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The phantom limb syndrome is the sensation that an amputated or missing limb is still attached to the body and is moving appropriately with other body parts.
Many individuals with amputations have a sensation that they are able to move their missing limbs voluntarily but others experience the missing limb as paralyzed in a painfully awkward position. But the most important feature of this syndrome is the painful condition of the amputated limb, called Phantom Limb Pain (PLP).
It seems to be more severe in the distal portions of the phantom and can have a number of characteristics such as cramping, shooting, stabbing or burning. Its onset can be immediate, but it may also appear for the first time many years after the amputation.
Although phantom limb pain is more common after the amputation of an arm or leg, it may also occur after the surgical removal of other body parts, such as a breast, rectum, penis, testicles, eyes, tongue or teeth (Phantom pain after eye amputation, 2011; Phantom phenomena in mastectomized patients and their relation to chronic and acute pre-mastectomy pain, 2004). Interestingly, phantom limb pain is more frequent when the amputation occurs in adulthood, less frequent in child amputees and virtually non existent in congenital amputees (Phantom limb sensations and phantom limb pain in child and adolescent amputees, 1998). Approximately 60 to 80% of individuals with an amputation experience phantom sensations in their amputated limb, and the majority of the sensations are painful. Since the beginning of the fire conflicts in the world, there has been a dramatic increase in the number of military service members with single and multiple-limb amputations.
In other parts of the world, civil wars and landmine explosions result in many unfortunate cases of traumatic amputations in otherwise healthy people (Phantom limb pain: theories and therapies, 2010). Recent studies report the prevalence of PLP to be more common among upper limb amputees than lower limb amputees; upper limb amputees are significantly more likely to suffer post-amputation pain which is more frequent, longer lasting and more severe in intensity when compared to lower limb amputees. Other risk factors are the presence of pre-amputation pain (Preamputation pain and acute pain predict chronic pain after lower extremity amputation, 2007) or even the time after amputation: phantom pain and phantom sensations are often long-term consequences of amputation. Female are hypothesized to report greater pain intensity and pain interference, and are also expected to report using a greater number of pain coping strategies and engaging in more frequent pain catastrophizing (Sex Differences in Pain and Psychological Functioning in Persons with Limb Loss, 2009).
Finally, the psychological aspect (such as stress, anxiety, depression) highly likely contribute to the persistence or exacerbation of PLP.
In a historical perspective, PLP had been considered mostly of psychological origin, with the prevalent belief that PLP was generated “in the patient’s head.” However, the development of advanced diagnostic methods, recently including neuroimaging, has facilitated explorations of changes in peripheral and central neural networks after amputation and their putative contribution to the development of PLP. Until recently, the dominant theory for cause of phantom limbs was irritation in the severed nerve endings (called neuromas).
As a consequence of injury, terminal swelling and regenerative sprouting of the injured axon end occurs and neuromas form in the residual limb that display spontaneous and abnormal evoked activity to mechanical and chemical stimuli.
The increased excitability of injured nerves that result in ectopic discharge seems to be due to alterations in the electrical properties of cellular membranes, such as an alteration of voltage-gated sodium channels and a decreasing of potassium channel expression in the neuroma (Sodium channels and mechanisms of neuropathic pain, 2006). This is caused by an accumulation of molecules enhancing the expression of sodium channels in these neuromas, that results in hype-excitability and spontaneous discharges.
Some neurons in the areas of spinal cord that are not responsible for pain transmission also sprout into the Lamina II of the dorsal horn of the spinal cord which is the area involved in the transmission of nociceptive afferent inputs.
Inhibitory GABA-containing and glycinergic interneurons in the spinal cord could be destroyed by rapid ectopic discharge, or might change from having an inhibitory to an excitatory effect under the influence of Brain-Derived Neurotrophic Factor (BDNF) released from the microglia, thereby contributing to a hyperexcitable spinal cord (BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain, 2005).
During this process, there is also an increase in the activity at NMDA receptors mediated by neurotransmitters such as substance P, tachykinins, and neurokinins at the dorsal horn of the spinal cord. These factors are normally expressed only by C-afferents and A? afferents, most of which are nociceptors. This process brings about a complicated change in the firing pattern of the central nociceptive neurons (Phantom Limb Pain: Mechanisms and Treatment Approaches, 2011).
Recent studies demonstrate some changes in the funcional and structural architecture of the primary somatosensory cortex (SI), subsequent to amputation; this is called cortical reorganization, and it's perhaps the most cited reason for the cause of PLP in recent years. Ramachandran, one of the most famous scientists about this topic, showed a point-to-point correspondence between stimulation sites and areas of sensation from the face to the phantom in arm amputees. This happens because the sensory input from face invade the original hand area in the brain, so the simple action of touching the face of the amputee evokes tactile sensations on the phantom (e.g. These sensory referrals from the face to phantom hand occur in a stable, topographically organized manner (Dynamic reorganization of referred sensations by movements of phantom limbs, 2010).
Multiple imaging studies using functional MRI (fMRI) have correlated greater extent of somatosensory cortex involvement with more intense phantom limb experience; activation in primary somatosensory and motor cortices is unaltered in amputees without pain and is similar to that in healthy controls. Phantom limb pain, cortical reorganization and the therapeutic effect of mental imagery, 2008). Very recently (december 2012), a study reveals the importance of the cortical plasticity in the Anterior Cingulate Cortex (ACC), a critical cortical area for pain sensation, including Phantom Limb Pain.
Nerve injuries or amputations trigger a series of plastic changes in pain-related cortical areas including the ACC. A number of different therapies relying on different principles have been proposed for the management of Phantom Limb Pain; however, specific treatment guidelines are yet to evolve and most successful measures employ multidisciplinary approaches in the management of pain and in rehabilitation.
A cross sectional study found that Acetaminophen (or Paracetamol) and Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) were the most common medications used in the treatment of PLP. NSAIDs inhibit the enzymes needed for the synthesis of prostaglandin and decrease the nociception peripherally and centrally.
Opioids bind to the peripheral and central opioid receptors and provide analgesia without the loss of touch, proprioception, or consciousness.
In particular, morphine has been shown to be very beneficial for the management of PLP, while methadone has received a differential treatment due to the additional concern about cardiac toxicity (The effects of methadone and its role in fatalities, 2004).
Comparative trials have also shown benefit with opioids when compared with tricyclic antidepressants, but the total amount of opioid required to achieve analgesia may be less when used together with these tricyclic antidepressants or anticonvulsants, which also have use in neuropathic pain modulation. TENS devices are portable, are easy to use, and have few side effects or contraindications. This can be explained by the existence in the brain of mirror neurons (neurons that are active not only during the execution of the task itself but also during the observation of the task), which fire in this occasion. A person without phantom limb pain and no amputations cannot feel these tactile sensations, because inputs from a non-mirror neuron block the mirror neuron, while a patient with an amputation does not have this non-mirror neuron system operating. Since the activation of these mirror neurons modulates somatosensory inputs, their activation may block protopathic pain perception in the phantom limb, and it is expected to decrease pain by resolving conflict between motor intention, proprioception and visual system. Mirror therapy is expected to be widely used for the treatment of phantom limb pain, because it's easy to use, even at patient's home (Mirror Therapy for Phantom Limb Pain, 2012).
This video shows a soldier using mirror therapy for his right leg that lost in Baghdad, during the war in Iraq, on December 17th 2007. A phantom limb is the sensation that an amputated or missing limb (even an organ, as the appendix) is still attached to the body and is moving appropriately with other body parts. Although not all phantom limbs are painful, patients will sometimes feel as if they are gesturing, feel itches, twitch, or even try to pick things up. A slightly different sensation known as phantom pain can also occur in people born without limbs, and people who are paralyzed.
In a historical perspective, PLP had been considered mostly of psychological origin, with the prevalent belief that PLP was generated “in the patient’s head”.
The axonal sprouts at the proximal section of the amputated peripheral nerve form connections with the neurons in the receptive field of the spinal cord. Another proposed mechanism of PLP is based on the “body schema” concept that was originally proposed by Head and Holmes in 1912. Most people who've had a limb removed report that it sometimes feels as if their amputated limb is still there. Phantom limb pain (PLP) is a complex phenomenon that includes a wide variety of symptoms ranging from tingling and itching to burning and aching. Although PLP occurs more often in adults, some studies demonstrated that it also occurs commonly in children and adolescents. The analgesic mechanism of acetaminophen is not clear but serotonergic and multiple other central nervous system pathways are likely to be involved. Tricyclic antidepressants are among the most commonly used medications for various neuropathic pains including PLP. Historically, there have been multiple studies showing the effectiveness of TENS of the contralateral limb versus ipsilateral to decrease PLP.
A mirror box is a box with two mirrors in the center (one facing each way), invented by Vilayanur S. In a mirror box the patient places the good limb into one side, and the stump into the other. As concerns non-pharmacological treatments for phantom limb pain attacks, some have considered the idea of using calcitonin hormone infusions; it has been then considered a good analgesic for alleviating pain in this type of disease. After an above-knee leg amputation, a 29-year-old pregnant woman (at eight weeks gestation) reported severe PLP.
In another study instead, conducted on patients with chronic phantom limb pain, the tested hypothesis was that calcitonin, ketamine, and their combination are effective in treating chronic phantom limb pain. This is called phantom limb awareness, that is often accompanied by specific sensory kinaesthetic sensations (phantom sensations); patients sometimes feel as if they are gesturing, feel itches, twitch, or even try to pick things up. Often, the patient feels to have a shorter limb than the other; this means that the exact sensation differs widely for individuals. The patients are elderly and have often suffered from long-lasting pre-amputation been observed as a consequence of the loss of other pain. Lower limb amputees fared better than upper limb amputees in terms of bodily pain, social function and mental health (A cross-sectional study of post-amputation pain in upper and lower limb amputees, experience of a tertiary referral amputee clinic, 2010). Amputees experience phantom sensations and phantom pain within 1 month after amputation, and a second peak occurs 12 months after amputation (Painful and nonpainful phantom and stump sensations in acute traumatic amputees, 2008). A study has found that amputees with depressive symptoms were more likely to characterize their pain as more severe than those without depressive symptoms (Phantom pain, residual limb pain, and back pain in amputees: results of a national survey, 2005).


The findings acknowledged the neuropathic nature of PLP and also suggested that both peripheral, as well as central mechanisms, including neuroplastic changes in central nervous system, can contribute to PLP. Ectopic discharges from stump neuromas represent a source of abnormal afferent input to the spinal cord and a potential mechanism for spontaneous pain and abnormal evoked pains. Studies reporting the reduction of phantom pain with drugs blocking the sodium channels lend further support to this theory (The use of prolonged peripheral neural blockade after lower extremity amputation: the effect on symptoms associated with phantom limb syndrome, 2010).
This is followed by increased neuronal activity (mechanical hyperalgesia) expansion of the neuronal receptive field, and hyperexcitability of other regions: this complicated process is called central sensitization.
But in the central sensitization, there is an injury-triggered expression of these factors (as Substance P) by A? fibres, that might contribute to Phantom Limb Pain. During reorganization, the cortical areas representing the amputated extremity are taken over by the neighboring representational zones in the primary somatosensory cortex.
In the amputees with PLP, the cortical representation of the mouth extends into the region of the hand and arm. The main event is a Loss of Long Term Depression (LTD) within the ACC and between cortical areas, that contributes to enhanced excitability of pain-processing and feeling cortical neurons. They may also diminish cortical reorganization and thus disrupt one of the proposed mechanisms of PLP.
There are some studies showing the effectiveness of TENS made on the contralateral limb versus ipsilateral (the phantom limb) to decrease PLP (Contralateral stimulation, using TENS, of phantom limb pain: two confirmatory cases, 2010). Mirror therapy was first reported by Ramachandran in 1996 and is suggested to help PLP by resolving the visual-proprioceptive dissociation in the brain.
The presence of mirror neurons in the brain is also supported by the phenomenon of tactile sensation in the phantom limb elicited by touching the virtual image of the limb (i.e. Approximately 60 to 80% of individuals with an amputation experience phantom sensation in their amputated limb, and the majority of the sensations are painful.
For example, Ramachandran and Blakeslee describe that some people’s representations of their limbs do not actually match what they should be: for example one patient reported that her phantom arm was about “6 inches too short”. However , the development of advanced diagnostic methods, recently including neuroimaging, has facilitated explorations of changes in peripheral and central neural networks after amputation and their putative contribution to the development of PLP.
This results in massive tissue and neuronal injury, causing disruption of the normal pattern of afferent nerve input to the spinal cord. Some neurons in the spinal cord areas which are not responsible for pain transmission also sprout into the Lamina II of the dorsal horn of the spinal cord, which is involved in the transmission of nociceptive afferent inputs.
During reorganization, the cortical areas representing the amputated extremity are taken over by the neighbouring representational zones in both the primary somatosensory and the motor cortex. The body schema can be thought of as a template of the entire body in the brain and any change to the body, such as an amputation, results in the perception of a phantom limb. This painless phenomenon, known as phantom limb sensation, can also occur in people who were born without limbs. They may also diminish cortical reorganization and disrupt one of the proposed mechanisms of PLP.
The analgesic action of tricyclic antidepressant is attributed mainly to the inhibition of serotonin-norepinephrine uptake blockade, NMDA receptor antagonism, and sodium channel blockade.
Ramachandran to help alleviate phantom limb pain , in which patients feel they still have a limb after having it amputated. The patient then looks into the mirror on the side with good limb and makes "mirror symmetric" movements, as a symphony conductor might, or as we do when we clap our hands. A case report relates the effectiveness of lesioning the dorsal root entry zone (DREZ) on upper limb phantom pain resulting from brachial plexus avulsions. The pain persisted for more than two weeks and was not relieved by multiple regimens of opioid and nonopioid medications.
Moreover, the pain can be made worse by stress, anxiety, and environmental changes (Rebecca Brightwell, AgrAbility in Georgia). The process and extent of cortical reorganization have been studied in both animal and human models following amputation and deafferentation. Some of these cortical changes may not require persistent peripheral sensory inputs; thus will not respond to any medical treatment that targeted at lower subcortical levels. Randomized controlled trials have demonstrated the effectiveness of opioids (oxycodone, methadone, morphine, and levorphanol) for the treatment of neuropathic pain, including PLP (Methadone for phantom limb pain, 2002).
The patient watches the reflection of his intact limb moving in a mirror placed parasagittally between their arms or legs (for the upper limb it's called mirror box), while simultaneously moving the phantom limb (moving the stump) in a manner similar to what he is observing so that the virtual limb replaces the phantom limb. It is often described as a burning or similarly strange sensation and can be extremely agonizing for some people, but the exact sensation differs widely for different individuals. This is followed by a process called deafferentation and the proximal portion of the severed nerve sprouts to form neuromas. This is followed by increased neuronal activity, expansion of the neuronal receptive field, and hyperexcitability of other regions.
A further expansion of the body schema concept is the “neuromatrix and neurosignature” hypothesis proposed by Ronald Melzack in 1989. Phantom limb sensations may include feelings of coldness, warmth or itchiness or tingling — but should not be confused with phantom pain. In addition to pain in the phantom limb, some people experience other sensations such as tingling, cramping, heat, and cold in the portion of the limb that was removed.
Randomized controlled trials have demonstrated the effectiveness of opioids (oxycodone, methadone, morphine, and levorphanol) for the treatment of neuropathic pain including PLP.
Because the subject is seeing the reflected image of the good hand moving, it appears as if the phantom limb is also moving. Cortical reorganization explains why the afferent nociceptive stimulation of neurons within the stump or surrounding area produces the sensation in the missing limb (Phantom limb pain: a case of maladaptive CNS plasticity?, 2006). In addition to contribution to pain or phantom pain, such cortical plastic changes may also triggers a series of brain disorders such as emotional fear, anxiety, mood depression, and impairment of cognitive functions (Cortical Depression and Potentiation: Basic Mechanisms for Phantom Pain, 2012).
Other induced sensations include warmth, cold, itching, squeezing, tightness, and tingling.
There is an increased accumulation of molecules enhancing the expression of sodium channels in these neuromas, that results in hype-excitability and spontaneous discharges. Cortical reorganization partly explains why the afferent nociceptive stimulation of neurons within the stump or surrounding area produces the sensation in the missing limb. The neuromatrix can be conceptualized as a network of neurons within the brain that integrates numerous inputs from various areas including somatosensory, limbic, visual, and thalamocortical components. Any sensation that the limb could have experienced prior to the amputation may be experienced in the amputated phantom limb. Through the use of this artificial visual feedback it becomes possible for the patient to "move" the phantom limb, and to unclench it from potentially painful positions. Intensity of phantom pain (visual analog scale) was recorded before, during, at the end, and the 48 h after each infusion.
The missing limb often feels shorter and may feel as if it is in a distorted and painful position.
So the most important feature of this syndrome is the painful condition of the amputated limb, called Phantom Limb Pain ( PLP ).
The extent of cortical reorganization has been found to be directly related to the degree of pain and the size of the deafferentiated region. Pain thresholds after electrical, thermal, and pressure stimulation were recorded before and during each infusion.
This is followed by a phenomenon called the “windup phenomenon” in which there is an upregulation of those receptors in the area. Multiple imaging studies have correlated greater extent of somatosensory cortex involvement with more intense phantom limb experience . The term “neurosignature” was proposed by Melzack to refer to the patterns of activity generated within the brain that are continuously being updated based upon one’s conscious awareness and perception of the body and self.
On postinfusion day 4, the patient reported reductions in the frequency and severity of PLP episodes, and a trend of improved PLP symptom control was noted over the next 48 hours, allowing the pain management team to begin tapering some medication dosages and thus reduce the woman's overall narcotic exposure. This process brings about a change in the firing pattern of the central nociceptive neurons. The deprivation of various inputs from the limbs to the neuromatrix causes an abnormal neurosignature to be produced that results in the generation of PLP.The other hypothesis relative to the mechanism of PLP has been derived from the research into illusory perceptions. The target neurons at the spinal level for the descending inhibitory transmission from the supraspinal centers may be lost. It has been shown that the parietal and frontal lobes are also involved besides the primary somatosensory cortex in the perception of the abnormal somatosensory phenomenon. There also may be a reduction in the local intersegmental inhibitory mechanisms at the level of the spinal cord, resulting in spinal disinhibition and nociceptive inputs reaching the supra spinal centers. Painful sensations, such as PLP, may be related to the incongruence of motor intention and sensory feedback and a corresponding activation of the parietal and frontal brain areas. Sensory assessments indicated that peripheral mechanisms are unlikely important determinants of phantom limb pain. This lack of afferent input and changes at the level of the spinal cord have been proposed to result in the generation of PLP. Ketamine, but not calcitonin, affects central sensitization processes that are probably involved in the pathophysiology of phantom limb pain.



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