Neuritis
Neuritis | |
---|---|
IVIG, Gabapentin, Amitriptyline |
Neuritis (/njʊəˈraɪtɪs/), from the Greek νεῦρον),[1] is inflammation of a nerve[2] or the general inflammation of the peripheral nervous system. Inflammation, and frequently concomitant demyelination,[3][4][5] cause impaired transmission of neural signals and leads to aberrant nerve function. Neuritis is often conflated with neuropathy, a broad term describing any disease process which affects the peripheral nervous system. However, neuropathies may be due to either inflammatory[6] or non-inflammatory causes,[7] and the term encompasses any form of damage, degeneration, or dysfunction, while neuritis refers specifically to the inflammatory process.
As inflammation is a common reaction to biological insult, many conditions may present with features of neuritis. Common causes include autoimmune diseases, such as multiple sclerosis; infection, either bacterial, such as leprosy, or viral, such as varicella zoster; post-infectious immune reactions, such as Guillain-Barré syndrome; or a response to physical injury, as frequently seen in sciatica.[8][9]
While any nerve in the body may undergo inflammation,[10] specific etiologies may preferentially affect specific nerves.[11] The nature of symptoms depends on the specific nerves involved, neuritis in a sensory nerve may cause pain, paresthesia (pins-and-needles), hypoesthesia (numbness), and anesthesia, and neuritis in a motor nerve may cause paresis (weakness), fasiculation, paralysis, or muscle wasting.
Treatment of neuritis centers around removing or managing any inciting cause of inflammation, followed by supportive care and anti-inflammatory or immune modulatory treatments as well as symptomatic management.
Causes
Infectious
Both active infections and post-infectious autoimmune processes cause neuritis.[12] Rapid identification of an infectious cause of neuritis dictates treatment approach and often has a much more positive long term prognosis than other etiologies.[13] Bacterial, viral, and spirochete infections all have been associated with inflammatory neural responses. Some of the bacterial agents most associated with neuritis are leprosy, lyme disease, and diphtheria. Viral causes of neuritis include herpes simplex virus, varicella zoster virus, and HIV.
Leprosy is frequently characterized by direct neural infection by the causative organism, mycobacterium leprae.[14] Leprosy presents with a heterogeneous clinical picture dictated by bacterial titer and inborn host resistance.[13] Tuberculoid leprosy, seen in cases where host immunity is high, is not commonly associated with neuritis. It presents with a low number of anesthetic, anhydrotic skin plaques with few bacilli, the result of a granulomatous process which destroys cutaneous nerves.[15] Lepromatous leprosy, seen when the host lacks resistance to the organism, presents with widespread skin lesions and palpably enlarged nerves.[15] Disease involvement in this form of leprosy characteristically progresses from cooler regions of the body, such as the tip of the nose and ear lobes, towards warmer regions of the body eventually resulting in extensive loss of sensation and destructive skin lesions. Rapid treatment is a critical component of care in patients affected with leprosy, delayed care results in permanent loss of sensation and tissue damage which requires an extensive treatment regime.[16]
Lyme disease, caused by the spirochete Borrelia burgdorferi, is a tick-borne illness with both peripheral and central neurological manifestations. The first stage of Lyme disease frequently presents with a pathognomonic "bull's eye" rash, erythema migrans, as well as fever, malaise, and arthralgias. Roughly 15% of untreated patients will then develop neurological manifestations, classically characterized by cranial neuropathy, radiculoneuritis, and a lymphocytic meningitis.[16] The nerve inflammation seen in neurological lyme disease is associated with a lymphoctyic infiltrate without evidence of direct infection of peripheral nerves.[15] While commonly self-limiting, treatment with antibiotics may hasten resolution of symptoms.[17][18]
Diphtheria, a once common childhood respiratory infection, produces a neurotoxin which can result in a biphasic neuropathy.[16] This neuropathy begins with paralysis and numbness of the soft palate and pharynx as well as bulbar weakness several days to weeks after the initial upper respiratory infection, followed by an ascending flaccid paralysis caused by an acute inflammatory demyelinating neuropathy after several more weeks.[15] While antibiotics are effective at eradicating the bacterium, neurological sequelae of infection must be treated with diphtheria antitoxin.[19]
Varicella zoster virus, the cause of chickenpox, can be found dormant throughout the nervous system after an initial infection. Reactivation of the virus cause herpes zoster, commonly known as shingles, is seen in a dermatomal or cranial nerve distribution corresponding to the ganglion in which the latent virus resided. After the herpetic rash resolves, an additional period of postherpetic neuralgia may persist for weeks to months.[15] Antiviral medications, including acyclovir, are effective at controlling viral reactivation. Management of ensuing neuropathic often requires further management possibly including gabapentin, amitriptyline, carbamazepine, or topical lidocaine.[22]
Autoimmune
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) is an inflammatory neuropathy, which while pathophysiologically similar to AIDP, progresses over a much more protracted time scale.[16] CIDP has an insidious onset and progresses over months to years, but is otherwise similar to AIDP in serological, CSF, and electrodiagnostic studies. Treatment consists of corticosteroids, with IV immunoglobulon or plasmapheresis as a bridge treatment until symptoms respond to corticosteroids.[28]
Paraneoplastic
Several different malignancies, particularly small-cell lung cancer and Hodgkin lymphoma, are associated with a paraneoplastic neuritis. This carcinomatous polyneuropathy is associated with the presence of antibodies against onconeural antigen, Hu, Yo, amphiphysin, or CV2/CRMP5, which recognize and bind to both tumor cells and peripheral nervous system neurons.[29] This paraneoplastic syndrome may present as either a sensory neuropathy, affecting primarily the dorsal root ganglion, resulting in a progressive sensory loss associated with painful paresthesias of the upper limbs, or a mixed sensorimotor neuropathy which is also characterized by progressive weakness. Treatment of paraneoplastic syndromes aim for both elimination of tumor tissue via conventional oncologic approach as well as immunotherapy options such as steroids, plasmapheresis or IVIG.[30]
Metabolic
Metabolic abnormalities and deficiencies in certain vitamin, particularly B vitamins, are associated with inflammatory degeneration of peripheral nerves.[31] Deficiency of vitamin B1, thiamine, causes beriberi which can be associated with a painful sensory neuropathy with muscle weakness and atrophy. Deficiency of niacine, vitamin B3, causes pellagra which can present with various peripheral neuropathies in addition to keratotic skin lesions. Vitamin B6, pyridoxine, has been associated with peripheral nerve damage both in cases of deficiency and excess.[32] Deficiency of vitamin B12 causes subacute combined degeneration, a disease classically associated with a central demyelinating process; however, it also presents with a painful peripheral neuropathy. Treatment of vitamin deficiencies focuses around repletion of specific deficiencies, recovery is often prolonged and some of the damage is often permanent.[33]
Toxic
Many classes of medication may have toxic effects on peripheral nerves, these
Diagnosis
The accurate diagnosis and characterization of a neuritis begins with a thorough physical exam to characterize and localize any symptoms to a specific nerve or distribution of nerves.[29] An exam will assess the time course, distribution, and severity and nerve dysfunction as well as whether the disease process involves sensory, motor, or both sensorimotor nerves. After the lesion has been localized, a more focused investigation may use specific techniques appropriate for the involved nerves. Blood tests should be performed to evaluate blood glucose and serum B12 levels with metabolites, additional measurement of specific vitamins or toxins may be performed as indicated if the history and physical exam are consistent. Medical tests which are often useful include: nerve biopsy, MRI, electromography, nerve conduction studies. fundoscopy, and lumbar punctures. However, the diagnosis of many of the disorders associated with neuritis is a clinical one which does not rely upon any particular diagnostic test.[16][3][27]
References
- ^ Chisholm, Hugh, ed. (1911). . Encyclopædia Britannica. Vol. 19 (11th ed.). Cambridge University Press. pp. 428–9.
- ^ "neuritis" at Dorland's Medical Dictionary
- ^ PMID 21527960.
- S2CID 26420981.
- PMID 28084646.
- )
- )
- PMID 26250643.
- OCLC 1048610895.)
{{cite book}}
: CS1 maint: location missing publisher (link - ^ Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health (Seventh ed.). 2003.
- )
- S2CID 35635940.
- ^ )
- ^ "Leprosy". The Lecturio Medical Concept Library. Retrieved 1 August 2021.
- ^ )
- ^ )
- OCLC 892787077.
- S2CID 22534091.
- PMID 31804499.
- OCLC 1021256616.
- )
- PMID 26478818.
- PMID 23931799.
- OCLC 1021256616.
- PMID 17282996.
- ISBN 978-3-319-98454-4.
- ^ PMID 31541214.
- S2CID 4961339.
- ^ OCLC 972843900.
- PMID 23937626.
- PMID 18646107.
- ^ )
- S2CID 3119130.
- S2CID 26056076.
- S2CID 3119130.