Phantom Limb Notes
Mercier, C., Reilly, K. T., Vargas, C. D., Aballea, A. & Sirigu, A. (2006). Mapping phantom
movement representations in the motor cortex of amputees. Brain, 129, 2202-2210.
 studies have found that if you stimulate the part of the brain associated with motor
movements of the amputated part results in movements or muscle contractions in the
adjacent body part (aka: stump).
 Perceived phantom movements were elicited by stimulating the part of the primary motor
cortex that represented the missing hand.
 Stimulating the corresponding part of the primary somotosensory cortex did not reliabiliy
result in sensations of phantom movement.
 86% of trials where subjects reported perceived phantom movement were accompanied
with muscle contractions in the stump.
 So, was it the movement of the muscles or something else that resulted in the perception
of phantom limb movement?
 “Our results show that TMS applied over the presumed hand area of the motor cortex
elicits sensations of movement in the phantom hand and that the amplitude of the
movement perceived is positively correlated with the intensity of stimulation” p. 2207.
 The representation of the amputated hand does not disappear from the motor cortex…
cortical neurons that previously targeted hand motoneurons controlling the missing hand
now target motoneurons in the remaining stump muscles.
 Activity in these “hand” cortical neurons continues to signal a movement of the missing
limb, even though this same activity now produces contractions in stump muscles.
 The activation of the hand area of the motor cortex continues to be associated with a hand
movement despite the fact that the descending motor commands generated by this
activation now result in stump muscle contractions.
 We believe that the sensation of phantom movement is related to activity in the motor
representation of the missing limb.
 CONCLUSION: When amputees voluntarily move their phantom limb, the interpretation
of the afferent information arising form the movement-related contraction of stump
muscles is modulated by the efferent motor command. That is, if the motor command
arises from the original biceps area, for example, the afferent feedback resulting from
biceps contraction will be interpreted as a stump movement, while if the motor command
arises from the original hand area, the same biceps contraction will now be interpreted as
a phantom hand movement.
 Loss of control over phantom movements is not due to the disappearance of the cortical
representation of those movements but rather due to a problem with voluntary access to
this representation.
Aglioti, S., Smania, N., Atzei, A., & Beerlucchi, G. (1997). Spatio-temporal properties of the
pattern of evoked phantom sensations in a left index amputee patient. Behavioral Neuroscience,
111, 867-872.
 Evoked phantom sensations are most likely to be ascribed to a new pattern of cerebral
organization that emerges after and because of amputation.
 Found that could stimulate parts of face and remaining fingers—created sensation in the
phantom finger reflecting the intensity and frequency of stimulus.
 Initially, the cortical representation of the lost finger was invaded by inputs from or
destined for the immediately adjacent portions of the somatosensory cortex.
 Facial areas eliciting sensations in an ipsilateral phantom arm or hand can develop
rapidly within weeks or even days of the amputation, become stabilized over several
weeks or months, and then undergo a gradual regression that may eventually lead to their
disappearance.
 The role of dominant and latent inputs: when the dominant input is removed (as in
removal of finger), then latent inputs become dominant – hence the continued sensation
of a finger brought forth by sensations in other fingers and face. Non-important inputs
eventually loose their synaptic activity (hence the regression of facially-created
sensations).
Richardson, C., Glenn, S., & Horgan, M. (2006). Incidence of phantom phenomena including
phantom limb pain 6 months after major lower limb amputation in patients with peripheral
vasular disease. Clinical Journal of Pain, 22, 353-358.
 out of 52 participants, all experienced phantom phenomena:
o kinetic, kinesthetic, exteroceptive (65.4% sporatic movement, 58% voluntary)
o phantom limb pain – 78.8%
o stump pain – 51.2%
o PLP and stump pain are linked
o PLP and ability voluntarily to move phantom are linked
 If PLP was absent immediately following amputation, did not develop
Flor, H., Nikolajsen, L., Jensen, T. S. (2006). Phantom limb pain: a case of maladaptive CNS
plasticity? Nature Reviews: Neuroscience, 7, 873-881.
 PLP “seems to be more severe in the distal portions of the phantom and can have a
number of characteristics such as stabbing, throbbing, burning, or cramping.”
 PLP is more common in adult amputees than children amputees; non-existent in
congential amputees.
 Possibly related to “neuromas” or bulbs that are formed in the damaged neurons – these
neuromas tend to have sporatic activity due to physical or chemical stimuli.
 “Damaged and reorganized nerve endings together with altered activity in the Dorsal
Root Ganglion represent a potential source of pain and abnormal evoked activity in nerve
injury.”
 Anaesthesia: local or epidural does not eliminate PLP in all patients.
 Spinal Cord: PLP could be related to disinhibition of components of the spinal cord –
including downregulation of opioid receptors, damage to inhibitory GABA interneurons,
and spinal remapping of the lost limb.
 Central Changes:
o reorganization of the primary somatosensory cortex – where hand used to be
represented in cortex is invaded by adjacent areas.
o Phantom pain and phantom sensation may be related to different cortical
processes.
o Magnitude of phantom pain seems to be related to degree of SI map
reorganization.
o Evidence of enhanced cortical exitability in patients with phantom limb pain.
o Abnormal painful sensations may be related to incongruence of motor intention
and sensory feedback.
o Visual, sensory, and motor feedback to the cortex might be an important
determinant of phantom limb phenomena and pain.
 Pain-Memory hypothesis:
o Chronic pain present in limb before amputation increases likelihood and severity
of phantom pain.
 Treatment:
o Current treatments (analgesic, antidepressants, stimulation) all ineffective.
o Use of motor-driven prosthesis correlated with reduction of phantom pain.
Cortical reorganization is probably the mediating variable.
o Discrimination training of stimuli by regimen of stimulation of stump = less pain
and reversal or cortical reorganization.
o Imagined movements of phantom also helped – including mirror treatment
(anecdotal evidence).
o Pharmacological: NMDA receptor agonists, GABA agonists.
o Stimulation of cortical areas by TMS or direct current may be viable options.