Mononeuritis Multiplex 

Updated: Feb 28, 2019
Author: Divakara Kedlaya, MBBS; Chief Editor: Dean H Hommer, MD 

Overview

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, 3]

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 Causes, Presentation, Workup, and Treatment):

  • Diabetes mellitus[1, 3]

  • Vasculitis[4, 5, 6, 7]

  • Amyloidosis[8]

  • Direct tumor involvement - Lymphoma, leukemia[9, 10]

  • Polyarteritis nodosa[11]

  • Rheumatoid arthritis[12, 13]

  • Systemic lupus erythematosus[14, 15]

  • Paraneoplastic syndromes[16, 17]

Pathophysiology and Etiology

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 causing destruction of the vessel wall and occlusion of the vessel lumen of small epineurial arteries.

Mononeuritis multiplex can be associated with many different conditions, as described below.

Mononeuritis multiplex can be associated with the following infections:

  • Lyme disease[18]

  • Leprosy[19, 20, 21]  - An Indian study, by Jaiswal et al, found mononeuritis multiplex to be the most common clinical presentation in a cohort of 18 patients with Hansen neuritis, with nerve conduction studies revealing the condition’s presence in 13 (72.2%) cases; severe sensory axonopathy was more prevalent than severe motor axonopathy[22]

  • Acute viral hepatitis A[23]

  • Hepatitis B[24]

  • Hepatitis C[25, 26]

  • Acute parvovirus B-19 infection[27]

  • Herpes simplex virus infection[28]

  • AIDS and HIV infection[29, 30]

Mononeuritis multiplex can be associated with the following rheumatologic disorders:

  • Wegener granulomatosis[31, 32]

  • Henoch-Schönlein syndrome[6, 33]

  • Sjögren syndrome[34, 35]

  • Behçet’s disease[36, 37]

  • Temporal (giant cell) arteritis[38]

  • Systemic lupus erythematosus[14, 15]

  • Rheumatoid arthritis[12, 13]

  • Polyarteritis nodosa - A retrospective study by Criado et al of 22 cases of cutaneous polyarteritis nodosa found that a quarter of the patients had mononeuritis multiplex[11, 39]

  • Scleroderma[40]

Mononeuritis multiplex can be associated with the following chronic conditions:

  • Diabetes mellitus[1, 3]

  • Amyloidosis[8]

  • Neurosarcoidosis[41, 42]

  • Celiac disease[43]

Mononeuritis multiplex can be associated with the following cancer-related conditions:

  • Chronic graft versus host disease (GVHD)[44]

  • Direct tumor invasion with intraneural spread - Lymphoma,[10] B-cell leukemia,[9] carcinoid tumor[45]

  • Paraneoplastic - Small cell lung cancer[16, 17]

Mononeuritis multiplex can be associated with the following hematologic conditions:

  • Churg-Strauss syndrome[46, 47]

  • Hypereosinophilia

  • Cryoglobulinemia[48]  - A single-center, retrospective study by Feldman et al found that of 131 patients with possible or definite cryoglobulinemia-associated neurologic symptoms, 16 (12.2%) had mononeuritis multiplex[49]

  • Hypereosinophilia[50]

  • Atopy-related peripheral neuritis (see below)[51]

  • Idiopathic thrombocytopenic purpura[52, 53]

Mononeuritis multiplex can be associated with the following miscellaneous conditions:

  • Amphetamine angiitis[54]

  • Gasoline sniffing[55]

In addition, mononeuritis multiplex can be associated with the genetic disorder Tangier disease[56, 57] and with multiple compression neuropathies.

Moreover, in a study of 157 patients with eosinophilic granulomatosis with polyangiitis, Cottin et al found mononeuritis multiplex to be associated with cases that included systemic vasculitis and the presence of antineutrophil cytoplasmic antibodies.[58]

Persons with one 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.[59]

In a cross-sectional, Japan-wide survey, Isobe et al found that patients with atopy-related peripheral neuritis (n = 133) tended to develop mononeuritis multiplex, with their lower limbs predominantly affected. The investigators also determined that most patients with atopy-related peripheral neuritis were female and that individuals with the disease tended to have a higher eosinophil count than did patients in the study with atopic myelitis.[51]

Epidemiology

The actual incidence of mononeuritis multiplex in the United States and rest of the world 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.

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.

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

A Danish study by Al-Zuhairy et al found that compared with healthy controls, patients who had suffered from multifocal motor neuropathy, a form of mononeuritis multiplex, for a median period of 24 years had a 9% decrease in the Rasch-built Overall Disability Scale for Multifocal Motor Neuropathy, a three-fold increase in the Neuropathy Impairment Score, a 29% reduction in isokinetic strength, a 56% decrease in grip strength, a 13% prolongation of the Timed 25-Foot Walk, and a 20% impairment measured via the EQ-5D-DL index value.[60]

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. In addition, 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 ensure 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).

 

Presentation

History

A detailed and complete medical history is vitally important in determining the possible underlying cause of mononeuritis multiplex. Pain often begins in the low back or hip and spreads to the thigh and knee on one side. The pain usually is characterized as deep and aching, with superimposed lancinating jabs that are most severe at night. Individuals with diabetes 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 knee reflex. Other possible symptoms that 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

Physical Examination

Loss of sensation 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. Some common findings of mononeuritis multiplex are as follows (not listed in order of frequency):

  • Sciatic nerve dysfunction

  • Femoral nerve dysfunction

  • Common peroneal nerve dysfunction

  • Axillary nerve dysfunction

  • Radial nerve dysfunction

  • Median nerve dysfunction

  • 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

 

DDx

Diagnostic Considerations

Conditions to consider in the differential diagnosis of mononeuritis multiplex include the following:

  • Ischemic monomelic neuropathy

  • Meralgia paresthetica

  • Neoplastic brachial plexopathy

  • Neoplastic lumbosacral plexopathy

  • Piriformis syndrome

  • Post ̶ head injury autonomic complications

  • Postpolio syndrome

  • Posttraumatic syringomyelia

  • Radiation-induced brachial plexopathy

  • Radiation-induced lumbosacral plexopathy

  • Rheumatoid arthritis

  • Systemic lupus erythematosus

  • Thoracic outlet syndrome

  • Traumatic brachial plexopathy

  • Lyme disease

  • Sjögren syndrome

  • Cryoglobulinemia

  • Temporal arteritis

  • Scleroderma

  • Sarcoidosis

  • Leprosy (Hansen disease)

  • Acute viral hepatitis A

  • AIDS

  • Hypereosinophilia

  • Paraneoplastic peripheral neuropathy

Differential Diagnoses

 

Workup

Approach Considerations

The suspected cause of mononeuritis multiplex, as suggested by the patient’s history, symptoms, and pattern of symptom development, helps to determine which tests to perform. (Imaging studies are not indicated for the diagnosis of mononeuritis multiplex.) Laboratory tests ordered include 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

  • 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

  • Autoimmune profile

  • Herpes viridae serology

  • Parvovirus B-19 antibodies

Histologic Findings

In some cases, a nerve biopsy may be appropriate to determine the underlying cause of mononeuritis multiplex (eg, a combination of perivascular mononuclear inflammatory cells and multifocal axonal loss and axonal loss with multinucleated inflammatory cells).[4] A pattern of necrotizing vasculitis of epineural arteries may be observed in HIV-related mononeuritis.

Some studies have 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.[4] A 1988 study, for example, found that among patients known to have peripheral nerve vasculitis, up to 45% of them did not have demonstrable evidence of the condition in their superficial peroneal nerve but did show evidence of vasculitis in their peroneus brevis muscle.[61]

However, a 2008 study of patients with proven peripheral nerve vasculitis (most of whom presented with either asymmetrical axonal polyneuropathy or mononeuritis multiplex) found that the benefits of combining nerve and muscle biopsies for the diagnosis of peripheral nerve vasculitis seem to depend on which muscle and nerve are chosen.[4] When compared with results from sural nerve biopsies alone, the report's authors found no significant increase in diagnoses of peripheral nerve vasculitis derived from combined biopsies of the sural nerve and the vastus lateralis muscle.

Electrodiagnostic Studies

Electrodiagnostic studies are 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.

Sensory nerve conduction studies

Sensory nerve conduction studies (NCSs) show abnormalities of decreased amplitude in the presence of axonal disruption. Physical examination and history will direct the electromyographic examination. Sensory NCSs are beyond the reference range for amplitude and/or latency only if a large enough percentage of the sensory axons are damaged. A lesion that eliminates conduction in less than 10% of the sensory axons produces a loss of amplitude that may not be detectable. 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.

Motor nerve conduction studies

Abnormalities are similar 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.

Velocity may be slightly reduced compared with the reference range, but it does not usually decrease below 70-80% of the lower limit of the reference range. Abnormal findings directly depend on the severity and aggressiveness of the underlying disease. A decrement of motor amplitude may be seen if there is significant denervation.

Needle electrode examination

Findings on the needle electrode examination can vary, depending on the severity and time course of the disorder. Findings are typically 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 polyphasia. Additionally, the loss of motor axons should generate a reduced number of MUAPs firing at high rates (ie, reduced recruitment).

Procedures

The performance of any procedure, such as a nerve biopsy, is dictated by the patient’s history and physical examination results. The purpose of any procedure is to determine the primary pathologic process.[4] A nerve biopsy may be performed to help distinguish between demyelination (destruction of parts of the myelin sheath covering the nerve) and axonal degeneration (destruction of the axon portion of the nerve cell), to identify inflammatory nerve conditions (neuropathies), or to confirm specific diagnoses.

 

Treatment

Approach Considerations

The physician must try to elucidate the underlying cause and initiate appropriate treatment according to the established protocols for the specific disease condition. Disorders such as vasculitis[4, 5, 6] can be fatal if not treated. (A study by de Luna et al of plasma exchange in the treatment of systemic necrotizing vasculitides found that in patients with mononeuritis multiplex, improvement in severe motor weakness occurred.[62] )

In addition, the physician and the patient should have the understanding that the nerve pain may be persistent for an extended period and may require ongoing treatment, with possible referral to a comprehensive pain treatment center. Both must have realistic expectations.

Other treatment considerations include the following:

  • Use caution in treating the patients who are insensate, especially with the use of modalities (eg, ice, heat)

  • Monitor and help control blood sugar levels in individuals with diabetes

  • Institute nutritional supplementation

  • Monitor bony prominences for pressure points

Safety is an important consideration, and appropriate safety measures must be provided. These may include, but are not necessarily limited to, installation of railings, removal of obstacles (eg, loose rugs that may slip on the floor), installation of low-level lighting, and testing of water temperatures before bathing.

Consultations

Consultations in the treatment of mononeuritis multiplex can include the following:

  • Neurologist - If an underlying neurologic condition is suspected

  • Rheumatologist - If an underlying rheumatologic condition is suspected

  • Infectious disease specialist - If evidence of an infectious etiology is present

  • Pain management specialist and physiatrist referrals may be needed in selected cases

Follow-up

The patient should follow up with the primary physician for underlying disorders (eg, diabetes). In addition, the patient should follow up with the primary physician or with the rehabilitation physician for pain medications and/or monitoring of laboratory tests.

Rehabilitation Therapies

Physical therapy

Physical therapy (PT) may be recommended for patients with mononeuritis multiplex, with the specific treatment generally depending on the site involved. PT can help to prevent contractures and maintain strength through the use of range of motion (ROM) and strengthening exercises, as appropriate. The physical therapist can assist the patient with positioning issues and recommend braces or splints (static and functional) to increase his/her independence with mobility.

Patients with mononeuritis multiplex often exhibit problems with diminished sensation and require instruction to improve their safety awareness. In some cases, a transcutaneous electrical nerve stimulation (TENS) unit may be recommended for pain control in patients with this condition. The physical therapist can instruct the patient in the appropriate setup and use of the unit.

Occupational therapy

Occupational therapy is directed toward maintaining functional independence in patients with mononeuritis multiplex. This training may include instructing the patient in the use of adaptive techniques for activities of daily living (ADLs). Built-up handles on eating utensils and adaptive aids (eg, long shoehorns, reachers) may be used to help the patient perform ADLs such as dressing and eating. A job-site analysis may need to be completed by the physical therapist and/or occupational therapist to ensure occupational safety. Therapy can incorporate job-specific training for those individuals who would benefit.

Recreational therapy

The primary focus of recreational therapy is to maintain the patient's activity level and self-esteem during recovery.

 

Medication

Medication Summary

The clinician must integrate the patient’s symptoms, signs, and clinical evaluation when considering the treatment of neuropathic pain in mononeuritis multiplex. The reduction of inflammation around the epineurium is the primary goal of treatment. Additional treatments are aimed at treating the primary cause and/or associated symptomology.

Over-the-counter analgesics are used for pain control. Various other medications may be used to reduce dysesthetic pain, which typically is a stabbing, burning pain.

Traditional medical models for treating chronic and neuropathic pain are based on the use of tricyclic antidepressants (eg, amitriptyline, nortriptyline, desipramine). When appropriate, anticonvulsant drugs have been used to treat lancinating pain. Gabapentin and pregabalin are medications of choice if tricyclic antidepressants are not effective. Despite its significant adverse effects profile, carbamazepine is the first-line medication for trigeminal neuralgia.

Advances in understanding of the pathophysiology of acute and chronic neuropathic pain states may lead to newer, more effective pharmacologic approaches to treatment.

More effective and safer antiepileptic drugs have continued to benefit patients with chronic pain conditions. Neurotransmitters such as serotonin, glutamate, substance P, calcitonin gene-related peptide (CGRP), and gamma-aminobutyric acid (GABA) are the targets of research and development of pharmacologic therapies for acute and chronic pain. In addition, sodium activity and calcium activity play important roles in the pathology and treatment of these chronic medical problems.

Medications that increase gastric motility (eg, metoclopramide) may be administered. Gastric motility also may be increased if the patient eats small, frequent meals and sleeps with his/her head elevated. Medications for bladder dysfunction include bethanechol and oxybutynin.

A report by Samson et al on two randomized, controlled trials indicated that in patients with eosinophilic granulomatosis with polyangiitis, non-hepatitis B virus polyarteritis nodosa, or microscopic polyangiitis (specifically, those patients whose five-factor score does not indicate a poor prognosis), the presence of mononeuritis multiplex can predict whether medical treatment other than corticosteroid therapy alone will be needed for a good outcome. The study involved 193 patients; 86 of them—as a result of corticosteroid failure, corticosteroid dependence, or relapse—required treatment in addition to corticosteroids (ie, intravenous immunoglobulins, biotherapies, cytotoxic agents, plasma exchanges). Univariate and multivariate analyses revealed that only the presence of initial mononeuritis multiplex was significantly associated with the need for add-on therapy.[63]

Opioids

Opioid analgesics, including tramadol, have been found to be efficacious in several high-quality randomized controlled trials in patients with various types of neuropathic pain (grade A recommendation). However, owing to concerns over their long-term safety (relative to first-line medications), they are recommended principally for patients who have not responded to the first-line medications, except in certain clinical circumstances (ie, for the treatment of acute neuropathic pain, episodic exacerbations of severe neuropathic pain, neuropathic cancer pain, and during titration of a first-line medication when prompt relief of pain is needed).[64, 65]

Corticosteroids

Class Summary

These can be helpful if mononeuritis multiplex is associated with vasculitis. Failure to recognize and treat vasculitis can result in fatal consequences.[4, 5, 6]

Prednisone

Prednisone is an immunosuppressant used for the treatment of autoimmune disorders. It may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte activity. The drug stabilizes lysosomal membranes and also suppresses lymphocytes and antibody production. Long-term treatment with corticosteroids may be necessary in individuals with mononeuritis multiplex.

Immunosuppressants

Class Summary

If the overlying condition is inflammatory or autoimmune in nature, immunosuppressants may be of limited benefit to patients who are intolerant of steroids.

Intravenous immunoglobulin (IVIG; Carimune Gammagard S/D, Gamunex-C, Octagam)

Intravenous immunoglobulin (IVIG) uses anti-idiotypic antibodies to neutralize circulating myelin antibodies. IVIG down-regulates proinflammatory cytokines, including interferon-gamma. It blocks Fc receptors on macrophages, suppresses inducer T cells and B cells, and augments suppressor T cells. In addition, IVIG blocks complement cascade, promotes remyelination, and may increase cerebrospinal fluid (CSF) immunoglobulin G (10%).

Anticonvulsants, Other

Class Summary

These agents are used to treat associated symptoms of dysesthesia and neuropathic pain.

Gabapentin (Neurontin)

Gabapentin has anticonvulsant properties and antineuralgic effects; however, its exact mechanism of action is unknown. It is structurally related to GABA but does not interact with GABA receptors. Titration to effect can take place over several days (300 mg on day 1, 300 mg twice on day 2, and 300 mg 3 times on day 3).

Carbamazepine (Tegretol, Equetro, Epitol, Carbatrol)

Carbamazepine may reduce polysynaptic responses and block posttetanic potentiation. It is a first-line medication for trigeminal neuralgia.

Topiramate (Topamax)

Topiramate is a sulfamate-substituted monosaccharide with a broad spectrum of antiepileptic activity; it may have state-dependent sodium channel blocking action. It potentiates the inhibitory activity of the neurotransmitter GABA. In addition, topiramate may block glutamate activity. It is not necessary to monitor plasma concentrations of topiramate to optimize therapy. On occasion, the addition of topiramate to phenytoin may require adjustment of the phenytoin dose to achieve optimal clinical outcome.

Pregabalin (Lyrica)

Pregabalin is a structural derivative of GABA. Its mechanism of action is unknown. Pregabalin binds with high affinity to the alpha2-delta site (a calcium channel subunit). In vitro, it reduces the calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function. The US Food and Drug Administration (FDA) approved pregabalin for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as adjunctive therapy in partial-onset seizures.

Zonisamide (Zonegran)

Zonisamide is indicated for adjunctive treatment of partial seizures with or without secondary generalization. Evidence suggests that it is effective against myoclonic and other generalized seizure types.

Tricyclic Antidepressants

Class Summary

These agents have analgesic properties useful for chronic and neuropathic pain.

Amitriptyline

Amitriptyline inhibits the reuptake of serotonin and/or norepinephrine at the presynaptic neuronal membrane, which increases their concentration in the central nervous system (CNS). Amitriptyline may increase or prolong neuronal activity, since reuptake of these biogenic amines is important physiologically in terminating transmitting activity.

Imipramine (Tofranil)

These agents have been suggested to act by inhibiting reuptake of noradrenaline at synapses in central descending pain-modulating pathways located in the brainstem and spinal cord.

Nortriptyline (Pamelor)

Nortriptyline has demonstrated effectiveness in the treatment of chronic pain.

Desipramine (Norpramin)

This is the original TCA used for depression. These agents have been suggested to act by inhibiting reuptake of noradrenaline at synapses in central descending pain-modulating pathways located in the brainstem and spinal cord.

Prokinetic Agents

Class Summary

Medications that increase gastric motility (eg, Reglan) may be administered. Gastric motility also may be increased if the patient eats small, frequent meals and sleeps with his or her head elevated.

Metoclopramide (Reglan, Metozolv)

The antiemetic effect of metoclopramide appears to be due to its ability to block dopamine receptors in the chemoreceptor trigger zone (CTZ) of the central nervous system (CNS). This agent also enhances gastrointestinal motility and accelerates gastric emptying time.

Cholinergic Agonists

Class Summary

Medications for bladder dysfunction include bethanechol and oxybutynin.

Oxybutynin chloride (Ditropan IR, Ditropan XL, Gelnique)

Both the immediate-release and the extended-release forms of oxybutynin have both an anticholinergic and a direct smooth muscle relaxant effect on the urinary bladder. In addition, oxybutynin provides a local anesthetic effect on the irritable bladder.

The human detrusor has M2 and M3 muscarinic receptors. The M3 receptor mediates contractile response of the human detrusor. Oxybutynin has greater affinity for the M3 receptor. Urodynamic studies have shown oxybutynin increases bladder size, decreases frequency of symptoms, and delays initial desire to void.

Ditropan XL has an innovative drug delivery system: oral osmotic delivery system (OROS). The Ditropan XL tablet has a bilayer core that contains a drug layer and a "push layer" that contains osmotic components. The outer tablet is composed of a semipermeable membrane with a precision laser-drilled hole that allows the drug to be released at a constant rate.

When the drug is ingested, the aqueous environment in the gastrointestinal tract causes water to enter the tablet via the semipermeable membrane at a constant rate. The introduction of water inside the tablet liquefies drug and causes the push layer to swell osmotically. As the push layer swells, it forces the drug suspension out the hole at a constant rate over a 24-h period.

Ditropan XL achieves steady-state levels over a 24-h period. It avoids first pass metabolism in liver and upper gastrointestinal tract to avoid cytochrome P450 enzymes. It has excellent efficacy, with minimal adverse effects.

Bethanechol (Urecholine)

The stimulation of the parasympathetic nervous system by bethanechol increases bladder muscle tone, causing contractions that initiate urination.

 

Questions & Answers

Overview

What is mononeuritis multiplex?

Which systemic disorders are associated with mononeuritis multiplex?

What is the pathophysiology and etiology of mononeuritis multiplex?

Which infections are associated with mononeuritis multiplex?

Which rheumatologic disorders are associated with mononeuritis multiplex?

Which chronic conditions are associated with mononeuritis multiplex?

Which cancer-related conditions are associated with mononeuritis multiplex?

Which hematologic conditions are associated with mononeuritis multiplex?

Which miscellaneous conditions are associated with mononeuritis multiplex?

Which genetic disorders are associated with mononeuritis multiplex?

What is the relationship between vasculitis and mononeuritis multiplex?

What is the likelihood of recurrence of mononeuritis multiplex?

What is the relationship between atopy-related peripheral neuritis and mononeuritis multiplex?

What is the incidence of mononeuritis multiplex?

What is the typical age of onset of mononeuritis multiplex?

What is the prognosis of mononeuritis multiplex?

What are the complications of mononeuritis multiplex?

What educational information should be provided to patients with mononeuritis multiplex?

Presentation

Why is a detailed patient history important in mononeuritis multiplex?

What are the common findings of mononeuritis multiplex?

DDX

What are the diagnostic considerations for mononeuritis multiplex?

What are the differential diagnoses for Mononeuritis Multiplex?

Workup

Which lab tests are used in the workup of mononeuritis multiplex?

What is the role of a nerve biopsy in the workup of mononeuritis multiplex?

What is the role of a muscle biopsy in the workup of mononeuritis multiplex?

When are electrodiagnostic studies used in the workup of mononeuritis multiplex?

How are sensory nerve conduction studies (NCSs) used in the workup of mononeuritis multiplex?

How are motor nerve conduction studies used in the workup of mononeuritis multiplex?

How are needle electrode exams used in the workup of mononeuritis multiplex?

What is the purpose of procedures used in the workup of mononeuritis multiplex?

Treatment

What are the approach considerations for the treatment of mononeuritis multiplex?

Which safety measures are indicated in the management of mononeuritis multiplex?

Which consultations are indicated in the workup of mononeuritis multiplex?

What are the follow-up considerations in the treatment of mononeuritis multiplex?

How is physical therapy used to treat mononeuritis multiplex?

How is a TENS unit used to treat mononeuritis multiplex?

What is the role of occupational therapy in the treatment of mononeuritis multiplex?

What is the purpose of recreational therapy in the treatment of mononeuritis multiplex?

Medications

What is the goal of medication in the treatment of mononeuritis multiplex?

Which medications are used to treat mononeuritis multiplex?

What are the traditional medical models for the treatment of mononeuritis multiplex?

Which agents are in development for the treatment of mononeuritis multiplex?

How are medications that increase gastric motility used on the treatment of mononeuritis multiplex?

When is add-on therapy indicated in the treatment of mononeuritis multiplex?

Which medications in the drug class Corticosteroids are used in the treatment of Mononeuritis Multiplex?

Which medications in the drug class Immunosuppressants are used in the treatment of Mononeuritis Multiplex?

Which medications in the drug class Anticonvulsants, Other are used in the treatment of Mononeuritis Multiplex?

Which medications in the drug class Tricyclic Antidepressants are used in the treatment of Mononeuritis Multiplex?

Which medications in the drug class Prokinetic Agents are used in the treatment of Mononeuritis Multiplex?

Which medications in the drug class Cholinergic Agonists are used in the treatment of Mononeuritis Multiplex?