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. 2011 Sep 26;589(Pt 23):5775–5784. doi: 10.1113/jphysiol.2011.219949

Dynamic changes in the perceived posture of the hand during ischaemic anaesthesia of the arm

N Inui 1,2, L D Walsh 1,3, J L Taylor 1,3, S C Gandevia 1,3
PMCID: PMC3249049  PMID: 21946853

Non-technical summary

Even when the hand is stationary we know its position. This information is needed by the brain to plan movements. If the sensory input from a limb is removed through an accident, or an experiment with local anaesthesia, then a ‘phantom’ limb commonly develops. We used ischaemic anaesthesia of one arm to study the mechanisms which define the phantom hand. Surprisingly, if the wrist and fingers are held straight during anaesthesia, the perceived phantom hand becomes bent at the wrist and fingers, but if they are bent during anaesthesia, the final phantom is extended at the wrist and fingers. There is no ‘default’ posture for the phantom hand. Further, the hand appears to increase gradually in size as anaesthesia develops. The start of these perceptual changes occurs when input from large-diameter sensory nerve fibres is declining. These results provide new information about how the brain generates phantom limbs.

Abstract

Abstract

Contorted ‘phantom’ limbs often form when sensory inputs are removed, but the neural mechanisms underlying their formation are poorly understood. We tracked the evolution of an experimental phantom hand during ischaemic anaesthesia of the arm. In the first study subjects showed the perceived posture of their hand and fingers using a model hand. Surprisingly, if the wrist and fingers were held straight before and during anaesthesia, the final phantom hand was bent at the wrist and fingers, but if the wrist and fingers were flexed before and during anaesthesia, the final phantom was extended at wrist and fingers. Hence, no ‘default’ posture existed for the phantom hand. The final perceived posture may depend on the initial and evolving sensory input during the block rather than the final sensory input (which should not differ for the two postures). In the second study subjects selected templates to indicate the perceived size of their hand. Perceived hand size increased by 34 ± 4% (mean ± 95% CI) during the block. Sensory changes were monitored. In all subjects, impairment of large-fibre cutaneous sensation began distally with von Frey thresholds increasing before cold detection thresholds (Aδ fibres) increased. Some C fibres subserving heat pain still conducted at the end of cuff inflation. These data suggest that changes in both perceived hand size and perceived position of the finger joints develop early when large-fibre cutaneous sensation is beginning to degrade. Hence it is unlikely that block of small-fibre afferents is critical for phantom formation in an ischaemic block.

Introduction

The ability to feel and move a limb requires the brain to use an ‘image’ of the body which constitutes part of our self-awareness (James, 1890). Such a representation underlies our conscious experience and it can become distorted in many neurological and psychiatric conditions (e.g. Frith et al. 2000). To make accurate movements, information is required about the lengths of body segments and the position and movement of joints (Sanes et al. 1984; Sainburg et al. 1993). This is derived from a modifiable body ‘schema’ (e.g. Head & Holmes, 1911; Cole & Paillard, 1995; Giummarra et al. 2007). The terminology for these central representations is controversial (de Vignemont, 2010; Longo et al. 2010).

The body schema derives from multiple sensory inputs (somatosensory, visual, and vestibular contributions) and is generated in parietal areas (e.g. Freund, 2003; Blanke & Arzy, 2005; Lewis, 2006; Pellijeff et al. 2006; Corradi-Dell'Acqua et al. 2009) as well as in more distributed cortical networks (Schwoebel & Coslett, 2005). It includes inputs related to central motor commands (or efference copies) (Gandevia et al. 2006). Such commands are mapped onto the body schema in the parietal cortex to generate expected sensory output (McGonigle et al. 2002) and reach the premotor cortex to drive movement corrections when errors arise (Wolpert et al. 1995).

A central body representation provides a template for perception of phantom limbs after amputation and deafferentation. The phantom generally adopts a habitual posture such as flexion at the elbow with the forearm pronated, often in a posture that resembles that prior to amputation or deafferentation (e.g. Ramachandran & Hirstein, 1998; Paqueron et al. 2004b). Spontaneous changes in posture of the phantom limb can occur in amputees (Ramachandran & Hirstein, 1998) and normal participants in whom a phantom arm arises after local anaesthesia (Melzack & Bromage, 1973). However, the extent to which this depends on afferent input and the mechanisms underlying any perceptual lability and distortion of phantom limbs are poorly understood (Isaacson et al. 2000). At least one report suggests that the posture of an experimental phantom is close to the posture of the limb when the nerve block was induced (Gentili et al. 2002).

When the sensory input from a body part is removed by peripheral anaesthesia, the part is not excised from perception. The part usually remains and is commonly described as swollen. As examples, anaesthesia of the thumb with a nerve block markedly increases the apparent size of the thumb (Gandevia & Phegan, 1999) while a brachial plexus block produces illusory swelling of the arm (Paqueron et al. 2004a). Such distortions of body segment size have been linked to loss of input from small-diameter afferents (Calford & Tweedale, 1991; Paqueron et al. 2003, 2004a). However, it is unclear whether the background firing of large-diameter afferents is involved.

Acute ischaemic anaesthesia of the upper limb was used to generate a phantom hand (e.g. Gandevia et al. 2006; Walsh et al. 2010) and we studied the perceptual changes as it developed. This form of anaesthesia was chosen because it develops slowly with loss of conduction in large-diameter axons occurring before that in small-diameter axons. Our aim was to determine whether the initial posture of the wrist and fingers before anaesthesia systematically influenced the posture of the phantom. In addition, we determined whether the perceived size of the hand increased, as this has not been studied with this form of anaesthesia. Finally, to gain some insight into the underlying mechanisms, we compared the timing of impairment of different sensory modalities with development of changes in the body representation of the hand. Preliminary results from the study have been presented (Walsh et al. 2011).

Methods

Participants

Studies were performed on 10 adult male and female participants who were healthy without any apparent neurological disorders (age range, 24–54 years). Informed written consent was obtained and the local ethics committee approved the procedures. The work conformed to theDeclaration of Helsinki.

Study 1

Subjects (n = 10) were comfortably seated and the right hand held in mid-pronation in a manipulandum that rotated in the flexion–extension plane of the wrist. The apparatus, hand and arm to above the elbow were screened from the subject. This experiment was conducted twice in all 10 subjects, once with the fingers taped fully extended to a plate attached to the manipulandum in full extension and once with the fingers taped in full flexion and the wrist comfortably flexed. Five subjects were studied first in full extension and the other five first in full flexion. Three sites for sensory testing were marked: the dorsum of the thumb, just proximal to the dorsum of the wrist, and the volar surface of the forearm just distal to the elbow.

A wide cuff with two chambers (Zimmer, Dover, OH, USA) was positioned on the upper arm and connected to a regulated pressure source (dual pneumotourn no. 030, ULCO Engineering, NSW, Australia) so that the cuffs could be simultaneously inflated to 300 mmHg in less than 1 s. This produces more consistent blocks than gradual manual inflation of a sphygmomanometer cuff. Sensory tests included assessments of tactile sensation with von Frey hairs and the ability to detect light touch with a cotton swab. After 10 min with the hand in the test posture (flexed or extended), control tests were carried out on the participants with their eyes closed 4 times before inflation of the cuff and at intervals of ∼5 min after inflation. About 30 min after inflation, voluntary movement was abolished for wrist and finger movements. A control study in four subjects revealed that there was no significant adaptation of the subject's perceived position of their intact wrist and fingers over a period of 40 min when the hand was maintained in the test posture with the wrist and fingers held comfortably extended.

To measure the development of the phantom hand, subjects indicated the perceived angular positions of their phantom fingers and wrist using a wooden hand, the posture of which allowed positioning in flexion and extension at the metacarpophalangeal and interphalangeal joints of the fingers. To assess perceived position at the wrist, a rotating pointer on the model was used. The model was positioned on the table about 20 cm in front of the subjects and 30 cm to the left of the midline. Subjects were asked to ‘signal the perceived finger positions of your right hand by using the wooden hand’ and to ‘think about each finger individually’. The wooden hand and wrist pointer were photographed with a digital camera mounted above the model to provide an indication of the perceived angular positions of the fingers and wrist. After each estimate of wrist and finger posture, the joints of the model hand were alternately placed in full extension or full flexion. Six points on the wooden hand were marked to measure joint angles using a software package (GNU image manipulation program): the tip of the index, the distal interphalangeal (DIP) joint, the proximal interphalangeal (PIP) joint, the metacarpophalangeal (MCP) joint, the metacarpal base and the wrist. Data for the angles of the index finger were analysed quantitatively. However, similar changes in angles occurred for the other fingers. Wrist angle was deemed to be at 180 deg with the metacarpal in line with the forearm. Angles <180 deg indicate flexion and >180 deg extension. Extension of the fingers was deemed to be 180 deg with the fingers straight.

The first study indicated that the initial posture of the hand (held for 10 min prior to cuff inflation) at either full flexion or full extension was critical for the change in perceived joint angles of a phantom hand (see Results). Hence, in two participants, we repeated the block with the hand in the fully flexed position for 10 min and then moved to the fully extended position only at the time at which the cuff was inflated. Again, subjects signalled the perceived angular positions of their phantom and simple sensory testing for light touch was conducted after cuff inflation.

Study 2

Perceived size of the hand was estimated by selection of a simple two-dimensional outline or template of the hand, in a neutral position, which best matched its ‘size’. Templates of different sizes were randomly arranged on sheets (Gandevia & Phegan, 1999; Longo & Haggard, 2010). The range of magnifications was 50–190% in 10% increments, with 100% being the size of a typical adult hand. Participants were asked to ‘select the template which best matches how big your hand feels or the perceived size of your hand’. Subjects chose one template from each of three sheets on each occasion. Subjects gave their responses within 10–15 s. Template selections were made 4 times prior to cuff inflation and at intervals of ∼5 min after inflation.

Prior to each estimate of perceived hand size, light touch sensation was assessed with a cotton swab as in the first study. In addition, temperature sensation was assessed. Again, the tests were conducted 4 times before inflation and at ∼5 min intervals thereafter. A computer-driven thermode was used to assess thermal and pain thresholds (TSA-2001 Model TSA II, Medoc Ltd, Ramat Yishai, Israel). A 30 × 30 mm thermode was placed on three sites: on the hand just proximal to the thumb, just proximal to the wrist, and just distal to the elbow. A cold detection threshold and the threshold for heat pain were assessed. Subjects were given thermal stimulation (from a baseline of 30°C, rate of change of 1.0°C s-1 (cooling) and 1.5°C s-1 (heat pain)) and were asked to say ‘Stop’ as soon as cool or heat pain was detected. The same wrist and elbow locations were used for thermal testing as for sensory testing in Study 1. However, due to the size of the thermode the most distal site was not on dorsum of the proximal phalanx of the thumb, but about 2 cm proximal to the first metacarpophalangeal joint.

Data analysis

Because the changes in perceived position and size began soon after the onset of cuff inflation, the data for the joint angles and for perceived hand size were fitted with a simple linear regression. Values for the perceived size were expressed as a percentage of initial values prior to cuff inflation.

To assess development of the ischaemic block, for each of the three testing sites on the arm, the time at which the cutaneous sensory threshold increased for von Frey filaments was determined in each subject in Study 1, along with the time at which the detection of light touch was abolished. To assess the change of cold detection, we measured the total increase in threshold over the whole duration of the block and determined the time at which a 10% elevation in threshold had occurred. Changes in the temperature at which heat pain was reported were small and variable between subjects. The absolute values are given. Because of the variation in times of sensory change in individual subjects the data are presented as a median and interquartile range.

Results

Development of a phantom wrist and fingers

Study 1

In the main experiment the hand and wrist were held in a fully flexed or fully extended position for 10 min prior to cuff inflation. Pilot testing revealed that over this time the subjects correctly signalled that their fingers were flexed or extended with minimal adaptation. However, the major new finding was that, after cuff inflation, despite the position of the hand and wrist being fixed (in either flexion or extension), the perceived position of the wrist and fingers changed systematically. This change was evident after 10–15 min, and surprisingly, thedirectionof the change depended on the posture in which the hand was held. If the actual hand posture was one of extension, then the perceived position of the wrist and fingers moved towards flexion. Conversely, if the posture was one of flexion, then the perceived position of the wrist and fingers moved towards extension. This slow change in position did not involve hand postures which were anatomically impossible and changes were in the same direction, but not always of the same magnitude for each of the fingers. In all subjects, the perceived position moved away from the real position of the hand. Data are shown for a typical subject in Fig. 1A and for the group in Fig. 1B. In Fig. 2, mean (± 95% confidence intervals) and individual subject data are shown for the absolute changes in perceived joint angle (at the wrist and three index finger joints). They emphasize that the final perceived postures differed depending on the maintained hand posture. Although hand position was maintained throughout the period of cuff inflation, the final perceived position of the hand was more flexed when the hand was held in extension than when it was held in flexion.

Figure 1. Actual and perceived posture of the hand during development of an ischaemic block.

Figure 1

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A, data from one subject for the two versions of study 1 (wrist and hand extended on left, wrist and hand flexed on right). Perceived position of a developing phantom during the ischaemic block. Shaded hands show the true maintained posture of the hand. Thick black lines show the perceived starting position of the hand prior to cuff inflation and the perceived final position of the phantom hand at the end of the block. Times are given relative to the time of cuff inflation. The direction of the perceived change is given by the curved arrow.B, data from 10 subjects. The dashed lines are the mean perceived position of the developing phantom at intermediate times of ∼13 min and ∼27 min. Data at these times were determined from the regression fitted for each subject. When the ischaemic block develops with the wrist and finger joints held extended (left), subjects perceive that these joints become more flexed as the block and the phantom develop. The final perceived position of the phantom hand is curled in flexion. However, if the block is applied with the wrist and finger joints flexed (right), then they are perceived to become more extended as the block develops.

Figure 2. Perceived angle of the wrist and index finger joints as a phantom hand develops during an ischaemic block.

Figure 2

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Mean data from 10 subjects (solid black lines) with 95% confidence intervals (thin black lines) for the wrist, metacarpophalangeal joint (MCP), proximal interphalangeal joint (PIP) and distal interphalangeal joint (DIP). Data from individual subjects are shown as thin grey lines. 180 deg represents a straight joint and decreasing angles indicate more flexion of the joint. When the ischaemic block is applied with the wrist and finger joints extended (top panels), these joints appear to become gradually more flexed as the block develops. In contrast, the wrist and finger joints are perceived to become progressively more extended when the block is applied with them in a flexed position (bottom panels). For the pooled data, the progression of these changes in joint angle is approximately linear until a final stable posture is reached (data not shown). The magnitude of the perceived changes in joint angle is less when the hand is flexed than when it is extended. However, after about 40 min of ischaemia, the final perceived position of the wrist and finger joints has ‘crossed over’.

To determine whether the changes in posture of the hand once the cuff was inflated depend on it being held in one posture for 10 minprior toinflation, we repeated the block in two subjects. Again, the hand was fixed in the fully flexed position for 10 min but just before the cuff was inflated the hand was moved into the fully extended position and held there. The perceived posture of the wrist and fingers curled into flexion in a qualitatively similar way to when the hand had been held for 10 min in the extended posture prior to cuff inflation. Hence, holding the wrist and hand positions constant for 10 min prior to cuff inflation is not critical for generation of the subsequent illusory changes in position.

Study 2

In addition to changes in the perceived posture of the hand during the development of anaesthesia and paralysis, the perceived size of the hand also changed. This is shown in Fig. 3. Across subjects, there was a progressive increase in perceived size which began shortly after cuff inflation. By the end of cuff inflation the mean increase was 34 ± 4% (mean ± 95% CI).

Figure 3. The mean for all subjects (n = 10) in study 2.

Figure 3

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Mean data from 10 subjects (thick black lines) with 95% confidence intervals (thin black lines) for change in perceived size of the hand. Data from individual subjects are shown as thin grey lines. The hand was perceived to increase in size during the ischaemic block. The insets show two templates of the hand to illustrate the magnitude of the average increase in (two-dimensional) perceived size.

Changes in sensation following cuff inflation

During the development of the ischaemic block, there was a progressive degradation in sensation. Measurements of touch (detection of light touch and von Frey hair thresholds) in the hand, just proximal to the wrist, and just distal to the elbow changed systematically. Cutaneous touch sensation was impaired progressively, beginning distally (Fig. 4). The initial impairment (an increase in von Frey threshold) began at 16.5 [15.0–18.5] (median [IQR]) min for the hand and at 20.5 [16.5–25.5] min for the elbow. Complete loss of detection of light touch followed the same pattern, again occurring earlier at the hand (19.5 [18.3–20.6] min) than at the elbow (37.5 [29–39] min). At 20–25 min, thresholds for cold sensation began to change throughout the arm. Cold was initially reported a means of 28.3–28.8°C at the three sites. These temperatures dropped by 5–9°C at the end of cuff inflation, with the change being slightly greater distally than proximally. Then, when detected, cold stimuli were commonly reported as painful. Changes in von Frey thresholds preceded changes in cold sensation for all 10 subjects at the hand, nine subjects at the wrist and for six subjects at the elbow. Even after 30–40 min of ischaemia, high skin temperatures still elicited a distinct sensation of heat pain. This index of C-fibre function changed only slightly at each site. The thresholds rose from ∼43 to ∼44°C by the end of cuff inflation.

Figure 4. Summary of the timing of changes in sensation measured during the two studies.

Figure 4

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Data are shown for assessments made over the base of the thumb (upper panel), just proximal to the wrist (middle panel) and just proximal to the elbow (lower panel). Mean and IQR plotted for the start of a change in von Frey threshold and the loss of light touch (Study 1), and the onset of elevation in cold thresholds (Study 2).

Discussion

The present studies have documented major changes in the perception of the body during an acute intervention, ischaemic deafferentation and paralysis. First, there is a progressive change in the perceived posture of the wrist and hand away from the maintained posture: when the joints are flexed, the hand appears to become extended, but when the joints are extended, the hand appears to become flexed. These final perceived postures are not the same, being more flexed for the fingers when the hand is held in extension than when it is held in flexion. Given that the posture of the wrist and fingers is unlikely to alter the way in which ischaemic anaesthesia is produced by a cuff proximal to the elbow, our results suggest that there is no fixed or default neural representation of a phantom wrist and hand. The posture of the final phantom is dramatically affected by the maintained posture of the hand. Second, with progressive ischaemic anaesthesia there is an accompanying illusion that the limb increases in size and becomes swollen. Perceived swelling of a deafferented body part has been documented previously after complete anaesthesia of the thumb (Gandevia & Phegan, 1999) and partial anaesthesia of the face (Turker et al. 2005) produced by lignocaine, as well as during clinical nerve blocks affecting large regions of the limb produced by similar compounds (Paqueron et al. 2003, 2004a,b;). Because the nerve blocks induced by lignocaine and by ischaemia do not affect axonal function in the same way (see below and Grosskreutz et al. 1999), the present results suggest that loss of large-fibre input from the hand is sufficient to initiate both the illusion of limb swelling and the alterations in perceived posture of the hand and wrist. We note that some formal assessments of sensation show early changes prior to changes in the perceived posture of the limb (Silva et al. 2010) and that this is corroborated by subjective changes in limb size (Paqueron et al. 2004a).

While the mean increase for the perceived size of the hand was 34% in the present study, the increase for the finger was 60–70% in the previous study (Gandevia & Phegan, 1999). It is unclear whether the smaller increase for the hand reflected an intrinsic difference between the body part (handvs. finger) or the specific progress of the afferent block. The illusory subjective swelling of a limb during a nerve block provides an early sign that anaesthesia is developing (Paqueron et al. 2004a).

The conventional view is that ischaemia and focal pressure over nerves innervating the arm produce their effect differentially on fibres of different diameter (e.g. Gasser & Erlanger, 1929; Mackenzie et al. 1975), with those of larger diameter being affected earlier than those of smaller diameter. Axonal diameter is not the only factor determining the effect of ischaemia because populations of large-diameter sensory and motor axons have slightly different responses to ischaemia (e.g. Mogyoros et al. 1997). Furthermore, the behaviour of different classes of C fibres is not uniform (Serra et al. 1999). Our result showing resistance to prolonged ischaemia of some C fibres, which signal heat pain, supports this view. By contrast, local anaesthesia produced by lignocaine and related compounds preferentially disrupts the function of small-diameter axons while large-diameter axons take longer to block (e.g. Paqueron et al. 2004a). The results from our method of ischaemic block by cuff inflation on the upper arm show that it produced a progressive disruption of the afferent input from the forearm and hand. In all subjects changes in sensory testing began first in the large-diameter cutaneous fibres, particularly those innervating the hand, and after 30–40 min large-fibre function, assessed by cutaneous touch, was lost up to just below the cuff at elbow level. Smaller fibres in the Aδ range include the main population of cold fibres (Johnson et al. 1973; Mackenzie et al. 1975), and by the end of the ischaemic period, we found a marked impairment of cold thresholds (by 5–10°C). In contrast, there was little impairment of heat pain, which indicates residual input from a population of C fibres subserving the sensation of pain to heating. These observations make it likely that both the distortions in perceived size of the limb and in its posture can be initiated and driven by loss of background input from large-diameter sensory axons. They do not reveal the additional role of classes of Aδ and C fibres in these illusions because it is difficult to abolish their background discharge selectively. Studies using local anaesthetic block and subjective reports suggest that illusions of perceived size of the limb can also be initiated by changes occurring in small-diameter afferents (e.g. Paqueron et al. 2004b).

What is the mechanism for the progressive change in posture as the ischaemic block develops? The brain has access to different central representations of the limb (e.g. Sirigu et al. 1991; Aglioti et al. 1995; Kammers et al. 2006; Longo et al. 2010) which subserve different sensory, motor and other functions, but those with sensorimotor roles depend on the background sensory input. Psychophysical studies have shown that the sensory input generating the proprioceptive image of the body is likely to be derived from specialized muscle receptors, particularly muscle spindle endings (e.g. Goodwin et al. 1972; Roll & Vedel, 1982; Gandevia, 1985) with a contribution also from cutaneous stretch receptors (Edin & Johansson, 1995; Collins et al. 2005). This image is sustained over the minutes prior to cuff inflation and induction of anaesthesia. We propose that, as the input from sensory receptors ‘fades’ during the anaesthesia, the perceived hand moves away from its initial maintained position (cf. Paqueron et al. 2004b).

More than one process may contribute to drive the change in perceived posture during development of ischaemic anaesthesia. One plausible contributory mechanism is that there is a peripheral contribution to the illusory changes in wrist and finger posture. This would require a differential effect of cuff inflation on the population response of activity in afferents signalling joint position. When the hand is fully flexed, it is likely that the firing rate of receptors which encode flexion will be greater than that of receptors signalling extension. For example, muscle spindles in the extensor muscles of the wrist and fingers will fire because they are stretched, whereas those in the flexors will fire at low rate or be silent. Similarly, proprioceptive cutaneous afferents innervating skin stretched over the dorsum of the hand will fire more than those on the palmar surface (Edin, 1992). As conduction block progressively develops, the reduction in the firing rate for the population of ‘flexion encoding’ receptors will be greater than for the extension encoding receptors. Such a differential response would lead to a perception that the hand is moving away from its initial extreme position. We propose that the progressive loss of sensory input which signals that the fingers are extended is interpreted as the phantom hand folding into flexion andvice versa. This process may coexist with other short-term central changes accompanying the ischaemic block (e.g. Brasil-Neto et al. 1993). Additional mechanisms are needed to explain the fact that the final postures produced by holding the hand in extension or in flexion are not the same but have actually ‘crossed over’ (see Fig. 2). For example, the changing peripheral inputs during the ischaemic block from a strong flexion population input or a strong extension population input may induce different levels and degrees of adaptation in channels signalling flexion and extension. For some aspects of proprioception there is evidence for the operation of directionally sensitive opponent channels (Seizova-Cajic et al. 2007).

These results raise some additional questions about the effects of progressive deafferentation on the body image. The first concerns the use of the term ‘phantom’. When should it be used? It is commonly applied to circumstances when there is a massive loss of afferent input, for example, from an amputation, a surgical nerve block or a central lesion such as spinal injury. In many of these situations some input from the periphery is preserved (e.g. Henderson & Smyth, 1948; Hunter et al. 2003), and voluntary commands can still be issued to move and change the position of the (paralysed) limb. In the present study in which there was a deliberately protracted loss of sensory inputs, the subjects maintain a clear perception of their extremity (and can signal its posture in detail), but this perceived limb should probably not be considered a ‘true’ phantom as there are substantive peripheral inputs which can signal its existence. Here, our observations were on body regions (wrist and hand) which ultimately became anaesthetised, while in some studies of development of phantom limb sensations after anaesthetic blocks, innervation of the joints (e.g. shoulder) often remained intact, depending on the type of brachial plexus block used (e.g. Paqueron et al. 2004b). Second, although the limb remained completely stationary during the period of cuff inflation, its perceived posture changed progressively. After 30–40 min, passive movements of the limb go undetected, yet, if subjects command their wrist to flex or extend, the phantom shifts its position in the direction of the intended movement (Gandevia et al. 2006; see also Smith et al. 2009) and the speed of this illusory movement grades with the level of subjective effort (Walsh et al. 2010). This highlights the ease with which the ‘phantom’ hand is incorporated into the systems which plan and execute movement.

In conclusion, the results provide insight into the formation of phantom limbs. First, there is no single default posture generated by the brain – the final posture of the phantom depends on the history of sensory input as the phantom evolves, rather than simply on the final input. Second, when anaesthesia is produced by ischaemic block, there is a seamless progression from a veridical perception of limb posture to the perception of a phantom. Finally, while the formation of phantom limbs occurs much more quickly here than in most clinical situations, the results emphasise the need to know how the sensory input from both large- and small-diameter afferents evolves during this process.

Acknowledgments

This work was supported by the National Health and Medical Research Council of Australia and the Japan Society for Promotion of Science (21500544). We are grateful to Dr Seizova-Cajic for comments on a draft of the manuscript.

Glossary

Abbreviations

CI

confidence interval

DIP

distal interphalangeal

IQR

interquartile range

MCP

metacarpophalangeal

PIP

proximal interphalangeal

Author contributions

Each author contributed to all aspects of the study. All experiments were performed at Neuroscience Research Australia (formerly Prince of Wales Medical Research Institute) in Sydney, NSW, Australia.

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