Phantom Limb Pain

Original Editor - Peter Le Feuvre as part of the World Physiotherapy Network for Amputee Rehabilitation Project

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Introduction

Phantom limb pain (PLP) is defined as "pain that is localised in the region of the removed body part". It is a poorly understood clinical phenomenon that remains the subject of intense research due to the acute and chronic nature of the condition. The incidence is reported to be as high as 60-80% in patients post-amputation and risk factors include chronic pre-amputation pain, post-operative surgical pain and psychological distress.

• Phantom pains often described as crushing, toes twisting, hot iron, burning, tingling, cramping, shocking, shooting, “pins & needles”
• Tends to localise to more distal phantom structures (e.g. fingers and toes)
• Prevalence in early stages 60-80%
• Independent of age in adults, gender, level or side of amputation

Phantom sensation

Individuals with amputation may also experience phantom sensation, which is different from PLP. Phantom sensation is almost universal and doesn't correlate with pain reports. There are three types of phantom sensations:

• Kinetic (movement)
• Kinesthetic (size, shape, position)
• Exteroceptive (touch, pressure, temperature, itch, vibration)

Onset

Onset is mostly immediate after amputation, some at a few weeks, rarely months later. A US study has found that for 3 to 4% percentage of individuals with amputation, onset of PLP occurred more than a year after amputation. One-third of patients experience maximal symptoms immediately post-op and generally resolved by 100 days, a half experience pain that slowly peaks and is improved within 100 days, a quarter of patients experience a slower rise towards maximal pain.

Natural history

PLP tends to diminish in severity and frequency over time, with resolution over several weeks to 2 years. One study showed 72% had PLP at 8 days, 65% at 6 months, 59% at 2 years. Also, the duration of episodes vary.  One study showed continuous PLP in 12%, days 2%, hours 37%, seconds 38%), 50% had decreasing PLP with time, 50% no change or increase over time.

Aetiology

There are numerous theories about the causes of phantom limb pain including peripheral, central and spinal theories:

Peripheral Theories

• Remaining nerves in the stump grow to form neuromas, which generate impulses. These impulses are perceived as pain in the limb which has been removed.
• After changes in the severity of phantom limb pain were noted in different temperatures, another theory says that cooling of the nerve endings increases the rate of firing of the nerve impulses, which are perceived by the patient as phantom limb pain

Central Theories

• Melzack proposed that the body is represented in the brain by a matrix of neurons. Sensory experiences create a unique neuromatrix, which is imprinted on the brain. When the limb is removed, the neuromatrix tries to reorganise, but the neurosignature remains due to the chronic pain experienced prior to the amputation. This causes phantom limb pain after amputation.

Spinal Theories

• When peripheral nerves are cut during amputation, there is a loss of sensory input from the area below the level of amputation. This reduction in neurochemicals alters the pain pathway in the dorsal horn

Drivers and treatment options

When PLP is present it is important to establish the principle driver(s). These may be centrally driven adaptation, peripheral sensitisation, mental state or social concerns, and musculoskeletal factors. Treatment should target these drivers.

Potential drivers of PLP and treatment options (please note this is not a conclusive list, but the table should stimulate ideas)

	Treatment options	Drivers
Central Adaptation	Mental imagery (also included within GMI) Graded Motor Imagery (GMI) (incl. mirror therapy) Anti-neuropathic medication/opioids Physical exercise/limb mobility Prosthetic use Acupuncture/TENS Machine Irritant management Self massage Education	PLP appears to coexist with a reorganisation of the cortical map. For example, in upper limb amputees, the greater the shift of the mouth and face representation into the deafferented hand and arm amputation zone, the greater the PLP. Stimulation of facial muscles, including mastication or eye movements, will then elicit PLP. In lower limb amputations this phenomenon can manifest in the migration of the representation areas for the bladder, bowel and genitals into the amputation zone. Again, stimulation of these organs will elicit PLP.
Peripheral Sensitisation	Irritant management with attention to excluding differential diagnosis, poor wound dressings, stump oedema. Pharmacology: Follow the pain ladder Stump sock/juzo/relax sock Education Prosthetic (if applicable): Ensure good alignment and fitting. Scar management Self massage/desensitisation Acupuncture/TENS Machine Sleep hygiene	Nociceptive input from the residual limb appears to correlate with the level of PLP. The dorsal root ganglion can amplify discharge from the residual limb or cross-excite neighbouring neurons. Increased circulating epinephrine resulting from sympathetic discharge will also trigger or exacerbate neuronal activity. Such sympathetic discharge can result from emotional distress, and may also be due to temperature or inflammation. Continued nociceptive stimulation will cause the peripheral nervous system to become more efficient at transmitting these signals and in turn contribute to neuropathic excitation.
Psychological and Social Factors	Education Sleep hygiene Acupuncture Physical exercise Relaxation techniques CBT Referral for formal mental health/social support	Is pain influenced by memory of the incident, memory of pain proceeding the amputation, mood state, social concerns or sleep pattern? Circulating epinephrine resulting from emotional distress can contribute to the sensitisation of the peripheral nervous system.
Musculoskeletal (MSK) Factors	Joint ROM/muscular Maintenance of control and function of the limb by working segmental stabilisers as well as global mobilisers. Trigger points/myofascial release Neural mobilisation	Joint dysfunction and MSK referral can contribute to the presence of PLP. In addition, prosthetic use significantly aids the resolution of PLP, especially with the upper limb. Preparatory work to ensure the maintenance of joint range, normal symmetrical movement and proximal stabilisation will aid prosthetic fitting and successful use, This will potentially enhance the beneficial effect of limb wearing upon PLP.

Resources

• Khan TW, Braun EE. Phantom Limb Pain. Encyclopedia of Trauma Care. 2015:1235-40.
• Odell R.H., Sorgnard R, Mile R.D., Cary R.M. Novel Treatment Device for Phantom-Limb Pain
  This case report describes the use of a promising and relatively new electric cell signaling treatment device for phantom limb pain.
  Practical Pain Managment Vol 15 #4.
• Mayo Clinic. Phantom limb pain.
• Amputee Coalition. Phantom limb pain.
• Finn SB, Perry BN, Clasing JE, Walters LS, Jarzombek SL, Curran S, Rouhanian M, Keszler MS, Hussey-Andersen LK, Weeks SR, Pasquina PF. A randomized, controlled trial of mirror therapy for upper extremity phantom limb pain in male amputees. Frontiers in neurology. 2017 Jul 7;8:267.
• Preißler S, Thielemann D, Dietrich C, Hofmann GO, Miltner WH, Weiss T. Preliminary evidence for training-induced changes of morphology and phantom limb pain. Frontiers in human neuroscience. 2017 Jun 20;11:319.
• Rothgangel A, Braun S, Witte L, Beurskens A, Smeets R. Development of a Clinical Framework for Mirror Therapy in Patients with Phantom Limb Pain: An Evidence‐based Practice Approach. Pain Practice. 2016 Apr 1;16(4):422-34.
• Pinto CB, Velez FG, Bolognini N, Crandell D, Merabet LB, Fregni F. Optimizing Rehabilitation for Phantom Limb Pain Using Mirror Therapy and Transcranial Direct Current Stimulation: A Randomized, Double–Blind Clinical Trial Study Protocol. JMIR research protocols. 2016 Jul;5(3).
• Kikkert S, Mezue M, Slater DH, Johansen-Berg H, Tracey I, Makin TR. Motor correlates of phantom limb pain. cortex. 2017 Oct 1;95:29-36.