Peripheral factors

Several clinical studies support the notion that mechanisms in the periphery (i.e. in the residual limb or in central parts of sectioned afferents) play a role for the phantom limb concept.

• Residual limb pathology with altered residual limb sensibility is a common feature.13

• Phantom pain and pressure pain thresholds at the residual limb are inversely correlated early after amputation.57

• Phantom sensations can be modulated by various residual limb manipulations.62

• Tapping neuromas may increase phantom pain.58

• Phantom limb sensations are temporarily abolished after local residual limb anesthesia.63

• Changes in blood flow may alter the phantom limb

perception.41

These clinical observations are supported by experimental studies. Following a nerve transection, formation of neuromas is seen universally. Such neuromas show spontaneous and abnormal evoked activity following mechanical or chemical stimulation (for review, see Devor64). The ectopic and increased spontaneous and evoked activity from the periphery is assumed to be the result of an increased expression of sodium channels.65 In the dorsal root ganglion (DRG) cells, changes also occur following a complete nerve cut. Cell bodies in the DRG show abnormal spontaneous activity and increased sensitivity to mechanical and neurochemical stimulation.66

The sympathetic nervous system may also play an important role. From animal studies it is known that application of norepinephrine (noradrenaline) at the residual limb or activation of the postganglionic sympathetic fibers excites and sensitizes damaged, but not normal, nerve fibers.67 Sympathetic-sensory coupling at the level of the DRG may also contribute to the increased pain response following changes in sympathetic activity.64

• Phantom pain is significantly more frequent in amputees with long-term residual limb pain than in those without persistent pain.23

Figure 31.2 Patient with severe residual limb pain. Areas of allodynia and hyperalgesia are indicated.
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