Neuralgia: Wikis


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Classification and external resources
ICD-10 M79.2
ICD-9 729.2
MeSH D009437

Neuralgia is pain in one or more nerves[1] that occurs without stimulation of pain receptor (nociceptor) cells. Neuralgia pain is produced by a change in neurological structure or function rather than by the excitation of pain receptors that causes nociceptive pain. Neuralgia falls into two categories: central neuralgia and peripheral neuralgia. This unusual pain is thought to be linked to four possible mechanisms: ion gate malfunctions; the nerve becomes mechanically sensitive and creates an ectopic signal; cross signals between large and small fibers; and malfunction due to damage in the central processor[2].

Neuralgia was first recognized by Silas Weir Mitchell, a neurologist in the American Civil War, who noticed hyperalgesia and chronic pain in patients who had nerve lesions in the extremities and also some cases where no lesion was observed: These causalgias were certainly major by the importance of the symptoms, but stemmed from minor neurological lesions" [3]. Mitchell termed the condition “causalgia” which has since become known as “Complex Regional Pain Syndrome Type 1 and Type 2” (CRPS). CRPS Type I is a syndrome that develops after an initiating noxious event .[4], and Type 2 describes a case when nerve damage is clear[5].

Neuralgia is often difficult to diagnose, and most treatments show little or no effectiveness. 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 more difficult to treat than other types of pain because it does not respond well to normal pain medications. Special medications have become more specific to neuralgia and typically fall under the category of membrane stabilizing drugs or antidepressants such as Cymbalta. The antiepileptic medication(AED) Lyrica was developed specifically for neuralgia and other neuropathic pain as a successor to Neurontin (gabapentin).

Under the general heading of neuralgia are trigeminal neuralgia (TN), atypical trigeminal neuralgia (ATN), and postherpetic neuralgia (caused by shingles or herpes). Neuralgia is also involved in disorders such as sciatica and brachial plexopathy with neuropathia. Neuralgias that do not involve the trigeminal nerve are occipital neuralgia and glossopharyngeal neuralgia[6].

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[6].

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). The attacks can occur in clusters, as an isolated attack, or be completely constant. Some patients will have a muscle spasm which led to the original term for TN of "tic douloureux" ("tic", meaning 'spasm', and "douloureux", meaning 'painful', in French).

Neuralgia is a form of chronic pain and can be extremely difficult to diagnose. Postherpetic neuralgia is the easiest to diagnose because it follows an obvious cause (shingles). Neuralgia is a rare disease. Women are more likely to be affected than men, and those over 50 are at the greatest risk. 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[7].



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[8].


Peripheral nerve injury

A neuron’s response to trauma can often be determined by the severity of the injury, classified by Seddon's classification. In Seddon’s Classification, nerve injury is described as either neurapraxia, axonotmesis, or neurotmesis. Following trauma to the nerve, a short onset of afferent impulses, termed “injury discharge”, occurs. While lasting only minutes, this occurrence has been linked to the onset of neuropathic pain[2].

When an axon is severed, the segment of the axon distal to the cut degenerates and is absorbed by Schwann cells. The proximal segment fuses, retracts, and swells, forming a “retraction bulb.” The synaptic terminal function is lost, as axoplasmic transport ceases and no neurotransmitters are created. The nucleus of the damaged axon undergoes chromatolysis in preparation for axon regeneration. Schwann cells in the distal stump of the nerve and basal lamina components secreted by Schwann cells guide and help stimulate regeneration. The regenerating axon must make connections with the appropriate receptors in order to make an effective regeneration. If proper connections to the appropriate receptors are not established, aberrant reinnervation may occur. If the regenerating axon is halted by damaged tissue, neurofibrils may create a mass known as a neuroma[2].

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[2].

Central neuronal injury

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. The damaged nerve terminal begins to swell and glial cells push the defective terminal away from connections to other neurons[2]. Often, aberrant sprouting of damaged CNS neurons, specifically sensory neurons, results in neuralgia.


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 a peripheral nerve is stimulated and recordings are taken from a purely-sensory portion of the nerve[5][9].

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 [10]. 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 [8].

Laser evoked potentials

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[11].

Quantitative sensory testing

Another method for testing the proper function of a nerve is Quantitative sensory testing (QST). QST relies on analysis of a patient’s response to external stimuli of controlled intensity. A stimulus is applied to the skin of the nerve area being tested in ascending and descending orders of magnitude. Clinicians can quantify the mechanical sensitivity of the tactile stimulus using von Frey hairs or Semmes-Weinstein monofilaments. Also, weighted needles can be used to measure pin-prick sensation, and an electronic vibrameter is used to measure vibration sensitivity. Thermal stimuli are quantified by using a probe that operates on the Peltier principle[9].

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[9].

Punch skin biopsy

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[9].

Atypical (trigeminal) neuralgia

Atypical trigeminal neuralgia (ATN) is a rare form of neuralgia and may also be the most misdiagnosed form. The symptoms can be mistaken for migraines, dental problems such as TMJ, musculoskeletal issues, and hypochondriasis. ATN can have a wide range of symptoms and the pain can fluctuate in intensity from mild aching to a crushing or burning sensation, and also to the extreme pain experienced with the more common trigeminal neuralgia. ATN pain can be described as heavy, aching, and burning. Sufferers have a constant migraine-like headache and experience pain in all three trigeminal nerve branches. This includes aching teeth, ear aches, feeling of fullness in sinuses, cheek pain, pain in forehead and temples, jaw pain, pain around eyes, and occasional electric shock-like stabs. Unlike typical neuralgia, this form can also cause pain in the back of the scalp and neck. Pain tends to worsen with talking, facial expressions, chewing, and certain sensations such as a cool breeze. Vascular compression of the trigeminal nerve, infections of the teeth or sinuses, physical trauma, or past viral infections are possible causes of ATN[6].

Glossopharyngeal neuralgia

Glossopharyngeal neuralgia consists of recurring attacks of severe pain in the back of the throat, the area near the tonsils, the back of the tongue, and part of the ear. The pain is due to malfunction of the 9th cranial nerve (glossopharyngeal nerve), which moves the muscles of the throat and carries information from the throat, tonsils, and tongue to the brain.

Glossopharyngeal neuralgia, a rare disorder, usually begins after age 40 and occurs more often in men. Often, its cause is unknown. But sometimes glossopharyngeal neuralgia results from an abnormally positioned artery that compresses the glossopharyngeal nerve near where it exits the brain stem. Rarely, the cause is a tumor in the brain or neck[6].

Occipital neuralgia

Occipital neuralgia, also known as C2 neuralgia, or Arnold's neuralgia, is a medical condition characterized by chronic pain in the upper neck, back of the head and behind the eyes.


Treatment options include medicines, surgery, and complementary approaches.

High doses of anticonvulsant medicines—used to block nerve firing— and tricyclic antidepressants are generally effective in treating neuralgia. If medication fails to relieve pain or produces intolerable side effects, surgical treatment may be recommended[5][12].

Neural augmentative surgeries are used to stimulate the affected nerve. By stimulating the nerve the brain can be “fooled” into thinking it is receiving normal input. Electrodes are carefully placed in the dorsal root and subcutaneous nerve stimulation is used to stimulate the targeted nerve pathway. A technician can create different electrical distributions in the nerve to optimize the efficiency, and a patient controls the stimulation by passing a magnet over the unit[5].

Some degree of facial numbness is expected after most of these surgical procedures, and neuralgia might return despite the procedure’s initial success. Depending on the procedure, other surgical risks include hearing loss, balance problems, infection, and stroke. These surgeries include rhizotomy (where select nerve fibers are destroyed to block pain) and Microvascular decompression (where the surgeon moves the vessels that are compressing the nerve away from it and places a soft cushion between the nerve and the vessels)[7].

Some patients choose to manage neuralgia using complementary techniques, usually in combination with drug treatment. These therapies offer varying degrees of success. Options include chiropractic, acupuncture, biofeedback, vitamin therapy, nutritional therapy, hot-cold compress, and electrical stimulation of the nerves[7][13].


Sleep deprivation and malnutrition have also been reported as byproducts of the pain. It is possible that there are other triggers or aggravating factors that patients need to learn to recognize to help manage their health. Bright lights, sounds, stress, and poor diet are examples of additional stimuli that can contribute to the condition. The pain can cause nausea, so beyond the obvious need to treat the pain, it is important to be sure to try to get adequate rest and nutrition[14].


  • Shankland, Dr. Wesley E. Face the Pain - The Challenge of Facial Pain, (Omega Publishing, 2001) [1] Dr. Shankland is a former associate editor of The Journal of Craniomandibular Practice [2].
  • In R. C. Sherriff's play Journey's End, the character Hibbert lies about having neuralgia to his commanding officer, and demands to be sent home. [15]

See also


  1. ^ neuralgia at Dorland's Medical Dictionary
  2. ^ a b c d e L. A. Colvin. Raj's Practical Management of Pain.BJA Advance Access published on December 1, 2000, DOI 10.1093/bja/aen312.Br. J. Anaesth. 101: 119-127.
  3. ^ Mitchell, S.W. (1872) Injuries of Nerves and their Consequences. Philadelphia: JB Lippincott Co§
  4. ^ Stanton-Hicks et al. (1995) RSD: changing concepts and taxonomy. Pain, 63, 127-133
  5. ^ a b c d Stechison, Michael. Personal INTERVIEW. 18 November 2008.
  6. ^ a b c d Gilron I, Watson CPN, Cahill CM, Moulin DE. 2006. Neuropathic pain: a practical guide for the clinician. Canadian Medical Association Journal 175:265-75
  7. ^ a b c Dworkin RH, Backonja M, Rowbotham MC, Allen RR, Argoff CR, et al. 2003. Advances in neuropathic pain - Diagnosis, mechanisms, and treatment recommendations. Archives of Neurology, 60:1524-34
  8. ^ a b Jensen TS. 2002. An improved understanding of neuropathic pain. European Journal of Pain-London, 6:3-11
  9. ^ a b c d Daniel HC, Narewska J, Serpell M, Hoggart B, Johnson R, Rice ASC. 2008. Comparison of psychological and physical function in neuropathic pain and nociceptive pain: Implications for cognitive behavioral pain management programs. European Journal of Pain 12:731-41
  10. ^ Melzack, R. (1975). The McGill Questionnaire: Major Properties and Scoring Methods. Pain, 1, 277-229
  11. ^ Garcia-Larrea L. 2008. Laser-evoked potentials in the diagnosis of central neuropathic pain. Douleur Et Analgesie 21:93-8
  12. ^ Galer BS. 1995. Neuropathic pain of peripheral origin: Advances in pharmacologic treatment. Neurology 45:S17-S25
  13. ^ Breivik H. 2002. Advances in treatment of neuropathic pain. European Journal of Pain-London 6:V-V
  14. ^ Backonja. 2004. Defining neuropathic pain (vol 97, pg 785, 2003). Anesthesia and Analgesia 98:67
  15. ^ Sherriff, Robert Cedric (1983). Journey's end. Harmondsworth [Eng.]: Penguin. pp. 53–58. ISBN 014 11 8326 8.  

External links

1911 encyclopedia

Up to date as of January 14, 2010

From LoveToKnow 1911

Medical warning!
This article is from the 1911 Encyclopaedia Britannica. Medical science has made many leaps forward since it has been written. This is not a site for medical advice, when you need information on a medical condition, consult a professional instead.

NEURALGIA (Gr. vfUpov, nerve, and iiXryos, pain), a term denoting strictly the existence of pain in some portion or throughout the whole of the distribution of a nerve without any distinctly recognizable structural change in the nerve or nerve centres. This strict definition, if adhered to, however, would not be applicable to a large number of cases of neuralgia; for in not a few instances the pain is connected with some source of irritation, by pressure or otherwise, in the course of the affected nerve; and hence the word is generally used to indicate pain affecting a particular nerve or its branches from any cause. There are few ailments which give rise to greater human suffering. The existence of neuralgia usually betokens a depressed or enfeebled state of health. It is often found to affect the hereditarily rheumatic or gouty. In weakened conditions of the system from improper or insufficient food, or as a result of any drain upon the body, or in anaemia from any cause, and in such diseases as syphilis or malaria, neuralgia is a frequent concomitant. Any strain upon the nervous system, such as mental overwork or anxiety, is a potent cause; or exposure to cold and damp, which seems to excite irritation in a nerve already predisposed to suffer. But irritation may be produced by numerous other causes besides this - such as a decayed tooth, diseased bone, local inflammations in which nerves are implicated, by some source of pressure upon a nerve trunk, or by swelling of its sheath in its passage through a bony canal or at its exit upon the surface.

The pain is generally localized, but may come to extend beyond the immediate area of its first occurrence. It is usually of paroxysmal character, and not unfrequently periodic, occurring at a certain time of the day or night. It varies in intensity, being often of the most agonizing character, or less severe and more of a tingling kind. Various forms of perverted nerve function may be found co-existing with or following neuralgia. Thus there may be hyperaesthesia, anaesthesia, paralysis, or alterations of nutrition, such as wasting of muscles, whitening of the hair, &c.

The forms in which neuralgia most commonly shows itself are facial neuralgia or tic douloureux, migraine (hemicrania or brow ague), intercostal neuralgia and sciatica.

Facial neuralgia, or tic douloureux, affects the great nerve of sensation of the face (fifth nerve), and may occur in one or more of the three divisions in which the nerve is distributed. It is usually confined to one side. When the first or upper division of the nerve is involved the pain is mostly felt in the forehead and side of the head. It is usually of an intensely sharp, cutting or burning character, either constant or with exacerbations, and often periodic, returning at a certain hour each day while the attack continues. The skin over the affected part is often red and swollen, and, even after the attack has abated, feels stiff and tender to the touch. In this, as in all forms of neuralgia, there are certain localities where the pain is more intense, these "painful points," as they are called, being for the most part in those places where the branches of the nerves emerge from bony canals or pierce the fascia to ramify in the skin. Hence, in this form, the greater severity of the pain above the eyebrow and along the side of the nose. There is also pain in the eyelid, redness of the eye, and flow of tears. When the second division of the nerve is affected the pain is chiefly in the cheek and upper jaw, the painful points being immediately below the lower eyelid, over the cheek bone, and about the upper lip. When the third division of the nerve suffers the pain affects the lower jaw, and the chief painful points are in front of the ear and about the chin.

Hemicrania, migraine, brow-ague' and sick headache are various terms employed to describe what by some is considered to be another form of neuralgia. An attack may come on suddenly, but, in general, begins by a dull aching pain in the brow or temple, which steadily increases in severity and extent, but remains usually limited to one side of the head. It attains at times an extreme degree of violence, and is apt to be aggravated by movement, loud noises or bright light. Accompanying the pain there is more or less of nausea, and when the attack reaches its height vomiting may occur, after which relief comes, especially if sleep supervene. An attack of this kind may last for a few hours or for a whole day, and after it is over the patient feels comparatively well. It may recur periodically, or, as is more common, at irregular intervals. During the paroxysms, or even preceding them, certain sensory disturbances may be experienced, more especially affections of vision, such as ocular spectra, hemiopia, diplopia, &c. Gout, eyestrain and intestinal toxaemia have been put forward as causes of migraine, and Sir W. Gowers regards it as the equivalent of a true epileptic attack.

Intercostal neuralgia is pain affecting the nerves which emerge from the spinal cord and run along the spaces between the ribs to the front of the body. This form of neuralgia affects the left side more than the right, is much more common in women than in men, and occurs generally in enfeebled states of health. It might be mistaken for pleurisy or some inflammatory affection of the lungs; but the absence of any chest symptoms, its occurrence independently of the acts of respiration, and other considerations well establish the distinction. The specially painful points are chiefly at the commencement of the nerve as it issues from the spinal canal, and at the extremities towards the front of the body, where it breaks up into filaments which ramify in the skin. This form of neuralgia is occasionally the precursor of an attack of shingles (Herpes zoster) as well as a result of it.

Sciatica is another of the more common forms of neuralgia. It affects the great sciatic nerve which emerges from the pelvis and runs down the leg to the foot. It is in most instances traceable to exposure to cold or damp, to overuse of the limbs in walking, &c. Any source of pressure upon the nerve within the pelvis, such as may be produced by a tumour or even by constipation of the bowels, may excite an attack of sciatica. It is often connected with a rheumatic or gouty constitution. In general the nerve of one side only is affected. The pain which is felt at first a little behind the hip-joint steadily increases in severity and extends along the course of the nerve and its branches in many instances as far as the toes. The specially painful points are about the knee and ankle joints; besides which a feeling of numbness is experienced throughout the whole limb. In severe cases all movement of the limb aggravates the pain, and the patient is obliged to remain in bed. In prolonged attacks the limb may waste and be drawn up and fixed in one position. Attacks of sciatica are often attended with great suffering, and are apt to be very intractable to treatment.

In the treatment of all forms of neuralgia it is of first importance to ascertain if possible whether any constitutional morbid condition is associated with the malady. When the attack is periodic the administration of a large dose of quinine two or three hours previous to the usual time of the seizure will often mitigate, and may even prevent the paroxysm. Many topical applications are of great efficacy. Liniments containing opium, belladonna or aconite rubbed into the affected part will often soothe the most severe local pain. And antipyrin, phenacetin, aspirin and similar analgetics are commonly taken. The plan at one time resorted to of dividing or excising a portion of the affected nerve is now seldom employed, but the operation of nerve-stretching in some forms of neuralgia, notably sciatica, is sometimes successful. It consists in cutting down upon and exposing the nerve, and in seizing hold and drawing upon it so as to stretch it. Such an operation is obviously justifiable only in cases where other less severe measures have failed to give relief. The employment of electricity, in long continued and intractable forms of neuralgia, proves in many instances eminently serviceable. In the severest forms of tic doloureux complete relief has followed the extirpation of the Gasserian ganglion. (F. W. MO.)

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