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    Unit 58. Neuropathic Pain

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    sorin niky mocanu
    This document discusses neuropathic pain (NP), which is pain caused by damage or disease of the somatosensory nervous system. NP affects about 8% of the population. The principal mechanisms of NP include ectopic activity, peripheral and central sensitization, and impaired inhibitory modulation. Diagnosis relies on clinical criteria and screening tools based on pain descriptors. Treatment approaches include anatomic therapies to correct structural abnormalities, ablative therapies to interrupt pain pathways, and augmentative neuromodulation therapies like spinal cord stimulation. Specific types of orofacial NP are also discussed such as trigeminal neuralgia, peripheral neuritis, and postherpetic neuralgia.

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    Unit 58. Neuropathic Pain

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    sorin niky mocanu
    16 views26 pages
    This document discusses neuropathic pain (NP), which is pain caused by damage or disease of the somatosensory nervous system. NP affects about 8% of the population. The principal mechanisms of NP include ectopic activity, peripheral and central sensitization, and impaired inhibitory modulation. Diagnosis relies on clinical criteria and screening tools based on pain descriptors. Treatment approaches include anatomic therapies to correct structural abnormalities, ablative therapies to interrupt pain pathways, and augmentative neuromodulation therapies like spinal cord stimulation. Specific types of orofacial NP are also discussed such as trigeminal neuralgia, peripheral neuritis, and postherpetic neuralgia.

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    This document discusses neuropathic pain (NP), which is pain caused by damage or disease of the somatosensory nervous system. NP affects about 8% of the population. The principal mechanisms of NP include ectopic activity, peripheral and central sensitization, and impaired inhibitory modulation. Diagnosis relies on clinical criteria and screening tools based on pain descriptors. Treatment approaches include anatomic therapies to correct structural abnormalities, ablative therapies to interrupt pain pathways, and augmentative neuromodulation therapies like spinal cord stimulation. Specific types of orofacial NP are also discussed such as trigeminal neuralgia, peripheral neuritis, and postherpetic neuralgia.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    16 views26 pages

    Unit 58. Neuropathic Pain

    Uploaded by

    sorin niky mocanu
    This document discusses neuropathic pain (NP), which is pain caused by damage or disease of the somatosensory nervous system. NP affects about 8% of the population. The principal mechanisms of NP include ectopic activity, peripheral and central sensitization, and impaired inhibitory modulation. Diagnosis relies on clinical criteria and screening tools based on pain descriptors. Treatment approaches include anatomic therapies to correct structural abnormalities, ablative therapies to interrupt pain pathways, and augmentative neuromodulation therapies like spinal cord stimulation. Specific types of orofacial NP are also discussed such as trigeminal neuralgia, peripheral neuritis, and postherpetic neuralgia.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 26

    NEUROPATHIC PAIN

    MEDICAL&SURGICAL PATHOLOGY 1
    PAIN

    Pain : survival mechanism that warns of the presence of a


    persistent / imminent tissue damage

    • Neuropathic pain (NP) : pain provoked by damage or


    disease(s) of the somatosensory nervous system
    • NP affects about 8% of the general population
    PA I N A N D
    PA I N F I B E R S

    A-alpha : proprioception
    A-beta : touch
    PAIN GENERATION

    Transduction Transmission Transformation Perception


    • Conversion of • nociceptive signals • Modulation of signals • Integration of
    noxious stimuli to arrive to the CNS in the synapses cognitive and
    nociceptive signals through nerve fibres through facilitation affective responses
    and inhibition
    USEFUL DEFINITIONS FOR PAIN
    ASSESSMENT

    • Nociceptive pain : pain resulting from the activation of peripheral nerve endings
    that respond to noxious stimuli. Derives from potential or actual damage to non-
    neural tissue; can be visceral or somatic.
    • Allodynia : painful response to a normally innocuous stimuli
    • Deafferentation pain : condition that results from a partial/complete loss of
    sensory input from a part of the body after lesions in the somatosensory pathways,
    often resulting from reorganization in the CNS (eg. Phantom limb pain)
    • Neuroplasticity : changes in neural pathways that results form bodily injuries OR
    changes in behaviour, environment or neural processes
    Ectopic activity – hyperexcitability with spontaneous
    discharges in afferent neurons

    Peripheral sensitization – reduced activation


    threshold of primary afferent neurons

    PRINCIPAL Central sensitization – increase in excitability and


    MECHANISMS OF synaptic efficacy of neurons in central nociceptive
    NEUROPATHIC PAIN pathways
    Impaired inhibitory modulation

    Activation of microglial cells


    Anamnesis and clinical history

    Confirm the diagnosis of NP

    APPROACH TO
    NEUROPATHIC Rule out treatable conditions
    PAIN
    Identify clinical factors that can help individualize
    treatment

    Clos follow-up to identify response to treatment


    and change the strategy according to it
    NEUROPATHIC PAIN
    DIAGNOSIS

    • Diagnosis of pain relies on clinical criteria (no biochemical markers available)


    • Identification of pain descriptors suggestive of neuropathic pain :
    o Burning pain
    o Electric shock-like pain
    o Dysesthesia
    o Brush allodynia

    • Clinical screening tools (questionnaires) based on pain descriptors are used in daily
    clinical practice, with good sensitivity and specificity
    • Pain intensity assessment : visual analog or numerical scales
    Anatomic therapies : procedures that correct
    structural abnormalities that cause specific
    pain syndromes

    NEUROSURGICA Ablative therapies : procedures that interrupt


    L TREATMENT the afferent pathways of pain, reserved for
    intractable cases of chronic NP
    OF NP

    Augmentative neuromodulation therapies


    (stimulation) : based on the gate theory
    (Melzak&Wall 1965) – changing the balance
    between excitatory and inhibitory fibers
    NEUROSURGICAL TREATMENT OF NP
    A N AT O M I C A L P R O C E D U R E S

    • Spinal decompression and reconstruction • Microvascular decompression :


    For mielo/radiculopathy generated by For craneal nerves-related NP (classic
    compression (disc hernia, osteophytes, trigeminal, glossopharyngeal or nervus
    spondylolisthesis, ligamentous hypertrophy) intermedius neuralgia)
    NEUROSURGICA
    L TREATMENT
    OF NP
    ABLATIVE
    PROCEDURES
    TRIPLE
    N E U R E C TO M Y
    FOR NP AFTER
    INGUINAL HERNIA
    R E PA I R
    SELECTIVE
    DORSAL
    RHIZOTOMY
    GANGLIONECTOMY
    FOR OCCIPITAL
    NEURALGIA
    DREZ LESIONING
    AUGMENTATIVE NEUROMODULATION
    TECHNIQUES

    Peripheral nerve stimulation Spinal cord stimulation


    AUGMENTATIVE NEUROMODULATION
    TECHNIQUES

    Brain
    stimulation
    TYPES OF OROFACIAL NEUROPATHIC
    PAIN
    TRIGEMINAL NEURALGIA

    • Paroxystic, unilateral and short-lasting facial pain


    • Types :
    1) Classical – no clear etiology (though commonly associated with vascular
    compression : superior cerebellar artery)
    2) Symptomatic (painful) – caused by tumors, cysts, viral infections, trauma, multiple
    sclerosis, systemic disease
    • Clinical diagnosis is completed with MRI and MR angiography to identify
    possible causes for type 2 TN or vascular impingement in the case of type 1 TN
    TRIGEMINAL NEURALGIA
    S U R G I C A L T R E AT M E N T
    PERIPHERAL NEURITIS

    • Localized neural pathologic condition induced by inflammation


    • Caused by :
    o Axonal damage – misdirected dental implant, periapical dental inflammatory lesion
    near a nerve
    o Proinflammatory cytokine secretion - temporomandibular joint pathology, paranasal
    sinusitis, tumors
    • Clinical presentation – tactile allodynia
    • Treatment – early administration of corticosteroids/NSAIDs
    HERPES ZOSTER AND POSTHERPETIC
    NEURALGIA

    • HZ results from the reactivation of the varicella zoster virus in the cranial sensory
    ganglia with inflammatory changes extending along the peripheral nerve : painful
    vesicular rash in the associated unilateral dermatome
    • Presents in patients with autoimmune diseases, immunosuppression, cancer
    • Postherpetic neuralgia is reported 3-6 months after the acute attack of HZ
    o Severe, fluctuating burning/throbbing/stabbing pain
    o Results from scarring induced by the viral infection in the nerves/ganglia and destruction of
    large myelinated fibers
    o Usually treated with antidepressant drugs +/- opioids, with low efficacy especially in the older
    age group

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