Neuralgia

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Neuralgia
Specialty Neurology

Neuralgia (Greek neuron, "nerve" + algos, "pain") is pain in the distribution of a nerve or nerves, [1] as in intercostal neuralgia, trigeminal neuralgia, and glossopharyngeal neuralgia.

Contents

Classification

Under the general heading of neuralgia are trigeminal neuralgia (TN), atypical trigeminal neuralgia (ATN), occipital neuralgia, glossopharyngeal neuralgia and postherpetic neuralgia (caused by shingles or herpes). The term neuralgia is also used to refer to pain associated with sciatica and brachial plexopathy. [2]

Atypical (trigeminal)

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 temporomandibular joint disorder, 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. Affected individuals 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. [2]

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 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).[ citation needed ]

Glossopharyngeal

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 glossopharyngeal nerve (CN IX), which moves the muscles of the throat and carries information from the throat, tonsils, and tongue to the brain.[ citation needed ]

Glossopharyngeal neuralgia, a rare disorder, usually begins after age 40 and occurs more often in men. Often, its cause is unknown. However, glossopharyngeal neuralgia sometimes 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. [2]

Occipital

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.[ citation needed ]

Mechanisms

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

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. This occurrence lasts only minutes, but has been linked to the onset of neuropathic pain. [4]

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 connect to the appropriate receptors 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. [4]

If an injured neuron degenerates or does not regenerate properly, then 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]

Diagnosis

When assessing neuralgia to find the underlying mechanism, a history of the pain, description of pain, physical examination, and experimental examination are required. Pain is subjective to the patient, but pain assessment questionnaires, such as the McGill Pain Questionnaire can be useful for evaluation. [5] Physical 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. [3] Additional tools may be used, predominantly in research settings including Laser Evoked Potentials and Quantitative Sensory testing.[ citation needed ]

Laser evoked potentials

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. LEP abnormalities may be indicative of neuropathic pain, while a normal LEP is often more ambiguous. LEPs can assess damage to both central and peripheral nervous systems. [6]

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 (SWMFs). 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. [7]

Treatment

Treatment options include medicines and surgery.

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 duloxetine (Cymbalta). The antiepileptic medication pregabalin (Lyrica) was developed specifically for neuralgia and other neuropathic pain as a successor to gabapentin (Neurontin).[ citation needed ]

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. [8] [ non-primary source needed ] [9]

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. [8]

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). [10]

History

The earliest cited instance of the term [11] is the French, névralgie, which, according to Rowland, [12] was coined by François Chaussier in his 1801 Table Synoptique de la Névralgie, for "...an affection of one or more nerves causing pain which is usually of an intermittent but frequently intense character". [13] The features and assumed etiology found in the medical literature have varied significantly over time. [13]

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 [14] and TJ Graham [15] 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 [16] 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. [13]

Society and culture

See also

Related Research Articles

<span class="mw-page-title-main">Nerve</span> Enclosed, cable-like bundle of axons in the peripheral nervous system

A nerve is an enclosed, cable-like bundle of nerve fibers in the peripheral nervous system.

<span class="mw-page-title-main">Cranial nerves</span> Nerves that emerge directly from the brain and the brainstem

Cranial nerves are the nerves that emerge directly from the brain, of which there are conventionally considered twelve pairs. Cranial nerves relay information between the brain and parts of the body, primarily to and from regions of the head and neck, including the special senses of vision, taste, smell, and hearing.

<span class="mw-page-title-main">Parasympathetic nervous system</span> Division of the autonomic nervous system

The parasympathetic nervous system (PSNS) is one of the three divisions of the autonomic nervous system, the others being the sympathetic nervous system and the enteric nervous system. The enteric nervous system is sometimes considered part of the autonomic nervous system, and sometimes considered an independent system.

<span class="mw-page-title-main">Brainstem</span> Posterior part of the brain, adjoining and structurally continuous

The brainstem is the stalk-like part of the brain that interconnects the cerebrum and diencephalon with the spinal cord. In the human brain, the brainstem is composed of the midbrain, the pons, and the medulla oblongata. The midbrain is continuous with the thalamus of the diencephalon through the tentorial notch.

<span class="mw-page-title-main">Trigeminal nerve</span> Cranial nerve responsible for the faces senses and motor functions

In neuroanatomy, the trigeminal nerve (lit. triplet nerve), also known as the fifth cranial nerve, cranial nerve V, or simply CN V, is a cranial nerve responsible for sensation in the face and motor functions such as biting and chewing; it is the most complex of the cranial nerves. Its name (trigeminal, from Latin tri- 'three', and -geminus 'twin') derives from each of the two nerves (one on each side of the pons) having three major branches: the ophthalmic nerve (V1), the maxillary nerve (V2), and the mandibular nerve (V3). The ophthalmic and maxillary nerves are purely sensory, whereas the mandibular nerve supplies motor as well as sensory (or "cutaneous") functions. Adding to the complexity of this nerve is that autonomic nerve fibers as well as special sensory fibers (taste) are contained within it.

<span class="mw-page-title-main">Trigeminal neuralgia</span> Neurological pain disorder

Trigeminal neuralgia, also called Fothergill disease, tic douloureux, trifacial neuralgia, or suicide disease is a long-term pain disorder that affects the trigeminal nerve, the nerve responsible for sensation in the face and motor functions such as biting and chewing. It is a form of neuropathic pain. There are two main types: typical and atypical trigeminal neuralgia. The typical form results in episodes of severe, sudden, shock-like pain in one side of the face that lasts for seconds to a few minutes. Groups of these episodes can occur over a few hours. The atypical form results in a constant burning pain that is less severe. Episodes may be triggered by any touch to the face. Both forms may occur in the same person. It is regarded as one of the most painful disorders known to medicine, and often results in depression and suicide.

<span class="mw-page-title-main">Nociceptor</span> Sensory neuron that detects pain

A nociceptor is a sensory neuron that responds to damaging or potentially damaging stimuli by sending "possible threat" signals to the spinal cord and the brain. The brain creates the sensation of pain to direct attention to the body part, so the threat can be mitigated; this process is called nociception.

<span class="mw-page-title-main">Solitary nucleus</span> Sensory nuclei in medulla oblongata

The solitary nucleus is a series of sensory nuclei forming a vertical column of grey matter in the medulla oblongata of the brainstem. It receives general visceral and/or special visceral inputs from the facial nerve, glossopharyngeal nerve and vagus nerve ; it receives and relays stimuli related to taste and visceral sensation. It sends outputs to various parts of the brain, such as the hypothalamus, thalamus, and reticular formation. Neuron cell bodies of the SN are roughly somatotopically arranged along its length according to function.

Postherpetic neuralgia (PHN) is neuropathic pain that occurs due to damage to a peripheral nerve caused by the reactivation of the varicella zoster virus. PHN is defined as pain in a dermatomal distribution that lasts for at least 90 days after an outbreak of herpes zoster. Several types of pain may occur with PHN including continuous burning pain, episodes of severe shooting or electric-like pain, and a heightened sensitivity to gentle touch which would not otherwise cause pain or to painful stimuli. Abnormal sensations and itching may also occur.

Neuropathic pain is pain caused by a lesion or disease of the somatosensory nervous system. Neuropathic pain may be associated with abnormal sensations called dysesthesia or pain from normally non-painful stimuli (allodynia). It may have continuous and/or episodic (paroxysmal) components. The latter resemble stabbings or electric shocks. Common qualities include burning or coldness, "pins and needles" sensations, numbness and itching.

<span class="mw-page-title-main">Headshaking</span> Horse behaviour

Headshaking is a behaviour displayed by horses, where the horse continuously shakes its head vertically and/or horizontally. In the 1980s it was considered a bad behaviour, but instead it turned out to be a painful medical condition.

<span class="mw-page-title-main">Nerve injury</span> Damage to nervous tissue

Nerve injury is an injury to a nerve. There is no single classification system that can describe all the many variations of nerve injuries. In 1941, Seddon introduced a classification of nerve injuries based on three main types of nerve fiber injury and whether there is continuity of the nerve. Usually, however, nerve injuries are classified in five stages, based on the extent of damage to both the nerve and the surrounding connective tissue, since supporting glial cells may be involved.

<span class="mw-page-title-main">Cranial nerve examination</span> Type of neurological examination

The cranial nerve exam is a type of neurological examination. It is used to identify problems with the cranial nerves by physical examination. It has nine components. Each test is designed to assess the status of one or more of the twelve cranial nerves (I-XII). These components correspond to testing the sense of smell (I), visual fields and acuity (II), eye movements and pupils, sensory function of face (V), strength of facial (VII) and shoulder girdle muscles (XI), hearing and balance, taste, pharyngeal movement and reflex, tongue movements (XII).

Geniculate ganglionitis or geniculate neuralgia (GN), also called nervus intermedius neuralgia, Ramsay Hunt syndrome, or Hunt's neuralgia, is a rare disorder characterized by severe paroxysmal neuralgic pain deep in the ear, that may spread to the ear canal, outer ear, mastoid or eye regions. GN may also occur in combination with trigeminal or glossopharyngeal neuralgia.

<span class="mw-page-title-main">Group C nerve fiber</span> One of three classes of nerve fiber in the central nervous system and peripheral nervous system

Group C nerve fibers are one of three classes of nerve fiber in the central nervous system (CNS) and peripheral nervous system (PNS). The C group fibers are unmyelinated and have a small diameter and low conduction velocity, whereas Groups A and B are myelinated. Group C fibers include postganglionic fibers in the autonomic nervous system (ANS), and nerve fibers at the dorsal roots. These fibers carry sensory information.

<span class="mw-page-title-main">Gustatory nucleus</span> Rostral part of the solitary nucleus located in the medulla

The gustatory nucleus is the rostral part of the solitary nucleus located in the medulla. The gustatory nucleus is associated with the sense of taste and has two sections, the rostral and lateral regions. A close association between the gustatory nucleus and visceral information exists for this function in the gustatory system, assisting in homeostasis - via the identification of food that might be possibly poisonous or harmful for the body. There are many gustatory nuclei in the brain stem. Each of these nuclei corresponds to three cranial nerves, the facial nerve (VII), the glossopharyngeal nerve (IX), and the vagus nerve (X) and GABA is the primary inhibitory neurotransmitter involved in its functionality. All visceral afferents in the vagus and glossopharyngeal nerves first arrive in the nucleus of the solitary tract and information from the gustatory system can then be relayed to the thalamus and cortex.

<span class="mw-page-title-main">Atypical trigeminal neuralgia</span> Medical condition

Atypical trigeminal neuralgia (ATN), or type 2 trigeminal neuralgia, is a form of trigeminal neuralgia, a disorder of the fifth cranial nerve. This form of nerve pain is difficult to diagnose, as it is rare and the symptoms overlap with several other disorders. The symptoms can occur in addition to having migraine headache, or can be mistaken for migraine alone, or dental problems such as temporomandibular joint disorder or musculoskeletal issues. 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.

<span class="mw-page-title-main">Wide dynamic range neuron</span>

The wide dynamic range (WDR) neuron was first discovered by Mendell in 1966. Early studies of this neuron established what is known as the gate control theory of pain. The basic concept is that non-painful stimuli block the pathways for painful stimuli, inhibiting possible painful responses. This theory was supported by the fact that WDR neurons are responsible for responses to both painful and non-painful stimuli, and the idea that these neurons could not produce more than one of these responses simultaneously. WDR neurons respond to all types of somatosensory stimuli, make up the majority of the neurons found in the posterior grey column, and have the ability to produce long range responses including those responsible for pain and itch.

<span class="mw-page-title-main">Outline of the human nervous system</span> Overview of and topical guide to the human nervous system

The following diagram is provided as an overview of and topical guide to the human nervous system:

Ocular neuropathic pain is a spectrum of disorders of ocular pain which are caused by damage or disease affecting the nerves. Ocular neuropathic pain is frequently associated with damaged or dysfunctional corneal nerves, but the condition can also be caused by peripheral or centralized sensitization. The condition shares some characteristics with somatic neuropathic pain in that it is similarly associated with abnormal sensations (dysesthesia) or pain from normally non-painful stimuli (allodynia), but until recent years has been poorly understood by the medical community, and frequently dismissed by ophthalmologists who were not trained to identify neuropathic pain as a source of unexplained eye pain beyond objective findings noted on slit-lamp examination.

References

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  7. ↑ 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. S2CID   28750350.
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  12. ↑ Richard Rowland (1838). A treatise on neuralgia. p.  3 . Retrieved 5 August 2012.
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  14. ↑ Warren JC (19 February 1928). "Cases of neuralgia or painful afflictions of the nerves". Boston Med. Surg. J. (i): 1–6.
  15. ↑ Graham TJ (1928). Treatise on indigestion. London: W. Joy. pp. 256–7.
  16. ↑ Teale TP (1830). A treatise on neuralgic diseases. Philadelphia: E. L. Carey & A. Hart.
  17. ↑ Sherriff, Robert Cedric (1983). Journey's end. Harmondsworth: Penguin. pp. 53–58. ISBN   0-14-118326-8.
  18. ↑ Aces High. 1976. Event occurs at 12:39.

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