Members: J. Tang, S. H. Hu, S. Ng, & A. Quach

Neuropathic pain, as defined by the International Association for the Study of Pain (IASP), is the pain induced by primary lesions or dysfunctions of the central or peripheral nervous system. It is often described as a tingling, burning or shooting pain. Neuropathic pain (NP) is studied in order to alleviate pain in those who suffer from neurological damage caused by amputation, virus infections, cancer, diabetes, brainstem infarctions and many other diseases[1] . These patients may suffer from abnormal perceptions of pain from stimuli, caused by hyperalgesia and allodynia, and may also suffer from other comorbidities[2] , essentially making it difficult to treat. There are three mechanisms that induce neuropathic pain: peripheral sensitization, central sensitization, and deafferentation. These are characterized, respectively, as the excessive excitation of peripheral non-nociceptors, the enlargement of receptive fields of dorsal horn neurons, and the disinhibition of those neurons by a loss of afferent signals, all which ultimately elevate the perception of pain[3] . NP is often treated with pharmacological drugs or other therapy in order to alleviate symptoms or target the causal mechanism of pain. However many treatments are still ineffective for a large percentage of those who suffer from NP. Recent research has identified various genes that confer protection or susceptibility to the development of NP. The identification of these genes and the study of the causal mechanisms of pain will allow the development of more effective treatment.

  1. Mechanisms of Neuropathic Pain (Shun-Hsiang Hu)

    1. Peripheral & Central Sensitization
    2. Case studies (post-surgery effects, diabetics, alcoholism)
    3. Venom inducing mechanism
    4. Immunity mechanism for pain
  2. Causes of Neuropathic Pain (Joyce Tang)

    1. Causes of polyneuropathy
    2. Causes of mononeuropathy
  3. Genes involved in neuropathic pain development (Joyce Tang)

    1. Genes that confer susceptibility
    2. Genes that confer protection
  4. Signs, Symptoms, Diagnosis (Sheena Ng)

    1. Spontaneous pain
    2. Stimulus-evoked pain
    3. Medical History and Clinical Examinations
    4. Laboratory Testing
    5. Neuroimaging ToolsVisit
  5. Comorbidities (Sheena Ng)

    1. Triad: Chronic pain, Sleep interference, Psychological functioning
    2. Neuroplasticity
  6. Treatment and Therapy (Alexa Quach)

    1. Non-pharmacological treatment
    2. Pharmacological treatment
    3. Interventional treatment
    4. Treatment guidelines
    5. Current research for new treatment
      • 5.1 Inhibition of astrocyte activation


References:
  1. ^ Baron R. Mechanism of disease: neuropathic pain – a clinical perspective. Nature Clinical Practice Neurology. (2011) 2(2): 95-106
  2. ^ Nicolson B, Verma S. Comorbidities in chronic neuropathic pain. Pain Med. (2004) 5 Suppl 1: S9-S47
  3. ^ Baron R. Mechanism of disease: neuropathic pain – a clinical perspective. Nature Clinical Practice Neurology. (2011) 2(2): 95-106