Polyneuropathy

From Wikipedia, the free encyclopedia
  (Redirected from Distal axonopathy)
Jump to: navigation, search
Polyneuropathy
Vasculitic neuropathy - plastics - low mag.jpg
Micrograph showing peripheral neuropathy (vasculitis).Polyneuropathy is peripheral neuropathy occurring in the same area on both sides of the body.
Classification and external resources
Specialty neurology
ICD-10 G60-G64
ICD-9-CM 356.4, 357.1-357.7
Patient UK Polyneuropathy
MeSH D011115

Polyneuropathy (poly- + neuro- + -pathy) is damage or disease affecting peripheral nerves (peripheral neuropathy) in roughly the same areas on both sides of the body, featuring weakness, numbness, and burning pain.[1] It usually begins in the hands and feet and may progress to the arms and legs; and sometimes to other parts of the body where it may affect the autonomic nervous system. It may be acute or chronic. A number of different disorders may cause polyneuropathy, including diabetes and some types of Guillain-Barré syndrome.[2][3][4]Sensory polyneuropathy is the condition of having multiple sensory neuropathies, while motor polyneuropathy refers to multiple motor neuropathies, sensorimotor polyneuropathy is the combination of both conditions.[medical citation needed]

Classification[edit]

Polyneuropathies may be classified in different ways, such as by cause, by speed of progression, or by the parts of the body involved. Classes of polyneuropathy also are distinguished by which part of the nerve cell is affected mainly: the axon, the myelin sheath, or the cell body.

Action potential propagation in myelinated neurons is faster than in unmyelinated neurons(left)

Signs/symptoms[edit]

Causes[edit]

Acute polyneuropathy may have various causes, including infections, autoimmune reactions, toxins, certain drugs (especially chemotherapy agents), and cancer. When the cause cannot be determined it is called "idiopathic." With drug-induced polyneuropathy, there is a trade-off of risk, benefit, and adverse effects; for example, chemotherapy may cause problems (nausea, vomiting, polyneuropathy, and others), but survival may be longer with it than without it.Chronic polyneuropathy often is caused by diabetes mellitus or by the excessive alcohol consumption (alcoholic polyneuropathy), or by degeneration of connective tissue protecting the nerves as in connective tissue diseases,but a variety of other less common causes are known, including nutritional deficiencies, and liver or kidney failure.

Polyneuropathies usually are caused by processes that affect the body as a whole. Diabetes and impaired glucose tolerance are the most common causes. Other causes relate to the particular type of polyneuropathy, and there are many different causes of each type, including inflammatory diseases such as lyme disease, vitamin deficiencies, blood disorders, and toxins (including alcohol and certain prescribed drugs).

Diagnosis[edit]

Micrograph of a muscle biopsy

Evaluation and classification of polyneuropathies begins with a history and physical examination in order to document what the pattern of the disease process is (arms, legs, distal, proximal, symmetric), when they started, how long they have lasted, if they fluctuate, and what deficits and pain are involved. If pain is a factor, and it often is, determining where and how long the pain has been present is important. One also needs to know what disorders are present within the family and what diseases the patient may have. This is vital in forming a differential diagnosis.

Although diseases often are suggested by the physical examination and history alone, testing is still a large part of the diagnosis. Tests that may be employed include electrodiagnostic testing using electromyography, nerve conduction studies, muscle biopsy, serum creatine kinase (CK) and antibody testing. Nerve biopsy rarely is used to establish a diagnosis, but is helpful in determining small fiber neuropathy. Other tests may be used, especially tests for specific disorders associated with polyneuropathies.Quality measures have been developed to diagnose patients with distal symmetrical polyneuropathy (DSP).[5]

Differential diagnosis[edit]

There is a large differential for polyneuropathies: vitamin deficiency, cancer, toxins, infections (ex. Guillain–Barré syndrome, Lyme disease), liver disease, endocrine disease (including diabetes with diabetic and pre-diabetic neuropathy), amyloidosis, genetic disorders, motor neuron disorders, motor neuropathies, kidney failure,[6] paraneoplastic, polio, porphyria (some types), neurosarcoidosis, spinal muscular atrophy, catecholamine disorders, psychological disorders and many others.[citation needed]

Treatment[edit]

Most types of polyneuropathy progress fairly slowly, over months or years, but rapidly progressive polyneuropathy also occurs. It is important to recognize that glucose levels in the blood may spike to nerve-damaging levels after eating even though fasting blood sugar levels and average blood glucose levels may still remain below normal levels (currently they typically are considered below 100 mg/dL for fasting blood plasma and 5.7% for HgbA1c, the test commonly used to measure average blood glucose levels over an extended period).[citation needed]

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 before a diagnosis of diabetes or pre-diabetes. Such damage often is reversible, particularly in the early stages, with changes in diet, exercise, and weight loss.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.If possible, treatment focuses on the underlying disease. Further, pain medications may be given and physical therapy is used to retain muscle function. Vyndaqel or Tafamidis is a European Medicines Agency approved drug for the treatment of familial amyloid polyneuropathy caused by transthyretin amyloisis.

See also[edit]

References[edit]

  1. ^ "Polyneuropathies. Medical inforamtion about polyneuropathy | Patient". Patient. Retrieved 2016-07-17. 
  2. ^ Richard A C Hughes (23 February 2002). "Clinical review: Peripheral neuropathy". British Medical Journal 324: 466. doi:10.1136/bmj.324.7335.466. 
  3. ^ Janet M. Torpy; Jennifer L. Kincaid; Richard M. Glass (21 April 2010). "Patient page: Peripheral neuropathy". Journal of the American Medical Association 303 (15). doi:10.1001/jama.303.15.1556. 
  4. ^ "Peripheral neuropathy fact sheet". National Institute of Neurological Disorders and Stroke. 19 September 2012. 
  5. ^ England, John D.; Franklin, Gary; Gjorvad, Gina; Swain-Eng, Rebecca; Brannagan, Thomas H.; David, William S.; Dubinsky, Richard M.; Smith, Benn E. (13 May 2014). "Quality improvement in neurology". Neurology 82 (19): 1745–1748. doi:10.1212/WNL.0000000000000397. ISSN 0028-3878. Retrieved 17 July 2016. 
  6. ^ Chronic renal failure, Medline Plus

Further reading[edit]