Phantom Limb Syndrome
Diseases

Author: Simone Pizzini
Date: 15/02/2013

Description

DEFINITION

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. 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.

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. Often, the patient feels to have a shorter limb than the other; this means that the exact sensation differs widely for individuals. Moreover, the pain can be made worse by stress, anxiety, and environmental changes (Rebecca Brightwell, AgrAbility in Georgia).
But the most important feature of this syndrome is the painful condition of the amputated limb, called Phantom Limb Pain (PLP).

SYMPTOMS

Phantom pains occur when nerves that would normally innervate the missing limb cause pain.
PLP has many features: at one end of the spectrum it is limited to simple, short-lasting and rarely occurring painful shocks in a missing body part; at the other end of the spectrum it can be a constant, excruciatingly painful experience during which the individual has a vivid and intense perception of the missing body part.
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).

EPIDEMIOLOGY

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. Phantom limb pain (PLP) frequently develops in these individuals.
In Western countries, the main reason for amputation is chronic vascular disease. The patients are elderly and have often suffered from long-lasting pre-amputation been observed as a consequence of the loss of other pain.
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).

RISK FACTORS

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. 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).
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. 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).
It was also reported to be more common among females than males.

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. 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).

NEUROLOGICAL BASES

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. 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.

PERIPHERAL CHANGES

Until recently, the dominant theory for cause of phantom limbs was irritation in the severed nerve endings (called neuromas). When a limb is amputated, many severed nerve endings are terminated at the residual limb.

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. 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.
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. 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).

CENTRAL CHANGES

SPINAL CORD

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. 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.
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 Aδ afferents, most of which are nociceptors. But in the central sensitization, there is an injury-triggered expression of these factors (as Substance P) by Aβ fibres, that might contribute to Phantom Limb Pain.
This process brings about a complicated change in the firing pattern of the central nociceptive neurons (Phantom Limb Pain: Mechanisms and Treatment Approaches, 2011).

CORTICAL REORGANIZATION

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. During reorganization, the cortical areas representing the amputated extremity are taken over by the neighboring representational zones in the primary somatosensory cortex. The process and extent of cortical reorganization have been studied in both animal and human models following amputation and deafferentation. 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).

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. there is a "thumb in cheek" map of stimulation on the face; this is the reason why an amputee who shaves, stimulating his cheek, might have phantom limb pain or phantom hand sensations).
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. In the amputees with PLP, the cortical representation of the mouth extends into the region of the hand and arm.
Phantom limb pain, cortical reorganization and the therapeutic effect of mental imagery, 2008).

NEW STUDIES IN THE ACC

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. 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. 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. 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).

THERAPIES

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.
Treatment guidelines used for other neuropathic pain conditions are probably the best approximation for now, especially for the treatment of stump pain (Postamputation pain: studies on mechanisms, 2012)

PHARMACOLOGICAL TREATMENTS

PARACETAMOL AND NSAIDS

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. The analgesic mechanism of acetaminophen is not clear but serotonergic and multiple other central nervous system pathways are likely to be involved. Acetaminophen has a little anti-inflammatory activity as compared to NSAIDs.
NSAIDs inhibit the enzymes needed for the synthesis of prostaglandin and decrease the nociception peripherally and centrally.

OPIOIDS

Opioids bind to the peripheral and central opioid receptors and provide analgesia without the loss of touch, proprioception, or consciousness. They may also diminish cortical reorganization and thus disrupt one of the proposed mechanisms of PLP. 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).
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.

NON PHARMACOLOGICAL TREATMENTS

TENS

Transcutaneous Electrical Nerve Stimulation has been found to be helpful in PLP.
It's a therapy generally used for neuropathic pain.

Low-frequency and high-intensity TENS is thought to be more effective than other doses. 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).
TENS devices are portable, are easy to use, and have few side effects or contraindications.

MIRROR THERAPY

It's maybe one of the most interesting and important treatments for the Phantom Limb Pain. 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 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. Most of the patients reported a decreasing of the Phantom Limb Pain.

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. 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. touching the contralateral limb, reflected in the mirror).
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.

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2014-06-25T10:14:43 - virginia bobbio
2014-06-25T09:57:42 - virginia bobbio

Virginia Bobbio
Luca Dalla Santaca'

PAIN PERCEPTION IN PHANTOM LIMB

DEFINITION

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. Approximately 60 to 80% of individuals with an amputation experience phantom sensation in their amputated limb, and the majority of the sensations are painful. Phantom sensations may also occur after the removal of body parts other than limbs, e.g. after breast amputation, extraction of a tooth (phantom tooth pain) or eye removal (phantom eye syndrome). The missing limb often feels shorter and may feel as if it is in a distorted and painful position. Occasionally, the pain can be worsened by stress, anxiety, and weather changes. Phantom limb pain is usually intermittent. The frequency and intensity of attacks usually declines with time.
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. 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”.
A slightly different sensation known as phantom pain can also occur in people born without limbs, and people who are paralyzed. Phantom pains occur when nerves that would normally innervate the missing limb cause it. 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. Other induced sensations include warmth, cold, itching, squeezing, tightness, and tingling. So the most important feature of this syndrome is the painful condition of the amputated limb, called Phantom Limb Pain ( PLP ).

Phantom phenomena and body scheme after limb amputation, 2014

NEUROLOGICAL BASES

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. 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.

PERIPHERAL MECHANISM

During amputation, peripheral nerves are severed. This results in massive tissue and neuronal injury, causing disruption of the normal pattern of afferent nerve input to the spinal cord. This is followed by a process called deafferentation and the proximal portion of the severed nerve sprouts to form neuromas. There is an increased accumulation of molecules enhancing the expression of sodium channels in these neuromas, that results in hype-excitability and spontaneous discharges. This abnormal peripheral activity is thought to be a potential source of the stump pain, including phantom pain. Studies reporting the reduction of phantom pain with drugs blocking the sodium channels lend further support to this theory. However, this cannot explain the mechanism of PLP in patients with congenital absence of limbs.

CENTRAL NEURAL MECHANISMS

CHANGES AT SPINAL CORD LEVEL

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. 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. This is followed by increased neuronal activity, expansion of the neuronal receptive field, and hyperexcitability of other regions. This process is called central sensitization. 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. This is followed by a phenomenon called the “windup phenomenon” in which there is an upregulation of those receptors in the area. This process brings about a change in the firing pattern of the central nociceptive neurons. The target neurons at the spinal level for the descending inhibitory transmission from the supraspinal centers may be lost. 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. This lack of afferent input and changes at the level of the spinal cord have been proposed to result in the generation of PLP.

CHANGES AT BRAIN LEVEL


Cortical reorganization is perhaps the most cited reason for causing PLP in recent years. 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 process and extent of cortical reorganization have been studied in both animal and human models following amputation and deafferentation. 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 extent of cortical reorganization has been found to be directly related to the degree of pain and the size of the deafferentiated region. Multiple imaging studies have correlated greater extent of somatosensory cortex involvement with more intense phantom limb experience .
Another proposed mechanism of PLP is based on the “body schema” concept that was originally proposed by Head and Holmes in 1912. 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. A further expansion of the body schema concept is the “neuromatrix and neurosignature” hypothesis proposed by Ronald Melzack in 1989. 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. It then results in an output pattern that evokes pain or other meaningful experiences. 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. 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. 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. 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.

Phantom-limb pain: characteristics, causes, and treatment, 2002

Sodium channels and mechanisms of neuropathic pain, 2006

SYMPTOMS

Most people who've had a limb removed report that it sometimes feels as if their amputated limb is still there. This painless phenomenon, known as phantom limb sensation, can also occur in people who were born without limbs. Phantom limb sensations may include feelings of coldness, warmth or itchiness or tingling — but should not be confused with phantom pain.
Phantom limb pain (PLP) is a complex phenomenon that includes a wide variety of symptoms ranging from tingling and itching to burning and aching. Its onset can be immediate, but it may also appear for the first time many years after the amputation. 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. Any sensation that the limb could have experienced prior to the amputation may be experienced in the amputated phantom limb. Phantom limb pain may cause sensations of:

  • Shooting, stabbing, piercing or burning pain
  • Pleasure
  • An article of clothing or jewelry
  • The limb still being attached and functioning normally
  • Numbness, tickling or cramping

By definition, phantom pain feels as if it comes from a body part that no longer remains.
Characteristics of phantom pain include:

  • Onset within the first few days of amputation
  • Tendency to come and go rather than be constant
  • Usually affects the part of the limb farthest from the body, such as the foot of an amputated leg
  • May be described as shooting, stabbing, boring, squeezing, throbbing or burning
  • Sometimes feels as if the phantom part is forced into an uncomfortable position
  • May be triggered by weather changes, pressure on the remaining part of the limb or emotional stress
    Although PLP occurs more often in adults, some studies demonstrated that it also occurs commonly in children and adolescents.

The prevalence of phantom limb sensation and pain in pediatric amputees, 1995

THERAPIES

For some people, phantom pain gets better over time without treatment. For others, managing phantom pain can be challenging. 
There are different types of treatments for PLP:

Pharmacological treatments

  • Acetaminophen and NSAIDs
    The analgesic mechanism of acetaminophen is not clear but serotonergic and multiple other central nervous system pathways are likely to be involved. NSAIDs inhibit the enzymes needed for the synthesis of prostaglandin and decrease the nociception peripherally and centrally.
  • Opioids
    Opioids bind to the peripheral and central opioid receptors and provide analgesia without the loss of touch, proprioception, or consciousness. They may also diminish cortical reorganization and disrupt one of the proposed mechanisms of PLP. Randomized controlled trials have demonstrated the effectiveness of opioids (oxycodone, methadone, morphine, and levorphanol) for the treatment of neuropathic pain including PLP.
  • Antidepressants
    Tricyclic antidepressants are among the most commonly used medications for various neuropathic pains including 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.

Non-pharmacological treatments

  • Transcutaneous Electrical Nerve Stimulation (TENS)
    Historically, there have been multiple studies showing the effectiveness of TENS of the contralateral limb versus ipsilateral to decrease PLP. Low-frequency and high-intensity TENS is thought to be more effective than other doses.
  • Mirror therapy
    A mirror box is a box with two mirrors in the center (one facing each way), invented by Vilayanur S. Ramachandran to help alleviate phantom limb pain , in which patients feel they still have a limb after having it amputated.
    In a mirror box the patient places the good limb into one side, and the stump into the other. 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. Because the subject is seeing the reflected image of the good hand moving, it appears as if the phantom limb is also moving. 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.
  • Surgical intervention
    Surgical interventions are usually employed when other treatment methods have failed. A case report relates the effectiveness of lesioning the dorsal root entry zone (DREZ) on upper limb phantom pain resulting from brachial plexus avulsions.

Phantom Limb Pain: Mechanisms and Treatment Approaches, 2011

HORMONAL USAGE FOR TREATING PHANTOM LIMB SYNDROME: THE USE OF CALCITONIN FOR TREATING PLP

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.
Example:
After an above-knee leg amputation, a 29-year-old pregnant woman (at eight weeks gestation) reported severe PLP. The pain persisted for more than two weeks and was not relieved by multiple regimens of opioid and nonopioid medications. On postamputation day 16, a 30-minute i.v. infusion of 200 IU of calcitonin (salmon) was administered; the woman reported transient excruciating pain during the final 5 minutes of the infusion. There was little overall change in her pain status over the next three days. 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.

Calcitonin for phantom limb pain in a pregnant woman, 2012

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. Twenty patients received, in a randomized, double-blind, crossover manner, 4 i.v. infusions of: 200 IE calcitonin; ketamine 0.4 mg/kg (only 10 patients); 200 IE of calcitonin combined with ketamine 0.4 mg/kg; placebo, 0.9% saline. Intensity of phantom pain (visual analog scale) was recorded before, during, at the end, and the 48 h after each infusion. Pain thresholds after electrical, thermal, and pressure stimulation were recorded before and during each infusion. Ketamine, but not calcitonin, reduced phantom limb pain. The combination was not superior to ketamine alone. question the usefulness of calcitonin in chronic phantom limb pain and stress the potential interest of N-methyl-D-aspartate antagonists. Sensory assessments indicated that peripheral mechanisms are unlikely important determinants of phantom limb pain. Ketamine, but not calcitonin, affects central sensitization processes that are probably involved in the pathophysiology of phantom limb pain.

Chronic phantom limb pain: the effects of calcitonin, ketamine, and their combination on pain and sensory thresholds., 2008

2014-04-03T08:27:08 - virginia bobbio
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