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This article is about nerve pain in general. For the similarly named nerve pain in the thigh, see Meralgia paresthetica.
Classification and external resources
ICD-10 M79.2
ICD-9 729.2
MedlinePlus 001407
MeSH D009437




Atypical (trigeminal)[edit]


In the case of trigeminal neuralgia the affected nerves are responsible for sensing touch, temperature sensation and pressure sensation in the facial area from the jaw to the forehead. The disorder generally causes short episodes of excruciating pain, usually for less than two minutes and usually only one side of the face. The pain can be described in a variety of ways such as "stabbing," "sharp," "like lightning," "burning," and even "itchy". In the atypical form of TN, the pain presents itself as severe constant aching along the nerve. The pain associated with TN is recognized as one of the most excruciating pains that can be experienced.[2]

Simple stimuli—such as eating, talking, making facial expressions, washing the face, or any light touch or sensation—can trigger an attack (even the sensation of a cool breeze). Attacks may be lone occurrences, clusters of attacks, or constant episodes. Some patients experience muscle spasm, which led to the original term for TN of "tic douloureux" ("tic", meaning 'spasm', and "douloureux", meaning 'painful', in French).







By understanding the neuroplastic changes following nerve damage, researchers may be able to better understand the mechanism of hyperexcitability in the nervous system that is believed to cause neuropathic pain.[3]

Peripheral nerve injury[edit]



In the event that an injured neuron degenerates or does not regenerate properly, the neuron loses its function or may not function properly. Neuron trauma is not an isolated event and may cause degenerative changes in surrounding neurons. When one or more neurons lose their function or begin to malfunction, abnormal signals sent to the brain may be translated as painful signals.[4]

Central neuronal injury[edit]

Neuronal injury in the central nervous system (CNS) typically leads to local degeneration of the nerve axon and myelin sheath. Axonal debris in the CNS is eliminated by macrophages. Trauma to neurons in the CNS also causes a proliferation of glial cells that form a glial scar. Development of the glial scar is thought to inhibit regeneration of central neural connections.[citation needed] The damaged nerve terminal begins to swell and glial cells push the defective terminal away from connections to other neurons.[4] Often, aberrant sprouting of damaged CNS neurons, specifically sensory neurons, results in neuralgia.


Diagnosis typically involves locating the damaged nerve by identifying missing sensory or motor function. This may involve tests such as an EMG test or a nerve conduction test.

Neuralgia is a form of chronic pain that can be difficult to diagnose. Postherpetic neuralgia is the easiest to diagnose because it follows an obvious cause (shingles).

Diagnosis of neuralgia is difficult, and misdiagnosis is common. Diagnosis typically involves locating the damaged nerve by stimulation of the specific damaged pathway or by identifying missing sensory function. The most common test for neuralgia is a nerve conduction study, such as using microneurography in which the peripheral nerve is stimulated and recordings are taken from a purely sensory portion of the nerve.[5][6]

When assessing neuralgia to find the underlying mechanism, a history of the pain, description of pain, clinical examination, and experimental examination are required. Since pain is subjective to the patient, it is important to use a pain assessment scale, such as the McGill Pain Questionnaire.[7] Qualifying the severity of the pain is essential in diagnosis and in evaluating the effectiveness of the treatment. Clinical examinations usually involve testing responses to stimuli such as touch, temperature, and vibration. Neuralgia can be further classified by the type of stimuli that elicits a response: mechanical, thermal, or chemical. Response to the course of treatment is the final tool used to determine the mechanism of the pain. Future research must focus on the relationships between all of these categories.[3]

In some cases, multiple sclerosis is related to nerve damage, causing the pain, so doctors will likely ask about family history to help diagnose. Nothing unusual can be seen in brain scans, so diagnosis is usually based on the description of the symptoms and the response to the medication or procedures.[8]

Laser evoked potentials[edit]

Neuropathic pain is often the result of a lesion in spinothalamic pathways. Laser evoked potentials (LEPs) are measurements of cortical responses using lasers to selectively stimulate thermonociceptors in the skin. Lasers can emit a radiant-heat pulse stimulus to selectively activate A-delta and C free nerve endings. By specifically targeting pain and temperature pathways and measuring cortical responses, clinicians can identify even minute lesions in the spinothalamic pathways. LEP abnormalities are strongly indicative of neuropathic pain, while a normal LEP is often more ambiguous. LEPs have high sensitivity and are very reliable in assessing damage to both central and peripheral nervous systems.[9]

Quantitative sensory testing[edit]


One problem with QST is that abnormalities may be observed in non-neuralgia pains, often making it inconclusive in diagnosis. Also, QST is very time consuming and relies on expensive equipment.[6]

Punch skin biopsy[edit]

Recently, skin biopsy has been used to investigate mechanoreceptors and their myelinated afferents. Though available in only a few research centers, skin punch biopsy is an easy procedure and is minimally invasive. Punch skin biopsy is used to quantify nerve fibers C fibers and A-delta nerve fibers through measurement of the density of intra-epidermal nerve fibers (IENF). Loss of IENF has been observed in several cases of neuropathic pain.[6]


Treatment options include medicines and surgery.





Marijuana: The American Medical Association stated in Report 3 of the Council on Science and Public Health (I-09) that "...Results of short term controlled trials indicate that smoked cannabis reduces neuropathic pain...".[11]


Neuralgia is a rare disease. Women are more likely to be affected than men.


The earliest cited instance of the term[12] is the French, névralgie, which, according to Rowland,[13] was coined by François Chaussier in his 1801 Table Synoptique de la Névralgie, for " affection of one or more nerves causing pain which is usually of an intermittent but frequently intense character".[14] The features and assumed etiology found in the medical literature have varied significantly over time.[14]

Various locations were proposed for the primary lesion during the nineteenth century, including nerve roots, ganglia, trunks and branches, as well as the brain and spinal cord. In 1828, JC Warren[15] and TJ Graham[16] placed the cause in the trunk or branch of the nerve innervating the perceived site of the pain, though Graham also attributed neuralgia to "morbid sensibility of the nervous system" due to "great disorder of the general health." Teale in 1830[17] and many after him argued that it may be located in the spinal cord or nerve root. Later in the century some proposed it may be an affliction of organs such as the uterus or liver, while others classed certain headaches as neuralgias, and proposed that emotional distress may promote the condition.[14]

Literature and film[edit]

See also[edit]


  1. ^ "Definition: neuralgia". International Association for the Study of Pain taxonomy. Retrieved 5 August 2012. 
  3. ^ a b Jensen, T. S. (2002). "An improved understanding of neuropathic pain". European Journal of Pain (London) 6 (Supplement): 3–11. doi:10.1016/S1090-3801(02)90002-9. 
  4. ^ a b c d P. Prithvi Raj (14 June 2000). Practical Management of Pain. Mosby. ISBN 978-0-8151-2569-3. 
  5. ^ a b c Stechison, Michael. Personal INTERVIEW. 18 November 2008.[non-primary source needed]
  6. ^ a b c d Daniel, H. C.; Narewska, J.; Serpell, M.; Hoggart, B.; Johnson, R.; Rice, A. S. C. (2008). "Comparison of psychological and physical function in neuropathic pain and nociceptive pain: Implications for cognitive behavioral pain management programs". European Journal of Pain 12 (6): 731–741. doi:10.1016/j.ejpain.2007.11.006. PMID 18164225. 
  7. ^ Melzack, R. (1975). "The McGill Questionnaire: Major Properties and Scoring Methods". Pain 1 (3): 277–299. doi:10.1016/0304-3959(75)90044-5. PMID 1235985. 
  8. ^ a b Dworkin, R. H.; Backonja, M.; Rowbotham, M. C.; Allen, R. R.; Argoff, C. R.; et al., GJ; Bushnell, MC; Farrar, JT et al. (2003). "Advances in neuropathic pain - Diagnosis, mechanisms, and treatment recommendations". Archives of Neurology 60 (11): 1524–1534. doi:10.1001/archneur.60.11.1524. PMID 14623723. 
  9. ^ Garcia-Larrea, L. (2008). "Laser-evoked potentials in the diagnosis of central neuropathic pain". Douleur et Analgesie 21 (2): 93–98. doi:10.1007/s11724-008-0092-5. 
  10. ^ Galer, B. S. (1995). "Neuropathic pain of peripheral origin: Advances in pharmacologic treatment". Neurology 45 (129): S17–S25. doi:10.1212/WNL.45.12_Suppl_9.S17. PMID 8538882. 
  11. ^ Head, Alvin. C. (2009). "Use of Cannabis for Medicinal Purposes" (PDF). Report 3 of the Council on Science and Public Health (I-09). 
  12. ^ Murray JAH. Bradley H, Craigie WA & Onions CT (1933). Oxford English Dictionary. Clarendon Press. 
  14. ^ a b c Alam C & Merskey H. What's in a name? The cycle of change in the meaning of neuralgia. History of psychiatry. 1994:129–174.
  15. ^ Warren JC. Cases of neuralgia or painful afflictions of the nerves. Boston Med. Surg. J.. 19 February 1928;(i):1–6.
  17. ^ Teale TP. A treatise on neuralgic diseases. Philadelphia: E. L. Carey & A. Hart; 1830.
  19. ^ Aces High. 1976. Event occurs at 12:39. 

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