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Paresthesia

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Paresthesia
SpecialtyNeurology Edit this on Wikidata

Paresthesia (/ˌpær[invalid input: 'ɨ']sˈθziə/ or /ˌpær[invalid input: 'ɨ']sˈθʒə/) (British English paraesthesia; plural paraesthesiae /ˌpærrɪsˈθzɪ/ or paraesthesias), is a sensation of tingling, tickling, pricking, or burning of a person's skin with no apparent long-term physical effect. The manifestation of a paresthesia may be transient or chronic.

The most familiar kind of paresthesia is the sensation known as "pins and needles" or of a limb "falling asleep". A less well-known but still fairly common paresthesia is formication.

Etymology

The word paresthesia comes from the Greek para ("beside", i.e., abnormal) and aisthesia ("sensation").

Cause

Stroke survivors and those with Traumatic Brain Injury (TBI) may experience paresthesia from damage to the central nervous system.

Transient

Paresthesias of the hands, feet, legs and arms are common, transient symptoms. The most common, everyday cause is temporary restriction of nerve impulses to an area of nerves, commonly caused by leaning or resting on parts of the body such as the legs; other causes include conditions such as hyperventilation syndrome and panic attacks. A cold sore outside the mouth (not a canker sore inside the mouth) can be preceded by tingling—an interesting observation because a cold sore is caused by herpes simplex virus. Viruses also notably may cause tingling along with shingles on the chest.

Other common examples occur when sustained pressure has been applied over a nerve, inhibiting/stimulating its function. Removing the pressure typically results in gradual relief of these paresthesias.[1]

Tingling in the feet after orgasm for some people is caused by a temporary reduction of blood flow to the extremities. [2]

Chronic

Chronic paresthesia indicates a problem with the functioning of neurons or poor circulation.

In older individuals, paresthesia is often the result of poor circulation in the limbs (such as in peripheral vascular disease), most often caused by atherosclerosis, the buildup of plaque within artery walls, over decades, with eventual plaque ruptures, internal clots over the ruptures and subsequent clot healing but leaving behind narrowing of the artery openings or closure, both locally and in downstream smaller branches. Without a proper supply of blood and nutrients, nerve cells can no longer adequately send signals to the brain. Because of this, paresthesia can also be a symptom of vitamin deficiency and malnutrition, as well as metabolic disorders like diabetes, hypothyroidism, and hypoparathyroidism. It can also be a symptom of mercury poisoning.

Irritation to the nerve can also come from inflammation to the tissue. Joint conditions such as rheumatoid arthritis, psoriatic arthritis, and carpal tunnel syndrome are common sources of paresthesia. Nerves below the head may be compressed where chronic neck and spine problems exist and can be caused by, among other things, muscle cramps that may be a result of clinical anxiety or excessive mental stress,[citation needed] bone disease, poor posture, unsafe heavy-lifting practices or physical trauma such as whiplash. Paresthesia can also be caused simply by putting pressure on a nerve by applying weight (or pressure) to the limb for extended periods of time.

Another cause of paresthesia, however, may be direct damage to the nerves themselves, i.e., neuropathy, which itself can stem from injury or infection such as frostbite or Lyme disease, or may be indicative of a current neurological disorder. Neuropathy is also a side effect of some chemotherapies (see Chemotherapy-induced peripheral neuropathy).[3] Benzodiazepine withdrawal may also cause paresthesia as the drug removal leaves the GABA receptors stripped bare and possibly malformed. Chronic paresthesia can sometimes be symptomatic of serious conditions, such as a transient ischemic attack, or autoimmune diseases like multiple sclerosis or lupus erythematosus.[citation needed]

The herpes zoster disease (shingles) can attack nerves causing numbness instead of pain commonly associated with shingles. A diagnostic evaluation by a medical doctor is necessary to rule these out.[clarification needed]

Demyelinating diseases may also cause cross-talk between adjacent axons and lead to paresthesia. During impulse conduction some aberrant current that escaped a demyelinated axon can circulate in the exterior and depolarize an adjacent demyelinated, hyperexcitable axon. This can generate impulses conducted in both directions along this axon since no part of the axon is in a refractory state. This becomes very serious in conditions such as multiple sclerosis and Guillain–Barré syndrome.

Acroparesthesia

Acroparesthesia is severe pain in the extremities, and may be caused by Fabry disease, a type of sphingolipidosis.[4]

It can also be a sign of hypocalcemia.

Dentistry

Paresthesia or "persistent anesthesia" is a transient or potentially permanent condition of extended numbness after administration of local anesthesia and the injected anesthetic has terminated.[5]

Potential causes include trauma induced to the nerve sheath during administration of the injection, hemorrhage about the sheath, type of anesthetic used, or administration of anesthetic potentially contaminated with alcohol or sterilizing solutions. [6]

Other

Other causes may include: Template:Multicol

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Diagnostic approach

The nerve conduction study usually provides useful information for making diagnosis. A CT scan is sometimes used to rule out some causes from the central nervous system.

Treatment

Medications offered can include the immunosuppressant prednisone, intravenous gamma globulin (IVIG), anticonvulsants such as gabapentin or Gabitril and antiviral medication, according to the underlying cause[medical citation needed].

In addition to treatment of the underlying disorder, palliative care can include the use of topical numbing creams, such as lidocaine or prilocaine. Care must be taken to apply only the necessary amount, as excess can contribute to the condition. Otherwise, these products offer extremely effective, but short-lasting, relief from the condition. Paresthesia caused by stroke may receive some temporary benefit from high doses of Baclofen multiple times a day[citation needed]. HIV patients who self-medicate with cannabis report that it reduces their symptoms[10]

Paresthesia caused by shingles is treated with appropriate antiviral medication[medical citation needed].

References

  1. ^ Paresthesia Information Page: National Institute of Neurological Disorders and Stroke. (NINDS)
  2. ^ "Why do my feet tingle when I ejaculate?".
  3. ^ "Chemotherapy-induced Peripheral Neuropathy". National Cancer Institute. Retrieved 1 December 2011.
  4. ^ Marks, Dawn B.;Swanson, Todd; Kim, Sandra I.;Glucksman, Marc (2007). Biochemistry and Molecular biology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 0-7817-8624-X.{{cite book}}: CS1 maint: multiple names: authors list (link)
  5. ^ Paresthesia dental definition: The Free Dictionary. (TheFreeDictionary)
  6. ^ Garisto, G; Gaffen, A; Lawrence, H; Tenenbaum, H; Haas, D (Jul 2010). "Occurrence of Paresthesia After Dental Local Anesthetic Administration in the United States". The Journal of the American Dental Association. 141 (7): 836–844. doi:10.14219/jada.archive.2010.0281. PMID 20592403.
  7. ^ Ietsugu, T; Sukigara, M; Furukawa, TA (Dec 2007). "Evaluation of diagnostic criteria for panic attack using item response theory: findings from the National Comorbidity Survey in USA". Journal of Affective Disorders. 104 (1–3): 197–201. doi:10.1016/j.jad.2007.03.005. PMID 17434598.
  8. ^ Nitrous Oxide
  9. ^ Vijverberg, H.P., van den Bercken, J. Crit. Rev. Toxicol. (1990) Neurotoxicological effects and the mode of action of pyrethroid insecticides.
  10. ^ Woolridge, Emily, et al. "Cannabis use in HIV for pain and other medical symptoms." Journal of pain and symptom management 29.4 (2005): 358-367.
  • [Clinical and neurological abnormalities in adult celiac disease, G. Cicarelli • G. Della Rocca • M. Amboni • C. Ciacci • G. Mazzacca • A. Filla • P. Barone,

Neurol Sci (2003) 24:311–317 DOI 10.1007/s10072-003-0181-4]