The idea that a person can retain an awareness of an amputated limb may not be surprising but to consider the claim that a missing limb can still move and feel intense pain raises both serious questions and skeptical eyebrows. How can a person feel pain in a limb that no longer exists? A residual consciousness of a dismembered limb in the form of sensation, movement and even pain is the essence of phantom limb syndrome.
Yet despite such historical cynicism, phantom limb syndrome is now widely accepted in the scientific community owing to a wealth of clinical studies and modern experimental evidence using advanced neuroimaging techniques (Bear et. al, 2006). Scrutiny of this phenomenon has yielded valuable insights into both the mechanics of brain function and our understanding of pain perception while revealing enticing clues as to how the human brain constructs our conscious experience.
Phantom limb syndrome is differentiated into three general areas according to the nature of the experience: phantom awareness (including sensations such as touch, temperature, vibration and pressure); phantom movement (either 'voluntary', like waving or 'involuntary', like pains and needles); and phantom pain, which can be distinguished from residual stump pain as a distinct pain of any form that seems to emanate from where the arm or leg used to be (Flor et al, 1995). It is also known to affect the majority of amputees irrespective of age, gender or site of amputation (Bear et al, 2006).
It is important to define phantom awareness as more than just an arbitrary 'sense' that the limb is still present. Despite connotations of the supernatural in its name, the value of studying phantom limb comes from the fact that it is the product of a tangible event in the sensory cortex, a fact that has been verified through detection of electrical activity in the missing limb areas of the brain using magnetoencephalography (Brugger et al, 2000; MacIver et al, 2008). Phantom limbs give rise to experience such as vibrations, perceptions of hot and cold and even more complex sensations like 'trickling' of water (Ramachandran, 1998; Bear et. al, 2006). Since no sensory input can be originating from the body - the limb of course being absent -it suggests that the quality of these subjective experiences is independent of a physical contribution.
Phantom movement is known to affect approximately 80% of amputees and can take many forms (Finger, 2001). For example, a patient called Tom who had his arm amputated just above the elbow following a car accident described being able to use his phantom arm to reach out for items such as the telephone receiver (Ramachandran, 1998). Admiral Lord Nelson claimed that he could feel fingernails digging into his phantom hand and was able to pull his arm away (Herman, 1998). Other patients describe phantom movement such spontaneous jerking, swinging arms while walking and gesticulating hand movements when talking (Bear et al, 2006; Finger et al, 2001). Such a diverse spectrum of symptoms establishes the subjective experiential nature of phantom movement.
The phenomenon of phantom pain presents many challenges, particularly with regards to the clinical aspect of medical treatment. How do you treat localised pain in a tissue that no longer exists? Pharmacological treatment involves a host of drugs (e.g. anti-depressants, pain-killers and analgesics) but specific combinations are largely experimental and they do not relieve phantom pain in the long-term (Flor, 2002). This is a dilemma both from the patients and the physician's perspective. Staggering incidence rates of up to 80% of amputees suffer from chronic phantom pain and treatment has been "notoriously difficult" (Flor, 2002). As a result, phantom limb pain has had a lasting impact on medical science as it endeavours to understand the underlying mechanisms to find an adequate prevention or treatment.
Some studies suggest that phantom pain is caused by inflammation of nerve endings in the stump but treatment by further amputation only alleviates the pain temporarily and often returns with greater ferocity (Melzack, 1990). Some suggest that the remaining nerves send physical signals through the spinal chord which are then misinterpreted by the brain as originating from the missing limb (Melzack, 1990). Other theories suggest that phantom pain may be a type of reminiscence or 'memory imprint' of pain felt in the real arm before amputation. It was this latter theory that gained the most popular support as a number of influential studies suggested a correlation between pre and post amputation pain (e.g. Katz et al, 1996). Yet there is some compelling evidence to indicate why these 'explanations' for phantom limb pain do not tell the whole story. Whereas explanations based on learned memories or a relationship to pre-operative pain may explain phantom pain in amputees, the recognition that phantom limb occurs in people born without limbs implies that pain perception originates from the brain itself and there is an innate mechanism for experiencing it which is not dependant on our body (Flor, 2002).
This observation has had a significant impact on modern pain theory. It directly challenges prevailing theories based on Descartes specificity theory which state that pain is expressed through the brain from received signals of injury to the body (Benini & DeLeo, 1999). Since phantom limb pain arises without sensory signals from the body, it strongly indicates that it is the brain itself, and not our body, which plays the central role in pain perception.
Current explanations for phantom limb syndrome are based around Wilder Penfield's homunculus. In the 1950's he demonstrated that specific areas of the sensory cortex tissue in the brain will activate specific areas of the body and there is in fact a precise map on the surface of brain which corresponds to each and every part of the human body (Bear et al, 2006). The relationship between this cortical map and phantom limb syndrome was discovered in the last decade by V.S. Ramachandran (Bear et al, 2006). He knew from Penfield's research that the area corresponding to the human hand on the brain lies directly beside the face area. He also knew that unrelated animal research had verified 're-mapping' of brain regions that had been deprived of sensory input from the corresponding limb (Pons 1987, 1991). He hypothesised that if the unused hand area in the human brain had re-wired to the face area, then phantom limb sensation could arise from constant movement of the face: a misinterpretation of the origin of the signal (Ramachandran, 1998).
This idea was revolutionary because it contradicted the central dogma of neurology which stated that the neuronal circuitry of the human brain was fixed (Bear et al, 2006). Ramachandran tested his theory by touching his patient Tom's face and asking him to report where he could feel the sensation on his body. As suspected, the patient reported feeling the touch both in his face and his phantom hand. In fact, Ramachandran was able to sketch out an entire detailed map of Tom's phantom hand on his face (Ramachandran, 1998). Subsequent tests using magnetoencephalography verified these results by showing that the brain area previously responding to sensory input in the patient's hand was now re-mapped to fire in the adjacent face area, just as it had re-mapped in the monkey studies (Ramachandran, 2000).
The discovery of this cortical plasticity from phantom limb research offers an experimental method of investigation into how phantom pain is represented in the brain: if phantom pain arises from erroneous re-mapping, could the pain be alleviated by reorganisation or correction of the map? After all, if the brain can re-wire in one direction with such malleability then it can be assumed to be equally flexible in the opposite direction (Flor et al, 1995; 2006). Current endeavours to find treatments for phantom pain are based on this idea (Flor, 2007).
The various insights gained from the research described in this paper emphasise the value of studying such mind-brain anomalies like phantom pain. Analysis of such neurological 'abnormalities' presents a convenient opportunity to investigate normal brain function without the need for invasive surgery. In addition to its contribution in a medical and scientific context as outlined, it also has much broader significance for our understanding of human perception. Phantom limb tells us that conscious experience like touch and movement do not require our physical body or input from the physical world. It tells us that their must be an innate or "genetically determined substrate" for sensation that can be modified by sensory input but is not dependant on it (Melzack, 1990). Moreover, it begs the question: if our brain can detect our body parts regardless if they are there are not, what other aspects of our reality are merely constructed by the brain?
The significance of phantom pain research to such fundamental questions about the nature of human consciousness is clear when considered in the context of related research. For example, observations of phantom limb have been used to formulate other theories pertaining to other subjective experiences such as sound, colour and numbers. In a condition named synaesthesia, the quality of colour is actually experienced as a sound and sometimes instead of seeing a number they instead see a colour. Realising that the processing areas for these sensations are next to each other in the brain - just like Tom's phantom hand and face - scientists were able to predict the same sort of re-mapping that exists in phantom limb syndrome (Rouw & Scholte, 2007; Rich et al, 2005; Ramachandran, 2005). Current research is extending such insights from phantom limb research into understanding more intricate areas of the human experience such as memory (Yaro & Ward 2007), language (Ramachandran, 2005) and even the concept of time (Smilek et al, 2007). Therefore, perhaps the most significant element of phantom research is its impact on brain function research and its influence on opening up our minds to discover the substance of our own consciousness.
Author: Kellieanne McMillan (Glasgow University, BSc Neuroscience)
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