Scalp pruritus, commonly known as an itchy scalp, is a widespread and often distressing symptom that can significantly impact an individual's quality of life. While occasional scalp itching is a common experience, persistent or excessive itchiness, especially when accompanied by hair loss, can be a cause for concern. It is normal to lose 50 to 100 hairs a day, according to the American Academy of Dermatology.
Scalp pruritus is a frequent complaint considered a diagnostically and therapeutically challenging situation. The scalp's skin possesses a unique neural structure, densely populated with innervated hair follicles and dermal vasculature. Despite advancements in understanding itch pathophysiology, scalp itching remains relatively understudied. Scalp pruritus can arise from various dermatologic, systemic, neurologic, and psychogenic diseases. Among patients with psychogenic pruritus, the most commonly affected sites are the scalp and face.
In a study conducted on a quantitatively representative sample of the French population, scalp itching was reported in 25% of the population.
The sensory innervation of the scalp is conducted through branches from the trigeminal nerve, cervical plexus, and dorsal rami of the cervical nerves. Hair follicles (HFs) are highly innervated with four types of specific nerve endings: free nerve endings (nociceptors), lanceolate nerve endings (acceleration detectors), Merkel nerve endings (pressure detectors), and pilo-Ruffini corpuscles (tension detectors). The free nerve endings innervating the HF are from A-delta (thinly myelinated) or C fibers (unmyelinated) that emerge from the superficial nerve plexus. These nerves terminate as free nerve endings in the connective tissue between the sebaceous gland and HF. Furthermore, HF development and cycling do affect the HF innervations. Initially, epidermal innervation is very dense, while it decreases and gains neuropeptide expression after penetration of HFs through the epidermis.
In addition to HF, the scalp has abundant blood vessels more than in any other body region. There are also cyclic changes of perifollicular vascularization. There is a significant increase in perifollicular vascularization during the anagen phase of HF, followed by regression of angiogenic blood vessels during the catagen and telogen phases.
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Pruritus involves different classes of cutaneous unmyelinated, slowly transmitting, sensory C-NFs that are distributed in the epidermis and papillary dermis. They are of two types; mechano-insensitive that are activated by histamine, and mechano--sensitive that cause pruritus with burning when induced activated by cowhage spicules (Mucuna pruriens). Informative data, namely distribution of C-fibers at various body sites, is lacking. Although the scalp is considered extremely itchy in many cutaneous inflammatory diseases and as mentioned above highly innervated, experimental itch studies in humans were not able to demonstrate lower itch thresholds.
Histamine, the prototype of endogenous itch mediator secreted from MCs, can induce pruritus via H1 and H4 receptors on NFs, whereas H3 receptors appear to be involved in the suppression of pruritus. MC can induce pruritus directly also through the release of other mediators such as chymase, tryptase and cytokines. MC also secrete neurotrophins such as nerve growth factor (NGF) that contribute to hyperplasia of NFs in chronic pruritus forms, as has been observed in Atopic dermatitis (AD). MCs function also as hair cycle regulators and are involved in the control of HF regression in murine system. MC density in scalp skin does not differ significantly from that in forearm skin.
PAR-2 is a G-protein coupled receptor that plays a major role in mediating chronic pruritus. During neurogenic inflammation, various endogenous serine proteases such as trypsins from keratinocytes and tryptase from MCs activate PAR-2 on sensory nerve ending to release calcitonin gene-related peptide (CGRP) and substance P (SP). PAR-2 signaling also stimulates the release of neuropeptides from central nerve endings thereby activating CGRP receptor and SP receptor (NK1R) to transmit itch responses to the central nervous system. Recently, it was shown that Cathepsin S which is an endogenous cystein protease evokes itch and activates PAR-2 and 4. Exogenous activators of PAR2 may be serine proteinases generated by bacteria, fungi, and house dust mites. PAR-2 interacts synergistically with transient receptor potential vanilloid-type 1 (TRPV1), thereby amplifying itch sensation. In the skin, PAR-2 is expressed by almost all cell types including keratinocytes, HF, sensory neurons, and MCs. In human HF, PAR-2 is confined to the Inner root sheath (IRS). PAR-2 activation is likely to be involved in pruritus of AD. In addition, skin exposure to exogenous microbial proteases could also induce itch and inflammation via PAR-2. This could explain why staph folliculitis in the scalp is extremely itchy.
TRPV1 receptor is activated by capsaicin, the key ingredient of hot chilli peppers. In addition to capsaicin, TRPV1 can also be activated by heat, acidosis and endogenous endovanilloids such as arachidonic acid derivatives, lipid peroxidation metabolites, and endocannabinoids. When TRPV1 is activated, it causes burning pain, itching and heat sensation, which is suppressed by continuous activation. TRPV1-expressing neurons are required for the behavioral responses to several different pruritic compounds including histamine, serotonin, and endothelin-1. TRPV1-expressing neurons have multiple intracellular mechanisms that generate or mediate itch. TRPV1 is highly expressed on sensory NFs, epidermal keratinocytes, HFs, dermal blood vessels, MCs, sebaceous glands and eccrine sweat glands. In human HF, TRPV1 is confined mainly to the Outer root sheath (ORS) and hair matrix. TRPV1 has a significant role in human hair growth control. In organ culture, TRPV1 activation by capsaicin resulted in hair shaft elongation, suppression of proliferation, induction of apoptosis, premature HF regression (catagen), and up-regulation of intrafollicular transforming growth factor-B2. Cultured human ORS keratinocytes also expressed functional TRPV1, whose stimulation inhibits proliferation, induces apoptosis, up-regulate known endogenous hair growth inhibitors (interleukin-1B, transforming growth factor-B2), and down-regulate known hair growth promoters (hepatocyte growth factor, insulin-like growth factor-I, stem cell factor). In rat skin, hair growth retardation, along with alopecia and a decrease in hair shaft thickness, follows as a consequence of capsaicin-induced sensory denervation. Pirt gene was recently identified as a regulator of TRPV1, in both histaminergic and nonhistaminergic itch. Tacrolimus has been reported to have anti-itch property, unrelated to its anti inflammatory property. This was explained possibly by a desensitization of TRPV1 and calcium currents through the phosphatidylinositol 4,5-bisphosphate regulation pathway. It would be of great interest to examine the role of TRPV1 receptor and its ligands in itchy scalp. Another thermosensitive Transient Receptor Potential channel which has been shown to have a role in itch in mice is TRPV3. TRPV3 is abundantly expressed in keratinocytes and scalp HF, mainly the ORS. Activation of TRPV3 shown recently to inhibit human hair growth.
Mrgpr family can be activated directly by peptides with common C-terminal motifs like RFamide, -RYamide, -RYG or -RLamide, neuropeptide AF, γ2-melanocyte-stimulating hormone, bovine adrenal medulla8-22 peptide [BAM8-22] and chloroquine. Recently, direct evidence proved the involvement of some of these peptides in itch sensation. Mouse MrgprA3 and MrgprC11 act as itch receptors in the skin for the pruritogens chloroquine, and bovine adrenal medulla 8-22 peptide (BAM8-22) and synthetic peptide Ser-Leu-Ile-Gly-Arg-Leu (SLIGRL) respectively. In human MrgprXs expression was detected exclusively in DRG neurons.
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Opioids and their receptors in the skin comprise part of the endogenous opioid system. It includes three opioid receptors: Mu (MOR), Delta (DOR) and Kappa (KOR), and the opioid peptides, such as enkephalins, endorphins, dynorphins and endomorphins. It is widely accepted that KOR signaling suppresses itch, while MOR signaling can stimulate itch. MOR seems to be important in chronic forms of pruritus, while KOR agonists are important in acute itching. Neuronal communication between pain- and itch-transmitting neurons underlies the role of opioids in pruritus. Many painful stimuli shown to inhibit itch by activating specific nociceptive pathways.
Several conditions and factors can contribute to both an itchy scalp and hair loss:
In severe cases, allergic reactions to things like hair dyes can cause an inflamed, itchy scalp and hair loss. In one study published in ISRN Dermatology, researchers found that up to 1 percent of the subjects were allergic to paraphenylendiamine (PPD), a common ingredient found in hair dyes. PPD is capable of causing severe hair loss in sensitive people. Inflammation and itching can also occur on the scalp around bug bites and can look like a rash or allergy. Allergic reactions to hair products can irritate the scalp and hair follicles, resulting in itching.People can have this type of allergic reaction to any product that they use on their hair, including: shampoos, conditioners, hair dyes, hair gel, hair mousses. A common cause of allergic scalp reactions is the chemical paraphenylenediamine, which is an ingredient in many dark hair dyes.
Neuropathic itch in scalp can be seen in association with diabetes mellitus, and herpes zoster. Scribner observed several patients whose primary complaint of pruritus confined to the scalp proved to be caused by unsuspected diabetes. Post herpetic neuralgia (PHN) has been historically associated with pain. However data emerged that PHN also induces Post herpetic itch (PHI). A large epidemiological study reported PHI in roughly half of PHN patients. PHI can coexist with PHN or occur alone. In a patient with PHI on the scalp, quantitation of PGP 9.5-immunoreactive epidermal nerves demonstrated loss of 96% of PGP 9.5 stained epidermal innervation in the itchy area. Concomitantly, quantitative sensory testing indicated severe damage to most sensory modalities except itch. Possible mechanisms include selective preservation of peripheral itch-fibers from neighboring unaffected dermatomes, imbalance between excitation and inhibition of second-order sensory neurons, and/or electrical hyperactivity of hypo-afferented central itch specific neurons. Oaklander has suggested that the excessive scratching observed in some patients with PHI may be due to a reduced sensation of pain. Normally, the act of scratching to relieve itch elicits mild pain, which provides a protective negative feedback to halt further scratching. In PHI, scratching the affected skin area elicits no pain, so that scratching persists unabated, sometimes to the point of severe skin damage. Ross et al. recently demonstrated the existence of itch inhibitory interneurons within the dorsal horn. Bhlhb5 mutant mice lacking these interneurons had persistent itch. Glutamate is one of the major excitatory neurotransmitters in the spinal cord and may have a role in these interneurons.
Sensitive skin is characterized by subjective complaints of discomfort without predictable classical visible signs of irritation and without an immunologic response. It was found that 36% of 400 subjects in 2 hospitals declared that they had sensitive skin on scalp. Further epidemiological studies revealed that 44% and 32% subjects declared suffering from sensitive scalp. Itching affects about 60% of subjects with sensitive scalp.
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Treatments vary depending on the cause of the itchiness and hair loss. Your doctor may recommend:
Common therapies to treat hair loss include:
Standard treatments for these conditions often include: immunotherapy, antifungal medications and ointments, steroids.
Not every itchy scalp with hair loss needs medical treatment. Here are some things you can do yourself to ensure that your scalp and hair stay healthy.
Some skin conditions that cause an itchy scalp and hair loss are beyond your control.A person should contact a healthcare professional if they experience any of the following: sudden hair loss, development of bald patches, hair falling out in clumps, severe itching and burning of the scalp, especially if the person also experiences hair loss.
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