Mononeuritis Multiplex 

  • Author: Divakara Kedlaya, MBBS; Chief Editor: Robert H Meier III, MD   more...
 
Updated: Jan 20, 2012
 

Background

Mononeuritis multiplex is a painful, asymmetrical, asynchronous sensory and motor peripheral neuropathy involving isolated damage to at least 2 separate nerve areas. Multiple nerves in random areas of the body can be affected. As the condition worsens, it becomes less multifocal and more symmetrical. Mononeuropathy multiplex syndromes can be distributed bilaterally, distally, and proximally throughout the body. (See Presentation.)[1, 2]

Mononeuritis multiplex actually is a group of disorders, not a true, distinct disease entity. Typically, the condition is associated with (but not limited to) systemic disorders such as the following (see Etiology, Presentation, Workup, and Treatment.):

Mononeuritis multiplex also may be associated with Lyme disease, Wegener granulomatosis, Sjögren syndrome, cryoglobulinemia, hypereosinophilia, temporal arteritis, scleroderma, sarcoidosis, idiopathic thrombocytopenic purpura,[7, 8] leprosy,[9] acute viral hepatitis A, acute parvovirus B-19 infection,[10] and acquired immunodeficiency syndrome (AIDS).[11, 12] Persons with one occurrence of mononeuritis multiplex are more prone to a recurrence. (See Prognosis, Presentation, and Workup.)

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Etiology

Mononeuritis multiplex most commonly is associated with diabetes mellitus and multiple nerve compressions. Mononeuritis multiplex involves damage to at least 2 separate nerve areas. This condition can become progressively worse over time. The damage to the nerves involves destruction of the axon (ie, the part of the nerve cell that is analogous to the copper part of a wire) and therefore interferes with nerve conduction. Common causes of damage include a lack of oxygen from decreased blood flow or inflammation of blood vessels. Approximately 33% of cases originate from unidentifiable causes.[13]

In a cross-sectional, Japan-wide survey, Isobe et al found that patients with atopy-related peripheral neuritis (APN, n = 133) tended to develop mononeuritis multiplex, with their lower limbs predominantly affected. The investigators also determined that most patients with APN were female and that individuals with the disease tended to have a higher eosinophil count than did patients in the study with atopic myelitis.[14]

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Epidemiology

The actual incidence of mononeuritis multiplex in the United States and elsewhere in the world is not known due to the widely varied underlying pathologies that may lead to the disorder. The primary disease process often is so dominant that the symptoms of mononeuritis multiplex simply are attributed to the initial disease and remain undiagnosed.

The age of onset for mononeuritis multiplex depends on the patient's age at occurrence of the associated disease process. For unknown reasons, however, this condition does tend to occur in older patients with relatively mild or unrecognized diabetes.

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Prognosis

If the cause of mononeuritis multiplex is identified early and is successfully treated, full recovery is possible, although it may take months to years. The same syndrome has a tendency to recur after an interval of months or years.

The extent of disability varies, ranging from no disability to partial or complete loss of function and movement. Complications in mononeuritis multiplex include the following:

  • Recurrent or unnoticed injury to any part of the body
  • Deformity
  • Atrophy
  • Disturbances of organ functions that are autonomically controlled (eg, cardiac, gastric, bladder)
  • Decreased self-esteem and decreased social interaction due to an inability to participate in activities because of pain or incoordination
  • Relationship problems associated with impotence
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Patient Education

If the causative factor for a patient's mononeuritis multiplex is discovered, education is directed toward avoidance of the initiating cause or pathogen. Additionally, recognition of early symptomology should be encouraged so that early treatment can be sought.

Persons with decreased sensation should be instructed to frequently check their feet or other affected areas for bruises, cuts, wounds, or other injuries. Also, patients who are insensate or incapacitated should be instructed to avoid prolonged pressure on various points on the body (eg, knees, elbows, sacrum) so as to discourage the development of pressure sores or ulcers.

Safety awareness instruction is important for these patients because of their impaired sensation and decreased ability to compensate for limitations. The patient should be instructed to assure that there is always adequate lighting, to test the water temperature before bathing or immersing body parts, and to wear protective shoes (no open toes or high heels).

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Contributor Information and Disclosures
Author

Divakara Kedlaya, MBBS  Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Loma Linda University School of Medicine; Medical Director, Physical Medicine and Rehabilitation and Pain Management, St Mary Corwin Medical Center

Divakara Kedlaya, MBBS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, and Colorado Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Paul V Brooks, MD  Medical Director, Department of Physical Medicine and Rehabilitation, Lexington Clinic, PSC; Assistant Professor, Department of Orthopedics, Division of Sports Medicine, Assistant Professor, Department of Surgery, University of Kentucky College of Medicine

Paul V Brooks, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Association of University Professors, American College of Sports Medicine, American Medical Association, American Pain Society, American Spinal Injury Association, Association for Academic Psychiatry, and Brain Injury Association of America

Disclosure: Nothing to disclose.

Chief Editor

Robert H Meier III, MD  Director, Amputee Services of America; Active Medical Staff, Presbyterian/St Luke's Hospital, Spalding Rehabilitation Hospital, Select Specialty Hospital; Consulting Staff, Kindred Hospital

Robert H Meier III, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists

Disclosure: Nothing to disclose.

References
  1. Vial C, Bouhour F. [Vasculitis multiple mononeuropathies]. Rev Prat. Nov 15 2008;58(17):1896-9. [Medline].

  2. Magy L. [What is a peripheral neuropathy?]. Rev Prat. Nov 15 2008;58(17):1873-7, 1880-1. [Medline].

  3. Bennett DL, Groves M, Blake J, et al. The use of nerve and muscle biopsy in the diagnosis of vasculitis: a 5 year retrospective study. J Neurol Neurosurg Psychiatry. Dec 2008;79(12):1376-81. [Medline]. [Full Text].

  4. Pagnoux C. Churg-Strauss syndrome: evolving concepts. Discov Med. Mar 2010;9(46):243-52. [Medline].

  5. Garzoni L, Vanoni F, Rizzi M, et al. Nervous system dysfunction in Henoch-Schonlein syndrome: systematic review of the literature. Rheumatology (Oxford). Dec 2009;48(12):1524-9. [Medline].

  6. Makol A, Grover M. Adalimumab induced mononeuritis multiplex in a patient with refractory rheumatoid arthritis: a case report. Cases J. Oct 30 2008;1(1):287. [Medline]. [Full Text].

  7. Greenberg MK, Sonoda T. Mononeuropathy multiplex complicating idiopathic thrombocytopenic purpura. Neurology. Sep 1991;41(9):1517-8. [Medline].

  8. Kumar S. Painful mononeuritis multiplex in idiopathic thrombocytopenic purpura. Indian Pediatr. Jun 2005;42(6):621-2. [Medline].

  9. Khadilkar SV, Benny R, Kasegaonkar PS. Proprioceptive loss in leprous neuropathy: a study of 19 patients. Neurol India. Oct-Dec 2008;56(4):450-5. [Medline]. [Full Text].

  10. Lenglet T, Haroche J, Schnuriger A, et al. Mononeuropathy multiplex associated with acute parvovirus B19 infection: characteristics, treatment and outcome. J Neurol. Jul 2011;258(7):1321-6. [Medline].

  11. Modi M, Vats AK, Prabhakar S, Singla V, Mishra S. Acro-osteolysis and mononeuritis multiplex as a presenting symptom of systemic angiitis of Wegener's type. Indian J Med Sci. Apr 2007;61(4):212-5. [Medline].

  12. Peshin R, O'Gradaigh D. Mononeuritis multiplex as a presenting feature of Wegener granulomatosis: a case report. Clin Rheumatol. Aug 2007;26(8):1389-90. [Medline].

  13. Mauermann ML, Ryan ML, Moon JS, et al. Case of mononeuritis multiplex onset with rituximab therapy for Waldenstrom's macroglobulinemia. J Neurol Sci. Sep 15 2007;260(1-2):240-3. [Medline].

  14. Isobe N, Kira J, Kawamura N, et al. Neural damage associated with atopic diathesis: a nationwide survey in Japan. Neurology. Sep 8 2009;73(10):790-7. [Medline].

  15. Said G, Lacroix-Ciaudo C, Fujimura H, et al. The peripheral neuropathy of necrotizing arteritis: a clinicopathological study. Ann Neurol. May 1988;23(5):461-5. [Medline].

  16. O'Connor AB, Dworkin RH. Treatment of neuropathic pain: an overview of recent guidelines. Am J Med. Oct 2009;122(10 Suppl):S22-32. [Medline].

  17. Finnerup NB, Sindrup SH, Jensen TS. The evidence for pharmacological treatment of neuropathic pain. Pain. Sep 2010;150(3):573-81. [Medline].

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