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Mononeritis multiplex
- 1. Prashant Shringi Senior residentNeurology Govt. Medical College Kota
- 2. Generalized termincluding disorders of any cause affecting PNS May involve sensory nerves, motor nerves, or both or autonomic nerves May affect one nerve (mononeuropathy), several nerves together (polyneuropathy) or several nerves not contiguous (Mononeuropathy multiplex)
- 3. Mononeuritis multiplexis a painful, asymmetrical, asynchronous sensory and motor peripheral neuropathy involving simultaneous or sequential damage to two or more noncontiguous peripheral nerves . : Bradely’s neurology in clinical practice 7th edition
- 4. As thecondition worsens, it becomes less multifocal and more symmetrical. Mononeuropathy multiplex syndromes can be distributed bilaterally, distally, and proximally throughout the body.
- 5. Mononeuritis multiplexactually 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 Leprosy Diabetes mellitus Vasculitis
- 6. The damageto the nerves involves destruction of the axon and therefore interferes with nerve conduction.
- 7. Common causesof damage include a lack of oxygen from decreased blood flow or inflammation of blood vessels causing destruction of the vessel wall and occlusion of the vessel lumen of small epineurial arteries.
- 8. Mononeuritis multiplexcan be associated with many different conditions. Infections Rheumatological disorders Chronic conditions Malingnancy Hematological conditions
- 9. Mononeuritis multiplexcan be associated with the following infections: Lyme disease Leprosy Acute viral hepatitis A Hepatitis B Hepatitis C Acute parvovirus B-19 infection Herpes simplex virus infection AIDS and HIV infection
- 10. Mononeuritis multiplexcan be associated with the following rheumatological disorders: Wegener granulomatosis Henoch-Schönlein syndrome Sjögren syndrome Behçet’s disease Temporal (giant cell) arteritis
- 11. Systemic lupuserythematosus Rheumatoid arthritis Polyarteritis nodosa Scleroderma
- 12. Mononeuritis multiplexcan be associated with the following chronic conditions: Diabetes mellitus Amyloidosis Neurosarcoidosis Celiac disease
- 13. Mononeuritis multiplexcan be associated with the following cancer-related conditions: Chronic graft versus host disease (GVHD) Direct tumor invasion with intraneural spread – Lymphoma, B-cell leukemia, carcinoid tumor Paraneoplastic – Small cell lung cancer
- 14. Mononeuritis multiplexcan be associated with the following hematologic conditions: Churg-Strauss syndrome Hypereosinophilia Cryoglobulinemia Hypereosinophilia Atopy-related peripheral neuritis Idiopathic thrombocytopenic purpura
- 15. Mononeuritis multiplexcan be associated with the following miscellaneous conditions: Amphetamine angiitis Gasoline sniffing In addition, mononeuritis multiplex can be associated with the genetic disorder Tangier disease and with multiple compression neuropathies.
- 16. Persons withone occurrence of mononeuritis multiplex are more prone to a recurrence. Mononeuritis multiplex can become progressively worse over time. Approximately 33% of cases originate from unidentifiable causes.
- 17. The actualincidence of mononeuritis multiplex is not known due to the widely varied etiologies that may lead to this 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.
- 18. The ageof 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.
- 19. If thecause 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.
- 20. Complications inmononeuritis 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
- 21. The suspectedcause of mononeuritis multiplex, as suggested by the patient’s history, symptoms, and pattern of symptom development, helps to determine which tests to perform.
- 22. A detailedand complete medical history is vitally important in determining the possible underlying cause of mononeuritis multiplex. The pain usually is characterized as deep and aching, with superimposed lancinating jabs that are most severe at night.
- 23. All patientsshould be questioned regarding - • HIV risk factors • possibility of a tick bite (Lyme disease) • Constitutional symptoms (malignancy) like weight loss, malaise, anorexia.
- 24. Individuals withDiabetes typically present with acute onset of severe, unilateral thigh pain that is followed rapidly by weakness and atrophy of the anterior thigh muscles and loss of the ankle reflex.
- 25. Other possible symptomsthat may be reported by the patient include the following: Numbness Tingling Abnormal sensation Burning pain - Dysesthesia Difficulty moving a body part - Paralysis Lack of controlled movement of a body part
- 26. Loss ofsensation and movement may be associated with dysfunction of specific nerves. Examination reveals preservation of reflexes and good strength except in regions that have been more profoundly affected.
- 27. Some commonfindings of mononeuritis multiplex are as follows Sciatic nerve dysfunction Femoral nerve dysfunction Common peroneal nerve dysfunction Axillary nerve dysfunction Radial nerve dysfunction
- 28. Median nervedysfunction Ulnar nerve dysfunction Peroneal nerve palsy Autonomic dysfunction - Dysfunction in the part of the nervous system that controls involuntary bodily functions, such as the glands, blood vessels, and heart.
- 29. Laboratory testsinclude the following: Complete blood count (CBC) with a differential Fasting blood glucose levels Borrelia burgdorferi antibody titer - If Lyme disease is suspected Human immunodeficiency virus (HIV) blood tests - If HIV infection is suspected
- 30. Hepatitis screen- If hepatitis is suspected as a causative agent Erythrocyte sedimentation rate (ESR) and C- reactive protein level - If a systemic inflammatory process is suspected. Herpes viridae serology Parvovirus B-19 antibodies
- 31. Autoimmune profile Extensive vasculitic and rheumatological workup include ANA, RF, Anti-dsDNA, Anti-Ro, Anti-La, ANCA screen, cryoglobulins Serum protein electrophoresis
- 32. In somecases, a nerve biopsy may be appropriate to determine the underlying cause of mononeuritis multiplex (usually a combination of perivascular mononuclear inflammatory cells and multifocal axonal loss and axonal loss with multinucleated inflammatory cells) .
- 33. A patternof necrotizing vasculitis of epineural arteries may be observed in HIV- related mononeuritis.
- 36. Some studieshave indicated that combining a nerve biopsy with a muscle biopsy can help clinicians to better diagnose peripheral nerve vasculitis, because it appears that in many cases, individuals with peripheral nerve vasculitis also have vasculitis in striated muscle.
- 37. Electrodiagnostic studiesare used only in conjunction with an accurate and complete history and physical examination. The lesion or lesions are distal to the motor and sensory cell bodies and result in either axonal disruption/degeneration or abnormal axonal conduction.
- 38. Sensory nerveconduction studies (NCSs) show abnormalities of decreased amplitude in the presence of axonal disruption. H-reflex latencies may be prolonged or absent in mononeuritis multiplex. However, the H-reflex is typically performed only in the tibial nerves, limiting its usefulness in investigating mononeuritis multiplex.
- 39. Abnormalities aresimilar to those seen in axonal polyneuropathies, with the exception of the anatomic distribution. A reduction in the motor action potential amplitudes and minimal alterations in nerve conduction velocity will be seen.
- 40. Findings onthe needle electrode examination can vary, depending on the severity and time course of the disorder..
- 41. Findings aretypically neuropathic and may include abnormal spontaneous membrane activity (positive sharp waves and fibrillation potentials) and, during and after reinnervation, increases in motor unit action potential (MUAP) duration, amplitude, and polyphasic potentials.
- 42. Slow progression -Treatcausative factors if possible Symptom Management
- 43. Tricyclic antidepressants ◦Amitryptilin, nortryptilin Calcium channel alpha-2-delta ligands ◦ Gabapentin, pregabalin Calcium channel blocker Prialt (Ziconotide) SNRI’s ◦ Duloxetine, venlafaxine Topical Agents ◦ Lidocaine, Capsaicin
- 44. Antiepileptic Drugs ◦Carbamazepine, phenytoin, lacosamide SSRI’s Opioid analgesics Tramadol Miscellaneous ◦ Botulinum toxin ◦ Mexiletine ◦ Alpha lipoic acid NMDA receptors unsuccessful ◦ Namenda, Dextromethorphan
- 45. First linedrugs Lidoderm 5% patch Tricyclic antidepressants Gabapentin Pregabalin p.o. Duloxetine Second line Carbamazepine Phenytoin Venlafaxine Tramadol
- 46. Physical Therapy ◦Gait and balance training Assistive devices Safe environment Footwear at all times Foot hygiene
- 47. If thecausative 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.
- 48.
- 49. Bradely’s neurologyin clinical practice 7th edition An Approach to the Evaluation of Peripheral Neuropathies;Mark B. Bromberg; SEMINARS IN NEUROLOGY/VOLUME 30, NUMBER 4 2010 Medscape.com