phantom limb pain: a review of the literature on attributes and potential mechanisms

© U.S. Cancer Pain Relief Committee, 1999 0885-3924/99/$–see front matterPublished by Elsevier, New York, New York PII S0885-3924(98)00136-5

Vol. 17 No. 2 February 1999 Journal of Pain and Symptom Management 125

Review Article

Phantom Limb Pain: A Review of the Literature on Attributes andPotential Mechanisms

Anne Hill, BSc, PhD

Department of Nursing and Midwifery, University of Stirling, Stirling, UK

Abstract

This study presents a review of the literature on the attributes and potential mechanisms involved in phantom limb pain, encompassing studies describing pain in the residual limb, phantom sensation and phantom limb pain, and the difficulties that may arise when making these distinctions. A variety of theories have been proposed to explain causal mechanisms for phantom limb pain. Conceptually, research into phantom limb pain is informed by the particular theory of chronic pain that is dominant at the time the research is undertaken. For example, early physiological theories on the etiology of phantom limb pain were grounded in specificity or pattern theories of pain. Later physiological research was based on the framework provided by Gate Control Theory and focused on identifying peripheral, spinal, and central neural mechanisms. Psychological explanations were grounded in psychoanalytic or personality theories of chronic pain which propose that phantom limb pain results from pre-amputation psychological disturbance. Despite numerous studies examining phantom limb pain, much of this research has both conceptual and methodological shortcomings. As such, the application of these research findings to clinical practice has limited utility.

J Pain Symptom Manage 1999;17:125–142.

© U.S. Cancer Pain Relief Committee, 1999.

Key Words

Phantom sensation, pain in the residual limb, phantom limb pain, Gate Control Theory, psy-

choanalytic theory, Neuromatrix Theory

Introduction

The presence of a phantom limb is now seenas a natural consequence of amputation. Thishas not always been the case. Throughout his-tory, phantom limbs have fascinated research-ers and prompted numerous investigations inan attempt to define phantom phenomenaand to understand why they occur. The pres-

ence of a phantom limb is seldom distressingfor an amputee, particularly when they are in-formed about its likely presence prior to ampu-tation.

1

In fact, many amputees welcome aphantom limb as it allows them to use a pros-thesis naturally. However, in addition to phan-tom sensation, a great many amputees sufferfrom phantom limb pain.

Many authors have found it useful to distin-guish between pain in the residual limb, phan-tom sensation, and phantom limb pain. Pain inthe residual limb is defined as pain at the siteof an extremity amputation. Phantom sensa-tion is defined as any sensation in the absentlimb except pain. Phantom limb pain is de-

Address reprint requests to:

Anne Hill, PhD, Departmentof Nursing and Midwifery, University of Stirling,Stirling FK9 4LA,UK.

Accepted for publication: March 31, 1998.

126 Hill Vol. 17 No. 2 February 1999

fined as painful sensations referred to the ab-sent limb.

2,3

Although these are defined as dis-crete categories, there are many commonfeatures across these definitions. Given thislack of distinction, examination of the litera-ture on phantom sensation and pain in the re-sidual limb is also necessary to explore the phe-nomenon of phantom limb pain.

This paper outlines the research that focuseson several specific issues. First, it defines phan-tom limb phenomena using the classificationthat distinguishes pain in the residual limb,phantom sensation, and phantom limb pain.Second, it examines the measurement of phan-tom limb pain and related phenomena. Third,it examines the literature on proposed causalmechanisms involved in phantom limb pain.The treatment of phantom limb pain is beyondthe scope of this review.

Phantom Phenomena

Pain in the Residual Limb

Pain in the residual limb is defined as pain atthe site of an extremity amputation. Pain in theresidual limb, not surprisingly, is particularlycommon in the early post-amputation phase.Parkes

4

noted that 50% of his nonselected sam-ple of 46 new amputees reported pain in theresidual limb in the first few weeks post-ampu-tation, but that this declined to 13% at 13-month follow-up. Similarly, Jensen et al.

5

notethat 57% of their sample of 58 amputees re-ported pain in the residual limb immediatelypost-amputation. This fell to 21% at the 2-yearfollow-up.

Pain in the residual limb also can persist be-yond the stage of post-surgery healing. In com-mon with many reports of immediate post-sur-gical pain, persistent pain in the residual limbis usually described as a “stabbing,” “shocking,”or “burning,” and is reported to occur at thelower end of the stump, close to the scar.

6

However, in contrast to immediate post-surgi-cal pain, pain in the residual limb continuesfor many years after the surgical incision hashealed and can occur in the absence of stimu-lation, or alternatively, in response to lightstimulation of the stump.

Occasionally, the intensity of pain experi-enced in the stump far exceeds any stimula-tion. This type of pain in the residual limb isdescribed as a “nerve storm” and is character-

ized by spontaneous movement, cold surfacetemperature, sweating, and reduced bloodflow to the stump.

7

Sliosberg

8

observed thiscondition in 50% of his sample of 251 ampu-tees. Movements ranging from slight, hardlyvisible jerks, to severe contractions were notedin those who reported pain in the residual limb.

Examination of stump frequently reveals pa-thology that may be related to the pain.

5,9,10

This includes skin pathology, infection, bonespurs, and neuroma.

2

There is also an associa-tion between stump pathology and increasedlevels of phantom limb pain.

4,11

Moreover,when phantom limb pain and pain in the resid-ual limb are both present, they are usually sim-ilar in nature and co-vary in intensity.

12

How-ever, it is important to note that both phantomlimb and pain in the residual limb are presentin many amputees who have no obvious stumppathology.

2,10

There are several problems with the litera-ture describing pain in the residual limb.Firstly, few studies make a distinction betweenstump and phantom pain. Of those that do, de-tails are not given of how pain in the residuallimb differs from phantom limb pain and ofhow these are measured. Secondly, studies thatdo examine the relationship between stumppathology and pain in the residual limb aregenerally retrospective. Because the develop-ment of pathology in relation to reported painin the residual limb is not examined in thesestudies, any relationship found may be spurious.

Phantom Sensation

Prevalence

As noted earlier, phantom sensation is de-fined as any sensation of the missing limb ex-cept pain and is experienced by virtually every-one who undergoes limb amputation.

13

AmbroseParé first reported this phenomenon in the lit-erature as early as the 16th century. However,it was not until the late 19th century that a de-tailed description was published and the con-cept of “phantom limb” became part of themedical literature.

14

Once a body part has been excised, either bytrauma or surgery, the feeling persists that thebody part is still present.

15

In addition, phan-tom sensation is reported in the absence of am-putation, for example, in patients with sensoryloss due to spinal cord injury where normal

Vol. 17 No. 2 February 1999 Phantom Limb Pain 127

sensation is absent.

16–22

Moreover, phantomlimbs have been induced in experimental situ-ations using an anesthetic block of an intactlimb.

23,24

For many years, it was thought that childrenborn with limb deficiencies, that is, without allor part of a limb, did not experience a phan-tom.

25–27

Given that the accepted basis of phan-tom sensation at that time was that prolongedsensory input from a limb is required for theformation of a cortical representation of thelimb,

27

it was proposed that those with congen-ital limb absence would not experience a phan-tom. However, several studies have found thatthis is not the case. In an early study, Weinsteinand Sersen

28

described five children with con-genital absence who experienced phantoms ofa limb they had never had. In a follow-up study,Weinstein et al.

29

reported another 18 cases inwhich phantoms were experienced in congeni-tally absent limbs. More recent research hasconfirmed these findings.

30,31

Localization

Immediately following amputation, the phan-tom limb resembles the pre-amputation limbin shape, length, and volume. In addition, it isreported to move in space and time in muchthe same way as the pre-amputation limb did.

32

The reality of a phantom limb is such thatmany amputees report trying to use the limb.

25

Despite the reality of a phantom limb, itdoes not remain a complete reproduction ofthe pre-amputation limb.

33,34

Over time, theproximal part of the phantom often fades. Theremaining phantom is comprised of the distalportion of the limb, usually those parts thathave the greatest representation in the soma-tosensory cortex. For example, in those with anupper limb amputation, the thumb is experi-enced more vividly than the remaining fingersand the balls of the fingers have greater claritythan the remaining part of the hand. Distalparts of the limb are felt more prominentlythan proximal parts. A similar distribution ofphantom sensation is found in lower limb am-putees.

The length of the phantom may also changeover time. In approximately one-third of am-putees, a process of “telescoping” occurs wherethe phantom is gradually felt to approach theresidual limb. Gradually, the distal part of thephantom may become attached to the residual

limb or indeed be experienced within the re-sidual limb.

33,35,36

Cronholm

33

reported that,while the phantom may shorten or telescope, itnever extends beyond the length of the pre-amputation limb. A telescoped phantom usu-ally extends to the length and volume of thepre-amputation limb under certain circum-stances, such as when the amputee wears aprosthesis. Furthermore, there is some evi-dence to suggest that only phantom sensation(not phantom pain) is experienced in a tele-scoped phantom limb and that the phantomextends beyond the stump to assume normalproportions when the individual experiencesan episode of phantom pain.

9,16

Melzack and Wall

32

proposed that changesin the “receptive fields” of dorsal horn neuronsaccount for some aspects of phantom sensa-tion. Expanded receptive fields of neurons inthe spinal cord have been observed in a num-ber of animal studies.

32

They propose that if astimulus is applied close to the end of the re-sidual limb, not only will it excite the cells inthe dorsal horn relating to the precise areastimulated, but the stimulus will also activatenearby neurons with receptive fields that in-clude the foot. Katz

37

suggested that thechanges in receptive fields may also explainthe phenomenon of telescoping. The per-ceived length and size of the phantom limbmay be a “perceptual marker” of the extent towhich cutaneous input from the stump andsurrounding tissue has occupied the area of so-matosensory cortex previously utilized by theamputated limb.

Evidence of a link with cortical reorganiza-tion is demonstrated in the differences in sen-sory acuity found in stumps of amputees witheither telescoped or extended phantom limbs.

35

In upper limb amputees, point localization isenhanced in those whose limb is experiencedin a telescoped position. In addition, lighttouch and two-point discrimination thresholdsalso show greater stump sensitivity in thosewith telescoped as opposed to extended phan-tom limbs.

35

Katz

37

suggested that these find-ings support the hypothesis that the distal re-gion of the stump takes over the tactile andsensory functions of the amputated limb.

Further evidence of cortical reorganizationfollowing amputation comes from experimen-tal studies with monkeys. In a microelectrodestudy, the area of somatosensory cortex previ-


ously occupied by a digit was shown to be takenover by cutaneous input from the stump andsurrounding tissue following amputation.

38

Cells identified in the area of sensory cortexwhich originally had receptive fields that in-cluded the amputated digit responded, afteramputation, to input of the adjacent digits, thepalm of the hand, and the amputation stump.These observations are consistent with studiescomparing the sensory acuity of the stump andthe intact, contralateral limb in human ampu-tees. For example, lower thresholds have beenobserved at the stump for light touch, two-point discrimination and point localization af-ter amputation of an upper limb.

35

There is also some evidence to suggest thatthe plasticity of the somatosensory cortex isuse-dependent, rather than a function of am-putation. A microelectrode study of the area ofsomatosensory cortex occupied by a digit of anonamputated monkey showed that the recep-tive field changed following prolonged non-noxious movement of the finger.

39

Thesechanges were indistinguishable from thechanges in receptive fields following amputa-tion.

38

This use-dependent aspect of corticalreorganization is not incompatible with the in-formation available on telescoped phantomlimbs. For example, Kallio

40

reported that tele-scoping is use-dependent in upper limb ampu-tations. A number of below-elbow stumps weresurgically cleaved so that, rather than use aprosthesis, the two branches of the residuallimb could be used as pincers by the amputee.After extensive training, the branches of thestump could be opened and closed at a ratethat approximated that of normal fingers.When patients were followed 2 to 6 years later,36% reported a phantom in which some fin-gers had fused together and others had disap-peared to accommodate the shape of thestump. Furthermore, the phantom arm hadtelescoped only to the extent that it shortenedto fit the amputation stump. Movement of thebranches of the residual limb resulted in simi-lar movement being felt in the phantom hand.

Beyond this, recent research by Flor and hercolleagues

41

suggests that the plasticity of thesomatosensory cortex is related to phantomlimb pain rather than nonpainful phantomphenomena. A strong relationship was foundbetween cortical reorganization (measured bya noninvasive neuroimaging technique) and

the magnitude of phantom limb pain followingarm amputation. No such relationship wasfound in relation to phantom sensation. Clearly,as technology improves, further research maybe undertaken to tease out the link betweenvarious phantom phenomena and cortical re-organization.

Quality

The predominant description of phantomsensation is that of a mild tingling or tightnesswhich is often described as “pins and nee-dles.”

25,35

Other qualities noted are touch, tem-perature, pressure, and itch.

2

In addition, mostamputees have a sense of the position, length,and volume of the phantom. Jensen andRasmussen

2

noted that the position of a phan-tom limb may be relaxed, fixed, or distorted.In upper limb amputees, the phantom arm isoften experienced as hanging loosely at theside of the body, moving freely when the per-son walks. However, in other cases, the phan-tom arm is fixed, bent at the elbow and the fistis held clenched towards the chest.

42

These fea-tures are also reported by lower limb ampu-tees.

33

In some cases, a phantom is distorted insuch a way that the position of the limb is theone that most closely resembles the immediatepre-amputation position.

14,43

This most com-monly occurs when a limb is traumatically lostand the limb was distorted by the accident. Dis-torted phantoms are also reported in cases ofparaplegia following accidents in which thephantom limb is perceived to be in a differentposition from the “intact” limb.

44

Although there is general agreement on thenature of phantom sensation, there are a num-ber of problems in evaluating the literaturewithin the definition of phantom sensation as“any sensation of the missing limb exceptpain.”

2,3

The primary obstacle is that it is fre-quently confounded with phantom limb painor pain in the residual limb. In part, this occursbecause subjects are frequently drawn frompopulations seeking treatment for phantomlimb pain or pain in the residual limb. Al-though these studies discuss phantom sensa-tion, they seldom measure or distinguish itfrom other phantom phenomena. For exam-ple, if the subject has phantom limb pain, whataspect of their experience is defined as non-painful? Moreover, does phantom sensation inthose who experience phantom limb pain


and/or pain in the residual limb differ fromphantom sensation in those who do not? In ad-dition, although recent research proposes thatphantom sensation may be a feature of corticalreorganization following amputation, thesefindings are also difficult to evaluate. For ex-ample, because the distinction between phan-tom sensation and other phantom phenomenais not explicit in these studies, it is not clearwhether cortical reorganization occurs only inthose with phantom sensation or whetherphantom limb pain or pain in the residuallimb is also part of this process.

Phantom Pain

Prevalence

In contrast with the literature on phantomsensation, there is little agreement concerningthe prevalence of phantom limb pain amongthe amputee population. Substantial litera-ture suggests that phantom limb pain israre.

4,26,42,45–48

However, many other studies in-dicate that 60–80% of amputees experiencephantom limb pain.

4,5,49–52

This lack of agree-ment has occurred, in part, because prevalencerates for phantom limb pain have been derivedfrom research studies in which the patient’s re-quest for treatment is the only indication oftheir pain status.

4, 26,42,45–48

When these figuresare compared to those acquired from ampu-tees who do not seek treatment for their pain,prevalence rates of phantom limb pain are esti-mated to be low. Recent studies indicate that ahigh percentage (54–85%) of amputees notseeking treatment for their pain also report sig-nificant levels of phantom limb pain.

10,52–54

Sherman et al.

52

have suggested that the differ-ence in prevalence rates reported in manystudies may also be a function of the amputee’sreluctance to report phantom limb pain tohealth care providers. Sherman and his col-leagues reported that 69% of the 2694 veteranamputees responding to a detailed survey ofphantom limb phenomena told the research-ers that their physicians had directly stated, orclearly implied, that the pain was “just in theirheads.” The great majority of amputees re-sponding to this survey were afraid to tell theirphysicians that they had phantom pain for fearthat the physician would think them insane orthat they would jeopardize the relationshipwith their physician. This relationship is partic-

ularly important in terms of obtaining treat-ment for stump problems at a stage when ver-bal report is frequently the only evidence thatsuch problems exist. Some support for this ten-dency to under report pain is found in a studyby Kolb

26

who noted that 0.5% of amputees ina large clinic spontaneously reported phantompain, but 5% acknowledged it when asked.

Sternbach et al.’s

55

analysis of the literaturesuggests that a 0.5–10% incidence for chronicphantom pain is the accepted norm. However,it is likely that this figure represents substantialunder reporting. In support of this, Shermanet al.’s

52

analysis showed that 85% of respon-dents reported experiencing significant levelsof phantom pain. This survey, which was car-ried out by a team of researchers who had noconnection with health care providers and noinfluence on treatment, had a 61% responserate. If all of the nonrespondents were pain-free, the prevalence of pain in this populationwould be 51%. These prevalence rates werefound in a military population and were repli-cated in a nonveteran sample.

54

Other research-ers have since confirmed similar rates of occur-rence in nonmilitary populations.

5,9,49,50,53,55

Itis likely that the higher incidence rates re-ported in studies that ask directly about phan-tom limb pain are more representative of thegeneral amputee population.

Intensity

Several studies report that “severe” phantomlimb pain occurs in only 0.5 to 5% of all ampu-tees.

21,42,46

These figures contrast with a studyof 2694 amputees, which reported that 51% ex-perienced phantom limb pain “severe” enoughto hinder lifestyle on more than 6 days permonth.

52

Twenty-seven percent of this sampleexperienced phantom limb pain for more than15 hours each day and a further 21% reporteddaily pain over a 10- to 14-hour period. Clearly,differences in the definition of “severe” phan-tom limb pain account for the differencesamong these studies.

The literature that discusses the intensity ofphantom limb pain is difficult to evaluate be-cause: (a) they are frequently case studies thatdo not describe how phantom limb pain ismeasured;

6,11,56–64

or (b) they describe howphantom limb pain is measured but the samplepopulation comprises only those seeking treat-ment for their pain.

4,26,42,45–48


One study assesses pain using the McGillPain Questionnaire and found that phantomlimb pain is similar in intensity to chronic lowback pain, nonterminal cancer pain, and laborpain.

65

More recent studies that used this mea-sure reported similar intensities.

66–68

Howeverthese studies comprised patients selected fromthose attending pain management programsand the results cannot be generalized to ampu-tees not seeking treatment for pain. Nonethe-less, a recent study using nonselected subjectsreported similar phantom limb pain intensityin a small sample of Scottish male amputees.

53

Localization

Like phantom sensation, which predomi-nates in distal portion of the phantom overtime, phantom limb pain is also primarily local-ized to the distal part of the missing limb. Inupper limb amputees, phantom pain is nor-mally felt in the fingers, palm of the hand, andoccasionally the wrist and in lower limb ampu-tees, phantom pain is generally experienced inthe toes, ball of the foot, instep, top of the footand ankle.

5,13,52,69,70

Given the similarity in loca-tion, it is possible that the changes in receptivefields and cortical reorganization observed fol-lowing limb amputation are related to bothphantom limb pain and phantom sensation.

Duration

There is a great deal of confusion concern-ing the duration of phantom limb pain. Manystudies suggest that phantom limb pain eitherdiminishes or disappears during the first 2years post-amputation. For example, Parkes

4

found that 84% of amputees experiencedphantom pain immediately post-amputationbut only 61% continued to experience somephantom pain. Of these cases, only 30% re-ported that their pain was “moderate to se-vere,” and 30% reported “mild” phantom pain.Similarly, in a prospective study, Jensen et al.

5

found that a small decline in pain prevalencefrom 72% 8 days post-amputation to 67% at a6-month follow-up was accompanied by a sig-nificant reduction in intensity to 50%. Boththese studies were carefully conducted, pro-spective studies following the course of phan-tom limb pain over the 2-year period followingamputation. In contrast, other research hasshown that phantom pain may be present in

those who were amputated up to 30 years pre-viously.

52,53

In the study by Sherman and hiscolleagues, 44% reported that their phantompain had not diminished over a 30-year period.The latter studies were also carefully con-ducted but differed from those reported byParkes

4

and Jensen et al.

5

in a number of ways.First, the study populations varied. Studies thatreported a decline in pain over the first 2 yearspost-amputation primarily described elderlyamputees. The latter studies were conductedon a younger population of amputees.

52,53

Sec-ond, the studies differed in the reasons for am-putation. In the Parkes

4

and Jensen et al.

5

stud-ies, the majority of subjects lost their limbs as aresult of vascular disease, whereas in the Sher-man et al.

52

study, the majority of the popula-tion underwent traumatic amputation follow-ing injury. Only Hill’s

53

study comprised subjectswho underwent amputation for a variety of rea-sons but the numbers in this study were smalland the subjects were all male. Finally, differ-ences in the research design of these studiesalso limit comparisons. Both Parkes

4

andJensen and colleagues

9

conducted prospectivestudies, collecting data at several time pointsover a 2-year period, whereas both Hill

53,72

andSherman et al.

52

employed a retrospective de-sign that collected data at only one time point.

Quality

Two of the most common descriptors ap-plied to phantom limb pain are “burning” and“cramping.” Other terms are also used. Phan-tom limb pain has been described as “numb,”“smarting,” “stinging,” “throbbing,” “piercing,”and “tearing.”

5,9–11,25,34,57,66,69,73,75

Evaluation of the qualities associated withphantom limb pain is difficult because a varietyof methods have been used to generate the de-scriptors. In many cases, the descriptors arespontaneously reported in single case studies.In others, the clinician, who may be familiarwith the literature, prompts the patient (i.e.,“is it a burning type of pain”?)

25

Some studiesprovide a list of descriptors from which the pa-tient selects those that are appropriate.

66,69,73,74

These studies too, are difficult to evaluate, asthe lists vary from study to study. In addition,many of these studies include patients seekingtreatment for their pain, and the resulting de-scription may not be applicable to the generalamputee population. Finally, phantom limb


pain descriptors may change over time. Insome of the above studies, descriptors aresought for immediate post-amputation pain,

69

whereas in others, the patient may have beenexperiencing phantom limb pain for manyyears.

66,73,74

Many patients report pain that resemblespre-amputation pain both in quality and loca-tion. For example, in a study of “somatosensorypain memories,” Katz and Melzack

70

noted thatamputees report pain that has similar qualitiesand is experienced in the same location as pre-amputation pain from surgical incisions, wounds,bedsores, ingrown toenails, ulcers, arthritis, corns,and calluses. This is graphically illustrated in acase study conducted by Bailey and Moersch

57

that reported on a male patient who had un-dergone amputation 22 years prior to the study.The patient had an accident that left a painfulsliver under his fingernail. One week later, hisarm was torn off in a machine accident at work.For 2 years following this accident, the patientexperienced pain of the same quality and inthe same location as that experienced when hehad the sliver under his fingernail. A more re-cent case study reported an individual who ex-perienced recurrences of pain during dress-ings of a wound prior to amputation.

76

The Role of Patient Characteristics in Phantom Limb Pain

In general, studies of phantom limb painpresuppose that amputees are a homogeneousgroup. Therefore, little is known about varia-tion within this population.

2,3

Although someresearch has examined the relationship be-tween patient characteristics (age, gender, du-ration of pain, reason for amputation, site ofamputation, etc.) and levels of phantom limbpain, many yielded mixed results because ofdifferences in sample selection, sample size,and study methods.

Bailey and Moersch

57

found that the inci-dence of phantom limb pain is greater in malethan female amputees, but other studies didnot identify a difference.

4,5,9

Similar difficultiescan be found in studies investigating the roleof age and medical status. For example,Buchannan and Mandel

49

found that older am-putees report the presence of phantom limbpain more often than younger amputees, butJensen et al.

5

found no such difference. Ka-shani et al.,

77

Kegel et al.,

78

Parkes,

4

and Parkes

and Napier

79

all report that the presence ofconcurrent medical conditions, such as arthri-tis or diabetes, predict increased phantomlimb pain, whereas Morgenstern

11

found thatmedical status is not related to phantom limbpain. The evaluation of this literature is diffi-cult because phantom limb pain is often in-ferred rather than measured

49,77,78

and whenphantom limb pain is measured, different in-struments are used. For example, Parkes

4

usedan interview method whereas Jensen et al.

5

used both interviews and a visual analoguescale (VAS) to measure phantom limb pain.

Measurement of Phantom Limb Pain

As discussed in the preceding sections, muchof what we know about phantom limb pain hasbeen derived from surveys of treatment out-comes in which the presence of phantom limbpain is inferred from the patient’s request fortreatment rather than measured.

6,11,57,59–61,63,64

Other surveys of patients requesting treatmenthave attempted to measure the intensity ofphantom limb pain using VAS

56,62

or verbal de-scriptor scales.

58

Studies designed to describe, rather thantreat, phantom limb pain have used a variety ofmeasures which assess both pain intensity andquality.80 Several studies have used the McGillPain Questionnaire53,65,66,67,72 and others haveused structured or semi-structured interviewsto quantify various aspects of phantom limbpain.1,5,9,52,66,69,81,82 These studies have yieldedsome useful data on the relationship betweenphantom limb pain and other variables, partic-ularly the initiating and exacerbating factorsinvolved in episodes of phantom limb pain.However, each of these measures has limita-tions. In addition, the diversity of measuresused in the literature does not permit mean-ingful comparison of research findings onphantom limb pain across studies.

A number of problems arise when making adistinction between phantom sensation, phan-tom limb pain, and pain in the residual limb.For instance, it is difficult to see how phantomsensation can be compared across subjects orstudies, given that the definition calls for theamputee to decide which sensations are notpainful. As discussed earlier, pain perception ismultifaceted and therefore directly related tothe individual’s unique history. While one am-


putee might report “tingling” as a sensation,another might define the same word as pain-ful. This makes it impossible to determinewhether it is the amputee’s interpretation ofthe word or some difference in the quality ofthe sensation that leads to different classifica-tions. Given these problems, it is not surprisingthat few studies make the distinction betweenphantom limb pain and phantom sensation ex-plicit.

Similarly, amputees are not always able todistinguish between stump pain and phantompain. Although sources of pain in the residuallimb are frequently obvious (for example, le-sions or scar tissue), this is not always the case.2

There is great variation in reported incidenceof pain in the residual limb whereas Cron-holm33 and Abramson and Feibel45 reportedthat 15% of their respective study popula-tions experienced pain in the residual limb,Sliosberg8 noted a prevalence of 27% andParkes4 reported a prevalence of 50%. Giventhese findings, it is possible that the disparity inprevalence rates for pain in the residual limband for phantom limb pain result from the am-putee’s inability to distinguish pain in the re-sidual limb from phantom limb pain. It is inter-esting to note that the prevalence rate of painin the residual limb in these studies is akin tothe prevalence rate of phantom limb pain.Cronholm33 and Abramson and Feibel45 reportthat a small proportion of their study popula-tions experience pain in the residual limb(15% respectively) and a small proportion alsoexperience phantom limb pain (35% and 2%,respectively). In contrast, Sliosberg8 and Parkes4

report that a large percentage of their studypopulations have pain in the residual limb(27% and 50%, respectively) and a large per-centage also have phantom limb pain (72.5%and 62%, respectively).

A further difficulty in disengaging stumppain from phantom limb pain comes fromstudies that have examined the difference intemperature between the stump and contralat-eral limb. In amputees with phantom limb pain,the temperature of the stump is significantlylower than in the contralateral limb.34,83,84

Sherman and Bruno84 found a consistent in-verse relationship between phantom limb painand the temperature of the residual limb rela-tive to the contralateral limb. This relationshiphas been demonstrated for throbbing, burn-

ing, and tingling descriptions of phantom limbpain, but not for any other descriptions (e.g.,tearing, cramping). Using thermography to ex-amine blood flow to the stump, Kristen et al.85

recorded a significant difference betweenstump temperature (288C) and the tempera-ture of the contralateral limb (318C). Thisstudy found that phantom limb pain is morelikely to occur if the distribution of stump tem-perature is patchy. Similarly, Katz73 found a sig-nificant difference in temperature between thestump (308C) and the same area on the con-tralateral limb (328C) in the group with phan-tom limb pain, and in a group with phantomsensation. No significant difference in temper-ature was found in the group who reportedneither phantom sensation nor phantom limbpain. Given the problems in classifying variousaspects of phantom phenomena outlined inpreceding sections, the findings of Katz73 show-ing differences between those reporting phan-tom sensation, phantom limb pain, and nophantom limb pain should be viewed withsome caution. Nonetheless, the research pro-viding concrete evidence of different physio-logical mechanisms underlying different quali-ties of phantom limb pain advances ourunderstanding of this phenomenon.

Limitations of Research in Phantom Limb Pain

A number of criticisms apply to studies con-cerned with pain in the residual limb, phan-tom sensation, and phantom limb pain. First,sample populations frequently comprise mili-tary veterans, primarily young men who havelost limbs as a result of trauma.1,51,69,84,86–88

Other studies assess elderly amputees, who cus-tomarily have a primary diagnosis of peripheralvascular disease.5,9,81,86,89,90 Given that elderlyamputees with vascular disease make up thelargest proportion of the overall amputee pop-ulation, this is not surprising. However, as thisparticular group has additional problems asso-ciated with age and medical conditions, thefindings of these studies cannot be generalizedto younger amputees. A final group consists ofthose requesting treatment for phantom limbpain. Again, it is difficult to generalize findingsabout pain and distress in this patient group tothose amputees who are not actively seeking


treatment. Nonetheless, research findings fromthese limited populations are habitually gener-alized to the amputee population as a whole.91

A second criticism is that even in those stud-ies that involve a more general amputee popu-lation, sample sizes are too small to draw con-clusions about the variables of interest. Forexample, of the studies in which gender wasthe variable of interest, few had a sample ofmore that 50 subjects. Of these, only 5% to 7%were female.57,58,92

A final criticism is that studies of phantomphenomena do not distinguish between imme-diate post-amputation and chronic phantomphenomena. This creates particular problemsin that immediate and chronic phantom limbpain will clearly be very different, as are acuteand chronic pain. For example, in terms ofGate Control Theory, pain is conceived of as aperceptual experience whose quality and in-tensity are influenced by the unique history ofthe individual, by the meaning they give to thepain-producing situation, the meaning theygive to the consequences of pain, and by theindividual’s state of mind.93 In addition to on-going physiological changes, clearly these fea-tures of pain perception will vary tremendouslyas a function of adjustment to amputation.

Causal Explanations for Phantom Limb PainPhysiological Mechanisms

A number of physiological mechanisms havebeen offered to explain the development ofphantom phenomena. Early theories of phan-tom limb pain are grounded in “specificity”theories of pain and explain phantom limbpain entirely in terms of peripheral factors. Forexample, based solely on the observation thatmanipulation of the stump influences phan-tom limb pain, a number of researchers pro-posed that stimulation of the nerve endings inthe amputation stump transmits informationto the brain that is interpreted as phantomlimb pain.43,57 However, this formulation doesnot explain the reason that manipulation ofthe stump results in the perception of painrather than sensation, or the reason that theoutput of this manipulation should be experi-enced as a phantom rather than at the site ofthe manipulation.

Recent research has also highlighted therole of peripheral nerve fibers in the explana-tion of phantom limb pain. Following amputa-tion, fibers from the cut end of nerves growinto nodules (neuromas) which generate ab-normal impulses. These impulses activate cen-tral nervous system neurons and may result inthe perception of phantom pain (ref. 12, page123; ref. 94). This hypothesis receives supportfrom examination of stumps, which frequentlyreveal pathological findings (skin pathology,circulatory disturbances, infection, bone spurs,or neuroma). Phantom pain is reported morefrequently by patients with observable stumppathology1 and co-occur in terms of frequencyand intensity with pain in the residual limb.10,52

Moreover, surgical removal of neuromas some-times provides relief from phantom limb pain.2

Mechanical, chemical, and electrical irritantsapplied to the nerve ending in the stump havebeen shown to exacerbate phantom limb pain,and local anesthesia has been shown to elimi-nate phantom limb pain.34

Although these studies show that peripheralfactors undoubtedly play a role in phantomlimb pain, there is evidence to suggest thatthey are not the primary eliciting factor. Paincan also occur in the absence of stumppathology2 and surgical revision of the stump,including removal of neuromas, has only lim-ited success in alleviating phantom pain.7

Phantom pain can occur in the absence ofnerve damage, such as when a limb is congeni-tally absent, and when information from theperiphery is blocked, such as when there hasbeen a complete transection of the spinalcord.13,95 The observation that one injection oflocal anesthetic will occasionally eliminatephantom limb pain beyond the active life ofthe anesthetic is inconsistent with the notionthat phantom limb pain is caused by chronicactivity in peripheral nerves.96 Moreover, theobservation that phantom sensation and phan-tom limb pain may be present immediately af-ter amputation rule out the causal role of neu-romas, as these have not yet formed in theamputation stump.

As early as the 1940s, a number of authorswere proposing that phantom limb pain couldnot be explained by peripheral mechanismsalone.34,57 This led to a search for alternativemechanisms. Livingston proposed that phan-tom limb pain can be attributed to abnormal


firing patterns in the internuncial neurons inthe spinal cord.34 In a study of 36 upper limbamputees suffering from phantom limb pain,he injected a local anesthetic into the sympa-thetic ganglia in the spinal cord. Althoughnine of these patients reported a permanentreduction in their pain, more than two-thirdsreported a temporary reduction in pain. Liv-ingston suggested that “closed, self-sustaining,reverberating circuits” are set up by chronicperipheral irritation or by the release of spinalcord cells from inhibitory control through theloss of afferent input. When these abnormalimpulses reach the brain, they are experiencedas painful. Furthermore once these circuits areestablished surgical removal of the peripheralsource has no effect on them and, therefore,will not abolish the pain.

Other authors have supported this hypothe-sis. For example, Carlen and his colleagues69

proposed that peripheral and spinal factorsalone account for phantom limb pain. Theseresearchers argue that if higher central mecha-nisms, released from the inhibition of periph-eral input, were critical to the experience ofphantom limb pain, it would follow that phan-toms experienced by paraplegics should bemore vivid as they have lost more input thanamputees. The literature suggests that this isnot the case, as paraplegics report fewer andless vivid phantom phenomena than ampu-tees.69

The mechanisms by which disinhibition inthe spinal cord results in phantom limb painhave been examined in detail by Wall,94 whoproposed that the sudden lack of afferent in-put following amputation results in a numberof changes at both the peripheral and spinallevel. Furthermore, Wall proposed that thereare both immediate and chronic changes. Theprocess described by Wall94 suggests that the ef-fects of peripheral nerve lesions spread beyondthe damaged cells into the spinal cord itself. Assuch, it addresses some of the observations onphantom phenomena not explained by pe-ripheral theories.

Although disinhibited spinal cord neuronsmay be responsible for phantom sensation, it isunlikely that this is the primary cause of phan-tom limb.3,95 Wall94 confined his analysis ofphantom phenomenon to those that occur fol-lowing amputation. However, as noted above,phantom limb pain has also been reported in

cases where there is no nerve damage and incases where there has been a complete transec-tion of the spinal cord.13 Accordingly, some re-searchers have gone on to postulate a role forhigher brain centers in phantom limb pain.For example, Melzack96 and Melzack andLoeser21 have proposed that the reticular acti-vating system plays an important role in phan-tom limb pain. These studies propose thatwhen peripheral fibers are destroyed, therebyreducing input, inhibition is decreased andsynchronous, self-sustaining activity develops atall neural levels. Thus, lack of input from theperiphery following amputation will result indisinhibition not only at the spinal level de-scribed above, but also at the cortical level.This model would account for some of the puz-zling aspects of phantom limb pain. It has notbeen empirically tested.

Psychological Explanations for PhantomLimb Pain

Some researchers propose that the puzzlingaspects of phantom limb pain can be ex-plained by looking at the psychologicalmakeup of the amputee. Psychological theo-ries have attributed chronic pain to personalitydisorders, masked depression, guilt, childhooddeprivation or trauma, defense against loss, orrepressed hostility and aggression.97–104

Preexisting personality has also been cited asan important feature in the development ofphantom limb pain. For example, a study byParkes4 found that those who have persistentphantom pain scored highly on a personalitymeasure of “compulsive self-reliance” and “ri-gidity.” Parkes proposed that those with a“rigid” personality dislike and resist changeand therefore experienced persistent phantompain because they found it difficult to deal withthe changes that are an inevitable conse-quence of amputation. In addition, Parkesnoted those who were “compulsively self-reli-ant” were also likely to experience persistentpain because of the helplessness that often ac-companies amputation. If these individualshave to rely on others for things they previ-ously did themselves, they become distressedand this leads to pain.

Parkes and Napier79 concluded that the “de-nier” or “defiant type” of amputee has a “com-pulsive need to do everything at least as well ashe could before the operation and if possible,


better, as if to convince himself and everyoneelse that he is not incapacitated at all” (p. 443).These authors believed that if this defensemechanism is disrupted, for example, by post-amputation disability, psychological conse-quences, such as phantom pain would follow.In a similar vein, Friedmann25 reported that“sensitive,” “intelligent,” and “neurotic” indi-viduals are more prone to phantom sensationand phantom pain than less imaginative andmore emotionally balanced people. It is inter-esting to note that this entire body of literaturereports on “personality types” that are associ-ated with increased phantom limb pain, whereasnone discuss personality types that are lesslikely to experience phantom limb pain.

The assumption in these retrospective stud-ies is that emotional disturbance precedes theonset of phantom limb pain and is, therefore,significant in its etiology. This assumption isquestionable. Sherman et al.88 proposed thatpsychological explanations of phantom limbpain have less to do with personality and moreto do with the post-amputation experience ofmany amputees suffering from phantom limb.For example, research has shown that despitenumerous treatments for phantom limb pain,few are successful.106 Sherman and his col-leagues suggested that this low success rate oftreatment for phantom limb pain will ulti-mately deter all but the most “persistent,” “self-reliant individuals” from continuing to insiston treatment. However, by continuing to seektreatment, these individuals are more likely tohave their pain labeled as “psychogenic” andbe referred to mental health clinics.106 As manystudies of the relationship between personalityand phantom pain recruit subjects from men-tal health clinics, this self-selection bias resultsin a tendency for individuals with these charac-teristics to dominate the clinical picture of atypical patient with phantom limb pain.

Studies that utilize representative samples ofsubjects do not support the hypothesis that pa-tients with phantom limb pain are more likelyto have personality problems. For example,Shukla et al.75 found no difference on a num-ber of personality measures between those withand without phantom limb pain. Other recentstudies indicate that among nonselected sam-ples of amputees, those with phantom limbpain cannot be distinguished from those withphantom limb sensation or no pain by their

scores on a questionnaire designed to measurepsychological “rigidity.”70,74

In the chronic pain literature, study of therole of personality types has been replaced, toa degree, by examination of the role of ap-praisal in pain perception. These studies havebetter explanatory power in relation to theemotions and behavior of individuals withchronic pain. Unfortunately, the role of ap-praisal has, to date, not been examined in stud-ies of individuals with phantom limb pain.

Another class of psychological explanationproposes that phantom limb pain results fromthe use of defense mechanisms such as “denial”or “repression.”26,27,36,105 Weiss and Fishman36

suggested that the phantom results from theindividual’s denial of limb loss. Phantom painis explained as functional in this situation, as itserves to reinforce the presence of the limb. Incontrast, Simmel27 proposed that phantomsensation was not caused by denial, but was thefocus for it. Phantom pain occurs because theindividual is overwhelmed by the emotions andanxiety associated with loss of a body part.Kolb,26 who proposed that phantom sensationwas, in fact, a healthy response to amputation,advanced another denial mechanism. Thoseindividuals who do not experience a phantomare denying their loss in contrast to those whodo experience phantom limb pain. Kolb sug-gests that the more important the body part isto the individual (emotionally), the more likelythey will be to deny their loss. Although he at-tributes the lower incidence of phantom breastto this mechanism of denial, recent studieshave shown that the incidence of phantom sen-sation following mastectomy actually is as highas it is following limb amputation.27,29,108–110 Itis possible that “denial” is a feature of the im-mediate post-amputation process,107,109 whichhas been likened to the grieving process associ-ated with any loss,82 but it is difficult to see howa concept such as “denial” is empirically test-able.

Loss of a limb for whatever reason is a majorevent with profound implications for the psy-chological health of the individual involved.Given this, it is not surprising that 20–60% ofamputees attending surgical or rehabilitationclinics are assessed as being clinically de-pressed.75,77,111 However, there are major diffi-culties in establishing a causal link betweenpsychological distress, such as depression, and


phantom limb pain. Few studies actually mea-sured psychological distress in amputees andthose that do seldom examine distress in rela-tion to phantom limb pain. In the studies de-scribed above, depression was examined in re-lation to amputee status rather than phantompain.75,77,111 Other reports of psychological dis-tress come from pain management programswhere those seeking treatment for phantomlimb pain may be expected to experience moredistress.58,112,113 Lindesay114 divided his studypopulation into those who requested treat-ment for phantom pain and those who did notand found that those who requested treatmentfor phantom pain were significantly more de-pressed than those who did not.

A further difficulty in establishing the role ofpsychological distress comes from the itemsthat appear in many of the instruments used tomeasure psychological distress. For example,difficulty in getting to sleep is regarded as asymptom of depression. It is also a feature ofchronic pain. Similarly, endorsement of itemsrelating to fatigue is indicative of depression,but is also associated with chronic pain in theabsence of depression.115

The relationship between phantom pain andpsychological distress is also confounded by avariety of post-amputation factors. Parkes116

noted that the psychological distress that oc-curs following loss of a limb is similar to thatnoted following loss of a spouse. Others havenot specifically reported grief, but have sug-gested there are a number of psychological ad-justments to be made in the immediate post-amputation phase.25 One consequence ofthese confounding factors is that they will varyas a function of time since amputation. A studyby Frank et al.86 suggested that a significantproportion of amputees succumb to depres-sion only after they have left the medical sys-tem. However, psychological distress often hasbeen measured in the early post-amputationphase while amputees are still being seen regu-larly at rehabilitation clinics. Research on therelationship between psychological distressand phantom limb pain has been retrospectiveand cross sectional, rather than longitudinal.As such, nothing is known about the variationand/or changes in psychological distress fromthe early to the chronic post-amputation pe-riod. The complexity of this literature makes itdifficult not only to determine causal connec-

tions, but also to determine how prevalent psy-chological distress is in amputees.

Thus the literature may present a misleadingpicture of the psychological status of amputeeswith phantom limb pain. This situation hasarisen, in part, because many researchersbased their conclusions on unintentionally bi-ased samples drawn from those amputees re-questing treatment for phantom pain. This hasresulted in unsubstantiated assumptions beingmade about the general population of ampu-tees. These difficulties are further exacerbatedby the failure to differentiate clearly betweenacute adjustment reactions following amputa-tion and chronic problems.88 For example, it iscommon to find reactions of shock, grief, an-ger, frustration, or denial in those who have re-cently undergone amputation.25,82 Indeed, theenormity of amputation is such, that thesesymptoms of distress will be expected in theimmediate post-amputation phase. More re-cent research suggests that psychological fac-tors do not play a causal role in phantom limbpain.88,117 Rather, these studies suggest that ep-isodes of phantom limb pain can be exacer-bated by stress, fear, fatigue, and insomnia asmay occur in other types of chronic pain. How-ever, these are the only studies to date thathave examined the role of psychological fac-tors in ongoing phantom limb pain and bothhave utilized samples comprised of military vet-erans.

Multicausal TheoriesBoth physiological and psychological theo-

ries may explain some aspects of phantom limbpain. Even combined however, they do notprovide a comprehensive explanation of phan-tom phenomena, including phantom limbpain. This is, perhaps, not surprising given themulticausal nature of pain proposed by theGate Control Theory. Beyond a multicausal ex-planation, Sherman1 argues that phantomlimb pain itself is not a unitary syndrome but anumber of symptom classes. Each class is quali-tatively different and is subserved by differentetiological mechanisms. To support this argu-ment, Sherman and his coworkers draw on theresults of recent research showing that oneclass of phantom limb pain, which is character-ized by “thermal” qualities, is associated withdecreased blood flow to the stump and is de-scribed as burning phantom limb pain.83–85 A


separate class of phantom limb pain character-ized by a “cramping” quality is associated withspike activity recorded from electromyography(EMG) of muscles within the stump. In thesame study, no association was found betweenEMG spike activity and “thermal” descriptorsof phantom limb pain.1

Further evidence that phantom limb painmay comprise a variety of symptom classescomes from a study of “somatosensory painmemories” in phantom limb pain.70 Soma-tosensory pain memories are characterized bythe qualities of pain experienced in the intactlimb prior to amputation. Many authors havereported that some amputees experiencephantom limb pain that closely resembles painthat was experienced in the limb prior to am-putation (e.g., ref. 57). For example, phantomlimb pain may be experienced as similar inquality and location to a painful wound beingdressed, an ingrown toenail, a painful foot ul-cer, or pain resulting from deep tissue injuriesin the limb prior to amputation. Amputees as-sert that it is real pain that they are experienc-ing, not merely a recollection of the pain theyhad prior to amputation. Moreover, this typeof phantom limb pain differs from that whichis experienced in the distal part of the phan-tom limb.76

The pain experienced in a limb prior to am-putation also may influence the course ofphantom limb pain many months later. For ex-ample, pain in the limb prior to amputationpredicts phantom limb pain at a 6 month fol-low-up.5 However, if pain is relieved by the ad-ministration of a continuous epidural block for3 days prior to amputation, the incidence ofphantom limb pain is decreased at 6 monthsfollow-up.81 Jensen et al.9 reported that 74% ofthe patients in their study had pain in a similarlocation to pre-amputation pain 8 days afteramputation. Forty-five percent still had pain inthe same location 2 years later. The characterof their phantom limb pain was similar to pre-amputation pain in 53% and 35% of patientsafter 8 days and 2 years, respectively. Whenboth location and quality were examined,phantom limb pain resembled pre-amputa-tion pain in 36% of patients at 8 days and 10%of patients after 2 years. Similarly, Katz andMelzack70 report that 42% of their sample hada “somatosensory pain memory” that resem-bled the quality and location of pre-amputa-

tion sensations. Recent findings suggest thatthe reason for these “somatosensory painmemories” may lie in functional or structuralchange within the central nervous system in re-sponse to noxious somatosensory input.70,118

Neuromatrix TheoryGiven the diversity of phantom limb phe-

nomena, no one causal mechanism can ex-plain phantom limb pain. Melzack13,70 has pro-posed that this diversity can be betterexplained using the concept of a neuromatrix.

The neuromatrix is defined as a “network ofneurons that extends throughout widespreadareas of the brain, composing the anatomicalsubstrate of the physical self” (ref. 71, p. 91). Itis suggested that the neuromatrix extends to atleast three major neural circuits. One is thesensory pathway that travels through the thala-mus to the somatosensory cortex. It is thispathway that primarily carries informationfrom the periphery. A second is the pathwaythat goes through the reticular formation tothe limbic system. This system is critical foremotion and motivation and may account forthe affective descriptions of their phantomsused by paraplegics who have completetransection of the spinal cord and psychologi-cal distress that is commonly seen in patientswith phantom limb pain.89,117 Manipulating thelimbic system in an animal model can relievepain.119 A third circuit incorporates the pari-etal lobe, an area that is significant in evaluat-ing sensory signals and in the recognition ofthe self. The importance of the parietal lobe inthe sense of self has been shown in studies ofbrain-damaged patients. For example, Sacks120

reported that patients with damage to the pari-etal lobe often refuse to accept that their limbis part of them. The limb itself is not damaged,but the patient does not accept it as part of thebody. A brain-damaged patient cried out inpain when his leg was strongly pinched but stillwould not accept that it was his leg that waspinched.

Input to the above systems, either from theperiphery or from within the neuromatrix it-self, is processed simultaneously and thenshared with other brain systems, producingoutput which is transformed into consciousawareness. Melzack describes the basic outputfrom the neuromatrix as a “neurosignature”which is particular to the individual. It is


thought to be determined by the pattern andstrength of connections between neuronswithin the neuromatrix. It is this pattern thatindicates that “the body is intact and unequivo-cally one’s own” (ref. 71, p. 91). In normal cir-cumstances, sensory signals are processed bythese systems then modulated by the ongoingpattern of the neuromatrix (the neurosigna-ture). The resulting output of the system con-tains information about the sensory input andthe conviction that the sensation is occurringin the body.

Melzack suggests that this postulated processis much like the working of “cell assemblies”proposed by Hebb.121 Hebb argued that thestrength of the connection between any twocells simultaneously activated by sensory inputwill become stronger. This in turn will lead toan assembly of neurons in which a signal goinginto one part of the group will spread throughthe rest. Hebb’s model suggests that cells acti-vated by environmental stimuli will becomepart of the cell assembly when paired withother active cells. Melzack13 argues that, interms of the neuromatrix, the primary compo-nents must be genetically prewired, althoughexperience will “add or delete, strengthen orweaken existing synapses” (p. 124). He citescases where a limb is congenitally absent yetthe individual still experiences a vivid phantomas evidence of the genetic or “hard wired” basisof the neuromatrix. In these cases, the limb it-self has never provided input to the matrix(ref. 13, p. 124).

This theory proposes that abnormal input tothe neuromatrix following amputation altersthe pattern generated by the neuromatrix andresults in output which is experienced as apainful phantom. Abnormal input can eitherresult from lack of normal sensory input fol-lowing amputation or from high levels of inputcaused by excessive firing in damaged nerves.The phantom itself appears to be felt becauseof the basic pattern of the neuromatrix, theneurosignature. The painful aspect of the out-put may occur for a variety of reasons. For ex-ample, the cramping or shooting quality ofphantom limb pain might occur because limbmovement will be a prewired aspect of the neu-romatrix. Following amputation, the neuroma-trix no longer receives signals from the periph-ery that the limb is moving. The output fromthe neuromatrix then will include the basic

neurosignature which has been modulated toinclude strong messages for the limb to move.This results, not only in the report of a cramp-ing type of pain, but also in the EMG spike ac-tivity associated with this aspect of phantomlimb pain.1,13

One illustration of the way that experiencecan shape the pattern produced by the neuro-matrix is highlighted by research on soma-tosensory pain memories.70 It is suggested thata neural representation of the pre-amputationpain is formed subsequent to one very intensepain experience or is formed and graduallystrengthened as a result of multiple occur-rences of pain. Given that “pain memories” areexperienced as both sensory and affectiveevents, it is reasonable to assume that boththese aspects of the original experience havebeen encoded within the neuromatrix. This issupported in a recent study by Hill et al.72

Because the neuromatrix extends over sucha wide area of the brain, this is a difficult the-ory to test. Some work is currently being un-dertaken.119,122–124 Nonetheless, it does providea framework that is consistent with peripheral,spinal, and central mechanisms identified inthe literature and incorporates many previ-ously unexplained research findings. Notably,Neuromatrix Theory implies that many facetsof an amputee’s experience might contributeto the quality and intensity of his or her phan-tom limb pain by initiating activity within theneuromatrix. In particular, this theory suggeststhat in addition to sensory input triggering theneuromatrix, psychological or social factorsmay also produce input that activates the ma-trix and results in the experience of phantomlimb pain. For example, research showing thatepisodes of phantom limb pain can be exacer-bated by stress, fear, fatigue, and insomnia88,117

might be explained by this theory. However,this possibility is not explicit in the expositionof this theory to date and no research has beenconducted examining the role of psychologicalfactors in phantom limb pain within thisframework.

In many respects, Neuromatrix Theory issimilar to Gate Control Theory and could beapplied to chronic pain in general, rather thanphantom limb pain in particular. Where it dif-fers from Gate Control Theory is in the postu-lation of a neural network across widespreadareas of the brain, in which activity of one area


will result in output from the entire network.As such, this theory provides a mechanism toexplain how numerous factors can result in theperception of pain. Gate Control Theory pro-poses that pain is a perception whose qualityand intensity are influenced by the unique his-tory of the individual, the meaning they give tothe pain-producing situation, the meaninggiven to the consequences of pain, and the in-dividual’s state of mind. This theory does not,however, explain how these factors influencepain perception. In contrast, NeuromatrixTheory not only suggests a possible mechanismto explain the diversity of factors involved inthe perception of pain, but also provides aplausible explanation for much of literature onthe psychological management of pain.

Neuromatrix Theory can be criticized onseveral grounds. First, because the neuroma-trix is postulated to extend over such a diffusearea of the brain, the proposed mechanismsare almost impossible to operationalize andtest. For example, it would be unworkable toisolate and examine any one proposed activat-ing stimulus when all aspects of experience aredescribed as potential stimuli within this ma-trix. Animal models of phantom limb pain maybe informative.119,122–124 Second, NeuromatrixTheory provides a plausible explanation forphantom sensation (particularly in the case ofcongenital limb absence where there is nodamage to the peripheral nervous system).However, it is not clear why phantom limb painrather than phantom sensation should occuras a response to the output from this matrix.Moreover, this theory provides no explanationof why some amputees do not experiencephantom limb pain. Future research is re-quired to develop the prediction that mecha-nisms can be operationalized and tested in am-putees experiencing phantom limb pain.

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