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Neuropathic Pain08

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  • 1. NEUROPATHIC PAIN R3 정고운
  • 2. I. Neuropathic Pain
    • Pain initiated or caused by a primary lesion or dysfunction of the nervous system
    • (eg, painful diabetic neuropathy, post-herpetic neuralgia)
  • 3.
    • Symptom
    • tactile allodynia(m/c)
    • Constant burning pain
    • Cramping /aching
    • Hyperpathia, hyperalgesia
    • Hyperesthesia
  • 4.
    • PERIPHERAL NEUROPATHIC PAIN
    • Due to anatomical,chemical or biochemical changes to peripheral nerves
    • Examples include: post-herpetic neuralgia,pain in HIV infections, trigeminal neuralgia, compression by a tumour , diabetic neuropathy, sciatica, post-surgery, following chemotherapy(eg vincristine), radiation
    • CENTRAL NEUROPATHIC PAIN
    • Due to pathophysiological changes in the brain or spinal chord ie the primary
    • lesion is in the CNS
    • Examples include phantom limb pain,pain following stroke, multiple sclerosis
  • 5. III. Pathophysiology
  • 6. Primary afferent neuronal mechanism
    • Ectopic activity votage gated NA+ channels 의 비정상적 증식
    • (neuroma) -> abnormal excitability
    • -> spontaneous sprouts
    • -> stimulate the connecting regenerative C-fiber
    • -> erratic impulse generation -> transmit to the CNS
    • -> dysesthesia, such as tingling, itching, electrifying sensitization
  • 7.
    • Abnormal expression of Na + channel - Increase density and up-regulation of Na channel(SNS(“sensory-nerve-specific, subtype α -Ⅲ(embryonic))
    • - action potential threshold ↓ & spontaneous ectopic discharge ↑ - fast recovery following inactivation - repetitive firing of injured neuron was facilitated
    • at low threshold (ectopic impulse generation)
  • 8.
    • Sensory-sympathetic coupling - noradrenaline released from near by sympathetic efferent fibers binds to α adrenoreceptors
    • on the injured afferent neuron & increased sensitivity
    • - causalgia - sympathetic block -> pain 감소 - sympathetic stimulus -> pain 증가
  • 9.
    • Ca channels in injured nerve endings
    • - entry of Ca ion into the nerve endings
    • N- or L type calcium channel -> calcitonin gene related peptide from injured nerve endings
    • - CCBs are effective to block neuropathic pain
  • 10.
    • Neuroimmune interaction - nerve injury -> MØ -> TNF α & IL1ß -> ectopic activity, inflammatory hyperalgesia
    • - higher TNF α immuoreactivities
  • 11.
    • Phenotypic change - DRG neuron - A-ß fiber (non-noxious) ->substance P (pronociceptive) / neuropeptide (antinociceptive) 生
  • 12.
    • Pathologic interaction c C & A-ß fiber - nerve injury -> disruption of glial ensheathment -> cross-excitation ∴ A-ß fiber (tactile) ↔ C fiber (noxious)
  • 13. Spinal mechanism
    • Central reorganization - small-diameter aff.(C fiber) -> superficial dorsal horn (lamina I/II) -> noxious stimuli - large-diameter aff.(A-ß fiber) -> deep dorsal horn (lamina III/IV) -> tactile stimuli - nerve injury 시 C fiber degeneration & A-ß fiber growth to lamina I/II
  • 14.
    • Disinhibition - inefficiency of endogenous inh. Sys.
    • continuous inhibitory control of brainstem ↓
    • loss of A- δ fiber
    • induce GABAnergic inhibitory interneuron apoptosis
    • transynaptic neural degeneration
    • (GABA receptor ↓ , opioid receptor ↓ )
  • 15.
    • Central sensitization
    • repetitive noxious stimulation leads to the increased activities of asparate & glutamte at NMDA & neurokinin 1 receptor
    • increased inctracellular CA & activation of PKC
    • -> activate DHC, phosphorylation of NMDA rec.
    • -> causes decreased Mg blockade at phys. resting potential
    • exp. Of c-fos -> neuropeptides -> central plasticity
  • 16. IV. Treatment
  • 17.  
  • 18.
    • Stimulation dependent pain (evoked pain)
    • pph. sensitization :
    • - local anesthetics( lidocaine patch 5%)
    • - capsaicin
    • abnormal exp. of Na channel
    • - antiepileptic, anticonvulsant, anti arrhythmic,
    • TCA(amitriptyline)
    • central sensitization
    • - Na channel blocker, local anesthetics
  • 19.
    • Stimmulous independent pain
    • Paresthesia & dysesthesia : spont. firing of A fiber
    • -> Na channel blocker
    • Peripheral sensitizaion, disinhibition, causalgia
    • -> local anesthetics, capsaicin, Na channel blocker, gabapentin, baclofen, clonidine
  • 20.  
  • 21. * Opiates
    • - - C fiber 에는 효과 & A-ß fiber 에는 효과 X < 용량 > - neuropathic>>nociceptive - center ↑: effect↓ - rotation 고려 - morphine : 300mg, oxycodein : 240mg, methadone : 80mg (sustained-release) fentanyl : 100 μ g (transdermal)
  • 22. * α 2 agonist
    • - opioid 와 작용 비슷
    • - sympathetic block -> opioid 보다 효과적 < 용량 > - clonidine : transdermal patch -> systemic delivery -> intraspinal delivery - intraspinal delivery : hypotension 주의
  • 23. * NMDA antagonist
    • - NMDA ionopore : glutamate (nerve injury 시 ↑ ), Mg 2+ , glycine, polyamine binding -> ionopore opening -> Ca 2+ influx < 용량 > - ketamine : 2~6 mg/kg/d(IV), 100~500mg/d(orla)
  • 24. * COX inhibitor & PG receptor antagonis
    • - tissue injury 시 PG release ↑ - ketorolac,parecoxib
  • 25. * Na + channel blocker
    • - nerve injury 시 ↑ < 용량 > - lamotrigine (choice) : ~400md/d - mexilletine : ~1200mg/d - lidocaine : 1~3mg/kg/h - non selective block
  • 26. *Ca 2+ channel blocker
    • - L, N, P/Q, R ,T - high threshold : L(cell body & dendritie), N, P/Q, R (synaptic site) < 용량 > - ziconotide : #1 0.1 μ g/h, #2 0.2 μ g/h, #3 0.3 μ g/h, #4 0.6 μ g/h, #5 1.2 μ g/h, #6 2.4 μ g/h - non selective & dose limiting side effect
  • 27. *Gabapentin
    • - unknown mechanism < 용량 > - starting dose : 900mg/d (#3) -> 2700~3600mg/d
  • 28. * Antidepressant
    • - cathecholamine reuptake ↓ < 용량 > - by sleep disturbance & at bedtime - amitriptyline, doxepin >> nortriptyline, imipramine - starting dose : 10mg/d (>65) : 25mg/d (<65) -> 200~300mg/d