Phantom Limbs
Tom lost his left arm above the elbow at the age of seventeen in a car accident. Weeks after the accident, Tom continued to feel the presence of the lost arm even though he knew that the arm was missing. He could move each “finger,” “grab” objects that were within reach of the lost arm, and do just about anything with his phantom arm as a real arm would have done (Ramachandran and Blakeslee 1998, pg 23). Tom’s impression of his phantom limb presents itself as an intriguing mystery of the brain.
Nearly 95 to 100% of amputees report experiencing a phantom limb that acts in much the same way their normal arm did. The phantom gesticulates when the person talks and moves when the person is walking or stretching. The vivid reality of the phenomena is that the phantom limb might even “feel” perfectly normal in size and shape, such that the amputee will attempt to use his phantom limb to perform tasks. In addition to the kinesthetic aspects of a phantom limb, patients report having a tingling sensation in their phantom limb known as phantom paraesthesia. About 50 to 80% of amputees also experience a more distressing and traumatic aspect of their phantom limb—pain. However, amputation is not the only means to experience a phantom. Patients whose limbs are intact yet are unable to transmit sensory input can also experience phantom limbs, like stroke victims and people who suffered brachial plexus avulsion or anesthetization of the spinal cord. Interestingly, paraplegics and even patients of congenital limb deficiency (aplasia) experience phantom kinesthesia and paraesthesia, as well as pain.
Phantom limb phenomena receives recognition within the general public because of its clinical connections as physicians find ways to ameliorate or eliminate phantom limb pain in patients. More significantly, phantom limb phenomena challenges the traditional view that the adult brain is incapable of extensive reorganization. Evidence supporting phantom limb phenomena indicates that the body schema produced by the brain is malleable. Moreover, phantom limb phenomena in congenital aplasia suggests that the body schema might be genetically predetermined and merely strengthened by sensory experience, which is contrary to the accepted idea that sensory inputs are essential to generate a body schema in the brain.
In the last two decades, there have been new insights into solving the mysteries of the phantom limb phenomena. One hypothesis that is gaining experimental support is the idea of cortical reorganization after deafferentation of a limb. In nonhuman primate studies, the primary somatosensory cortex (SI) shows expanded representation of the body schema where adjacent cortical areas move into the deafferentation zone, the cortical area lacking normal inputs. In human patients, tactile stimulation of other body parts, such as the face, can often elicit referred phantom sensation in the phantom limb. These data argue for the hypothesis that changes in structural and functional architecture of the area SI after deafferentation is the main cause of phantom limb phenomena. Besides the somatosensory cortex, studies showing similar changes in the thalamus and brainstem also provide evidence toward a reorganization hypothesis. Currently, there are two proposed explanations for the structural and functional changes after deafferentation: unmasking of existing silent synapses by disinhibition and the sprouting of new connections.
Tom lost his left arm above the elbow at the age of seventeen in a car accident. Weeks after the accident, Tom continued to feel the presence of the lost arm even though he knew that the arm was missing. He could move each “finger,” “grab” objects that were within reach of the lost arm, and do just about anything with his phantom arm as a real arm would have done (Ramachandran and Blakeslee 1998, pg 23). Tom’s impression of his phantom limb presents itself as an intriguing mystery of the brain.
Nearly 95 to 100% of amputees report experiencing a phantom limb that acts in much the same way their normal arm did. The phantom gesticulates when the person talks and moves when the person is walking or stretching. The vivid reality of the phenomena is that the phantom limb might even “feel” perfectly normal in size and shape, such that the amputee will attempt to use his phantom limb to perform tasks. In addition to the kinesthetic aspects of a phantom limb, patients report having a tingling sensation in their phantom limb known as phantom paraesthesia. About 50 to 80% of amputees also experience a more distressing and traumatic aspect of their phantom limb—pain. However, amputation is not the only means to experience a phantom. Patients whose limbs are intact yet are unable to transmit sensory input can also experience phantom limbs, like stroke victims and people who suffered brachial plexus avulsion or anesthetization of the spinal cord. Interestingly, paraplegics and even patients of congenital limb deficiency (aplasia) experience phantom kinesthesia and paraesthesia, as well as pain.
Phantom limb phenomena receives recognition within the general public because of its clinical connections as physicians find ways to ameliorate or eliminate phantom limb pain in patients. More significantly, phantom limb phenomena challenges the traditional view that the adult brain is incapable of extensive reorganization. Evidence supporting phantom limb phenomena indicates that the body schema produced by the brain is malleable. Moreover, phantom limb phenomena in congenital aplasia suggests that the body schema might be genetically predetermined and merely strengthened by sensory experience, which is contrary to the accepted idea that sensory inputs are essential to generate a body schema in the brain.
In the last two decades, there have been new insights into solving the mysteries of the phantom limb phenomena. One hypothesis that is gaining experimental support is the idea of cortical reorganization after deafferentation of a limb. In nonhuman primate studies, the primary somatosensory cortex (SI) shows expanded representation of the body schema where adjacent cortical areas move into the deafferentation zone, the cortical area lacking normal inputs. In human patients, tactile stimulation of other body parts, such as the face, can often elicit referred phantom sensation in the phantom limb. These data argue for the hypothesis that changes in structural and functional architecture of the area SI after deafferentation is the main cause of phantom limb phenomena. Besides the somatosensory cortex, studies showing similar changes in the thalamus and brainstem also provide evidence toward a reorganization hypothesis. Currently, there are two proposed explanations for the structural and functional changes after deafferentation: unmasking of existing silent synapses by disinhibition and the sprouting of new connections.
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