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Peripheral neuropathy
Classification and external resources
ICD-10 G64., G90.0
ICD-9 356
DiseasesDB 9850
MeSH D010523

Peripheral neuropathy is the term for damage to nerves of the peripheral nervous system,[1] which may be caused either by diseases of the nerve or from the side-effects of systemic illness.

The four cardinal patterns of peripheral neuropathy are polyneuropathy, mononeuropathy, mononeuritis multiplex and autonomic neuropathy. The most common form is (symmetrical) peripheral polyneuropathy, which mainly affects the feet and legs. The form of neuropathy may be further broken down by cause, or the size of predominant fiber involvement, i.e., large fiber or small fiber peripheral neuropathy. Frequently the cause of a neuropathy cannot be identified and it is designated idiopathic.

Neuropathy may be associated with varying combinations of weakness, autonomic changes and sensory changes. Loss of muscle bulk or fasciculations, a particular fine twitching of muscle may be seen. Sensory symptoms encompass loss of sensation and "positive" phenomena including pain. Symptoms depend on the type of nerves affected; motor, sensory, autonomic, and where the nerves are located in the body. One or more types of nerves may be affected. Common symptoms associated with damage to the motor nerve are muscle weakness, cramps, and spasms. Loss of balance and coordination may also occur. Damage to the sensory nerve can produce tingling, numbness, and pain. Pain associated with this nerve is described in various ways such as the following: sensation of wearing an invisible "glove" or "sock", burning, freezing, or electric-like, extreme sensitivity to touch. The autonomic nerve damage causes problems with involuntary functions leading to symptoms such as abnormal blood pressure and heart rate, reduced ability to perspire, constipation, bladder dysfunction (e.g., incontinence), and sexual dysfunction.[2]

Contents

Causes

The causes are broadly grouped as follows:

Many of the diseases of the peripheral nervous system may present similarly to muscle problems (myopathies), and so it is important to develop approaches for assessing sensory and motor disturbances in patients so that a physician may make an accurate diagnosis.

Types by pattern of nerve involvement

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Mononeuropathy

Mononeuropathy is a type of neuropathy that only affects a single nerve.[8] It is diagnostically useful to distinguish them from polyneuropathies, because the limitation in scope makes it more likely that the cause is a localized trauma or infection.

The commonest cause of mononeuropathy is by physical compression of the nerve, known as compression neuropathy. Carpal tunnel syndrome is one example of this. The "pins-and-needles" sensation of one's "foot falling asleep" (paresthesia) is caused by a compression mononeuropathy, albeit a temporary one which can be resolved merely by moving around and adjusting to a more appropriate position. Direct injury to a nerve, interruption of its blood supply (ischemia), or inflammation can also cause mononeuropathy.

Mononeuritis multiplex

Mononeuritis multiplex, or mononeuropathy multiplex, is the clinical result of damage to several different nerves, either serially or concurrently.

Mononeuritis multiplex typically presents with acute or subacute loss of sensory and motor function of individual peripheral nerves. The pattern of involvement is asymmetric.

Mononeuritis multiplex may also cause pain, which is characterized as deep, aching pain that is worse at night, is frequently in the lower back, hip, or leg. In people with diabetes mellitus, mononeuritis multiplex is typically encountered as acute, unilateral, severe thigh pain followed by anterior muscle weakness and loss of knee reflex.

Electrodiagnostic studies will show multifocal sensory motor axonal neuropathy.

It is caused by, or associated with, several medical conditions:

Polyneuropathy

Polyneuropathy is a pattern of nerve damage which is quite different from mononeuropathy. The term "peripheral neuropathy" is sometimes used loosely to refer to polyneuropathy. In a polyneuropathy, many nerve cells in different parts of the body are affected, without regard to the nerve through which they pass. Not all nerve cells are affected in any particular case. In one common pattern (distal axonopathy), the cell bodies of neurons remain intact, but the axons are affected in proportion to their length. Diabetic neuropathy is the most common cause of this pattern. In demyelinating polyneuropathies, the myelin sheath around axons is damaged, which affects the ability of the axons to conduct electrical impulses. The third and least common pattern affects the cell bodies of neurones directly. This usually picks out either the motor neurones (known as motor neurone disease), or the sensory neurones (known as sensory neuronopathy or dorsal root ganglionopathy).

The effect of this is to cause symptoms in more than one part of the body, often on left and right sides symmetrically. As for any neuropathy, the chief symptoms include weakness or clumsiness of movement (motor); unusual or unpleasant sensations such as tingling or burning, reduction in the ability to feel texture, temperature etc., and impaired balance when standing or walking (sensory). In many polyneuropathies, these symptoms occur first and most severely in the feet. Autonomic symptoms may also occur, such as dizziness on standing up, erectile dysfunction and difficulty controlling urination.

Polyneuropathies are usually caused by processes that affect the body as a whole. Diabetes (or impaired glucose tolerance) is the most common cause. Other causes relate to the particular type of polyneuropathy, and there are many different causes of each type, including inflammatory diseases, vitamin deficiencies, blood disorders, and toxins (including alcohol and certain prescribed drugs). Most types of polyneuropathy progress fairly slowly, over months or years, but rapidly progressive polyneuropathy also occurs. Sometimes this has an identifiable cause; when it does not it is often referred to as Guillain–Barré syndrome. It is important to recognize that glucose levels in the blood can spike to nerve-damaging levels after eating even though fasting blood sugar levels and average blood glucose levels can still remain below normal levels (currently typically considered below 100 for FBP, Fasting Blood Plasma, and 6.0 for HGBA1c, hemoglobin A1C the test commonly used to measure average blood glucose levels over an extended period). Studies have shown that many of the cases of peripheral small fiber neuropathy with typical symptoms of tingling, pain and loss of sensation in the feet and hands are due to glucose intolerance prior to a diagnosis of diabetes or pre-diabetes. Such damage is often reversible, particularly in the early stages, with diet, exercise and weight loss. 17

The treatment of polyneuropathies is aimed firstly at eliminating or controlling the cause, secondly at maintaining muscle strength and physical function, and thirdly at controlling symptoms such as neuropathic pain.

Other classifications

Peripheral neuropathy may also be classified according to the type of nerve cell affected (motor, sensory, autonomic), or the process affecting the nerves (e.g. inflammation in neuritis).

Autonomic neuropathy

Autonomic neuropathy is a form of polyneuropathy which affects the non-voluntary, non-sensory nervous system (i.e. the autonomic nervous system) affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a person's conscious control and function automatically. Autonomic nerve fibers form large collections in the thorax, abdomen and pelvis outside spinal cord, however they have connections with the spinal cord and ultimately the brain. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and 2. In most but not all cases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy.

Autonomic neuropathy is one cause of malfunction of the autonomic nervous system, but not the only one; some conditions affecting the brain or spinal cord can also cause autonomic dysfunction, such as multiple system atrophy, and therefore cause similar symptoms to autonomic neuropathy.

The signs and symptoms of autonomic neuropathy include the following:

Neuritis

Neuritis is a general term for inflammation of a nerve[9] or the general inflammation of the peripheral nervous system. Symptoms depend on the nerves involved, but may include pain, paresthesia, paresis, hypoesthesia (numbness), anesthesia, paralysis, wasting, and disappearance of the reflexes. Causes include:

  • Underlying conditions causing localized neuritis (affecting a single nerve):

Types of neuritis include:

Signs and symptoms

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 opioid (narcotic) drugs (i.e., morphine, oxycodone).

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 bedsheet 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. Ankle jerk reflex is classically absent in peripheral neuropathy.

Treatment

Many treatment strategies for peripheral neuropathy are symptomatic. Some current research in animal models has shown that neurotrophin-3 can oppose the demyelination present in some peripheral neuropathies.[10]

A range of drugs that act on the central nervous system such as drugs originally intended as antidepressants and antiepileptic drugs have been found to be useful in managing neuropathic pain. Commonly used treatments include using a Tricyclic antidepressant (such as amitriptyline) and antiepileptic therapies such as gabapentin or sodium valproate. These have the advantage that besides being effective in many cases they are relatively low cost.

A great deal of research has been done between 2005 and 2010 which indicates that synthetic cannabinoids and inhaled cannabis are effective treatments fo a range of neuropathic disorders. [11] Research has demonstrated that the synthetic oral cannabinoid Nabilone is an effective adjunct treatment option for neuropathic conditions, especially for people who are resistant, tolerant, or allergic to common medications.[12] Orally, opiate derivatives were found to be more effective than cannabis for most people.[13] Smoked cannabis has been found to provide relief from HIV-associated sensory neuropathy. [14] Smoked cannabis was also found to relieve neuropathy associated with CRPS type I, spinal chord injury, peripheral neuropathy, and nerve injury. [15]

Pregabalin (INN) (pronounced /prɨˈgæbəlɨn/) is an anticonvulsant drug used for neuropathic pain. It has also been found effective for generalized anxiety disorder. It was designed as a more potent successor to gabapentin but is significantly more expensive, especially now the patent on gabapentin has expired and gabapentin is available as a generic drug. Pregabalin is marketed by Pfizer under the trade name Lyrica.

As noted above in the section on Polyneuropathies and their causes, symmetric small fiber neuropathy, commonly called peripheral neuropathy, can often be reversed, particularly in the early stages before a diagnosis of diabetes or pre-diabetes with diet, exercise and weight loss. It is also suggested that, because alcohol is a neurotoxin, even individuals with neuropathies from causes other than alcoholism may benefit from limiting or eliminating their alcohol intake.

TENS (Transcutaneous Electrical Nerve Stimulation) can be an effective in some cases as a non-pharmacological treatment and is free from adverse effects. It is believed to work via stimulating large afferent fibers, which in turn leads to an inhibition of small pain afferent fibers.[16]

References

  1. ^ "Peripheral Neuropathy Fact Sheet: National Institute of Neurological Disorders and Stroke (NINDS)". http://www.ninds.nih.gov/disorders/peripheralneuropathy/detail_peripheralneuropathy.htm. Retrieved 2008-11-30. 
  2. ^ http://www.neurologychannel.com/neuropathy/symptoms.shtml
  3. ^ Gabriel JM, Erne B, Pareyson D, Sghirlanzoni A, Taroni F, Steck AJ (1997). "Gene dosage effects in hereditary peripheral neuropathy. Expression of peripheral myelin protein 22 in Charcot-Marie-Tooth disease type 1A and hereditary neuropathy with liability to pressure palsies nerve biopsies". Neurology 49 (6): 1635–40. PMID 9409359. 
  4. ^ Kiziltan ME, Akalin MA, Sahin R, Uluduz D (2007). "Peripheral neuropathy in patients with diabetes mellitus presenting as Bell's palsy". Neuroscience Letters 427: 138. doi:10.1016/j.neulet.2007.09.029. PMID 17933462. 
  5. ^ Cohen JS (December 2001). "Peripheral Neuropathy Associated with Fluoroquinolones" (PDF). Ann Pharmacother 35 (12): 1540–7. doi:10.1345/aph.1Z429. PMID 11793615. http://fqvictims.org/fqvictims/News/neuropathy/Neuropathy.pdf. 
  6. ^ Gonzalez-Duarte A, Cikurel K, Simpson DM (2007). "Managing HIV peripheral neuropathy". Current HIV/AIDS reports 4 (3): 114–8. doi:10.1007/s11904-007-0017-6. PMID 17883996. 
  7. ^ Wilkes G (2007). "Peripheral neuropathy related to chemotherapy". Seminars in oncology nursing 23 (3): 162–73. doi:10.1016/j.soncn.2007.05.001. PMID 17693343. 
  8. ^ "Dorlands Medical Dictionary:mononeuropathy". http://www.mercksource.com/pp/us/cns/cns_hl_dorlands_split.jsp?pg=/ppdocs/us/common/dorlands/dorland/five/000067367.htm. 
  9. ^ neuritis at Dorland's Medical Dictionary
  10. ^ Liu N, Varma S, Tsao D, Shooter EM, Tolwani RJ (2007). "Depleting endogenous neurotrophin-3 enhances myelin formation in the Trembler-J mouse, a model of a peripheral neuropathy". J. Neurosci. Res. 85 (13): 2863–9. doi:10.1002/jnr.21388. PMID 17628499. 
  11. ^ http://www.cannabis-med.org/data/pdf/en_2010_01_special.pdf
  12. ^ Skrabek RQ, Galimova L, Ethans K, Perry D (2008). "Nabilone for the treatment of pain in fibromyalgia". J. Pain 9 (2): 164-73. 
  13. ^ Frank B, Serpell MG, Hughes J, Matthews JN, Kapur D (2008). "Comparison of analgesic effects and patient toleration of nabilone and dihydrocodeine for chronic neuropathic pain: randomized, crossover, double blind study". BMJ 336 (7637): 119-201. 
  14. ^ Abrams DI, Jay CA, Shade SB, Vizozo H, Reda H, Press S, Kelly ME, Rowbotham Mc, Petersen KL (2007). "Cannabis in painful HIV-associated sensory neuropathy: a randomized placebo-controlled trail". J. Neurology 68 (7): 515-21. 
  15. ^ Wilsey B, Marcotte T, Tsodikov A, Millman J, Bentley H, Gouaux B, Fishman S (2008). "A randomized, placebo-controlled, crossover trail of cannabis cigarettes in neuropathic pain". J. Pain 9 (6): 506-21. 
  16. ^ Ro, LS.; Chang, KH. (Sep 2005). "Neuropathic pain: mechanisms and treatments." (PDF). Chang Gung Med J 28 (9): 597-605. PMID 16323550. http://memo.cgu.edu.tw/cgmj/2809/280901.pdf. 

17. Latov, Norman; 'Peripheral Neuropathy: When the Numbness, Weakness, and Pain Won't Stop; American Academy of Neurology Press Demos Medical Publishing; N.Y., N.Y.; 2007

External links


Neuritis
Classification and external resources
ICD-10 M79.2
ICD-9 729.2
MeSH D009443

Neuritis is the general inflammation of the peripheral nervous system.

Contents

Symptoms

Symptoms depend on the nerves involved, but may include pain, paresthesia, paresis, hypoesthesia (numbness), anesthesia, paralysis, wasting, and disappearance of the reflexes.

Causes

  • Underlying conditions causing localized neuritis (affecting a single nerve):

Types

See also

Sources

External links


1911 encyclopedia

Up to date as of January 14, 2010

From LoveToKnow 1911

Medical warning!
This article is from the 1911 Encyclopaedia Britannica. Medical science has made many leaps forward since it has been written. This is not a site for medical advice, when you need information on a medical condition, consult a professional instead.

NEURITIS (Gr. veupov, nerve), a term applied to the inflammation of one or more bundles of nerve fibres. Two varieties are known, the localized and the multiple. The localized form frequently follows on exposure to cold and may attack a single nerve. Facial paralysis (Bell's palsy) is commonly seen following a neuritis of the facial nerve. Neuritis may follow blows and wounds of a nerve, injuries involving stretching of a nerve or long continued pressure such as may occur in a dislocation of the elbow joint, or the nerve may share in the extension of a neighbouring inflammation. The first symptom of a localized neuritis is pain of a boring character along the course of a nerve and its distribution, the part being sensitive to pressure. There may be slight redness and oedema along the course of the nerve, movement becomes painful in the muscles to which the nerve is distributed, numbness may follow and the tactile sense be impaired, finally the muscles atrophy, and degenerative changes may take place in the nerve or nerve sheath. Slight cases following cold or injury may pass off in a few days, while severe cases such as those following the pressure of an unreduced dislocation may last for months.

Multiple neuritis or polyneuritis is a disease which may affect many of the peripheral nerves symmetrically and at the same time. For the pathological changes see Neuropathology. Th e difference in these changes is due mostly to the difference in the aetiology of the neuritis. The causes may be divided as follows: (I) The toxins of acute infective diseases, such as diphtheria, influenza, typhoid fever, malaria, scarlet fever and septicaemia. (2) Acute or chronic poisoning by lead, arsenic, mercury, copper and phosphorus. (3) General disorders: gout, rheumatism, tubercle, carcinoma. (4) The local action of leprosy and syphilis. (5) Endemic disease: beri-beri. (6). Alcohol, the most common.

Alcoholic neuritis occurs as a result of constant steady drinking, particularly in those who drink beer rather than spirit. The earliest symptom is numbness of the feet and later of the hands, then painful cramps in the legs appear and there is pain on moving the limbs, or the patient complains of deadness, tingling and burning in the hands and feet, and superficial tenderness is occasionally present. In other varieties of the disease the earliest symptoms are weakness of the legs and extreme fatigue, leading to a characteristic "steppage gait," or marked inco-ordination of movement may occur and the gait become ataxic. Trophic changes soon appear, in some cases early and rapid muscular wasting occurs, the skin becomes dry and glossy, the nails brittle and the hair thin. In time actual contractures takes place, the hip and knee-joints become flexed and the foot dropped at the ankle. In cases that recover there may be permanent deformity. Should the case progress the patient may become bedridden and powerless, and degenerative mental changes may take place, loss of memory, irritability of temper and emotional instability. Various complications such as bronchitis, fatty changes in the heart, albuminuria and a liability to pulmonary tuberculosis, tend to carry off the victim of chronic alcoholic neuritis. Cases seen early in the progress of the disease, who can be placed under supervision, may recover under treatment, but those in whom the attacks have recurred several times and in whom there is much mental impairment rarely make a complete recovery. The treatment consists in putting the patient to bed, with the administration of strychnine hypodermically, and attention should be paid to the position of the limbs so as to avoid the development of contractures, cradles being used, the limbs kept in the correct positions by sandbags, and gentle massage being employed as soon as possible. Should contractures have already formed some mechanical device adapted to stretch the contracted muscle must be resorted to. Biers' hyperaemic suction apparatus is very useful in the painless stretching of contracted joints, or old-standing adhesions may have to be broken down under an anaesthetic, extension apparatus being afterwards worn. In the later treatment the galvanic and faradaic currents combined with massage are useful in helping to restore the wasted muscles, and hot-air baths and warm applications are appreciated.

Arsenical neuritis mostly affects the lower extremities, as contrasted with lead, which mainly paralyses the fingers and wrists; recovery is even slower than in alcoholic neuritis, the treatment being on the same lines, with the removal of the cause of the disease. In the neuritis of chronic lead poisoning a fine tremor of the hands is an early symptom and sensory symptoms are usually absent; the muscles affected are the extensors of the wrists, thumb and fingers (see Lead Poisoning). The course of the disease is long, and an attempt should be made to eliminate the lead from the system by purgatives and the administration of potassium iodide.

The diabetic neuritis paraesthesia is slight, and the legs are chiefly affected; weakness and ataxia may be present. Trophic sores on the feet are of frequent occurrence in this variety. The treatment is that of the disease.

Post-diphtheritic neuritis occurs in about Io % of all cases of diphtheria. In this form paralysis of the soft palate is the earliest symptom, and this may be the only one, or the pharynx may be affected. The limbs are affected much later, usually about the 5th or 6th week. Atrophy of the muscles is frequently rapid. If the respiratory muscles are unaffected the prognosis is good, but the paralysis of the limbs may last for several months. The treatment is complete rest, good food and the administration of strychnine.

Acute polyneuritis with numbness and motor weakness has been noted after influenza, together with slight muscular wasting and electrical degeneration. Later, loss of sensation in the peripheral portion of the limbs is complained of, and the motor weakness may affect the muscles of the trunk and face. Such cases tend towards complete recovery.


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