Academic Minute
5:00 am
Tue September 24, 2013

Dr. Tamar Makin, University of Oxford – The Source of Phantom Limb Pain

In today’s Academic Minute, Dr. Tamar Makin of the University of Oxford explains how the brain creates pain in phantom limbs. 


Tamar Makin is a postdoctoral research fellow in the FMRIB unit at the University of Oxford. Her research utilizes functional magnetic resonance imaging of the brain to explore structural and functional plasticity in amputees.

About Dr. Makin

Read the full article

Dr. Tamar Makin – The Source of Phantom Limb Pain

What happens to the brain cells responsible for operating the hand following arm amputation? We studied how brain changes following amputation may relate to a mysterious phenomenon termed “phantom limb pain” – pain that is perceived to be arising from the missing hand. We wanted to study the “phantom” cortex. But we were facing a problem – how would we identify which brain areas belonged to the hand, now missing? We took advantage of the fact that most of our participants experienced vivid phantom sensations, and we asked them to move their phantom fingers, while scanning their brains.

We were astonished to find, that in amputees that have suffered long-term phantom pain, the brain’s response to phantom hand movements was indistinguishable from that seen in people with intact limbs. This was despite the fact that our participants typically lost their hand many years prior to the experiment. We then looked at the structure of this brain area – to see whether it had shrunk, or degenerated, after amputation. While the amputees tended to have degeneration of this cortex compared to intact participants, we found less degeneration in amputees who experienced more pain.  In fact, the hand-area in the brain of a typical amputee suffering from chronic phantom pain looked indistinguishable from that of a typical intact participant.

However, the apparent preservation of the hand area does not indicate that the brain is functioning normally. People with more phantom pain had disrupted communication between the hand are and other brain areas, responsible for interaction with our external environment. In other words, the dissociation between phantom sensations and the physical world resulted in a functional detachment between the phantom cortex and the rest of the movement cortex.

Together, these findings shed new light on the neural correlates of the conscious experience of phantom pain. We found that the hand area of the brain seems to maintain its originally assigned role, despite the loss of original inputs and outputs. Our results may encourage rehabilitation approaches aimed at re-coupling the representation of the phantom hand with the external sensory environment.

 

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