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Chapman S (2010) Pain management in patients following limb amputation. Nursing Standard. 25, 19,35-40. Date of acceptance: February 5 2010.

or crushing phantom pain, described ascontinuous or intermittent.

Phantom pain is a type of neuropathic paincaused by the mechanical severing of nerves byamputation of a body part. Unlike nociceptivepain, which is generated by the activation ofnormal pain pathways and has a protectivefunction, neuropathic pain is generated by theabnormal activation of pain pathways in responseto damage or dysfunction in the nervous systemand does not have a protective function (Callin and Bennett 2008a). This damage or dysfunctioncan occur in the peripheral and/or central nervoussystem. The International Association for theStudy of Pain (1994) defined neuropathic pain as pain initiated or caused by a primary lesion ordysfunction of the nervous system. This definitionallows for the fact that a primary lesion does notnecessarily have to be evident and includes a widerange of pain syndromes that can disrupt activity in the nervous system and cause dysfunction orabnormal activity. Neuropathic pain can existwithout an identifiable cause (Johnson 2004).

Definitions and characteristics of painfollowing amputation

Definitions of pain and/or sensations experiencedfollowing amputation can vary, but can besubdivided into phantom limb pain, phantomlimb sensation and stump pain (Box 1). Theexperience of any of these types of pain orsensations has been described as a phantomcomplex (Nikolajsen and Jensen 2005).Phantom limb pain This is a painful sensationperceived in the missing limb. Pain may bedescribed as shooting, severe burning, ischaemic orcrushing in nature, or severe and agonising causedby the phantom limb being in a hyper-extended orunnatural posture (Bloomquist 2001, Schug 2008).

Pain management in patientsfollowing limb amputation

PAIN CAN OCCUR following the amputation of many body parts. Phantom limb sensation and pain after the amputation of upper or lowerlimbs is the most studied of these phenomena.Amputation of upper or lower limbs can beundertaken as a result of malignancy, trauma,diabetes, congenital deficiency or peripheralvascular disease.

The reported incidence of phantom limb painvaries in the literature from 2-97% (Schug 2008),but is thought to occur in 60-80% of amputees.This variability may arise because of differentdefinitions of pain and data collection techniques.Bloomquist (2001) reported that even seven yearsafter amputation, 50% of patients continue to experience burning, cramping, throbbing

If you would like to contribute to the art and science section contact: Gwen Clarke, art and science editor, Nursing Standard, The Heights, 59-65 Lowlands Road, Harrow-on-the-Hill, Middlesex HA1 3AW. email: gwen.clarke@rcnpublishing.co.uk

SummaryPhantom limb pain is common in patients who have amputations.This article outlines the different theories that explain thepathophysiology of phantom limb pain, including peripheral, spinaland central mechanisms. Treatment options are targeted ataddressing these mechanisms, combining analgesic techniques with physical and psychological rehabilitation.

AuthorSuzanne Chapman, clinical nurse specialist, pain management, The Royal Marsden NHS Foundation Trust, London.

KeywordsAmputation, neuropathic pain, phantom limb pain, urogenital painThese keywords are based on subject headings from the BritishNursing Index. All articles are subject to external double-blind peerreview and checked for plagiarism using automated software. Forauthor and research article guidelines visit the Nursing Standardhome page at www.nursing-standard.co.uk. For related articlesvisit our online archive and search using the keywords.

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Flor et al2006 described phantom limb pain ashaving many features that may be reportedanywhere along a spectrum from simple, short-lasting and rarely occurring, painful shocks in a missing body part to a constant, excruciatingpainful experience during which the individual hasa vivid, intense perception of the missing body part(Flor et al2006).Phantom limb sensation This is any sensation ofthe missing limb except pain. Sensations includepins and needles, tingling and prickling. Awarenessof movement and positional orientation of the limb are widely reported (Casale et al2009). Thephantom limb may move spontaneously or remainfixed, while some patients are able to move thephantom limb at will. Telescoping is a commonlyreported form of positional limb orientationwhere, over time, the phantom limb changes in size and length and in extreme cases, only the digitscan be felt on the end of or in the residual stump(Richardson 2008).Stump pain This is pain experienced in theresidual portion of the limb or stump (Prantl et al 2006). Causes of stump pain may includeneuromas scarred nerve endings or nodules thatmay cause abnormal ectopic firing of nerves(Bloomquist 2001) bony spurs in the residualstump, localised skin disease and infection (Prantlet al 2006). Residual limb and stump temperaturecan be affected by increased or decreased bloodflow to the stump (Siddle 2004). Often thetemperature in the stump and the remaining limb is lower. This low stump temperature iscorrelated to the burning sensation that may beexperienced as part of phantom pain (Schug2008). Muscle tension in the residual limb canincrease the cramping and squeezing sensationsassociated with phantom pain.

Risk factors proposed for the development of phantom limb pain include the severity of pre-amputation pain and post-operative pain(Nikolajsen and Jensen 2001), older age

(Schug 2008), and catastrophising and passivecoping styles (Richardson et al 2007).Catastrophising refers to a coping stylecharacterised by excessively negative thoughtsand emotions in relation to pain (Vase et al 2010).

Theories of phantom limb pain

The exact mechanism of phantom limb pain is not understood fully. There are several theoriesproposed to explain the mechanism orpathophysiology of phantom limb pain (Box 2). It is unlikely that phantom limb pain is generatedand maintained by one mechanism alone and it is more likely that elements from all theories are involved. A summary of key points for thesemechanisms is outlined in Box 3.Peripheral theories Wherever cell or tissuedamage occurs, chemicals and enzymes arereleased. These chemicals and enzymes contributeto the inflammatory process, sensitise theperipheral pain receptors (nociceptors) andstimulate nerves that carry pain signals (A deltaand C fibres) (Middleton 2003). As thenociceptors are continuously exposed to thesechemicals they start to respond to lowerconcentrations of these chemical mediators(Mann 2008) and start to produce a rapid numberof action potentials, which the central nervoussystem interprets as pain (Middleton 2003).

Structural changes in the nociceptive neuronescause the release of neurotransmitters from thenerve endings near the site of the damage, therebyactivating neighbouring nerve endings (Callinand Bennet 2008b). Therefore nerves notinvolved in the original damage are now involved,expanding the area of the body the brain perceivesis involved in pain (Mann 2008). Alteration andan increase in the sodium and calcium channelsplay a role in the generation of spontaneous nervedischarges from the peripheral damaged neurons(Callin and Bennett 2008b). This sensitisationprocess does not resolve spontaneously (as it doesin normal tissue healing) in neuropathic painstates such as phantom limb pain.

Patients often report pain and sensitivity tovibration and touch in the residual limb or stumpfollowing amputation. As a consequence of injury

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4Phantom limb pain: painful sensation perceived inthe missing limb.

4Phantom limb sensation: any sensation of themissing limb except pain, for example, pins andneedles, tingling or prickling.

4Stump pain: pain in the residual portion of the limbor stump.

(Richardson 2008, Schug 2008)

BOX 1

BOX 2

Phantom limb pain theories

4Peripheral theories: assume that phantom limb painoriginates at the nerves around the injury.

4Spinal theories: attribute the cause to changesinside the spinal cord.

4Central theories: assume that phantom limb pain is caused by some mechanism in the brain.

(Siddle 2004)

Pain and/or sensations that may beexperienced following amputation

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and subsequent tissue healing, swelling andregenerative sprouting of the injured nerve (axon)end occurs and can form nodules called neuromas(Siddle 2004). These neuromas displayspontaneous and abnormal activity to stimuli.Tapping of the stump neuroma can cause stumppain and phantom limb pain (Nikolajsen andJensen 2001). Local anaesthetic blockade ofneuromas can eliminate the spontaneous andstimulation-induced pain in the stump, but notongoing phantom limb pain, suggesting that thereare other mechanisms involved in the process (Flor et al 2006). Phantom pain is often presentsoon after amputation and long before neuromashave had time to develop so this theory does notexplain the early development of phantom pain(Nikolajsen and Jensen 2001).

Vascular mechanisms have also beenconsidered as a potential explanation for theperipheral mechanisms that relate to phantomlimb pain. As discussed previously, an increase ordecrease in blood flow to the stump can still causestimulation of the nerve endings (Siddle 2004).Lower temperatures can cause increased firing ofnerve impulses, which are perceived by the patientas phantom limb pain (Siddle 2004).Spinal theories Continuous stimulation of theperipheral pain receptors (nociceptors) will inturn lead to continuous transmission of painsignals to the spinal cord. In the presence of thiscontinuous transmission of signals from theperipheral nervous system, the central nervoussystem becomes more sensitive and responsive a process known as central sensitisation (Flor 2008, Mann 2008). Nerve injury, such asthat caused by amputation, can trigger a state ofhyperexcitability in the central nervous system,characterised by increased neuronal firing,changes within the structure of the peripheralsensory neurones as they arrive at the spinal cordand a reduction in the normal spinal cordinhibitory processes (Flor 2008).

Another theory proposes that the severing ofnerves in limb amputation modifies the receptionof impulses to the central nervous system from theareas distal to the site of the amputation there isa loss of sensory nerve input from the amputatedportion of the body (Stannard and Booth 1998).This results in a reduction in neurochemicals witha resulting change in how receptive the dorsalhorn neurons are and the pain pathway (Siddle2004). This causes neural reorganisation to occurat spinal cord and brain level. It is unclear atpresent how much these spinal mechanismscontribute to phantom limb pain. Central theories These include the reorganisationof the somatosensory cortex, known as corticalremapping or cortical reorganisation, andtheories regarding neurosignatures ormemories. Cortical remapping or cortical

reorganisation suggests that phantom limb pain is a process of abnormal reorganisation in theneuromatrix secondary to pre-existing pain or the amputation process (Richardson 2008). Theconcept of the neuromatrix was proposed byMelzack (1990) to explain phantom limb pain. It suggests that the human body is represented inthe brain by a matrix of neurones. Factors thatcontribute to this neuromatrix include sensorylife experiences including pain, which creates aneurosignature or memory of each body part inthe brain (Siddle 2004). Melzack (1990)proposed that following amputation phantomsensations or pain represent the persistence of thisneurosignature, despite the loss of the body part.

Amputation involves the severing of nervesand, as discussed previously, this results in areduction of impulses from the severed limb to the central nervous system. This causes neuralreorganisations to occur at both spinal cord andbrain level (Richardson 2008). As a result of thisreorganisation in the somatosensory cortex, thebrain undergoes changes where the area whichreceived or generated impulses for the missing

Peripheral changes4Structural changes in the nerves (neurones and axons).

4Ectopic impulses (abnormal firing of nerves).

4Changes in the function of neurotransmitters: increased function (up-regulation) or reduced function (down-regulation).

4Alterations in channels and transduction molecules (sodium andcalcium channels).

4Formation of neuromas.

Spinal changes4Continued input from peripheral nociceptors causes an increase in the

responsiveness of neurones in the spinal cord (central sensitisation).Central sensitisation process may include: increased firing of neurones in the spinal cord, a reduction in normal spinal inhibitory mechanisms, and structural changes in the nerve endings of the primary sensoryneurones as they arrive at the spinal cord.

4Severing of nerves for amputation modifies the reception of impulses to the central nervous system causing neural reorganisation at spinalcord and brain level.

Central changes4Cortical remapping or reorganisation: the somatosensory cortex of the

brain undergoes changes where the area of the brain that received or generated impulses for the missing body part is taken over by anadjacent area of the brain.

4Neuromatrix theory: a matrix of neurones that represent the body in thebrain can be influenced by experiences in life, which creates a memory or neurosignature. It is proposed that phantom limb pain or sensationsrepresent the persistence of this memory despite the loss of the body part.

(Melzack 1990, Stannard and Booth 1998, Siddle 2004, Flor et al 2006, Callin and

Bennett 2008b, Mann 2008, Richardson 2008)

BOX 3

Peripheral, spinal and central mechanisms involved in thegeneration of phantom limb pain

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body part is taken over by an adjacent area of the brain. An example of this is that non-painfulstimulation of another body part, such asbrushing a cheek, can produce phantomsensations or pain in the missing upper phantomlimb (Flor et al 2006, Richardson 2008).

A physical basis for this theory has beendemonstrated. Using neuroimaging techniquesFlor et al (2006) were able to demonstrate a pain memory and altered structure in thesomatosensory cortex in the brain that mayunderlie phantom pain while peripheral factorssustain the memory.

Flor et al (2006) listed the following as othercentral mechanisms, that may contribute tophantom limb pain:

4Alterations in sensory and motor feedback perception of abnormal somatosensoryphenomena such as telescoping, which refers to changes in the size and length of thephantom limb.

4A pain memory hypothesis pain in thephantom limb is similar to the pain that existedin the limb before amputation, which is part of the neurosignature or memory for theamputated limb.

4Affective and motivational aspects of pain depression and coping-related variables.

In summary, it is likely that the initiating eventsfor phantom limb pain, phantom limb sensationand stump pain start in the periphery, whichgenerates a chain of events at the spinal andcentral nervous system level.

Treatment options

In light of the theoretical mechanisms proposedfor phantom limb pain, a combination oftherapies should be considered. Treatmentusually consists of a combined approachincluding medication and rehabilitation withphysical and psychological components.Pre-amputation Analgesic medication such asopioids, non-steroidal anti-inflammatory drugs(NSAIDs) and paracetamol should be used tomanage pre-amputation pain as there remains a link between this pain experience and chronicpain such as phantom limb pain (Middleton2003, Flor et al 2006). Evidence for the use oflocal anaesthetics to reduce pre-amputation painin an effort to reduce phantom limb pain aftersurgery is equivocal, with some studies reportinga reduction in phantom limb pain (Bach et al 1988,Schug et al 1995) and others reporting no

reduction in phantom limb pain (Pinzur et al1996, Nikolajsen et al 1997). It may be beneficialto target patients identified as having passive orcatastrophising coping styles early and involvepsychological support teams to enable the patient to develop more active coping strategies(Vase et al 2010).Post-amputation Strong, effective analgesianeeds to continue in the peri-operative and post-operative period as there remains a weakcausal link between pain experienced in thisperiod and phantom limb pain (Richardson2008). Analgesic therapy with opioids such aspatient-controlled analgesia, local anaesthetics(such as epidural infusions) and NSAIDs shouldcontinue, providing a balanced combinedanalgesic approach. Patients should be assessedcarefully and if they are reporting phantom limbpain, specific medicines that target neuropathicpain should be commenced.

Antidepressants such as amitriptyline, used in lower doses than for treatment of depression,are now widely used for treating phantom limbpain. They work by inhibiting the re-uptake ofneurotransmitters serotonin and noradrenaline(norepinephrine) in the central nervous system.This allows more neurotransmitters to beavailable in the synaptic area to help inhibitfurther relay of the pain signal (Middleton 2003).Antidepressants also block sodium channelsperipherally and this reduces the ability of nervecells to transmit pain impulses.

Anticonvulsants such as gabapentin orpregabalin stabilise cell membranes and work bypreventing the spread of neuronal excitation or byenhancing the activity of neurotransmitters. Theyare thought to inhibit the spread of neural activityin the pain pathway by blocking synaptictransmission (Siddle 2004).

Other analgesics that may be consideredinclude N-methyl-D-aspartate receptorantagonists such as ketamine and membranestabilisers such as lidocaine and mexiletine. Topical agents, such as lidocaine plasters,capsaicin and eutectic mixture of localanaesthetics (EMLA) cream, can be applied tothe stump once the wound is healed. There maybe a role for nerve blocks in the management ofstump pain. The infiltration of local anaestheticinto a painful area can block the peripheralsodium channels. This can then reducespontaneous ectopic nerve firing (Middleton2003). Surgical treatment may be effective forspecific stump pathology, such as bone spurs andneuromas, but does not generally have a role inthe management of phantom limb pain(Nikolajsen and Jensen 2001).

Early involvement of acute and chronic painmanagement teams will optimise treatment ofpatients with this specific type of neuropathic

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pain. Pain management teams will also providesupport for the patient and for nurses and otherhealthcare professionals involved in the patientsday-to-day care. Unresolved pain issues canaffect a patients ability to engage in therehabilitation process so early intervention and management are essential.

Other therapies target the corticalreorganisation that occurs after amputation. One example is the visual feedback technique ofmirror therapy which, it is speculated, normalisesthe cortical reorganisations in the brain. Chan et al (2007) demonstrated that mirror therapyreduced phantom limb pain in patients who hadundergone lower limb amputation. Patientsattempt to perform movements of the phantomlimb while viewing the reflected image of themovement of the intact limb.

A study by MacIver et al (2008) used a mentalimagery technique with a group of 13 upper limbamputees with phantom limb pain. The amputeeshad six weeks of intensive training in mentalimagery. This involved a combination of a body-scan exercise and imagined movement and sensation in the phantom limb. MacIver et al(2008) demonstrated changes in corticalreorganisation using functional magneticresonance imaging (MRI) with a correspondingreduction in some aspects of phantom limb pain.

Flor et al (2001) reported that using anelectrical prosthetic limb moved by signals fromthe patients muscle in the residual portion of theamputated limb could reduce pain if used forseveral hours every day. The authors undertookMRI scans that demonstrated a reversion of thesensory cortex to its original state. In addition,patients were asked to touch the skin over thestump repeatedly to improve the sensorydiscrimination in that area. This reducedphantom pain, possibly by replacing some of thesensory input that was lost following amputation.

Transcutaneous electrical nerve stimulation mayalso be considered to relieve pain. The electricalcurrent between the skin electrodes stimulates thenerve fibres that transmit pain in the dorsal horn ofthe spinal cord and blocks pain impulses (Stannardand Booth 1998, Siddle 2004). Evidence isconflicting, but studies report a reduction in theseverity of phantom limb pain (Katz and Melzack1991). However, a recent Cochrane review foundno studies that met the eligibility criteria forinclusion in the review and recommended that alarge multicentre randomised controlled trial wasneeded (Mulvey et al 2010).

Rehabilitation is important in physical andpsychological adjustment, which will in turninfluence the patients pain experience. Physicaltherapy maximises function by training and

Bach S, Noreng MF, Tjllden NU (1988)Phantom limb pain in amputees duringthe first 12 months following limbamputation, after preoperative lumbarepidural blockade. Pain. 33, 3, 297-301.

Bloomquist T (2001) Amputation andphantom limb pain: a pain-preventionmodel. Journal of the AmericanAssociation of Nurse Anesthetists. 69, 3,211-217.

Callin S, Bennett MI (2008a) Diagnosisand management of neuropathic pain inpalliative care. International Journal ofPalliative Nursing. 14, 1, 16-21.

Callin S, Bennett MI (2008b)Assessment of neuropathic pain.Continuing Education in Anaesthesia,Critical Care and Pain. 8, 6, 210-213.

Casale R, Alaa L, Mallick M, Ring H(2009) Phantom limb related phenomenaand their rehabilitation after lower limbamputation. European Journal of PhysicalRehabilitation Medicine. 45, 4, 559-566.

Chan BL, Witt R, Charrow AP et al (2007) Mirror therapy for phantom

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Flor H (2008) Maladaptive plasticity,memory for pain and phantom limb pain:review and suggestions for new therapies.Expert Review of Neurotherapeutics. 8, 5,809-818.

Flor H, Denke C, Schaefer M, Grsser S(2001) Effect of sensory discriminationtraining on cortical reorganisation andphantom limb pain. The Lancet. 357, 9270, 1763-1764.

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Johnson L (2004) The nursing role inrecognizing and assessing neuropathicpain. British Journal of Nursing. 13, 18,1092-1097.

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group of patients as many healthcare professionalsare involved in the patients rehabilitation.

Conclusion

Phantom limb pain is common followingamputation. In addition, patients may experiencephantom limb sensations and stump pain. Thecause of phantom limb pain is unknown, but it isthought to result from a combination of differentmechanisms. A structured pain assessment andmanagement regimen is vital to allow the patient to embrace rehabilitation and return to a good quality of life following amputation. A combination of pharmacological and non-pharmacological techniques should be usedby the nurse and the multidisciplinary team to improve the patients peri-operative and post-operative pain experience and reduce therisk of any long-term negative effects NS

AcknowledgementEach of the articles in this series has been written by a member of the Royal College of NursingLondon Pain Interest Group. Nursing Standardwould like to thank Felicia Cox, senior nurse, pain management, Royal Brompton and HarefieldNHS Foundation Trust, and chair, Royal College of Nursing London Pain Interest Group, for co-ordinating and developing this series.

&art & science pain series: 17strengthening muscle groups to compensate for missing structures and adjusting balance foreveryday activities and function. Fitting andmaintaining a prosthesis and learning how to use or walk with the prosthesis are also vitalcomponents of care (Kelly and Dowling 2008).

Role of the nurse

Nurses play a pivotal role in the management of phantom limb pain. Early aggressivemanagement of pre-amputation pain and post-operative pain are acknowledged asimportant in reducing the risk of developingsevere chronic phantom limb pain (Middleton2003). Regular patient assessment for phantomlimb pain and initiating specific therapiestargeted at this type of pain are essential.Mortimer et al (2002) reported that patients feltinformation on phantom pain failed to meet theirneeds. Nurses are uniquely placed to preparepatients before surgery for the experience ofphantom limb pain and phantom limb sensation,and to reinforce that these phantom feelings arenormal post-operatively. Early recognition of the patients coping style and interventions ifnecessary will also help the patient to manage pain.The liaison role of the nurse is important for this

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