Trichodynia

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As Trichodynia (from the Greek. Trichos "Hair" and Odyne "pain", synonymous Burning scalp syndrome ) are at the discomfort (or sensory disturbances) scalp called. Popularly it is called "hair root catarrh ", but a " catarrh " is an inflammation of the mucous membranes (often respiratory organs). The term “Burning Scalp Syndrome” (or “Scalp Dysesthesia ”) was coined in 1998 in a scientific study. Before that, the existence of this clinical picture was still largely controversial among dermatologists. The causes are largely unknown and insufficiently researched. The expressions of the sensations range from tingling ("pins and needles"), itching, burning or tension to aching scalp. Trichodynia is often associated with hair loss , and an increased frequency of tension headaches is observed in patients with trichodynia. For this clinical picture it is classic that microscopic no changes on the scalp can be determined.

Pathogenesis

The pathogenesis of Burning Scalp Syndrome is not yet fully understood. Nevertheless, there are some hypotheses as to how the burning sensation on the scalp develops and why conventional therapies have so far failed.

Usually the life cycle of the hair is divided into three phases: the growth phase or anagen, the resting phase or telogen and the loss phase or catagen. There is some evidence that a change in the hair follicles occurs when it enters the resting or telogen phase, creating a burning or warm sensation in the scalp. The chemical mediator is suspected to be the substance known as substance P or neuropeptide P, which is responsible for pain and burning sensations in the skin and occurs, among other things, in many skin diseases .

It can also be seen that inflammatory reactions affect the hair follicle, causing the hair to switch to the telogen phase as a protective mechanism, which results in an increase in substance P in the hair follicles. This, in turn, results in burning and painful sensations, such as inflammation or progressive hair loss. Here are a few hypotheses on the pathogenesis of Burning Scalp Syndrome:

  1. Some hypotheses assume that the symptoms of Burning Scalp Syndrome are caused by irritation of nerve cells in the scalp.
    1. Among other things, inflammatory events on the scalp can lead to a congestion of the blood circulation in the scalp, whereby the sensory nerve endings in the scalp are irritated.
    2. A stasis of lymphatic drainage of the scalp caused by certain causes can also lead to nerve irritation, secondary to an accumulation of toxic waste materials.
    3. The permanent hair loss caused by Cicatricial alopecia , accompanied by the accumulation of inflammatory cells and fibrous tissue in the dermis, also leads to the irritation of nerve cells due to the resulting compression. The disease can be caused by lichen planus (lichen planopilaris), lupus erythematosus, and infections such as folliculitis decalvans. The Burning Scalp Syndrome can therefore be a syndrome that occurs with these diseases.
  2. It has been confirmed that the syndrome can occur from taking birth control pills , among other things .
  3. Some patients with severe scalp psoriasis and pustular psoriasis have symptoms of the syndrome.
  4. Patients who experience an allergic reaction from exposure to hair dye and develop dermatitis as a reaction may also experience the symptoms.
  5. Among other things, fear or depressive illnesses are also considered to be the cause of the Burning Scalp Syndrome.

Occurrence

"Due to the discrepancy between the sensation of pain and a lack of pathological-anatomical substrate as well as between an often existing fear of hair loss and the objective extent of hair loss, trichodynia is more often interpreted as a mental disorder from the group of somatoform disorders ."

Trichodynia is not an exceptional phenomenon. In a study published several years ago, these abnormal sensations are registered in up to 34% of patients who go to a hair clinic because of their hair loss.

Current studies by doctors at a Turkish university clinic confirm these figures. This study examined 248 people (95 men and 153 women) who suffered from hereditary hair loss (androgenetic alopecia, AGA) or diffuse hair loss (telogenem effluvium, TE). 29% of the patients reported the phenomenon of trichodynia. The abnormal sensations were described by people with both genetic and diffuse hair loss. The authors of the research report point out that with both forms of hair loss (AGA and TE), a possible influence by stress factors ( stress ) is very likely.

Trichodynia (and the associated hair loss) can subsequently be the cause of psychological problems. Patients often reported depression and anxiety disorders . So far it has been assumed that an overproduction of the substance P (a messenger substance for the transmission of pain) and a preceding inflammation could be the cause of the trichodynia. However, what the overproduction of substance P could result from is not clear.

treatment

The treatment of trichodynia is based on the underlying hair disease (AGA or TE) and any accompanying psychological components.

literature

  • JP Schade: Lexicon medicine and health . Published 2003, MedicaPress AG

Web links

Wiktionary: Trichodynia  - explanations of meanings, word origins, synonyms, translations

Individual evidence

  1. JP Schade: Lexicon Medicine and Health , p. 190, 2003
  2. Hanish Babu, Burning-Scalp-Syndrome ( Memento of the original from January 4, 2016 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. , Retrieved March 18, 2015  @1@ 2Template: Webachiv / IABot / suite.io
  3. ^ R. Trüeb: Trichodynie. In: The dermatologist . 12/1997, pp. 877-880.
  4. ^ A. Rebora, MT Semino, M. Guarrera: Trichodyniea. In: Dermatology . 1996, 192 (3), pp. 292-293.
  5. ^ I. Kivanc-Altunay et al .: The presence of trichodynia in patients with telogen effluvium and androgenetic alopecia. In: International Journal of Dermatology . 2003; 42 (9), pp. 691-693.