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Phantom Limb Pain

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Marcos Mills

on 14 November 2013

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Transcript of Phantom Limb Pain

What is it ?
Phantom Limb Pain is defined as being the sensation of pain that comes from a part of the body that is no longer there.

It is typically described as being stabbing, sharp, burning, squeezing or throbbing.

First described in 16th century by Ambrose Pare, a French military surgeon. The term itself was coined by Silas Mitchell, a famous Civil War surgeon. It remains a poorly understood and difficult to treat condition.
Mechanism of Pain
PLP once thought to be primarily a psychiatric illness. The paradigm has now shifted more towards changes at several levels of the neural axis, especially the cortex. Important to note, none of these constructs are able to fully explain PLP independently, and it is likely that multiple mechanisms are responsible. Proposed mechanisms include:
1. Peripheral Mechanism
2. Central Neural Mechanisms
3. Psychogenic Mechanism
The probable outcome of phantom limb pain is poorly understood. It is thought that phantom limb pain reduces or vanishes in most cases in the two years following amputation. However, persistent phantom limb pain may occur in approximately 5% of amputees. Even in these persistent cases, the pain usually becomes less severe over time.

Phantom Limb Pain
What it is NOT
Phantom limb pain should not be confused with "Phantom Limb Sensation," which is a painless phenomenon which may include feelings of warmth, cold, itchiness or tingling.

It is also not local pain of the soft tissues that are still present, which is important to differentiate.
Other Characteristics
Phantom limb sensation may be present as a result of spinal cord injury, amputation, or congenital deficiency.
Phantom pain is almost exclusively experienced after amputation.
Onset is usually within the first few days of amputation. Peak periods of pain tend to be within a month and the second year after amputation.
Tendency to come and go rather than be constant.
Usually affects the part of the limb that is farthers from the body.
May be triggered by weather changes, pressure on the remaining part of the limb, or emotional stress.
Can be present following amputation of different body parts, including eyes, teeth, tongue, nose, breast, penis, bowel, and bladder...but most common occurrence is following limb amputation.
A recent study estimated there were about 2 million people with limb loss in USA . This number has been projected to increase by more than double by the year 2050.

The incidence of PLP has been reported to range from 42.2-78.8% in patients requiring amputation.
Upper extremity amputation
Presence of pre-amputation pain
Residual pain in remaining limb
Time after amputation
Severity and duration of pre-amputation pain seem to be greatest predictors.
Peripheral Mechanism
The CNM is explained in terms of changes at the level of the spinal cord and changes at the level of the brain.

Central Neural Mechanism
During amputation, peripheral nerves are severed resulting 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 which have an increased expression of sodium channels resulting in hypre-excitability and spontaneous discharges. This abnormal peripheral activity is thought to be a potential source of PLP.

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
Psychogenic Mechanism
The assumption that PLP is of psychogenic origin has not been supported in the recent literature even though stress, anxiety, exhaustion, and depression are believed to exacerbate PLP. Most research on the relationship between psychological symptoms and PLP has been retrospective and cross sectional rather than longitudinal and thus limited inferences can be derived from these studies.

Risk Factors
Spinal Cord
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 areas of spinal cord that are not responsible for pain transmission also sprout into 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, 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.
-Cortical Reorganization
: in recent years, probably the most cited cause. During reorganization, cortical areas representing missing extremity are taken over by neighboring representational zones both in somatosensory and motor cortex. This explains why afferent nociceptive stimulation of neurons within stump or surrounding area produces the sensations felt. Extent of reorganization is 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.

-Body Schema
: A template of the whole body exists in the brain, and any change to the body can result in the perception of PLP. Further expanded as the "neuromatrix and neurosignature" hypothesis which conceptualizes that a network of neurons integrates all the inputs (somatosensory, limbic, visual, etc). It then results in an output pattern that evokes pain or other experiences. The deprivation of inputs from the limbs to the matrix causes an abnormal signature to be produced, which results in the generation of PLP.

-Illusory Perceptions
: It has been shown that the parietal and the frontal lobes are also involved in the perception of abnormal somatosensory phenomenon. Painful sensations, like PLP, may be the result of the incongruence of motor intention and sensory feedback and a corresponding activation of the parietal and frontal brain areas.
1. Pharmacotherapy
2. Surgical/Invasive Procedures
3. Adjuvant Therapy
(morphine, tramadol)
Tricyclic Antidepressants
(Amitriptyline, Nortriptyline, Imipramine)
(Carbamazepine, Gabapentin)
Sodium Channel Blockers
(Lidocaine, Bupivacaine)
NMDA Receptor Antagonists
(memantine, ketamine)
Propranolol (unknown mechanism)
Nifedipine (unknown mechanism)
Calcitonin (unknown mechanism)
Surgical/Invasive Procedures
Stump revision
Nerve block
Spinal cord stimulation
Deep brain/thalamus stimulation
Cortical Stimulation
Adjuvant Therapy
Mirror Therapy
Transcutaneous nerve stimulation
Sensory Discrimination training
Prosthesis training
Cognitive behavioral pain management
Electroconvulsive therapy
Mirror Box Therapy
The patient watches the reflection of their intact limb moving in a mirror between their arms or legs while simultaneously moving the phantom hand or foot in a manner similar to what they are observing so that the virtual limb replaces the phantom limb. Studies have shown the existence of mirror neurons in the brain which fire both at times when an animal performs an action or observes an action. Similar homologous neurons have also been discovered in humans. 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 in the mirror. Since the activation of these mirror neurons modulates somatosensory inputs, their activation may block pain perception in the phantom limb
PLP is a relatively common and disabling entity. Much has been learned much about the pathophysiology and management of PLP since it was first described about five centuries ago. However, there is still no one unifying theory relative to the mechanism of PLP. Specific mechanism-based treatments are still evolving, and most treatments are based on recommendations for neuropathic pain. The evolution of the mechanistic hypothesis from body schema and neuropathic theories to the recently proposed role of mirror neurons in the mechanism of pain have added to our understanding of PLP. Further research is needed to elucidate the relationship between the different proposed mechanisms underlying PLP. A synthesized hypothesis explaining the phenomenon of PLP is necessary in the future for the evolution of more specific mechanism-based treatment recommendations.

Pharmacologic Treatments Note
Of all these options, the most frequently prescribed medications for phantom pain includes tricyclic antidepressants, anticonvulsants, and opioids.
There is insufficient evidence to support the broad efficacy of any of these options.
Most of the positive results seen in literature are to be interpreted with caution, since a majority of the studies are based on limited sample sizes and lack of long-term efficacy and safety outcomes.
Pharmacologic therapy should be tailored to each individual patient based upon their unique complaints and circumstances.

In the News
Makin's study focused on the lingering representation of the limb itself. Makin's interpretation of her results is that the experience of pain is causing the brain reorganization rather than brain reorganization causing the pain.

But physiotherapist Lorimer Moseley of the University of South Australia, who was not involved in the study, disagreed. The two explanations of phantom pain are different paradigms, Moseley said — "there is no reason to suggest that one is true and the other is not." However, he challenged the interpretation that the pain causes the brain remapping, because the experience of pain arises from the brain, he said.

The problem, Moseley said, is the study shows that pain and remapping are correlated, but does not show that one causes the other.

What is it ?
Final Thoughts
Full transcript