central sensitization clinical implications for chronic head and neck pain n.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Central Sensitization: Clinical Implications for Chronic Head and Neck Pain PowerPoint Presentation
Download Presentation
Central Sensitization: Clinical Implications for Chronic Head and Neck Pain

Loading in 2 Seconds...

play fullscreen
1 / 45

Central Sensitization: Clinical Implications for Chronic Head and Neck Pain - PowerPoint PPT Presentation


  • 66 Views
  • Uploaded on

Central Sensitization: Clinical Implications for Chronic Head and Neck Pain. Arthur S. Roberts DDS, MD, MSc Indiana Craniofacial Center, PC Indiana University School of Dentistry Oral Medicine University of Edinburgh College of Medicine and Veterinary Medicine Pain Management. DISCLOSURES.

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Central Sensitization: Clinical Implications for Chronic Head and Neck Pain' - shakti


Download Now An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
central sensitization clinical implications for chronic head and neck pain

Central Sensitization: Clinical Implications for Chronic Head and Neck Pain

Arthur S. Roberts DDS, MD, MSc

Indiana Craniofacial Center, PC

Indiana University School of Dentistry

Oral Medicine

University of Edinburgh

College of Medicine and Veterinary Medicine

Pain Management

disclosures
DISCLOSURES
  • Innovative Health Solutions
  • American Academy of Pain Management
prototype
Prototype
  • 35-55 y/o female
  • Extensive PMH
  • Multiple prior providers
  • Polypharmacy
  • Often hypervigilant
  • Either non-communicative or circumstantial
  • May be none of the above!!!
chronic p ain i s n ot a cute pain
Chronic Pain Is Not Acute Pain
  • Pathologic not protective
  • Multidimensional (Biopsychosocial)
  • Entangled via neuromatrix
  • Pan-Systemic
chronic pain implies an altered neuromatrix
Chronic pain implies an altered neuromatrix
  • “The neuromatrix, which is genetically determined and modified by sensory experience, is the primary mechanism that generates the neural pattern that produces pain. Its output pattern is determined by multiple influences, of which the somatic sensory input is only a part, that converge on the neuromatrix.”Melzack2001

* Emphasis added

central sensitization
Central Sensitization
  • “Sensory-afferent signals overwhelm the body's ability to filter them”[1,2]
    • neuro-immune dysfunction,
    • neuro-endodrine dysfunction
    • NMDA (N-methyl-D-aspartate) dysregulation
    • Sympatho-afferent coupling
    • Altered serotonin and norepinephrine production and utilization

Melzach, Woolf 2001

common cs symptoms
Common CS symptoms
  • Depression
  • Anxiety
  • Sleep fragmentation
  • Allodynia
  • Hyperalgesia
  • Fatigue

[1,3-5]

two etiological p athways
Two Etiological Pathways
  • Chronification of nociceptive pain
    • Neuroplastic changes
    • Peripheral sensitization
    • Central sensitization
  • Chronic stress
    • Elevated levels of chronic stress
    • Anxiety
    • Sleep fragmentation
    • Decreased pain thresholds
    • Dysautonomia
slide11

Etiology of CSS

  • Genetic predisposition
  • Environmental
    • Trauma
      • Physical
      • Psychological
    • Infectious
      • Lyme disease
      • Chronic EBV
      • Parasites
    • Toxins
      • Heavy metal
      • Biotoxins
    • Medications
  • Sleep disturbances
    • Sleep apnea
    • Circadian rhythm disorders
  • Metabolic
    • Thyroid disease
  • Autoimmune
    • Celiac disease
slide12

Dysregulation of the hypothalamic pituitary adrenal axis

Damage to hippocampal neurons and reduced neurogenesis

  • Disruption of the normal circadian cycle
  • Reduced basal cortisol levels

Kaplan 2013

slide13

Depression and chronic pain share common neurophysiology and neurobiology. They are mutually reinforcingneuropathologicprocesses.

  • Bimodality
  • Pain
  • Depression

Kaplan 2013

slide14

Common genetic vulnerabilities

  • Common neurobiology
    • Neuroanatomy
    • Neuroendocrinology
    • Neuroimmunology
    • Neurotransmitters
from cs to css
From CS to CSS

Microglial Activation

slide16

Microglia Activation

Neurodegenerative Diseases

Ischemia

Hypoxia

Infections

Medication

Trauma

Toxins

Kaplan 2013

slide17

Central Sensitization Syndrome

CSS = Chronic Pain + Neuropsychiatric Condition

  • Neuroinflammatory
  • Neurodysregulatory
  • Neurodegenerative

Kaplan 2013

slide18

50% to 65%

1,2,3,4,5,7,9,11

slide19

When depression and chronic pain occur together, treatment success is dramatically lower and cost is dramatically higher than when these conditions occur separately.

central sensitization syndromes css
Central Sensitization Syndromes (CSS)

Adapted from Wallace and Clauw [2]

Tension-type HA

Migraine

Limb Movement Disorder

Fibromyalgia

Restless Leg Syndrome

Chronic Fatigue Syndrome

TMD

Atypical Odontalgia

Burning Mouth Syndrome

Post Traumatic Stress Disorder

Depression

Primary Dysmenorrhea

Irritable Bowel Syndrome

Multiple Chemical Sensitivities

Myofascial Pain Syndrome

characteristic sequelae central sensitization
Characteristic sequelae central sensitization
  • Vagal dysregulation [7, 18, 20]
  • Sympatho-afferent coupling of sensitized trigeminal complex [6,21-25]
  • Decreased medullary descending inhibition [8,11,12,15-17,23,26-32]
  • Hypoactivity of the hypothalamic-pituitary-adrenal axis
    • Autonomic nervous system alterations
      • Increased sympathetic tone
      • Low vagal tone

[5,12,14,20,21,23-25,33-38]

vagal dysregulation
Vagal dysregulation
  • Reduces endorphin release
  • Alters serotonin production and utilization
    • Altered accommodation of minimally painful events
    • Contributes to depression

[7, 18, 20]

sympatho afferent coupling
Sympatho-afferent coupling
  • Sensitized trigeminal complex
  • Lowered parasympathetic drive
  • Increased sympathetic drive
    • Altered norepinephrine levels
    • Dysfunctional sleep
    • Anxiety

[6,21-25]

decreased medullary descending inhibition
Decreased medullary descending inhibition
  • Increases effect of peripheral nociceptive input
    • Lowered pain thresholds
    • Hyperalgesia,
    • Allodynia
    • Greater impact of peripheral sensitization

[8,11,12,15-17,23,26-32]

hypoactivity of the hypothalamic pituitary adrenal axis
Hypoactivity of the hypothalamic-pituitary-adrenal axis
  • autonomic nervous system alterations
  • increased sympathetic tone
  • low vagal tone
  • Immune abnormalities
  • Fatigue
  • Malaise

[5,12,14,20,21,23-25,33-38]

indicators for central sensitization
Indicators for central sensitization.
  • depression
  • anxiety
  • hyperalgesia
  • allodynia
  • stress related pain exacerbation
  • fatigue
  • poor sleep
therapeutic problems
Therapeutic Problems
  • Polypharmacy
  • different prescribing specialists
  • iatrogenic contribution
    • failing to differentiate chronic from acute pain
  • Symptomatic - Acute symptoms of CSS disorders need to be addressed
  • Syndromic - Essential to treat the pathways in chronic pain disease

[2,5,7,8,13-15,17,19,20,32]

two approaches to css therapy
Two approaches to CSS therapy
  • Symptomatic approach: Address the effects of CS after it has occurred
  • Syndromic approach: Interrupt the CS
  • Optimal outcomes often depend on doing both.
    • Pharmacological
    • Non-pharmacological

[1,4,6,8,13,14, 40-44]

pharmacological approaches
. Pharmacological Approaches
  • Treating the effects
    • Acetaminophen
    • Serotonin (SSRI) and norepinephrine (SNRI) reuptake inhibitors and tricyclic antidepressants (TCA)
    • Opioids and Tramadol
  • Drugs that may treat the central sensitization itself:
    • N-methyl-D-aspartate (NMDA) receptor blockers
      • Namenda, Ketamine, Memantine
    • Calcium channel alpha(2) ligands
      • Gabapentin, Lyrica
non pharmacological approaches npt
Non-pharmacological Approaches (NPT)
  • Each element of neuromatrix is potential therapeutic target
  • Two broad operative groups:
    • Reducing CS itself
    • Responding to the effects of CS
repetitive transcranial magnetic stimulation rtms
Repetitive Transcranial Magnetic Stimulation (rTMS)
  • Safe and non-invasive
  • Stimulation of the motor cortex and prefrontal cortex
  • Limited application
    • Short duration of effects
    • Significant equipment costs
    • Greater efficacy in centrally, rather than peripherally, originated pain
    • Reverses intra-cortical motor dysfunction
    • Alters sensory-discriminative function
    • Restores of descending inhibition
    • Improves cognitive function [56,57]
    • Some investigators argue that the analgesic effects are independent of descending inhibitory control and are influenced by other elements of the neuromatrix [58]
manual therapy
Manual Therapy
  • Improves function
  • Improves descending inhibition
      • Widespread analgesia.
      • Short duration
      • Limited assistance in desensitizing the neuromatrix
      • Addresses functional rehabilitation

[4,13,60-64]

virtual reality
Virtual Reality
  • Limited evidence
  • Distraction in the hyper-vigilant patient
  • Potential benefit in patients with movement associated nociceptive etiology
  • Not in widespread use

[13,65]

improving stress tolerance and neuro feedback training
Improving Stress Tolerance and Neuro feedback Training
  • Stress
    • Etiologic and exacerbating factor for CS
    • Endogenous (chronic pain)
    • Exogenous (psychosocial changes)
    • Irritable, hyper-excitable chronic pain patient
    • Related to sympatho-afferent coupling in the hypothalamic-pituitary-adrenal axis of the neuromatrix.
    • neuro-immune changes from upregulated pronociceptive immune mediators in primary afferent nociceptors
  • Reduction of stress levels improves:
      • Pain threshold
      • Maladaptive behavior
      • Autonomic balance

[12,14,17,35,36,66-68]

transcutaneous electrical nerve stimulation
Transcutaneous Electrical Nerve Stimulation
  • Activates poly-segmental inhibitory feedback
  • Significant effect with focal, segmental chronic pain
  • Results in widespread pain are equivocal

[13,40, 69-73]

percutaneous electroneural stimulation pens
Percutaneous Electroneural Stimulation (PENS)
  • Percutaneous stimulation of peripheral branches of multiple cranial and cervical nerves
      • Trigeminal, Vagus, Occipital
    • Discreet
    • Stimulates afferents
  • improved autonomic regulation
  • Improves centrally mediated pain
  • Improves sensory - discriminatory functions
  • serotonin/norepinephrine production and utilization
  • endorphin production
  • analgesia and mood improvement appears to follow a ‘learning curve’[59]
  • cost-effective, non-invasive, low co-morbidity option

[1,2,5, 6,8-10,12-15,20-23,25-28,42-44,53, 55]

once initiated central sensitization can engender additional presentations
Once initiated central sensitization can engender additional presentations
  • Increased frequency and intensity of pain
  • Increased endogenous stress levels
  • Increased sympatho-afferent coupling
  • Autonomic dysfunction
    • anxiety
    • poor sleep
    • difficulty coping
    • lowered pain thresholds
    • increased risk of developing additional presentations of CS
  • Persistent microglial inflammation

[2,74]

removal of the initiating stimulus will not insure favorable outcomes
Removal Of The Initiating Stimulus Will Not Insure Favorable Outcomes
  • Continuing stimulus for the development and/or maintenance of CS
    • Extended disease course
    • Additional CS presentations (syndromes)
    • Devolves to dealing with the effects of the CS rather than control or eradication of the CS [2,3,74]
stress induced cs
Stress Induced CS
  • No biological axis may exist in the early stages
    • Maladaptive behavior
      • Engender biological issues
      • Contribute to maintenance and exacerbation of CS
        • PTSD
        • Depression
    • HPA induced changes
    • Microglial activation
conclusions
Conclusions
  • Potentially progressive
  • Devastating
  • Multimodal disease
  • Worldwide economic and social burden
effective intervention
Effective intervention
  • Fundamental differences in acute and chronic pain
  • Effects on and by the neuromatrix
  • biopsychosocial health of the individual patient
  • Integrate a comprehensive multidisciplinary therapeutic plan
slide43

The comorbidity of neuropsychiatric disease (depression, GAD, PTSD) and chronic pain are common.

slide44

When depression and chronic pain occur together, treatment success is dramatically lower and cost is dramatically higher than when these conditions occur separately.