cardiff University’s Electronic Resources) and Google Scholar for journals dated 1982-2012. The main key words used in the search included, “transcutaneous electrical nerve stimulation”, “pain”, “osteoarthritis”, “knee”, and “periphery”. Backchaining was also used to ensure all relevant literature was obtained.

Introduction

Osteoarthritis a very common joint disorder occurring in any joint but most commonly in the hip, knee, the joints of the hand and foot, and spine (Symmons et al. 2003). It mostly affects those aged 60 and over with approximately 40% of people over the age of 65 suffering symptoms associated with knee OA (Zhang et al., 2008) resulting in globally nearly 250 million people having osteoarthritis of the knee, 3.6% of the population (Vos et al. 2012). This resulted in osteoarthritis becoming the fourth leading cause of disability in the year 2000 (Symmons et al. 2003) and costing the NHS a total of 25 million pounds in 2008 (NICE 2008)

Arthritis knee

Osteoarthritis of the knee is a chronic degenerative disorder with a multifactorial aetiology (Felson, 2000). This includes general factors; such as age, sex and obesity, mechanical factors; such as alignment and trauma (cooper et al. 2000) and genetic factors (Reginato et al. 2002).

Osteoarthritis of the knee is characterised by both loss of articular cartilage and by central and marginal new bone formation (subchondral sclerosis, osteophytes) (Woolf and Pfleger, 2003). There is also often thickening of the capsule and low grade synovitis resulting in alterations in biomechanics of the joint. Osteoarthritis affects the whole joint with secondary changes including ligament laxity due to articular cartilage loss and muscle weakness around the joint due to disuse respectively (Felson 2000).

Osteoarthritis of the knee is associated with pain, joint stiffness and deformity, which in turn lead to limitations of daily activities for sufferers. Although there is currently no cure available, there are a number of treatment options open to sufferers to provide symptomatic relief, as well as joint function improvements. There are many non- pharmacological treatment options available such as education, rehabilitation exercises, manual therapies, acupuncture and electro-modalities such as TENS. There is also a wide range of pharmacological measures available, non-steroidal anti-inflammatory drugs, oral analgesia and topical treatments. Pharmacological treatments also include intra-articular modalities such as injections of corticosteroid and hyaluronic acid and tidal irrigation to reduce symptoms. In severe cases, where nonsurgical interventions have failed, more invasive approaches may be needed (Cooper et al 2000) including therapeutic arthroscopy and joint replacement.

Models of Pain

Pain something that the medical profession aims to alleviate in all patients suffering from it. In order to do this an understanding of the function of pain is needed as well as knowledge of the physiological processes the cause pain.

Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage (Bonica 1979). It serves as a stimulus to motivate an individual to cease or withdraw form damaging or potential damaging situations, or to protect a damaged body part during the healing process (Winlow et al. 1984). There are three main models of pain, the cognitive-behavioral model of pain, the gate control theory of pain and the neuromatrix theory of pain.

Gate control theory of pain

The gate control theory suggests there is a neurological “gate” in the dorsal horn of the spinal cord (Melzack and Wall 1967). This gate either blocks pain signals or allows them to continue to the brain. This “gate” in the spinal cord differentiates between the types of fibers carrying pain signals. Pain signals travelling down the larger C nerve fibers are blocked whereas pain signals travelling done the smaller a-delta nerve fibers are allowed to pass through and therefore continue up to the brain where the pain can be perceived (cord (Melzack and Wall 1967). This gating mechanism is influenced by descending nerve impulses from the brain in response to ascending pain stimuli.

Cognitive behavioral theory of pain

The cognitive behavioural pain theory explores the perception of pain by relating it to more than just the physical and physiological attributes of the pain mechanism, and explores the predisposing and perpetuating factors as well as the psycho-social aspects involved in pain perception (Letham et al. 1983). This model explains why some individuals continue to experience pain after trauma has healed, or display a pain response disproportionate to the original condition.

The theory states that the perception of pain is influenced by predisposing factors such as personality, coping style and previous history of illness, as well as perpetuating factors such as behaviour, emotions, and physical symptoms (Letham et al. 1983). This explains why some individuals suffer with continued pain after the original injury has resolved and are driven by fear of further pain leading to increasingly restricted activities despite the original injury being resolved, exhibit a maladaptive avoidance response. While other will experience very little pain in situations that would otherwise be excruciating, for example soldiers in battle (Letham et al. 1983)

Neuromatrix theory of pain

The pain neuromatrix theory is a development of the gate control theory of pain.

A widespread distribution of neurons imprint a ‘neurosignature’ upon nerve impulse patterns that pass through the sensory matrix (Melzack 2001). This neurosignature creates the experience of self and gives subsets of patterns that give unique experiences such as pain. The perception of pain in the brain would be as the end result of an activation of the pain neuromatrix with a characteristic pattern relating to the pain signature (Melzack 2001). This is part of a multi system response to a perceived threat. However there are many other inputs that can trigger the pain neuromatrix in the brain including movement, touch, fear and visual stimuli (Melzack 2001). This is due to the fact that the widespread neurons which make up the neuromatrix for pain perception are involved in many other activities so the pattern for pain perception can be triggered by other groups of neuromatirx being active during other activities not purely the pain neuromatrix

Pain and pathways

There are four basic processes involved in nociception(processing of pain), Transduction, transmission, perception and modulation (McCaffery and Pasero, 1999).

Transduction begins when nociceptors (free nerve endings) of either the A-delta fibres or C fibres of the primary afferent neurones respond to noxious stimuli. A noxious stimulai occurs when tissue is damaged and inflation occurs. The nociceptors are found in the somatic structures (skin, muscles, and joints) as well as the visceral structures (organs such as gastro-intestinal tract or the liver). (Wood 2008)

Although both the C fibre and A-delta fibres are Primary afferent fibres they have different cell structures and are associated with different pain qualities (table 1).

Table 1: Characteristics and functions of C fibres and A-delta fibres (Farquhar-Smith 2007)

C fibres

A-delta fibres

Characteristics:

Small diameter

Unmyelinated

Slow conducting

Receptor type:

Polymodal: respond to more than one type of noxious stimuli:

Mechanical

Thermal

Chemical

Pain quality:

Diffuse

Dull

Burning

Aching

Referred to as ‘slow’ or ‘second’ pain

Characteristics:

Large diameter

Myelinated

Fast conducting

Receptor type:

High-threshold mechanoreceptors: respond to mechanical stimuli over a certain intensity.

Pain quality:

Well-localised

Sharp

Stinging

Pricking

Referred to as ‘fast’ or ‘first’ pain

There are three stages to the transmission of pain; first the impulse is transmitted from the site of transduction along the nociceptor fibres (first order neurons) to the dorsal horn, in the spinal cord, where both C fibre and A delta fibres terminate. In the dorsal horn they synapse with the second order neurons and which then cross the spinal cord via the anterior white commissure and ascend to the thalamus via the two main nociceptive ascending pathways. These are the spinoparabrachial pathway and the spinothalamic pathway. The thalamus then directs the nervous impulse to multiple areas of the cortex and higher brain for processing as there is not a discrete pain centre (Wood 2008).

The end result of the pain transmission is the perception of pain. This is where pain becomes a conscious and multidimensional experience with affective-motivational, sensory-discriminative, emotional and behavioural components. When painful stimuli are transmitted to the brain stem and thalamus, three main cortical areas are activated, the reticular system, the somatosensory cortex, and the limbic system, each one is responsible for a different response to the pain stimuli. (McCaffery and Pasero, 1999)

The reticular system is responsible for the autonomic and motor response to pain, for example, automatically withdrawing from a painful stimulus. It also plays a role in the affective-motivational response to pain, such as assessing an injury after pain has occurred.

The somatosensory cortex is involved with the interpretation and perception of sensations. It identifies the location, type and intensity of the pain sensation and relates this sensation to past experiences before triggering a response.

The limbic system is responsible for the behavioural and emotional response to pain as well as past experiences of pain.

The modulation of pain involves altering or inhibiting the transmission of pain impulses in the dorsal horn of the spinal cord. The complex pathways involved in the modulation of pain are called the descending modulatory pain pathways (Ossipov et al. 2010). These pathways can lead to either an excitatory response (an increase in the transmission of pain impulses) or an inhibitory response (a decrease in transmission of pain impulses). Descending inhibition produces an analgesic effect by causing the release of inhibitory neurotransmitters which partially or completely block the transmission of pain impulses in the spinal cord (Ossipov et al. 2010).

Endogenous pain modulation helps to explain the wide variations in the perception of pain in different people as individuals produce different amounts of inhibitory neurotransmitters. Endogenous opioids are found throughout the central nervous system (CNS) and prevent the release of some excitatory neurotransmitters, for example, substance P, therefore, inhibiting the transmission of pain impulses.

Physiotherapy and treatment of Pain

Transcutaneous electrical nerve stimulation (TENS) – papers on TENS and Pain (critical review of the literature)

Transcutaneous electrical nerve stimulation (TENS) is an electro therapy procedure the aim of which is pain relief. During treatment a low amplitude and frequency alternating electric current is passed between two electrodes placed on the body resulting in stimulation of the nervous system. Research will be reviewed examining the theory that TENS is an effective pain reliving modality. Previous studies by Chesterton et al (2002, 2003) Vance et al (2012) and Chen et al (2010) have all shown TENS to be an effective form of pain relief against blunt pressure pain with. All however have used different parameters for both the TENS settings and application sites.

All of the previous studies looked at found TENS to be an effective method of pain relief based on pressure pain threshold measurement. Both of Chesterton’s and Vance’s studies found a statistically significant increase in pressure pain threshold after a twenty minute application of TENS (p=0.005, p=0.01, and p=0.002 respectively). Chen also found a significant difference in post TENS of p=<0.001. However unlike the other studies which looked at the difference between the pre and post treatment pressure pain values Chen’s study looked at the number of subjects that achieved a set increase in pressure pain value (10N). This does not take into account the normal distribution of the group, meaning that this set increase may not actually be a significant difference in pressure pain threshold in all of the subjects tested.

Vance was the only study to look at other forms of pain measurement s outcome measures, as well as the use of a pressure pin threshold measure similar to the other studies a cutaneous mechanical pain threshold measure using Von Frey filaments and heat pain threshold measure were also used. Although using these additional outcome measures to assess the effectiveness of TEN as a pain reliving modality it was only the pressure pain threshold measure that yielded a significantly change. Therefore the results of the study can still only be extrapolated to the pressure pain reliving abilities of TENS and no other forms of pain.

Both Vance and Chen explored the differences between the frequencies TENS applied. Chen uses 3Hz for low frequency and 80Hz for high frequency. Vance does not specify the actual frequency used and only states high and low frequency Tens was used with the definition of High frequency TENS >50Hz and Low frequency TENS <10 Hz. This reduces the validity of Vance’s results as the study cannot be repeated and the exact parameters are not known.

In Chesterton’s 2002 also explored the differences between the frequencies of TENS applied using 4Hz as the low frequency and 110Hz as the high frequency. The results were similar to Chen with the high frequency TENS proving a more affective pain reliving modality of TENS.

All three studies have good internal reliability, the same experimenter was used for every measurement, and standardised testing procedures were used. The rate of application of the algometer was kept constant when measuring the pressure pain threshold and the same point was used on each subject for the measurement. Chen and Vance, however, relied sole on the skill and consistence of the experimenter to ensure the pressure pin threshold reading was taken in the same manner for every subject. Chesterton’s studies used a special mounting frame for the algometer to ensure that it was perpendicular to the skin and that the rate of application was constant. This improved the internal reliability of the study as each subject will have had the reading taken in exactly the same way.

Chesterton and Chen both use healthy volunteers as the subjects in their studies. Both studies have a good sample size with an equal distribution of males and females. Chen’ subjects have a small age range (mean ± SD, age 26.7 ± 2.9 years) which is not representative of the population. Chesterton’s sample has a much larger are range (mean ± SD, age 30± 7 years, range 18-57 years) which is a far closer representation of the general population and makes the extrapolation and application of the results more reliable. However both of these studies, due to only using healthy subjects, cannot be reliable extrapolated to apply to people who are not healthy. Therefore it cannot reliably be said that anyone suffering with a painful condition, be it degenerative, trauma, or surgical, will benefit from the application of high frequency TENS or that it will reduce their pain. It can only reliable be said that it will reduce the pain perceived in healthy individuals. This however is addressed by Vance, although using smaller sample size than Chesterton all of the subjects used in the study all had a diagnosis of medial compartment osteoarthritis of the knee. Unlike the other studies Vance did not have an equal split of male to female subjects (29 male 46 female), however by using a stratified randomisation process it was ensure that each experimental group had the same ratio of male to female subjects. Therefore unlike the other studies Vance’s results can be reliably extrapolated to apply to a population with a diagnosis of medial compartment osteoarthritis of the knee, and high frequency TENS can be reliably used as a pain reliving modality.

Random allocation of groups

Not all subjects tens naive

Blinding

All have good baseline comparability between groups.

Chen

Good base line A paired t-test on this data found no significant differences (mean + SD = -1.50 ± 5.65N, P = .143)

Chesterton 2002

Good basleine similar This was confirmed by a one-way analysis of variance (ANOVA) for pre-treatment mean MPT (P 0:19

Chesterton 2003

Good One-way analysis of variance (ANOVA) showed no significant differences in PPT, between the groups at baseline (p 0:142)

Vance

Bad not equal gender split 29 male 46 femle.

But good that same ration in each group.

Good There were no significant differences between groups in demographic characteristics, with the exception of body mass indexes (P.027).

Algomiter reliability

Aim(s)

Hypothesis (hypotheses)

Does High-TENS affect pressure pain threshold (PPT) at the periphery?

Null Hypothesis: There will be no difference in the pressure pain threshold between the control group and experimental group.

Methods

Design

This study was an experimental repeated measures clinical trial. The independent variable being assessed was transcutaneous electrical nerve stimulation. The dependent variable was Pressure pain threshold. The study included 20 people who had no previous history of knee pain and had not previously experienced TENS. Subjects attended two sessions with a 48 hour interval. In the first session subjects were given a placebo TENS and in the second a single high frequency TENS treatment. Outcome measurements were obtained before and during each treatment. Ethical approval for the study was granted by the University Ethics Committee (Cardiff University, 2012).

Participants

A convenience sample of 20 subjects from Cardiff University School of Healthcare was used. The inclusion criteria consisted of being a healthy subject. Subjects were screened for relevant contraindications and exclusion criteria including: pacemakers, heart disease or arrhythmias, undiagnosed pain, epilepsy, peripheral neuropathy (Fox and Sharp, 2007), history of trauma or surgery to the dominant leg in the last 6 months, medication, history of pregnancy or knowledge or use of TENS treatment (Chesterton et al., 2002). No subjects were excluded. The experimental procedure was explained to each subject who then signed a consent form witnessed by an independent person (Appendix 4). At the first session, subjects were assessed for bilateral recognition of sharp versus dull pressure at the L3 dermatome to rule out loss of sensation.

Ethics

Ethical approval was obtained from The School of Healthcare Studies Ethics committee Cardiff University and a single blind experiment using repeated measures was used. A risk assessment was carried out for the pilot and data collection assess risk to the subjects and the investigator using the standard risk assessment method of the cardiff university Physiotherapy department. The risk is quantified by the Risk Rating Number which is calculated by multiplying the probable frequency by the potential severity. For this research the probable frequency is unlikley scoring two and the potential severity is negligible scoring one (appendix 1). The Risk Rating number is two which requires no further action (Cardiff Univeirsity 2012).

Individuals with a history of knee pain were excluded, reducing the likelihood of physical injury to the subjects during the PPT measurement process. In the event of an injury subjects would be withdrawn from the study and appropriate medical advice would be sought. The privacy and dignity of the subjects during electrode placement was ensured by using screens, and gaining informed consent before exposing the skin on the back. The information sheet given to the subjects (Appendix 3) informed them of what the study involved, and that the results would be analysed as part of this research project. Subjects were informed they were free to withdraw from the study at any time. All data was confidential and anonymous. All data stored on a computer was and password protected and anonymous.

Pilot study

A pilot study was conducted on 3 subjects not included in the main study prior to data collection. This was to ensure that the method to be used was satisfactory and to allow researcher to familiarize themselves with the equipment. It also allowed the researcher to estimate the time required, allowing appropriate time slots to be set. Another reason for the pilot study to be carried out was to expose any unforeseen errors or limitations in the design protocol allowing modification as necessary (Jenkins et al, 1998). The pilot study highlighted variations in subject foot placement in sitting, in turn effecting the knee positioning needed for a PPT reading to be taken. It was therefore decided to give subjects the following verbal command on how to sit, “sit with your feet flat on the floor and your knees at ninety degrees”, to minimize variance in knee position. The rest of the method was deemed sufficient and no further changes were made.

Apparatus

The pressure pain threshold was assessed using a handheld pressure algometer (Algometer commander, Jtech medical, United States) with a flat circular metal tip measuring 1.1 cm in diameter. The force was displayed digital in increments of 0.1N and applied at a rate of at 5N/s (Chesterton et al 2002). The subjects were instructed to say “stop” when the sensation first became painful. A practice test was first performed on the non-dominant knee to familiarize subjects with the procedure. The use of a pressure algometer for measuring pressure pain threshold has excellent test-retest reliability (r.70-94) (Fischer, 1987), and is a valid measure for deep-tissue hyperalgesia as discussed by Staud et al. (2007)

Electrical stimulation was generated via a commercially available a dual channel, TENS unit (200 plus, TPN), the unit uses an asymmetrical, biphasic waveform. The pulse width was set at 50 microseconds and the frequency 150Hz, and the intensity was increased to the subjects’ verbal report of when the feeling became strong but still comfortable.

Procedure.

Before taking part in the study, all subjects were given an information sheet (appendix 3) explaining research study and what would be expected from them if they participate and completed a consent form (Appendix 4).

Subjects came in on two separate occasions 48 hours apart; once for the control trial (sham TENS) and once for the application of TENS. In the first session demographic data was obtained, which included age and gender.

A standard ‘sharp/blunt’ discrimination test was performed, using neurotip at each stimulation site, to ensure intact skin sensation. The skin was then cleaned using an alcohol wipe before the application of electrodes (Chesterton et al., 2003).

Two TENS electrodes were then placed over the L3 spinal level. Each electrode was placed over the L3 Spinal nerve root the location of which was found by palpating to the L3 spinal level (Rhoades et al. 2009). The first electrode was positioned 10mm to the left of the L3 spinal process with the second positioned 10mm to the right. The center of each the electrode was placed level with the inferior aspect of the L3 spinal process (figure 1). Experimenter 1 was responible soley for the electrode psoiting nd TENS application to ensure internal reliability. Figure 1

Subjects were seated in a comfortable upright position with feet flat on the floor. The position of the pressure pain reading was then marked bilaterally. This was done by measuring 30mm superior to the central aspect of the superior border of the patella in flexion (figure 2). Experimenter 2 was responsible solely for the positioning of the pressure pain reading and the algometer application to ensure internal reliability. Figure 2

A practice pressure pain measurement was then performed on the subject’s non dominant side with subjects instructed to say “stop” when the sensation first became painful. At this point the experimenter immediately retracted the algometer. (Chesterton et al. 2003) This process was then repeat three times at 30 second intervals on the dominant side to establish a base line figure (Vance et al 2012).

The Tens machine was then turned on and the intensity increased to the subjects’ verbal report of when the feeling became strong but still comfortable. For the sham TENS subjects were told that some forms of TENS were imperceptible and, they might not feel any sensation. The battery in the TENS unit was inserted the wrong way round. The unit was still visibly switched on and the intensity turned up, but no current was flowing (Chesterton et al 2003). A 30 minute timer was started as soon as the intensity was correctly adjusted.

When the 30 minute time period had elapsed three further pressure pain threshold readings were taken again at 30 second intervals on the dominant side to a post treatment figure. Once these reading were taken the TENS machine was turned off and the electrodes removed. Subjects were monitored for a further 30 min after the end of the stimulation period (Chesterton et al 2002).

Subjects returned for the second session 48 hours later.

Data Analysis

All data was entered into Windows Excel version 2010 Descriptive analysis was carried out using means, standard deviations this was presented as tables and graphs. The data was then entered into SPSS (Statistical Package for Social Sciences version 20.0). The data was interval ratio and the study investigated one group of subjects. A paired t-test was conducted to compare the percentage change in pressure pain threshold between the control and high TENS conditions. A statistical significance level of 95% (p<0.05) was used (Hicks, 2004). All raw SPSS outputs can be found in Appendix 5.

Results

The demographic data can be seen in Table 1. The following tables and graphs present both descriptive and statistical analysis of the pressure pain threshold data. All SPSS outputs can be seen in appendix 5 and raw algometer data can be seen in Appendix 6.

Table 1: Demographic Characteristics of Sample

N

minimum

maximum

mean

S.D

Age

20

19

23

19.95

1.09904

Key: N = Number of subjects

S.D = Standard Deviation

A small standard deviation is seen for the age of subjects in Table 1. The male to female ratio was 1:1 with 10 female subjects and 10 male subjects. All subjects met the inclusion and exclusion criteria, and all were able to complete the study.

Discussion

There are two primary and related theories for explaining the efficacy of TENS in chronic or acute pain relief. The gate theory (Wall, 1965 (Melzack R, Wall P. Pain mechanisms: a new theory. Science. 150(699):971-979,1965)) proposes that pain transmission relies on a ‘gate’ to the thalamus and cortex for nocireceptive information to be interpreted as pain. This theory postulates that inhibition of nocireceptors can be caused by rapid impulse activation of myelinated nerve fibers. The second related theory postulates that neurotransmitter exhaustion can be caused by rapid nerve activation outside of its refractory period, and that the temporary exhaustion of neurotransmitters would provide pain relief until such time as neurotransmitter synthesis had ‘refilled’ the synaptic junctions (Kaye, 2007(Transcutaneous Electrical Nerve Stimulation: WebMD eMedicine. http://www.emedicine.com/pmr/topic206.htm January 26, 2007)).

Limitations

Clinical Implications

Further research

Conclusion