Phantom limb studies
Myolelectric
A prosthetic that can be controlled by the patient
Cosmetic
A prosthetic that is just for appearences
A patient had their index finger removed and after 5 months they had referred sensations in their face which were mapped; after 3 years they were retested and the finger map was virtually unchanged (suggests that the connections have grown in the 5 months since the amputation - REMAPPING)
Aglioti et al. (1997) Remapping case study
The phantom is a mirror image of the healthy contralateral limb which could have been learned in utero; a lot of movement occurs in utero (it is thought that left and right handedness is learnt in utero); doesn't account for those without healthy limb
Alternative explanation for congenital phantoms: mirror image
Learning by observation of full bodied others; would activate the mirror neuron system; action observation system particularly active for grasping; harder for this account to explain in legs
Alternative explanation for congenital phantoms: observation
A prosthesis could be integrated into the body image, a rubber hand illusion occurs in healthy people so the aplasics may take ownership of the prosthetic; been shown that to some extent we incorporate tools into our body; this doesn't account for those who have phantoms without prosthetics
Alternative explanation for congenital phantoms: prosthesis usage
for an innate organisation of sensorimotor cotices or they are due to viewing other's bodies
Aplasic phantoms may provide evidence for
Melzack's neuromatrix
Are aplasic phantoms evidence for an innate body schema (___) or is there another explanation?
congenital phantoms/ aplasia
Born without a tissue or an organ (these phantoms cannot be explained by memories)
Showed, after left arm amputation referred sensation in the left side of the face on 23 hours after surgery (this was specific to pain and touch); this would have been too early for new routes to have developed; an fMRI a month later showed referred sensations were associated with discrete activation
Borsook et al. (1998) unmasking case study
44 year old woman without forearms and legs, had a lot of use from her upper arms, more damage to her thighs; always experienced phantoms in all 4 limbs and her awareness of these was interrupted during interference or seeing her in a mirror
Brugger et al. (2000) aplasic case study AZ
Stimulated the motor cortex using TMS and recorded and MEP from the relevant muscle; in healthy adults should cause a movement/twitch, in AZ found what she thought "should" have moved was correct 13/18 times; she was consistent but not quite somatotopically accurate, there were also some latencies
Brugger et al., (2000) AZ MEPs
fMRI while moving phantoms showed no response in the hand area of S1 when moving phantoms but was when moving stump, activation in the premotor area and the SMA and parietal cortex showing a clear routing in the sensorimotor system when she is thinking about moving her phantoms (yet still differences to actually moving stumps)
Brugger et al., (2000) AZ fMRI results
High consistency of the interview of vividness of phantoms across sessions (3 weeks), no pain/temperature sensations; performed similar to controls in rotation task of body parts (all took longer when involved rotation that mirror image)
Brugger et al., (2000) behavioural tasks
could be learned via the mirror system (especially grasping motions) from infancy
Case 26: left phantom wrist, thumb and palm, congenital aplasic, no hand on either side
evidence that gesture must be learned along with phantoms as these hand actions could be learned through observation of others actions
Case 27: aplasic who gestures with their phantoms (both hands aplasic)
Reason for her loss of limb is unknown so thought she may have lost them in utero and so could have had some early sensorimotor input/experience
Case 28 (AZ): tetra-amelia: it is unclear whether the mirror system can produce leg phantoms, other cases of phantom legs thought to be due to prosthesis use but AZ never used them
Reasons for phantoms thought to come from sites in the nervous system (neuroma formation at the stump site -periphery explanation); the dorsal root ganglia has been implicated; targetted DRG stimulation has shown a positive effect; review of 135 patients, 33 had good outcomes and stated better than SCS; paresthesia in DRG stimulation was directed to the painful areas more so than in traditional SCS
Dorsal route ganglion stimulation in the treatment of phantom limb pain (Eldabe et al., 2015)
Uncontrolled retrospective data, small sample size and a short follow up time
Dorsal route ganglion stimulation in the treatment of phantom limb pain (Eldabe et al., 2015) -problems
Claims that phantom limbs are entirely psychological and it is a "mourning process"; psychological factors can contribute to the pain but not the etiology
Freudian denial explanation of phantom limbs
patient with and without phantoms and controls viewed impossible hand movements finding that the patient with phantom limb sensations performed like controls (showing his phantoms constrained him) whereas the patient without phantoms was not constrained (shows we represent the body in the brain physically)
Funk, Shiffrer and Brugger (2005) looked at hand movement observation in aplasics
Small sample, the 2 aplasics may have had different reasons and so hard to compare, association not causation, can't assume the effect is due to stored knowledge as the aplasic had phantoms but no stored knowledge
Funk, Shiffrer and Brugger (2005) looked at hand movement observation in aplasics - criticicms
8 cases where the phantom pain was triggered by thinking about, observing or inferring that another was in pain - shows role of the mirror system
Guimmarra et al., 2007 (phantom pain and mirror system)
Studied the representations of the hand during voluntary movements; using fMRI investigated and found that: similar non-symmetrical representations between hands in amputees and controls; challenges the view that the somatosensory area for the missing body part is completely reorganised (could there be reorganisation of inputs rather than S1)
Kikkert et al. (2016)
Patient CL (left hand aplasic phantom) used intact hand to indicate where the phantom hand was and repeated this 10 times; did the same for the right hand when covered. They 2 maps showed similar distortions, if phantoms arise from observing others we would expect them to be the same as their real hand (would expect it to be less distorted - which it wasn't); as they were distorted in the same way it is thought they are due to reorganisation of the S1
Longo, Long and Haggard (2012) developed a method to investigate the structure of a phantom
Using a myoelectric prosthesis may protect against the pain by preventing the reorganisation from occuring
Lotze et al. (1999) using a myoelectric prosthesis
Weather, minor surgery, cognition (thinking about the limb)
Melzack et al. (1987) found the strength of the phantom depended on:
Phantom pain is seen even following a complete transection of the spinal chord suggesting the pain is all in the brain and there is no sensory input needed for it; phantoms feel real because they are produced by the same brain processes as the intact body; neural networks in the brain generate experiences which are felt to originate in that part of the body (losing feeling to a body part doesn't lead to feeling there is a gap; it is innate so would explain aplasic phantoms
Melzack's neuromatrix explanation for phantom limbs
Neglect from posterior cingulate cortex can lead to patients denying ownership of the body; this is damage to the neuromatrix network
Melzack, 1997 (evidence for Melzack's neuromatrix)
Phantom sensations can survive S1 excision so sensory experience doesn't seem to be needed in order to experience phantoms
Melzack, 1997 (evidence for Melzack's neuromatrix) - S1 excision
The pain of phantoms is just a memory; often the pain is similar to pain felt there before the amputation; often patients can feel a phantom watch even phantom arthritic pain
Memory explanation for phantom limbs
Amputated the fingers of monkeys and found that the area of the S1 that was activated by the finger that had been removed was taken over representing the surrounding fingers; showed plasticity in the cortex
Mersenich (1984) amputation in primates
80 lower limb amputees, between subjects (all amputees, some mirror some not) finding that the mirror condition allowed participants to make more phantom movements but it didn't decrease their level of pain over the controls
Mirror box to relieve phantom pain (Ramachandran, 1996) -study
"learned paralysis" hypothesis of limb pain, suggests that the pain is due to not being able to move from a painful position, they aren't gatting any feedback that they aren't. Being able to see themselves moving the limb in the mirror tells them visually they can move it
Mirror box to relieve phantom pain (Ramachandran, 1996) -theory
7 amputees with phantom arms trained in visual imagery which defied usual constraints, 5 mins per hour everyday for 28 days and found that they were same as controls before training but after training could use the impossible movement to carry out left right judgement tasks: patients had a modified neural representation of limbs entirely through internally generated mechanisms
Moseley and Brugger (2009) Modifying phantom limbs (found visual imagery could modify body representations without a sensory input)
Reorgansiation
New connections are made over time which allows for the area that has lost it's sensory input to be reused by other areas
Used augmented reality to treat a phantom limb patient, individual and simultaneous phantom limb movements were predicted using myoelectric pattern recognition and were used as inputs, pain began to reduce, telescoping caused the phantom to return to its normal length however this is only one single case study
Ortiz-catalan et al. (2014) treatment of phantom limb pain using AR
Those which match the existing opposite limb -may have formed from bilateral BI in utero
Overlapping subtypes of congenital phantom limbs (Price, 2006) 1.
Aplasic phantoms which develop later in life learnt from sensory (visual) input
Overlapping subtypes of congenital phantom limbs (Price, 2006) 2.
Size and shape and posture illusionsreported in all 20 patients, 15 patients experienced illusions of the hand moving (opening and closing); viewing the arm abolished the kinaesthetic and postural illusion but not the size and shape ones; found the longer the loss of kinaesthesia the larger the illusion (likely to be due to thinking about the movement but having a lack of feedback (short time period)
Patients undergoing upper limb surgery given local anaesthesia had sensory testing (a pinprick, vibration, passive movement) and motor testing (voluntary movement) every 5 mins for 60 mins and patients asked to report sensations from their limbs: (also a problem with the study)
The arm may have been removed but the nerves at the stump of the limb are still there and are still producing the signals; the unmyelinated nerves regenerate or sprout into neuromas; can have surgery to remove the neuroma which can lead to lessening of pain
Peripheral explanation for phantom limbs
Found a greater incidence in phantoms the greater number of years experience with the limb - not congenital but the incidence of phantoms increases the older the individual is when the phantom is removed
Price (2006)
Hard to falsify
Problem with Freudian denial
Doesn't explain how aplasic patients feel phantoms
Problem with the memory explanation
Could be seen as a counterproductive approach as the patients don't need what is lost to be reinstated
Problem with the mirror box method (Guimmarra and Moseley, 2011)
Often phantom limbs and pain occur quickly and so this explanation cannot account as the neuromas take time to sprout
Problem with the peripheral explanation of phantom limbs
Persistence of hand representation is associated with pain; loss of input and experience of pain may drive plasticity (together); plasticity may not be the bad thing as it is adaptive, new therapies could address connectivity between representation of phantom and the rest of the body
Reorganisation does not equal pain (Makin et al., 2013)
that in a case with a patient with brachial plexus injury (dorsal route ganglia damage - no sensory input below the shoulder)
Representations in the brain reorganising are unlikely to be due to the peripheral nerve input as found
Mazue and Makin
Some patients could voluntarily extend the telescoped hand
Referred sensation (Ramachandran)
Stimulation of other body parts which caused the patients to feel as though they were being stimulated on their phantom
Tinel's signal
Tapping a neuroma in the stump of an amputated limb created a signal and sensation of the phantom
Unmasking
The branches of connectivity were already there but the amputation removes the dominantly connected element
Telescoping
The phantom moves closer to the stump over time; the more weakly represented part of the phantom may disappear (arm less represented than hand)
Phantom limb movements which increase vividness of sensations may be associated with reduced pain (general sensation and phantom pain may be driven by the same mechanism)
Treatments that target pain typically decrease overall vividness of limb sensations, BUT
Phantom limbs can occur despite reorganisation of the primary somatosensory cortex
Weiss, 1998 (evidence for Melzack's neuromatrix)
69%
___ of amputees report painful phantoms
95%
___ of amputees report phantoms
67%
___ of amputees report phantoms within 1 week of amputation
87%
___ of amputees report phantoms within 8 weeks of amputation
28%
___ of amputees who reported experiencing phantom limbs and phantom limb pain had heard of phantom limbs already
most people can't remember things from before we were 3 so perhaps it was in the fist 3 years of life that they developed the phantom limb from viewing others
only 3 cases in which the patient had no intact contralateral limb yet the phantom was there from their earliest memory but