Scalp psoriasis: symptoms, diagnosis, treatment

Scalp psoriasis is one of the most common and socially visible forms of psoriasis. The disease manifests as persistent erythematous-squamous plaques within and beyond the hairline, dense scales, itching, burning, pain when scratching, and severe cosmetic discomfort. Even with a limited area of involvement, sleep is impaired, productivity and quality of life are reduced. [1]

Scalp lesions are observed in 45-80% of patients with psoriasis at various stages of their lives. For some patients, this location is the first manifestation of the disease. The high visibility of the lesions, frequent pain and itching, and dandruff-like flaking cause a disproportionate impact on emotions and social interactions. [2]

The scalp is considered a difficult area to treat due to its dense hair growth, difficulty delivering medications to the lesions, and high relapse rates after treatment discontinuation. In practice, this requires specialized dosage forms, a long-term remission maintenance strategy, and a willingness to transition to phototherapy or systemic agents if there is an insufficient response to topical treatment. [3]

The current understanding of the disease relies on dysregulation of the interleukin-23-interleukin-17 axis, the involvement of memory T cells, and cytokine cascades with a key role for keratinocytes and dendritic cells. For the scalp, the contribution of lipophilic yeasts of the genus Malassezia is discussed, which partially explains the overlap with seborrheic dermatitis and the effectiveness of adjuvant antifungal shampoos in sebopsoriasis. [4]

Disease codes: ICD-10 and ICD-11

In the International Classification of Diseases (ICD-10), skin lesions in plaque psoriasis are coded in block L40, where L40.0 is used for typical plaques, and L40.9 for unspecified forms. There is no separate subtype of "scalp psoriasis" in ICD-10; localization is specified in the clinical diagnosis. [5]

In ICD-11, plaque psoriasis is coded EA90.0. If necessary, scalp and scalp localization is specified using post-coordination with anatomical modifiers. This approach is convenient for accounting for severity by location, choosing treatment strategies, and auditing treatment results. [6]

Table 1. Correspondence of codes for psoriasis localized on the scalp

Classification	Main code	What does it mean?	How to clarify localization
ICD-10	L40.0 or L40.9	Plaque or unspecified psoriasis	Specify "scalp" in the diagnosis
ICD-11	EA90.0	Plaque psoriasis	Add anatomical modifier "head, hairy part"

The use of post-coordination in ICD-11 improves patient pathway traceability and comparability of research data. [7]

Epidemiology and disease burden

The global prevalence of psoriasis is approximately 2-3% of the population, with a significant proportion of patients experiencing scalp involvement. In different samples, the proportion of scalp lesions varies from 45% to 80%. In dermatology registry cohorts, scalp localization is often associated with a higher quality-of-life impact score. [8]

The scalp can be affected in any psoriasis phenotype, and in some cases remains the only site of involvement. Despite the relatively small area, itching, visibility of lesions, and dandruff-like flaking are associated with anxiety, depression, and limited social activity. [9]

Head lesions often coexist with other "difficult" areas, such as the nails and palms, further complicating the course of the disease and reducing treatment satisfaction. The correct choice of dosage form and remission maintenance regimen is critical to long-term symptom control. [10]

The systemic nature of psoriasis requires an assessment of associated risks, including metabolic disorders and the likelihood of developing psoriatic arthritis, which is observed in a significant proportion of patients and requires early screening. [11]

Causes and triggering factors

Psoriasis is an immune-mediated chronic skin inflammation with a polygenic predisposition. The interleukin-23/interleukin-17 axis plays a leading role, as evidenced by the high efficacy of targeted blockers of these targets. At the scalp level, activated keratinocytes, dendritic cells, and memory T cells remain key players. [12]

Classic triggers for flare-ups include stress, mechanical trauma with the Koebner phenomenon, acute infections, weight fluctuations, smoking, and certain medications. For the scalp, the role of Malassezia yeast and the interaction of the skin microbiome with host immunity are discussed. [13]

Some patients report worsening symptoms with increased sweating or wearing tight hats, which is associated with friction, maceration, and changes in the skin barrier. Adequate care, gentle hygiene, and stress management help reduce the frequency of relapses. [14]

Some patients develop sebopsoriasis, a clinical phenotype on the border between seborrheic dermatitis and psoriasis, in which case it is logical to include antifungal shampoos in the treatment regimen as an adjuvant to anti-inflammatory therapy. [15]

Table 2. Most likely trigger factors and control measures

Factor	What's happening	What to do
Stress and lack of sleep	Increased itching and inflammation	Sleep hygiene, stressproofing techniques
Mechanical friction	Koebner phenomenon	Use soft brushes and avoid aggressive scrubbing.
Infections	Immune shift	Treatment of foci of infection, vaccination according to the calendar
Sebopsoriasis and Malassezia yeast	Adjuvant effect on inflammation	Ketoconazole shampoo 2-3 times a week in courses

Antifungal shampoos do not replace anti-inflammatory therapy, but they reduce itching and flaking in sebopsoriasis. [16]

Pathogenesis with a focus on the scalp

Dysregulation of the interleukin-23-interleukin-17 axis leads to the activation of T-helper cells type 17 and the production of interleukin-17 and associated mediators, which stimulate keratinocytes, enhance proliferation, and disrupt epidermal differentiation. The result is hyperkeratosis, parakeratosis, and dermal inflammation with vasodilation. [17]

The scalp is characterized by a high density of follicles and sebaceous glands, which influences the barrier and microbiome. The contribution of Malassezia products to maintaining inflammation through interactions with innate and adaptive immunity is discussed. This partially explains the clinical overlap with seborrheic dermatitis in some patients. [18]

Inflammatory maintenance loops include tissue memory T cells and local production of interleukin-23, which explains the tendency of scalp lesions to relapse after discontinuation of therapy and justifies the need for maintenance regimens. [19]

Understanding these mechanisms underlies targeted therapy and modern approaches to long-term symptom control with minimal drug burden. [20]

Clinical picture and possible complications

Classic signs include well-defined erythematous plaques under dense whitish scales, often extending beyond the hairline. Itching and pain when scratching are common and correlate with sleep disturbances. With extensive hyperkeratosis, dense, "armor-like" crusts may form. [21]

Unlike cicatricial alopecia, scalp psoriasis typically does not cause irreversible hair loss. Diffuse hair loss, such as telogen effluvium, is possible, as is pityriasis amianthus, a specific form of massive adhesion of scales and hair. Secondary infection of the lesions is most often associated with scratching. [22]

Associated risk areas include the face, ears, and neck. Comorbidities include anxiety, depression, and metabolic disorders, requiring screening and multidisciplinary management. [23]

Diagnostics: from examination to confirmation

The diagnosis is established clinically based on the characteristic appearance. Trichoscopy helps differentiate psoriasis from seborrheic dermatitis and dermatophytosis: psoriasis is characterized by regular red dots and globules, and diffuse white scales; seborrheic dermatitis is characterized by predominantly yellowish scales and irregular vessels. [24]

Microscopic examination of scales and fungal culture are indicated in cases of atypical presentation, significant hair fragility, areas of "blackheads," tenderness, and regional lymphadenopathy—symptoms typical of scalp dermatophytosis. Skin biopsy is rarely required, primarily when discoid lupus erythematosus or lichen planus follicularis are suspected. [25]

Assessing the impact of the disease on the patient's life is essential. The PSSI (Severity Index) is used for head localization, the PASI (Personal Identification Severity Index) is used for overall assessment, and quality-of-life indices are used for overall assessment. This is important for choosing treatment strategies and monitoring effectiveness. [26]

Table 3. Diagnostic minimum and indications for clarifying tests

Step	What to do	When is enough?	When to expand
Examination and trichoscopy	Typical plaques and vascular pattern	Typical picture without alopecia	Atypia, soreness, "black spots"
Mycology	KOH test and culture	If dermatophytosis is suspected	Before prescribing systemic steroids
Skin biopsy	Exclude DKV and cicatricial alopecia	Not required for typical picture	Persistent erythema, atrophy, follicular plugs
Severity assessment	PSSI, PASI, DLQI	To all patients	To monitor the response to therapy

PSSI is calculated based on the severity of erythema, infiltration and scaling, taking into account the area of the lesion, the range of scores is from 0 to 72. [27]

Differential diagnosis in difficult cases

Seborrheic dermatitis, tinea capitis, discoid lupus erythematosus, and lichen planus follicularis are the main symptoms. Seborrheic dermatitis is suggested by oily, yellowish scales and a rapid response to antifungal shampoos; tinea pedis is suggested by pain, brittle hair, blackheads, regional lymphadenopathy, and a positive mycology test. [28]

Discoid lupus erythematosus is characterized by atrophy, telangiectasias, follicular keratin plugs, and the risk of cicatricial alopecia; confirmation is by biopsy with immunopathology. Lichen planus follicularis produces inflammatory follicular papules, burning, and scarring. [29]

Table 4. Scalp psoriasis versus common "mimics"

Sign	Psoriasis of the scalp	Seborrheic dermatitis	Dermatophytosis of the head	DKV	Lichen planus follicularis
scales	White, dry	Yellow, fatty	Brittle hair, crusts	Dense horn plugs	Follicular keratotic plugs
Trichoscopy	Regular red spots, white scales	Irregular vessels, yellow scales	Blackheads, deformed hair	Telangiectasias, whitish spots	Perifollicular changes
Alopecia	Non-scarring, not always	No	Focal with fragility	Scar	Scar
Tests	Not required for typical picture	No	Positive mycology	Biopsy	Biopsy

Trichoscopy and mycology significantly reduce the risk of diagnostic errors and accelerate the start of correct therapy. [30]

Treatment

Basic care and keratolytics. Daily emollients and mild shampoos reduce itching and facilitate scale removal. Salicylic acid, in the form of ointments and shampoos, promotes dekeratinization but should not be applied simultaneously with calcipotriol, as it inactivates it; when combined, it is advisable to separate the two. [31]

Topical corticosteroids. High- and ultra-high-potency preparations in shampoo, foam, or solution form are first-line treatment for the scalp, administered in 2-4-week courses, followed by a maintenance regimen of 1-2 times per week. The efficacy and safety of short-term courses have been confirmed by randomized trials. [32]

Vitamin D analogs and fixed-dose combinations. Calcipotriol foam or solution and the combination of calcipotriol betamethasone dipropionate gel or foam provide a pronounced anti-inflammatory and antiproliferative effect and are suitable for hair growth. The combination often outperforms monotherapy in the speed and depth of response. [33]

New generation nonsteroidal anti-inflammatory topical agents. The phosphodiesterase-4 inhibitor roflumilast in 0.3% foam form has shown clinically significant improvement in scalp symptoms and pruritus in real-world practice and randomized trials. [34]

Phototherapy, including home devices. Narrowband ultraviolet-B (UVB) for the scalp is delivered using comb lamps, which deliver light to the skin between hairs. In randomized trials, the UVB comb was comparable in efficacy to betamethasone solution and was well tolerated. Home phototherapy with narrowband ultraviolet-B is as effective as outpatient therapy and often improves compliance. [35]

Systemic therapy for insufficient response or high impact on daily life. If topical therapy is insufficient or the impact on daily life is high, a transition to systemic agents is indicated according to the EuroGuiDerm guidelines and AAD-NPF recommendations. Biologics targeting interleukin-17 or interleukin-23 demonstrate a rapid and sustained scalp response as measured by the PSSI. [36]

Maintenance of remission. After achieving clearance, intermittent use of mild steroids or fixed combinations 1-2 times per week is recommended, along with continued use of topical treatment and keratolytics as needed. This reduces the risk of relapse without increasing safety risks. [37]

Table 5. External therapy for the scalp: forms, courses, notes

Class of product	Optimal shape for the head	Typical course	Important notes
High potency corticosteroids	Shampoo, foam, solution	2-4 weeks daily	Then 1-2 times a week for maintenance
Calcipotriol	Foam, solution	4-8 weeks	Do not combine with salicylic acid in the same application.
Combination of calcipotriol betamethasone	Gel, foam	4-8 weeks	Often faster and deeper than monotherapy
Salicylic acid	Ointment, shampoo	2-6 weeks	Separate with calcipotriol
Roflumilast	Foam 0.3%	According to the instructions	Non-steroidal option for sensitive areas

The choice of dosage form is critical for delivery to the interhairline and to improve treatment compliance. [38]

Table 6. Phototherapy for scalp psoriasis

Method	How to use	Efficiency	When it is especially useful
Narrowband UV-B comb	3-5 times a week	Comparable to betamethasone solution in small studies	Reluctance or contraindications to steroids
Home Narrowband Ultraviolet-B Panels	According to an individual protocol	Not inferior to outpatient phototherapy	Limited access to the clinic, low adherence to visits

The safety of narrowband ultraviolet-B when dosed correctly is high, the key risk being erythema, which can be controlled by dose adjustment. [39]

Table 7. Systemic agents with evidence of effect on the scalp

Class and examples	Head data	Comments
Interleukin-17 blockers: secukinumab, ixekizumab	High PSSI-90 proportions and complete clearance in subanalyses and individual studies	Rapid onset of action, stable control during long-term therapy
Interleukin-23 blockers: guselkumab, risankizumab, tildrakizumab	Strong overall skin response, compelling data in difficult areas	Convenient administration intervals
Traditional systemic means	The effect on the head is variable	Used taking into account the safety profile and comorbidities

The choice of systemic agent is based on the patient profile and goals for PSSI and quality of life, based on the EuroGuiDerm living guidelines and AAD-NPF recommendations. [40]

Security and Interactions

The main risks of topical steroids are atrophy, telangiectasia, and tachyphylaxis with long-term continuous use; these are mitigated by short courses and maintenance regimens. Salicylic acid is useful as a keratolytic, but it inactivates calcipotriol when applied concurrently, requiring dilution. [41]

Phototherapy requires dose control and consideration of the phototype. Home narrowband ultraviolet-B devices have demonstrated non-inferiority over outpatient phototherapy, with a higher incidence of resolved erythema, which can be corrected with training and titration. [42]

Systemic drugs require standard laboratory monitoring and assessment of comorbidities before initiation and over time. The choice of molecule is determined by the risk profile, desired response rate, and individual factors. [43]

When to see a doctor immediately

An urgent consultation with a dermatologist is necessary in case of severe pain, oozing and odor from the lesions, signs of a bacterial infection, rapid hair loss with brittleness and pain, suspected dermatophytosis, a sharp generalized deterioration, fever, as well as severe sleep disturbance and depressive symptoms. [44]

Treatment goals, response assessment and maintenance

Practical goals include reducing PSSI to low levels, relieving itching and normalizing sleep, and achieving an acceptable frequency of maintenance applications. If adequate topical therapy is ineffective or if the disease has a high impact on life, switching to phototherapy or systemic agents is indicated according to clinical guidelines. [45]

Table 8. Severity assessment and target benchmarks

Indicator	What do we evaluate?	Goal of therapy
PSSI	Erythema, infiltration, scaling and scalp area	Minimal PSSI, sustained improvement with maintenance
PASI and BSA	Overall severity	Maintaining low values with stable remission
DLQI	Impact on life	Reduction to low values and normalization of sleep

Using PSSI in routine helps to objectify the dynamics, switch strategies in time and explain to the patient the logic of the therapy steps. [46]