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Published On: Feb 22, 2016
Last Updated On: Oct 12, 2020
Itch is a symptom that 100 percent of people with eczema have to deal with — often on an ongoing basis, day and night.
Eczema is frequently referred to as “the itch that rashes.” Itch is said by many people to be the worst thing about eczema, as it can be so incessant and never goes away. Eczema flares are frequently triggered by the “itch-scratch cycle.” This is when itching leads to scratching, which results in the release of inflammatory mediators, leading to the development of eczema and more dry skin.
Dry skin and eczema flares lead, in turn, to more itching— and so the cycle continues. Itch is a complicated symptom of eczema. Multiple nerve pathways and chemical mechanisms have been identified—as well as other contributing factors, including a defective skin barrier, external triggers and human nature – in the search to answer the question “Why does eczema itch?”
Itch in atopic dermatitis generally originates in the skin. Medical names for itch starting in the skin can be pruritus, dermatological itch, or pruritoceptive itch. This type of itch begins when free nerve fibers are stimulated by nerve endings called C fibers in the top layer of the skin (the epidermis). The nerve endings can be stimulated by different factors, including external irritants, dry skin, eczema flares, or chemical mediators in the skin (more about chemical mediators later).
In response to itch in the skin, nerve pathways are activated and messages travel to the brain. People often respond to itch with a behavior (called the behavioral response), which is often scratching. However, itch in atopic dermatitis is not as straightforward as this; it is actually thought to be very complex. This is because there are two other types of itch—neurogenic itch and psychogenic itch—that are also thought to play a part.
Neurogenic itch is generated in the central nervous system (the brain and spinal cord interpret messages from nerve pathways) in response to circulating itch factors. Psychogenic itch is completely different as it relates to itch being stimulated by psychological factors. In eczema these include unconscious or conscious urges to scratch, habit, or a response to stress.
The epidermis (the top layer of the skin) consists of keratinocyte cells, which are constantly reproducing then moving upward and being shed as dead skin cells. In addition to keratinocytes, the epidermis contains nerve receptors and chemical mediators, which also appear to be involved with the sensation of itch. One theory concerns nerve endings in the epidermis, as it is thought that an itch sensation is generated through nerve receptors adjacent to the keratinocyte cells. specific nerve receptors for itch have not yet been identified in the epidermis. However, scientific experiments have shown that if the epidermis is removed, itch is abolished. This proves that itch must generate from the epidermis. In addition, itch is uniquely restricted to the skin, mucous membranes and the cornea of the eye, where there are epidermal layers. No other body tissue experiences itch.
In eczema, the skin barrier is altered compared to normal skin. The skin barrier is located in the uppermost layers of the epidermis (the stratum corneum). In normal skin, this is a resistant barrier that protects the underlying skin from irritants and prevents water loss from the body. In atopic dermatitis, the skin barrier is altered due to changes in the filaggrin gene, which determines the normal structure of the skin barrier, so the normal levels of natural moisturizing factors (NmFs) are decreased. As a result, the cells are not able to retain water and they shrink. This causes gaps between the skin cells. In addition, there is a breakdown of lipid lamellae from around the skin-cell walls. This leads to dry skin and a defective skin barrier, which allows the entry of irritants and the loss of water through the skin. This is known as trans-epidermal water loss (tewl). Interestingly, tewl has been shown to increase at night, which may be one explanation of why itching is frequently worse at night.
There is an interactive network between the skin, the nervous system and the immune system. When eczema flares, becoming red and sore, this causes itch. Inflammation is driven by a variety of chemical mediators, including a neuropeptide called substance-P. Inflammation increases blood flow, which also contributes to generating itch.
Sweat and perspiration induce itching and often aggravate eczema. This is thought to be due to altered sensations in the sweat gland nerve endings in the skin. Neuropeptides are chemical mediators involved in the control of sweat glands. If you have atopic dermatitis, you have increased amounts of neuropeptides compared to people with nonatopic skin. Another way in which sweating may induce itching in eczema is that there seems to be an IgE- mediated allergic reaction to the components of sweat. Sweat comprises mainly water, lactate, minerals, and urea. We know that IgE levels are raised in atopic dermatitis and reactions to IgE are complex.
There are many individual trigger factors in eczema that may cause itch due to irritant and allergic reactions. These may include soaps, perfumes, detergents, household cleaning products, chemical substances, synthetic and wool clothing, animal dander, household dust mites, tree and grass pollens, sudden changes in temperature, humidity, and contact allergy to metal, cement, or latex.
A chemical itch mediator is a substance in the body that acts as a messenger. When introduced into the skin, the chemical mediator acts on nerves endings in the upper layers of the skin, or indirectly through cells that play a role in causing itch. In atopic dermatitis, several chemical itch mediators have been identified.
Histamine is not a mediator of itch in atopic dermatitis, but its role remains controversial. In atopic dermatitis, it has been found that nerve fibers that transmit itch both peripherally and centrally are histamine insensitive. These peripheral nerve fibers have been found to be mechanically sensitive but unresponsive to histamine. It is thought that these specific nerve fibers may be more clinically relevant to atopic dermatitis itch rather than those nerve fibers that are histamine sensitive. This is the reason why even high doses of antihistamine do not relieve itch, unless they are centrally sedating antihistamines. Therefore sedating antihistamines are probably the only ones that help itch in eczema that does not have a urticarial component (e.g., Piriton or Atarax).
Skin conditions that cause an eczematous reaction including urticaria are histamine mediated, as are insect-bite reactions and allergic drug reactions. Histamine directly stimulates histamine type 1 (H1) receptors on itch-specific nerve fibers. This is why for these conditions antihistamines taken in tablet form (or given by injection or via a drip in emergencies) are the mainstay of treatment. several types of antihistamine drugs may be prescribed. Treatment generally starts with non-sedating H1 antihistamines (e.g., Cetrizine, Fexofenadine, or Neoclarityn), but there are several other treatment options available.
It is very interesting to compare the reaction to itch and pain as two different stimuli. pain and itch have very different behavioral patterns. The central processing of itch involves multiple areas of the brain. The specific brain areas activated by itch are also involved with the central processing of pain. This implies that neural networks activated by these two stimuli are not distinct. Yet itch and pain have different activation patterns and reflexes.
Pain causes a withdrawal reflex. If pain is experienced, we try to protect the painful part of the body and not touch or overuse it. For example, if you hurt your back, you become very protective, avoid bending, and move with trepidation. Itch has the opposite behavioral pattern; the scratch reflex draws us to the itchy area. Intense scratching helps to relieve the itch and indeed often becomes pleasurable — until damage is caused resulting in broken skin. Then itch is replaced by pain, and the person withdraws from the area.
Areas in the cortex activated in atopic dermatitis and associated with processing itch lead to the following functions relating to itch:
The cortex in the frontal brain is the area of reward and decision-making. this gives one explanation for the compulsive and often satisfying nature of scratching. therefore physical and emotional components of itch are linked together.
Scratching is also linked to behavioral psychology, and in particular to conditioning, which is part of human nature. Classical conditioning is a form of learning in which a given stimulus — itch — becomes increasingly effective in evoking a response — scratch. So when skin itches, the response is to scratch. The intensity of the relationship between the two stimuli means that whenever itch is felt as a sensation, scratch will become an automatic, conditioned response. This is a learned human behavior, and scratching — even for small babies — can quickly become an unconscious reaction, due to conditioning.
Itch is a complex symptom, with physical and psychological causes in eczema. In the process of answering the question “Why does eczema itch?” It has become very clear that it is impossible for anyone with eczema to resist the urge to scratch, or indeed to “stop scratching” when told to do so. It is just not that simple.
Original article written by Independent Dermatology Nurse Julie Van Onselen, for the United Kingdom’s National Eczema Society magazine Exchange, issue No. 147, Spring 2013. Edited for the U.S. audience and republished with permission.
The National Eczema Eczema Association, extends a special thank you to Julie Van Onselen, Independent Dermatology Nurse, and Margaret Cox, Chief Executive, National Eczema Society.