Phantom Limb Pain: - PowerPoint Presentation

Slide1

Phantom Limb Pain:

Current Theories and Evidence Based Treatments

Christopher V Boudakian, DO PGY-4

Rusk Rehabilitation

NYU

Langone

Medical CenterSlide2

ObjectivesIdentify the definition and characteristics of phantom painUnderstand the current theories in the etiology and pathophysiology of phantom painIdentify current evidence-based treatments for phantom painSlide3

What is phantom limb pain?The concept, first introduced by French military surgeon Ambrose Pare in the mid 16th century, is pain that is perceived in a region of the body that is no longer present.Later expanded by Silas Weir Mitchell in the mid 19th century who coined the term “phantom pain”

Traditionally described as two separate phenomenaPerhaps a spectrum disorder?In 1998, Weinstein proposed phantom sensations can be divided into 3 categories: kinetic sensations, kinesthetic components, and

exteroceptive

perceptionsSlide4

3 categories of sensationKinetic sensations are the perception of movement, both spontaneous and willedKinesthetic components refer to the size, shape, and position of the missing body partExteroceptive perceptions include touch, pressure, temperature, itch, and vibrationPain described in this category, however, distinguished by greater intensitySlide5

Characteristics of phantom painSeen in both patients with congenital and acquired limb deficiency.***Symptoms not limited to the limbsReports of phantom sensations and pain emanating from less common regions of the body including breast, nose, teeth and also visceral organs including rectum, uterus, and bladder.Recent studies report 50 to 85% of patients with limb loss experience phantom pain.

This is in contrast to earlier studies which report rates under 10% Incidence rates have been shown to be independent of gender, age, and location/level of amputation.Not likely affected by mechanism, elective vs

traumatic

1Slide6

Characteristics of phantom painCorrelations with residual limb pains remain unclearKooijman et al. (2000) and Nikolajsen et al. (1997) reported positive correlation between phantom pain and residual limb pain.

Estimates show 50% of people with acquired amputations experience phantom pain in the first 24 hours and an additional 25% in the in the first week following limb loss1Uustal and Meier report most people with amputations do not experience significant pain beyond 3 months.Slide7

Characteristics of phantom painOften described as burning, cramping, electrical shocks, severe itching, or stabbingEpisodes may last seconds to hours.Slide8

Theories of phantom painDespite numerous attempts to classify and define phantom pain, the pathophysiology and etiology of the condition remain unclear.Both central and peripheral theories have been proposed.Likely multifactorialSlide9

Central Nervous System TheoriesRevolves around the concept of neuroplasticity and cortical reorganization.Areas representing the amputated body part are taken over by neighboring representational zones in both the somatosensory and motor cortexExtent of remapping proportional to intensity of painSlide10

Central Nervous System TheoriesBody schema theory postulated by Head and Holmes in 1912, later expanded by Melzack and termed neuromatrix theoryInvolves the internal representation of spatial and biomechanical processes reflecting in bodily experience

Damage within any of the systems involved result in perceptual distortionNeuromatrix theory adds to this by including cognitive and emotional factors.Neurosignature refers 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.

Deprivation of various inputs from the limbs to the

neuromatrix

cause an abnormal

neurosignature

to be producedSlide11

Peripheral Nervous System TheoriesReinforced by correlation between residual limb pain and phantom painMechanism remains unclear, however, it is postulated phantom pain may stem from neuromas formed at the site of amputationNeuromas may exhibit abnormal activity following mechanical or chemical stimulation generating ectopic impulse discharge

Ectopia may drive neuroplasticity and sensitization leading to increased sympathetic tone that serves as a feedback loop to maintain phantom painPain is not consistently abated with neuroma or nerve/plexus blocks

Vaso

et al. (2014) propose the dorsal root ganglia, which remain intact after amputation may also be implicated in pain due to

ectopiaSlide12

Multifactorial TheoryRamachandran and Hirstein (1998) propose that there are at least 5 different sources that contribute to phantom pain:Residual limb neuromas

Cortical remappingCorrollary dischargeBody image

Somatic memories

All 5 components may work together and reinforce each otherSlide13

Treatment optionsLimited options without clear consensus on an optimal regimenCommon pharmacological treatment includes opioids, anticonvulsants, lidocaine/mexiletine, clonidine, ketamine, amitryptaline

, NSAIDs, and calcitonin. Opioids bind to central and peripheral receptors providing analgesia without loss of touch, proprioception, or consciousness.Slide14

Pharmacological treatmentStudies demonstrate opioids may diminish cortical reorganizationHuse et al. (2001) small, double-blind crossover trial (n=12) showing evidence of reduced cortical reorganization with morphine leading to reduced pain.

McCormick et al. (2014) reports the best evidence in the literature for use of IV ketamine and IV morphine perioperatively and PO morphine for long term treatment, 8 weeks to 1 year

Level

2

evidence for gabapentin, both oral (PO) and intravenous (IV) morphine, tramadol, intramuscular (IM)

botulinum

toxin, IV and epidural

Ketamine

Level

3

evidence for amitriptyline, dextromethorphan,

topiramate

, IV calcitonin, PO

memantine

, continuous

perineural

catheter analgesia with

ropivacaine

L

evel

4

evidence for methadone,

intrathecal

(IT) buprenorphine, IT and epidural fentanyl, duloxetine, fluoxetine, mirtazapine, clonazepam,

milnacipran

, capsaicin, and

pregabalin

.

Sympathetic targets and NSAIDS have not been well studiedSlide15

TENSKatz and Melzack demonstrated significant pain relief in patients with the use of transcutaneous electrical stimulationRCT (1991) demonstrated significant decrease in pain with auricular TENSCarabelli and Kellerman (1985) showed pain relief with application of TENS to unaffected side in 3 patients, no return of symptoms at 6 month follow up

Finsen et al. (1988) performed a single–blinded trial (n=51) and found no significant difference in post operative or chronic limb pain with the use of TENS.Phantom pain after TENS was significantly lower between four months and one year follow up

Mulvey

et al. (2012) performed a pilot study demonstrating reduction of pain on movement and at rest in 10 subjects.Slide16

Implantable StimulatorsTemporary and immediate relief found by deep brain stimulation of the ventral caudal thalamic nucleus and posterior columns.Bittar et al. (2005) showed mean reduction of pain by 62% at one year follow up for 3 patientsPerreira and Boccard

(2013) demonstrated efficacy in 5 amputee subjects at one year.Spinal cord stimulation does not appear to help reliably decrease the intensity or frequency of phantom pain. Largest study performed by Broggi et al in 1996 (n=26), with 58% success rate at 2 year follow up.

With advances in spinal cord stimulators, recent literature is limited to case reports regarding use in phantom limb pain

Katayam

et al. (2001) studied the effect of SCS, DBS, and MCS on 19 patients with phantom pain

Satisfactory long term

pain control

was

achieved in 6 of 19 (32%) by SCS, 6 of 10 (60%) by DBS and 1 (20%) of 5 by MCS.

No evidence of an advantage of MCS over SCS and DBS of the thalamusSlide17

Other modalitiesAcupuncuture has demonstrated mixed and inconsistent results.Other treatments reported to have mixed results include anesthetic and surgical neuroablation as well as psychologic

interventionsVaso et al. (2014) demonstrated spinal and intraforaminal block (n=31) consistently attenuated, and often completely eliminated both phantom pain and sensation in lower limb amputeesSlide18

Mirror TherapyRamachandran et al. proposed the use of mirrors in 1996Patient views the reflection of their intact limb moving in a mirror placed strategically to mimic movement on the affected sideChan et al. (2007) performed a randomized, sham-controlled crossover study showing significant decrease in pain for patients who underwent mirror therapy in comparison to 2 control groups

mental visualization was ineffective and may actually worsen painRamachandran poses that the mirror resolves the visual-proprioceptive dissociation proposed as an explanation for phantom pain.

Mechanism

remains unclearSlide19
Slide20

Mirror TherapyRizollati et al. (2006) demonstrated the existence of “mirror neurons” in macaques that fire both when the animal performs an action, as well as when it observes the same action performed.Ramachandran et al. (2008) further demonstrated that touching the virtual image in the mirror is sufficient to elicit tactile sensation in the phantom limb

Activation of mirror neurons modulates somatosensory inputs and may block pain perception in the phantom limb.Slide21

Mirror TherapyDeconinck et al. (2014) performed a systematic review to asses the effect of mirror therapy on brain activation during a motor taskMirror therapy increases neural activity in areas involved with allocation of attention and cognitive control (dorsolateral prefrontal cortex, posterior cingulate cortex, S1 and S2, precuneus). Evidence for ipsilateral

projections from the contralateral M1 to the untrained/affected hand as a consequence of training with mirrorsApart from activation in the superior temporal gyrus and premotor cortex, there is little evidence it activates

the mirror neuron system

.

Mirror therapy can

exert a strong influence on the motor network, mainly through increased cognitive penetration in action

control.

Variance

in methodology and the lack of studies that shed light on the functional connectivity between areas still limit insight into the actual underlying mechanismsSlide22

Conclusion Further research is needed to determine the relationship between proposed mechanisms of phantom painTreatment plan should be targeted to symptoms as well as underlying mechanismsSlide23

Thank YouSlide24

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McCormick et al. “Phantom limb pain: A Systematic Neuroanatomical-Based Review of

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preamputation

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