The pathogenesis of pruritus is multifactorial. Currently this phenomenon is considered as a separate type of sensation, although for many years it has been perceived as sub-modality of pain [21]. Pruritus can be interpreted as a defence mechanism directed against dangerous organisms or stimuli [5]. These comprise parasites, insects, sharp objects, irritants and allergens [22]. Various stimuli are transmitted from skin through cutaneous sensory unmyelinated C-nerve fibres but also via thinly myelinated Aδ fibers [23–25]. The transmission proceeds through dorsal root ganglia into the spinal cord, then due to lamina I neurons through the spinothalamic tract, thalamus and eventually reaches cerebral cortex. Several areas of cortex are activated, both sensory and motoric [26–28]. Regarding the crucial role of central nervous system (CNS) in generating itch sensation validates the following statement: it is the brain that itches.

Numerous chemical substances contribute to pathogenesis of itch. No universal mediator exists, rather disease-specific sets of mediators [5]. Neurotransmitters in the skin are synthesized by nerve fibers and numerous cells including Merkel cells, Langerhans cells, keratinocytes, melanocytes, granulocytes, lymphocytes, monocytes-macrophages and mast cells [29]. Histamine is commonly regarded as a classic mediator of itch although over the years other substances have been investigated. In general, pruritus transmission is divided into histaminic and non-histaminic [30]. The latter is associated with mediators such as acetylcholine (Ach), α-melanocyte-stimulating hormone (α-MSH), beta-endorphine, catecholamines, calcitonin gene related protein (CGRP), endothelin 1 (ET-1), gastrin-releasing peptide (GRP), interleukin 31 (IL-31), nerve-growth factor (NGF), neurokinin A (NK-A), opioids, prostaglandins, proteases, substance P (SP) and vasoactive intestinal peptide (VIP) [31–60]. Growing evidence concerning the mediators of itch contributes to the continuous appearance of selective therapeutic approaches, for example nalfurafine (kappa opioid receptor agonist) or aprepitant (NKR1 antagonist). It must be noted that administration of various drugs may also elicit pruritus, especially antimalarials, opioids and hydroxyethylstarch (HES) [61]. Although selective serotonine reuptake inhibitors (SSRI) may be used as a treatment modality in several forms of pruritus [62–65], they may also elicit pruritus in certain situations [66, 67]. Iatrogenic types of pruritus may occasionally result from the dermatologic treatment itself, for example due to contact irritant reaction (high concentrations of topical modalities) or phototherapy.

Interestingly, pruritus may also be regarded as a “contagious” phenomenon. This hypothesis has been evaluated in recent studies performed by Papoiu et al. [68], van Laarhoven et al. [69] and Bartels et al. [70]. The contagious pruritus is an example of a “nocebo effect” in which a subject expects a certain form of reaction from the organism based solely on a suggestion. In contrast to “placebo effect”, the reaction is considered as unfavourable. Holle et al. [71] suggested that the social contagion of itch is a normative response, being experienced by most people. Functional magnetic resonance imaging (fMRI) revealed that key areas of the brain responsible for experiencing and responding to itch were anterior insula, premotor cortex, primary somatosensory cortex and prefrontal cortex. Neuroticism as a personality trait was also postulated as factor influencing the itch contagion [71].

It is acknowledged that certain intrinsic personality factors combined with stressful life events make an individual more prone to develop pruritus [72]. Bandura [73] described the concept of perceived self-efficacy which is defined as people’s beliefs about their capabilities. These beliefs determine feelings, thoughts, motivation and behaviour. In consequence, perceived self-efficacy may influence the way in which an individual copes with difficult situations and stress. Furthermore, a possible influence is implied regarding skin disorders and itch. Dalgard et al. [72] have proven that adolescent individuals with poor self-efficacy complained of itch twice as often in highly stressful situations as those with high self-efficacy (30 % vs. 15 %; p = 0.072). The authors suggested that itch may possibly be alleviated by psychotherapeutic interventions that strengthen the general coping mechanisms.

Itch inhibition has many aspects. Thermal and mechanical counterstimuli may inhibit histamine-associated pruritus in human subjects [74, 75]. Spinal interneurons releasing glycine and gamma-aminobutyric acid (GABA) contribute to this phenomenon, as demonstrated by Akiyama et al. [76]. Recently, the role of spinal B5-interneurons and kappa-opioid agonist dynorphin as an itch inhibiting neuromodulator has been reported in mice [77]. Glutamate release associated with VGLUT-2 transporter and TRPV-1 receptors generates pain and inhibits pruritus [78, 79]. Tropomyosin-receptor kinase A (TrkA) functioning as NGF receptor has recently been targeted by novel CT327 antagonist [80].

Acute and chronic stressors trigger responses in skin as well. Stress exerts its influence on dermatological disorders and itch itself due to releasing neuropeptides and hormones [81]. Mediators released locally or systematically increase sensory innervation, promote the synthesis of pruritogenic substances, stimulate neurogenic inflammation and lower the threshold of itch [82]. An impaired parasympathetic response possibly links chronic stress and itch [83]. Stress influences itch whereas itch results in additional stress. Thus, vicious “itch-scratch-itch” cycle appears and perpetuates itself. The relationship between itch and stress has been evaluated directly in several researches, predominantly in those focusing on subjects suffering from atopic dermatitis or psoriasis.

Atopic dermatitis (AD) is a common chronic or recurrent inflammatory skin disease affecting 15–20 % of children and 1–3 % of adults worldwide [84]. Pruritus is a key feature of AD included in the classic diagnostic criteria proposed by Hannifin and Rajka [85] and by UK Working Party [86]. The pathogenesis of itch in AD is multifactorial. Pruritus threshold is diminished and various factors trigger itch in lower concentrations than in healthy subjects [87, 88]. Epidermal barrier dysfunction measured by increase in transepidermal water loss (TEWL) was reported by several authors [89, 90]. Altered pattern of cutaneous innervation was observed in skin specimens. In animal models of AD as well as in human subjects the density of epidermal and dermal nerve fibres was higher [37, 91]. Plasma concentrations of SP, CGRP, NPY, beta-endorphine, NGF, brain-derived neurotrophic factor (BDNF) were altered in patients with AD [92–96]. Increased levels of histamine were reported in plasma and skin of patients suffering from AD [87, 97]. Rukwied et al. [98] observed that histamine induced extravasation of proteins was lower in atopic subjects, implying that other mediators may elicit pruritus in this group of patients. This issue was reflected by inconsistent effectiveness of antihistamines in reducing itch. Interleukines were also investigated in the context of itching, such as Il-2, Il-6, Il-13 or Il-31 [99–101].

Yosipovitch et al. [102] reported that 87 % subjects suffering from AD experienced pruritus on a daily basis. The worst itch intensity reached 9.0 ± 1.2 points (VAS). Similar results were published by Dawn et al. [103] – 91 % subjects experienced pruritus at least once every day, whereas mean itch intensity was 8.3/10 (Likert scale). Several studies have proven that stress is important factor influencing pruritus in AD. In a previously mentioned study the severity of itch increased due to stress in 71 % respondents; 22 % identified stress as the most common factor initiating the onset of pruritus [102].

Oh et al. [104] observed that pruritus intensity (VAS) was positively correlated with state-anxiety and trait-anxiety values (r = 0.573; r = 0.525; respectively). Subjects with anxiety and pruritus levels presented with more intense NPY and NGF immunohistochemical staining.

A study conducted by our group proved that the intensity of pruritus assessed with VAS (mean 7.9 ± 2.2) was related to the stress experienced by AD patients prior to disease exacerbation (ρ = 0.37, p < 0.001) [105]. Stress was evaluated utilising Social Readjustment Rating Scale and Stress Self-assessment Scale. Moreover, pruritus intensity was higher in subjects presenting with symptoms possibly associated with depression (VAS 9.1 ± 1.6 vs. 7.6 ± 2.2 points, p = 0.004; 4-Item Itch Questionnaire: 17.3 ± 2.5 vs. 13.1 ± 4.4 points, p < 0.001).

Peters et al. [106] observed significant positive correlation between itch and NGF+ neurofilaments in non-lesional skin (tau 0.466, p = 0.028) and between itch and NF-mast cell contacts (tau 0.745, p = 0.022) in lesional skin in subjects suffering from AD who had performed TSST. Tran et al. [107] focused on autonomic nervous system dysfunction in AD. Heart rate variability (HRV) was measured after eliciting histamine-induced itch, after artificial scratching the itchy area of the skin using cytology brush and after performing TSST. AD patients presented higher heart rates than healthy subjects, marked sympathetic response to itch and scratching (based on very low frequency and low frequency spectrum of HRV) and dysfunctional parasympathetic response to itch and scratching (based on high frequency spectrum of HRV).

Schut et al. [108] investigated the influence of personality traits and depression on itch. Pruritus was induced using an experimental video “Itch – what is behind it?”, while a video “Skin – the communication organ” was used as a control. Predictor variables were assessed with The Neo Five-Factor Inventory (NEO-FFI; the questionnaire measures personality traits defined as neuroticism, extraversion, openness to experience, agreeableness and conscientiousness), The Hospital Anxiety and Depression Scale (HADS) and The Self-Consciousness Scale (SCS). The intensity of itch was measured using VAS and by observing the number of scratch movements. Unsurprisingly, AD subjects with high HADS scores were prone to experience more pronounced itch, whereas the increase in the number of scratch movements was associated with high public self-consciousness and low agreeableness (detailed results therein). A recent study attempted to determine the role of coping as a possible mediator influencing the relationship between stress and pruritus [109]. The instruments for assessing Itch intensity, perceived stress and disease specific coping included VAS, Recovery-Stress Questionnaire (REST-Q) along with postawakening cortisol levels in saliva, and Marburger Skin Questionnaire (MSQ), respectively. The latter focused on factors such as “social anxiety-avoidance”, “itch scratch cycle”, “helplessness” and “anxious depressive mood”. Cortisol levels were not significantly correlated with itch intensity, contrarily to perceived stress and coping mechanisms (detailed results therein). The results supported the hypothesis that pruritus-related stress leads to unfavourable coping mechanisms which further perpetuate this bothersome phenomenon.

Psoriasis is a chronic inflammatory disorder affecting approximately 0.73–2.9 % of European population [110]. Among adults aged 20–59 years in the US, the prevalence of psoriasis in Caucasians, African Americans and Hispanics was 3.6 %, 1.9 % and 1.6 %, respectively [111]. Frequency of pruritus in psoriasis patients ranges from 67 to 96.6 % [112–120].

The pathogenesis of pruritus in psoriatic subjects is associated, at least to some extent, with neurogenic inflammation. In a Japanese study an increased number of SP-positive nerves in the perivascular area, increased number of NGF-immunoreactive keratinocytes and increased NGF skin concentration was found [121]. High affinity receptor for NGF (TrkA) was observed in the epidermis and dermal nerve fibers, while protein gene product 9 (PGP-9.5) immunoreactive nerve fibers were more prevalent in the epidermis and upper dermis. These aspects were correlated with itch intensity as well. Moreover, the authors established that E-selectin immunoreactive vessels as well as endothelial leucocyte adhesion molecule 1 (ELAM-1) density in venules contribute to the pathogenesis of itch. Madej et al. [122] emphasized the role vascular adhesion protein-1 (VAP-1). Wiśnicka et al. [123] and Reich et al. [124] observed that pruritus intensity may be correlated with high CGRP and low NPY plasma levels. Several authors investigated the role of semaphorine-3A (axon-guidance molecule) in association with pruritus [125, 126]. Decreased level of semaphorine-3A upregulates NGF expression, further resulting in hyperinnervation of C-fibers. Additionally, downregulation of kappa-opioid receptor in epidermis was also observed in psoriasis. Nigam et al. [127] reported that Gamma-aminobutyric acid (GABA) and its receptor (GABA_A) participate in pathogenesis of psoriasis and development of pruritus in these individuals.

Individuals suffering from psoriasis regard pruritus as the most bothersome symptom [128, 129]. The intensity of pruritus in psoriasis is regarded as moderate one. Reich et al. [115] reported mean VAS scores of 4.2 ± 2.4, while in a study conducted by Yosipovitch et al. [113] the worst VAS scores reached 6.4 ± 2.5.

Many researchers focused on the relationship between stress and pruritus in psoriasis. A Swedish study revealed that 67 % of respondents deemed stress as an aggravating factor of pruritus; pruritus intensity (verbal four-point rating scale and VAS) and stress were positively correlated (r = 0.8, p < 0.05) [118]. Pruritus negatively impacted QoL of participants: 60 % complained of mood disturbances, whereas problems concerning concentration, sleep, sexual desire and appetite were declared by 47 %, 35 %, 21 % and 11 % of participants, respectively. Reich et al. [115] reported that patients suffering from heavy or extremely heavy stress (as assessed by Social Readjustment Rating Scale and self-assessment method) were more susceptible to the occurrence of itch (p < 0.05). The severity of stress and the intensity of pruritus were positively correlated (p = 0.015). Zachariae et al. [18] reported moderate correlation between stress reactivity and the degree of itching in a large group of Nordic subjects comprising members of psoriasis associations (n = 5795) and psoriasis patients (n = 702). A later study emphasized a significant decrease in HRQoL in patients suffering from itch (DLQI 12.2 ± 7.0 vs. 6.8 ± 7.1; p = 0.02) [117]. Over 70 % of patients had experienced at least one stressful event within 1 month before exacerbation of the disease. Regarding stress levels, no differences were observed between patients experiencing pruritus and those who did not (72.8 % vs. 70.0 %, respectively; p = 0.85). Similar itch levels were present in patients who had experienced at least one stressful life event prior to exacerbation as in patients who had not. In the majority of subjects itch intensity was significantly correlated with stress degree.

In a study by Chang et al. [116] pruritus was exacerbated by emotional stress in over 49 % of Korean outpatients (n = 152). Additionally, the authors performed skin biopsies and histologic examination along with immunofluorescent staining. Specimens from lesional, itchy skin presented with more pronounced staining for TrkA particles (high affinity receptor for NGF), SP-receptors (SPR) and CGRP-receptors (CGRPR) when compared to healthy areas of skin and lesional, non-pruritic areas. These observations serve as a link between pathogenesis and clinical symptomatology. However, in a study by Remrod et al. [130] pruritus intensity measured with VAS was not correlated neither with the number of SP positive fibers and SP positive cells, nor with salivary cortisol levels.

A recent study established that stress is the most important factor inducing and aggravating itch in psoriasis (49 % and 61 % of patients, respectively) [128].

Gupta et al. [131] reported that pruritus severity (10-point scale) was correlated with depression scores (Carroll rating scale for depression; CRSD) among outpatients suffering from psoriasis, atopic dermatitis and chronic idiopathic urticaria. The authors suggested that depressive symptoms may be regarded both as a primary feature of the skin disorder or as its consequence. Elevated levels of corticotropin-releasing factor associated with depression could intensify itch perception by increasing opiate levels in CNS.

Urticaria is a heterogenous group of disorders characterized by sudden appearance of urticarial wheals and/or angioedema. The prevalence rates vary according to different studies, ranging from 0.3 to 11.3 % of population [132]. Zuberbier et al. [133] conducted a study among German subjects reported lifetime prevalence of any urticarial lesions and chronic urticaria (CU) reaching 8.8 % and 1.8 %, respectively. Possibly up to 20 % of population will experience at least one episode of acute urticaria (AU) during their lifetime. In 40 % cases angioedema is also present [134]. Acute forms of urticaria subside within 6 weeks (most commonly within 24 h), whereas chronic forms last longer than 6 weeks. In chronic idiopathic urticaria (CIU) lesions appear spontaneously due to known or unknown causes [135]. Among chronic urticaria subtypes inducible urticaria is also mentioned along with its variants.

Itching in urticaria is almost invariable; some patients complain of more intense pruritus than the others [136]. Pruritus is described as pricking or burning in quality and exacerbates in the evening or during night. Although the lesions are itchy, patients tend to rub the skin rather than scratch it.

Quality of life is severely impaired in this group of patients, as reported in various studies [137–141]. Patients suffering from CIU present with impaired functioning in various daily activities and coexist with psychological co-morbidity. O’Donnell et al. [137] evaluated general health status of chronic urticaria patients (n = 142) utilizing the Nottingham health profile (NHP) questionnaire. The NHP scores obtained during the study were compared to NHP scores among patients suffering from ischemic heart disease. CU patients presented almost identical scores concerning energy, social isolation, emotional reactions and higher sleep disturbance.

Yosipovitch et al. [102] evaluated subjects suffering from CIU (n = 100). Pruritus intensity (VAS) at its worst state was more pronounced in patients that felt depressed (9.0 ± 1.6 vs. 7.7 ± 1.8, p = 0.018), agitated (8.4 ± 1.5 vs. 7.4 ± 2.1; p = 0.006) and anxious (9.1 ± 1.2 vs. 7.7 ± 1.9; p = 0.016). Moreover, 25 % respondents claimed that stress increased the perceived pruritus intensity.

Conrad et al. [142] researched the relationship between pruritus and anger in patients suffering from chronic idiopathic urticaria (n = 41) and psoriasis (n = 44). Eighty-five percent of the urticaria group presented at least moderate pruritus and more than 20 wheals day, while 82 % of subjects with psoriasis had at least 10 % of affected body surface area. Mean VAS scores for pruritus were similar in both groups (2.6 ± 1.1 and 2.2 ± 1.2, respectively). The authors assessed psychological distress and psychopathological symptoms perceived by the subjects as well. Symptom Checklist 90-R (SCL-90-R) questionnaire was utilized to assess nine psychopathological symptoms (somatization, obsessive-compulsive, interpersonal sensitivity, depression, anxiety, hostility, phobic anxiety, paranoid ideation, and psychoticism) and provide three global distress indices. Additionally, state anger, trait anger and anger expression were evaluated with State Trait Anger Expression Inventory (STAXI). Compared to healthy subjects (n = 49), both groups were characterized by higher emotional distress, depression and anxiety. Anger trait and anger state values were also more pronounced in the latter groups. In terms of pruritus severity, state anger was a significant predictor accounting for 19 % of its variance among the urticaria group. Among subjects suffering from psoriasis depression was the only significant predictor responsible for 12 % variance in pruritus severity.

Among adolescents with acne vulgaris (n = 108), 36.1 % subjects complained of pruritus that had occurred within the acne lesions in the past, while 13.9 % participants reported that their acne lesions were pruritic at the time of examination [143]. The latter group experienced pruritus intensity reaching approximately 3.1 ± 2.9 points (VAS). The maximal intensity of pruritus within acne lesions in the past had reached 4.0 ± 2.5 points. Itch aggravation associated with stress was reported by 33.3 % of subjects. Corresponding results were obtained by Lim et al. [144].

Peyri et al. [145] evaluated patients with seborrheic dermatitis (n = 2159). Over 90 % subjects complained of pruritus. Although no direct statistical correlation between stress and pruritus was reported, 76.4 % respondents reported that disease outbreak was triggered by factors such as stress, depression or fatigue.

A study by Niemeier et al. [17] conducted on 101 patients with hand dermatoses (26 with psoriasis, 33 with vesicular hand eczema and 42 with contact dermatitis) revealed that high stress responders experienced more severe pruritus intensity than low stress responders (VAS = 5.4 ± 2.2 and 4.0 ± 2.6 points, respectively; p ≤ 0.01). When evaluated with Coping with Chronic Skin Diseases Questionnaire (CSD), high stress responders were more likely to present social anxiety and avoidance (33.1 ± 10.0 points vs. 26.6 ± 9.8 points; p ≤ 0.001), vicious circle of itching or scratching (23.2 ± 6.3 points vs. 18.2 ± 6.6; p ≤ 0.001), helplessness (25.2 ± 7.9 points vs. 20.9 ± 7.2 points; p ≤ 0.01) and anxious-depressive mood (23.0 ± 5.9 points vs. 16.5 ± 6.2 points; p ≤ 0.001).

Certain studies revealed that wound healing is impaired by psychological factors including stress [146–148]. On the other hand, pruritus is a serious issue in patients suffering from burn injuries. The problem was addressed by van Loey et al. [149]. At 3 months postburn, 87 % subjects suffered from mild to severe itching. At 1 and 2 years postburn the percentages dropped to 70 % and 67 %, respectively. Itch intensity decreased from 2.8 ± 1.8 at 3 months postburn, through 1.8 ± 1.8 at 1 year postburn and eventually 1.5 ± 1.6 points at 2 years postburn. Additionally, the itching complaints seemed to be related to early post-traumatic stress symptoms. It is possible that pruritus experienced by patients suffering from chronic wounds may not only stem from the underlying disease but also induce additional stress and therefore impair the healing process. These theoretical speculations further encourage the application of treatment modalities that both alleviate itch and are aimed at psychological well-being of an individual.

Psychogenic, somatoform or idiopathic pruritus is a somewhat mysterious clinical entity. Also referred to as functional itch disorder (FID), this entity was defined by French Psychodermatology Group (FPDG) as an “itch disorder, where itch is at the centre of the symptomatology, and where psychological factors play an evident role in the triggering intensity, aggravation or persistence of the pruritus” [150]. More precise and accurate criteria were also proposed (Table 6.2). All compulsory criteria and at least three optional criteria are to be met in order to establish the diagnosis.

It is evident that the diagnosis of FID is based on excluding other possible causes of pruritus, both cutaneous and extracutaneous. This process is time- and cost-consuming, occasionally requiring prolonged hospitalization. If established, the diagnosis frequently remains unclear from patient’s perspective. However, physicians should bear in mind that regardless of its aetiology chronic pruritus is a very bothersome symptom, deteriorating the quality of life and possibly facilitating secondary psychological or even psychiatric problems. Therefore abnormalities detected during psychiatric evaluation in a patient suffering from chronic pruritus do not necessarily imply psychogenic aetiology.

Although studies evaluating psychiatric problems in subjects suffering from skin disorders are profuse, few focused specifically on the subject of psychogenic pruritus. In a German study 195 dermatological outpatients were evaluated [151]. Somatoform pruritus was diagnosed in over 10 % subjects. An interesting study was conducted by Kretzmer et al. [152]. Among 100 psychiatric ward inpatients idiopathic pruritus was diagnosed in 42 % of the subjects, more frequently among females (58 % vs. 34 %; p = 0.03). The diagnosis seemed to be associated with psychosocial stress as it was established in 48.5 % and 29 % patients without and with adequate social support, respectively (p = 0.02). Idiopathic pruritus was diagnosed in 76 % of patients regularly receiving opioids. Additionally, the diagnosis was more frequent in patients with higher scores on the anger-trait measure (p = 0.02), angry temperament measure (p = 0.02) and ruminative catastrophization (p = 0.04).

Therapy of itch frequently poses significant challenge to physicians. Regardless of itch aetiology, certain recommendations are widely acknowledged. Factors that increase skin dryness should be avoided, especially in AD individuals. These include dry climate, heat, excessive washing and bathing [8]. Likewise, contact with irritants, allergens, hot and spicy meals, hot beverages, alcohol and stressful situations is unadvisable. Washing should be prompt, performed with mild, non-alcaline soaps or syndets and followed by emollient application. The latter need to be prescribed in adequate amounts (e.g. 250 g per week) and ideally administered liberally and frequently [153]. In general, treatment of an underlying dermatological or systemic condition is fundamental in alleviating itch. Depending on the disease, topical therapy, phototherapy and systemic therapy are recommended. Numerous treatment modalities have been evaluated, whereas several require further description. H₁ antihistamines have been deemed as a mainstay of pruritus therapy in AD for many years. First generation antihistamines (hydroxyzine, clemastine) may improve sleep due to their sedative properties [153]. According to randomized controlled trials second generation antihistamines proved somewhat disappointing in relieving pruritus intensity in AD patients. They are, however, utilized as a treatment of choice in chronic urticaria [154]. Novel therapeutic modalities in AD (dupilumab) or psoriasis patients (apremilast) also significantly reduce itch [155, 156]. As depression symptoms frequently accompany chronic pruritus individuals (10 %) [10], SSRI therapy seems advisable in selected cases. Paroxetine proved useful in patients with polycythaemia vera, paraneoplastic pruritus or pruritus associated with psychiatric diseases [62, 64, 157], while sertraline was effective in cholestatic pruritus [65, 158] and uremic pruritus [159, 160]. In order to cease vicious itch-scratch cycle psychosomatic methods may also be instigated. Multidisciplinary programmes support the development of itch coping mechanisms [161–163]. Concerning the role of stress in itch development patient education, stress management and relaxation techniques are beneficial. Habit reversal therapy (HRT) is a subtype of cognitive therapy encompassing awareness training, inducing responses replacing dysfunctional behaviour and increasing the motivation to control the habits. AD patients utilizing HRT experienced an improvement in skin status and reduction in scratch behaviour [164–166].

The associations between itch and stress in dermatologic disorders constitute current and relevant issues in clinical practice. Stress initiates the onset of pruritus and frequently contributes to its exacerbation. Additionally, itch itself is a stressful symptom, negatively affecting quality of life. Many aspects still lack comprehensive explanation, although the interactions between nervous system, endocrine system and skin seem evident. Growing number of researches regarding pathogenesis of itch may contribute to the development of novel therapeutic approaches which may further turn out to be effective in clinical practice. Decreasing the intensity of itch will possibly result in reducing the stress perceived by an afflicted individual as well. Holistic approach towards the patient warrants utilization of different therapeutic modalities, including those originating from psychology and psychiatry.