Peripheral neuropathy
You don't need to be Editor-In-Chief to add or edit content to WikiDoc. You can begin to add to or edit text on this WikiDoc page by clicking on the edit button at the top of this page. Next enter or edit the information that you would like to appear here. Once you are done editing, scroll down and click the Save page button at the bottom of the page.
| Peripheral neuropathy Classification and external resources | |
| ICD-10 | G64., G90.0 |
|---|---|
| ICD-9 | 356 |
| DiseasesDB | 9850 |
| MeSH | D010523 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-525-6884
Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [2] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
Overview
Neuropathy is usually short for peripheral neuropathy, and refers the term for damage to nerves of the peripheral nervous system, which may be caused either by diseases of the nerve or from the side-effects of systemic illness.
Peripheral neuropathies vary in their presentation and origin, and may affect the nerve or the neuromuscular junction.
Types
The four major forms of nerve damage are polyneuropathy, autonomic neuropathy, mononeuropathy, and mononeuritis multiplex. The most common form is peripheral polyneuropathy, which mainly affects the feet and legs.
Often the form of neuropathy is further broken down as to cause (see below), or other type, such as small fiber peripheral neuropathy, which is idiopathic.
There are other less common forms of neuropathy, for example Enteric Neuropathy
Peripheral neuropathy is not a disease in itself, but a symptom or a complication of other underlying conditions. Peripheral nerves, either singly or in groups, are damaged through lack of circulation, chemical imbalance, trauma, or other factors.[1]
Peripheral neuropathies may either be symmetrical and generalized or focal and multifocal, which is usually a good indicator of the cause of the peripheral nerve disease.
Generalized peripheral neuropathy
Generalized peripheral neuropathies are symmetrical, and usually due to various systematic illnesses and disease processes that affect the peripheral nervous system in its entirety. They are further subdivided into several categories:
- Distal axonopathies are the result of some metabolic or toxic derangement of neurons. They may be caused by metabolic diseases such as diabetes, renal failure, deficiency syndromes such as malnutrition and alcoholism, or the effects of toxins or drugs.
- Myelinopathies are due to a primary attack on myelin causing an acute failure of impulse conduction. The most common cause is acute inflammatory demyelinating polyneuropathy (AIDP; aka Guillain-Barré syndrome), though other causes include chronic inflammatory demyelinating polyneuropathy (CIDP), genetic metabolic disorders (e.g., leukodystrophy), or toxins.
- Neuronopathies are the result of destruction of peripheral nervous system (PNS) neurons. They may be caused by motor neurone diseases, sensory neuronopathies (e.g., Herpes zoster), toxins or autonomic dysfunction. Neurotoxins may cause neuronopathies, such as the chemotherapy agent vincristine.
Causes
Aside from diabetes (see Diabetic neuropathy), the common causes of neuropathy are herpes zoster infection, HIV-AIDS, toxins, alcoholism, chronic trauma (such as repetitive motion disorders) or acute trauma (including surgery), various neurotoxins and autoimmune conditions such as celiac disease, which can account for approximately 16% of small fiber neuropathy cases.[1] Neuropathic pain is common in cancer as a direct result of the cancer on peripheral nerves (e.g., compression by a tumor), as a side effect of many chemotherapy drugs, and as a result of electrical injury. In many cases the neuropathy is "idiopathic," meaning no cause is found. A form of spinal nerve entrapment called Posterior Rami Syndrome can led to neuropathic pain.
- Genetic diseases:
- Metabolic / Endocrine:
- Toxic causes:
- alcoholism,
- drugs
- organic metals,
- Inflammatory diseases:
- Vitamin deficiency states:
- Others:
- malignant disease,
- radiation
Complete Differential Diagnosis for Peripheral Neuropathy
- Acromegaly
- Alcoholic polyneuropathy
- Atherosclerosis
- Amyloidosis
- Botulism
- Brucellosis
- Carpal Tunnel Syndrome
- Charcot-Marie-Tooth Disease
- Compression
- Diabetic polyneuropathy
- Diabetes Mellitus
- Diptheria
- Drugs
- Dysentery
- Dysproteinemia
- Fabry's Disease
- German Measles
- Hereditary Ataxia
- Herpes Zoster
- HIV
- Hypothyroidism
- Infectious Mononeucliosis
- Leukemia
- Lyme Disease
- Lymphoma
- Malaria
- Metachromatic leukodystrophy
- Multiple Myeloma
- Mycosis
- Paraneoplasia
- Paraproteinemia
- Paratyphus
- Pernicious anemia
- Polyarteritis Nodosa
- Polyrediculitis
- Porphyria
- Post-tetanus shot
- Primary biliary cirrhosis
- Refsum's Disease
- Rheumatoid Arthritis
- Sarcoidosis
- Scleroderma
- Sjogren's Syndrome
- Spinal process
- Spotted Fever
- Sprue
- Syphillis
- Systemic Lupus Erythematosus
- Thiamine deficiency
- Trauma
- Tuberculosis
- Typhoid Fever
- Uremic/Chronic Renal Failure
- Viral Hepatitis
- Vitamin B1 deficiency
- Vitamin B6 deficiency
- Vitamin B12 deficiency
Signs and symptoms
Neuropathy often results in numbness, abnormal sensations called dysesthesias and allodynias that occur either spontaneously or in reaction to external stimuli, and a characteristic form of pain, called neuropathic pain or neuralgia, that is qualitatively different from the ordinary nociceptive pain one might experience from stubbing a toe or hitting a finger with a hammer.
Neuropathic pain is usually perceived as a steady burning and/or "pins and needles" and/or "electric shock" sensations and/or tickling. The difference is due to the fact that "ordinary" pain stimulates only pain nerves, while a neuropathy often results in the firing of both pain and non-pain (touch, warm, cool) sensory nerves in the same area, producing signals that the spinal cord and brain do not normally expect to receive.
Those with diseases or dysfunctions of their peripheral nerves can present with problems in any of the normal peripheral nerve functions.
In terms of sensory function, there are commonly loss of function (negative) symptoms, which include numbness, tremor, and gait imbalance.
Gain of function (positive) symptoms include tingling, pain, itching, crawling, and pins and needles. Pain can become intense enough to require use of opiate drugs (i.e., morphine, oxycontin).
Skin can become so hypersensitive that patients are prohibited from having anything touch certain parts of their body, especially the feet. People with this degree of sensitivity cannot have a bed sheet touch their feet or wear socks or shoes, and eventually become housebound.
Motor symptoms include loss of function (negative) symptoms of weakness, tiredness, heaviness, and gait abnormalities; and gain of function (positive) symptoms of cramps, tremor, and fasciculations.
There is also pain in the muscles (myalgia), cramps, etc., and there may also be autonomic dysfunction.
During physical examination, those with generalized peripheral neuropathies most commonly have distal sensory or motor and sensory loss, though those with a pathology (problem) of the peripheral nerves may be perfectly normal; may show proximal weakness, as in some inflammatory neuropathies like Guillain-Barré syndrome); or may show focal sensory disturbance or weakness, such as in mononeuropathies, radiculopathies and plexopathies.
Common disorders of the peripheral nerves include focal entrapment neuropathies (e.g., carpal tunnel syndrome), generalized peripheral neuropathies (e.g., diabetic neuropathy), plexopathies (e.g., brachial neuritis) and radiculopathies (e.g., of cranial nerve VII; Facial nerve).
Treatment of neuropathic pain
Neuropathic pain can be very difficult to treat. Sometimes strong opioid analgesics may provide only partial relief. Opioid analgesics are to be considered only as a tertiary treatment. Several classes of medications not normally thought of as analgesics are often effective, alone or in combination with opioids and other treatments. These include tricyclic antidepressants such as amitriptyline (Elavil®), anticonvulsants such as gabapentin (Neurontin®) and pregabalin (Lyrica®).
In animal models of neuropathic pain it has been found that compounds which only block serotonin reuptake do not improve neuropathic pain.[1][1][1][1][1][1][1][1] Similarly, compounds that only block norepinephrine reuptake also do not improve neuropathic pain. Compounds such as duloxetine, venlafaxine, and milnacipran that block both serotonin reuptake and norepinephrine reuptake do improve neuropathic pain. Antidepressants usually reduce neuropathic pain more quickly and with smaller doses than they relieve depression. Antidepressants therefore seem to work differently on neuropathic pain than on depression, perhaps by activating descending norepinephrinergic and serotonergic pathways in the spinal cord that block pain signals from ascending to the brain.
Many of the pharmacologic treatments for chronic neuropathic pain decrease the sensitivity of nociceptive receptors, or desensitize C fibers such that they transmit fewer signals. The newer anticonvulsants gabapentin and pregabalin appear to work by blocking calcium channels in damaged peripheral neurons. Tricyclic antidepressants may also work on sodium channels in peripheral nerves. The anticonvulsants carbamazepine (Tegretol®) and oxcarbazepine (Trileptal®), especially effective on trigeminal neuralgia, are thought to work principally on sodium channels.
In general, the antidepressants seem to be most effective on continuous burning pain, while the anticonvulsants seem to work best on sudden, lancinating, "shock-like" pains that appear to involve large numbers of peripheral nerves improperly firing together.
In some forms of neuropathy, especially post-herpes neuralgia, the topical application of local anesthetics such as lidocaine can provide relief. A transdermal patch containing 5% lidocaine is available. Ketamine in a transdermal gel is also frequently effective when the neuropathy is localized. Neurontin 100mg/g PLO gel is also effective for treating peripheral neuropathy, including Carpal Tunnel Syndrome. Capsaicin cream can be beneficial in several neurogenic pain disorders, which causes release of the pain neurotransmitter Substance P, and eventually reduces the availability of Substance P.
Transcutaneous electrical nerve stimulation (TENS) is worth a trial in chronic neurogenic pain. Some pain management specialists will try acupuncture, with variable results. TENS, with certain electrical waveforms, appears to have an acupuncture-like function.
In some neuropathic pain syndromes, "crosstalk" occurs between descending sympathetic nerves and ascending sensory nerves. Increases in sympathetic nervous system activity result in an increase of pain; this is known as sympathetically-mediated pain. Reducing the sympathetic nerve activity in the painful region with local nerve blocks or systemic medications such as the alpha-blocker clonidine may provide relief. Other drugs, known for their ability to desensitize cardiac tissue, include beta-blockers such as propanolol and calcium channel blockers such as verapamil.
The NMDA receptor seems to play a major role in neuropathic pain and in the development of opioid tolerance, and many experiments in both animals and humans have established that NMDA antagonists such as ketamine and dextromethorphan can alleviate neuropathic pain and reverse opioid tolerance. Unfortunately, only a few NMDA antagonists are clinically available and their use is usually associated with unacceptable side effects.
Several opioids, particularly methadone, have NMDA antagonist activity in addition to their μ-opioid agonist properties that seems to make them effective against neuropathic pain, although this is still the subject of intensive research and clinical study. Methadone has this property because it is a racemic mixture; one stereo-isomer is a μ-opioid agonist; the other is a NMDA antagonist.
A recent study showed smoking marijuana is beneficial in treating HIV-associated periphial neuropathy.[1]
In addition to pharmacological treatment there are several other modalities that help some cases. While lacking double blind trials, these have shown to reduce pain and improve patient quality of life particularly for chronic neuropathic pain: Interferential Stimulation; Acupuncture; Meditation; Cognitive Therapy; and prescribed exercise.
In more recent years, infrared photo therapy has been used to treat neuropathic symptoms. Photo therapy devices emit near infrared light typically at a wavelength of 890nm. This wavelength is believed to stimulate the release of nitric oxide, an endothelium-derived relaxing factor into the bloodstream, thus vasodilating the capilaries and venuoles in the microcirculatory system. This increase in circulation has been shown effective in various clinical studies, to decrease pain and improve sensation in diabetic and non-diabetic patients.[citation needed] Note that the U.S. FDA has not approved any infrared photo therapy devices to treat neuropathy.[1]
Alternative medicine treatments
There are 2 dietary supplements that have clinical evidence showing them to be effective treatments of diabetic neuropathy; alpha lipoic acid and benfotiamine. In several studies using a variety of dosages and routes of administration, alpha lipoic acid was found to reduce the various symptoms of peripheral diabetic neuropathy. A recent review of the published data determined “ALA should be considered as a treatment option for patients with peripheral diabetic neuropathy.” Also a recent study using orally administered alpha lipoic acid found that 600 mg once a day caused a marked reduction in the symptoms of diabetic neuropathy including stabbing pain, burning pain, paresthesia, and asleep numbness of the feet. Benfotiamine is a lipid soluble form of thiamine that has several placebo controlled double blind trials proving efficacy in treating neuropathy and various other diabetic comorbidities. 400 mg a day was the most commonly studied dose.
See also
- Nerve
- Peripheral nervous system
- Neuritis
- Neuralgia
- Small fiber peripheral neuropathy
- Phantom limb
- Phantom pain
- Posterior Rami Syndrome
- Neuropathy
- Myopathy
- Myelinopathy
- Guillain-Barré syndrome
References
Additional Resources
- Dr. Lee Dellon: Pioneering Pain Relief Dr. Lee Dellon's research in the pain caused by Peripheral Neuropathy and other nerve disorders is highlighted in this recent article.
Neuropathy related organizations
- Special Interest Group on Neuropathic Painof the International Association for the Study of Pain (IASP)
- The Neuropathy Association
External links
- Nep Know More Provides Additional Help and Information on Neuropathic Pain
- A neuropathic series of articles from a neurologist who researches neuropathic pain
- Up to 16% of Patients with Small Fiber Neuropathy May Have Celiac Disease
- National Diabetes Information Clearinghouse
- Information about Neurology Article on marijuana's effect on neuropathic pain
- Nitric Oxide and its Role in Diabetes, Wound Healing and Peripheral Neuropathy
- National Diabetes Information Clearinghouse
Acknowledgements
The content on this page was first contributed by: C. Michael Gibson, M.S., M.D.
de:Neuropathiefr:Neuropathieit:Neuropatia nl:Neuropathieit:Neuropatia periferica
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
