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Orofacial pain a neuropathic pain syndrome

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Nerve sprouting and neuroma. DRG: Sprouting of sympathetic fibres ... Astrocytes in spinal cord activated after sciatic nerve damage. Garrison et al 1991 ... – PowerPoint PPT presentation

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Title: Orofacial pain a neuropathic pain syndrome


1
Orofacial pain - a neuropathic pain syndrome?
Gunnvald Kvarstein gunnvald.kvarstein_at_rikshospital
et.no
2
Which specialist should treat facial pain?
  • Challenge to medical and dental professions.
  • The patients have multiple diagnoses, requiring
    management by multiple disciplines
  • Neurology
  • Otolaryngology
  • Dentistry
  • Psychiatry

3
Differential diagnosis
  • Atypical facial pain
  • Trigeminal neuralgia (primary or secondary?)
  • Horton's syndrome (cluster headache)
  • Temporomandibular disorders
  • Dental pain
  • Sinusitis
  • Cancer
  • Cervical pain
  • Myofascial pain

4
Dental pain
5
Atypical odontalgia--a form of neuropathic pain
that emulates dental pain
  • Overtreatment - numerous invasive procedures
    and unnecessary treatment.
  • Dental extraction, injection or even the
    placement of a crown represents a tissue trauma
    and deafferentation.
  • A small percentage have a genetic predisposition
    to deafferentation pain.

6
Oral and maxillofacial surgery in patients with
chronic orofacial pain.
  • Pupulation 120 patients
  • Diagnoses
  • myofascial pain (50)
  • atypical facial neuralgia (40),
  • depression (30)
  • TMJ synovitis (14)
  • TMJ osteoarthritis (12)
  • trigeminal neuralgia (10)
  • TMJ fibrosis (2)
  • History of previous oral and maxillofacial
    surgical procedures (32).
  • Israel HA 2003

7
Oral and maxillofacial surgery in patients with
chronic orofacial pain.
  • Procedures performed
  • endodontics (30)
  • extractions (27),
  • apicoectomies (12)
  • temporomandibular joint (TMJ) surgery (6),
  • neurolysis (5)
  • orthognathic surgery (3)
  • debridement of bone cavities (2)
  • Surgery exacerbated pain in 55 of those operated
  • Israel HA 2003

8
Oral and maxillofacial surgery in patients with
chronic orofacial pain
  • Treatment recommendations
  • medications (91) TCA, anticonculsants, opioids?
  • physical therapy (36)
  • psychiatric management (30)
  • trigger injections (15)
  • oral appliances (13) (local anesthesia,
    capsaicain)
  • biofeedback (13)
  • acupuncture (8) TENS?
  • surgery (4)
  • Botox injections (1)
  • Israel HA 2003

9
Oral and maxillofacial surgery in patients with
chronic orofacial pain
  • Misdiagnosis and multiple failed treatments were
    common, and lead to sequelae, with delay of
    necessary treatment in 5
  • Surgery, may exacerbate the pain,
  • Surgery must be based on a specific diagnosis
    that is amenable to surgical therapy
  • Israel HA 2003

10
What is neuropathic pain (NP)?
  • Neuropathic pain initiated by a lesion or disease
    affecting parts of the nervous system that
    normally transmits pain related signals

11
Some characteristics of NP
  • The symptoms
  • Both stimulus independent and stimulus dependent
    pain
  • A delayed onset, but remain after healing
  • My change over time
  • Heterogeneous mechanisms not explained by a
    single etiology or a specific lesion
  • Difficult to treat, limited effect of TCA,
    anticonvulsants and opioids.

12
From simple sensory testing to Quantitative
sensory testing (QST )
  • Touch and Pin prik
  • Cold/heat
  • Pressure and vibration
  • Thermorollers (200C and 450C)
  • Von Frey hairs (standardized mechanical stimuli)
  • Hypo-/hyper- phenomena?
  • Temporal summation (response to repeated
    stimulation

Thermorollers
Von Frey hair Nylon filaments
13
Thermo test
Heat pain tolerance
Heat pain
Heat
Neutral
Cold
Cold pain
Patients respond to standardized thermal stimuli
14
Diagnostic dilemma
  • A specific symptom can reflect different
    pathophysiological mechanisms
  • To predict the underlying mechanism, we need a
    wider symptom profile and a battery of sensory
    stimuli.

15
Phenotypic mapping
  • Standardised QST protocol to determine the
    mechanisms and design a mechanism-based treatment
  • German Research Network on Neuropathic
    Pain, Baron R 2006

16
  • A standardized mapping of symptoms and signs
  • - to determine the mechanisms (target)
  • - to optimize therapy
  • Baron R.
  • Mechanisms of Disease ..
  • Nat Clin Pract Neurol 2006

17
Neuropathic pain based oncomplex mechanisms!
Central and peripheral mechanisms
18
Animal pain research- nerve injury models
provide new insight to the mechanisms
19
Mechanisms after a nerve injury
  • Peripherally
  • Nerve sprouting and neuroma
  • DRG
  • Sprouting of sympathetic fibres
  • Increased gene expression of ion-channels,
    transmittors and receptors
  • .
  • Decreased expression of opioid receptors.
  • Dorsal horn
  • Loss of inhibitory (GABA) interneurons
    (apoptosis)
  • Impaired central inhibition and increased central
    fascilitation

20
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21
New insight
  • Decreased function of unmyelinated fibres
  • Downregulation of
  • Nav1.8 channels
  • Bradykinin- (B2), substance P- and opioid-
    receptors
  • Increased function of myelinated fibres
  • Upregulation of
  • Ca a2d-1 channel subunits (gabapentin?)
  • Na 1.3 channels
  • Bradykinin (BK B1) and capsaicin (TRPV1)
    receptors
  • Future therapy Specific sodium channel blockers?

22
  • Ion channels and receptors are translocated to
    intact neurons
  • Na channels
  • TRPV1 (vanilloid)
  • adrenoceptors
  • Baron R 2006

23
Lysophosphatidic acid (LPA)
  • A small phospholipid
  • After tissue and nerve injury release from
    activated platelets, damaged nerve cells (cancer
    cells)
  • LPA activate LPA receptors (DRG) leading to
    demyelinisation and allodynia
  • In knockout mice (no LPA1 reseptor) or after
    pretreatment with antidot (AS ODN) no
    demyelinisation or allodynia

24
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25
Evidence for activated glia cells
  • Astrocytes in spinal cord activated after sciatic
    nerve damage
  • Garrison et al 1991

26
A close interplay
Glutamate
27
Marchand F et al Nature 2005
28
Are the activated glica cells neurodestructive?
  • Proinflammatory mediators lead to NP and
    allodynia
  • Antagonists of TLR4 (stopping cytokine
    production) reverses NP
  • Blocking glia activation a target for therapy?
  • Fluorocitrate, minicyclin, propentofylline
  • IL 1 beta and TNF a antagonists (Embrel)?

29
Marchand F et al Nature 2005
30
Opioids activate glia cells
  • TLR (toll like receptors) recognise opioids and
    release neuroexitatory pro-inflammatory cytokines
  • This counteracts opioid analgesia
  • Prevention of glial cell activation
  • enhances opioid analgesia
  • prevents opioid tolerance, depencence, withdrawal
    and respiratory depression!
  • Therapeutic target?
  • TLR antagonists (LPS- R/S naloxone)?

31
LPS
Naloxone
Marchand F et al Nature 2005
32
Glia activation - neurodestructive or
neuroprotective?
33
Glia cell activation neuroprotective?
  • Remove cell debris which prevents proinflammatory
    activation
  • Provide antiinflammatory cytokines IL2, IL4, and
    IL 10
  • Is blocking glial activation beneficial?
  • A neuroprotective activation the new target?
  • Cannabinoids (CB2) receptors on glial cells
  • Intrathecal administration IL-4 and IL 10
    suppresses chronic pain

34
Gene implantation the future treatment?
  • Implantation of cytokine genes may provide
    prolonged production
  • Genes enter the cell by endocytosis of a viral
    vector

Milligan 2009
35
At the time being
  • Keep the surgerions away!
  • Cognitive interventions
  • Symptomatic treatment?
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