Trichodynia refers to the painful sensation of the scalp related to the complaint of hair loss. Originally suggested to be distinguishing for telogen effluvium and related to hair loss activity and follicular inflammation, further studies have found trichodynia to be common in androgenetic alopecia as well and coexisting with psychopathologic findings. The respective studies failed to demonstrate correlations between trichodynia and quantifiable hair loss activity, nor histopathologic evidence for follicular inflammation. A symptomatic scalp is a frequent condition in specific dermatological conditions of the scalp. By definition of exclusion, we are not dealing with trichodynia in these cases. It is conceivable that neuropeptides are key players between the central nervous system and the skin immune and microvascular system. Such mechanisms would explain the noxious effects of both external stimuli and emotional distress in eliciting cutaneous nociception. Since we have begun to understand the diverse etiologies of trichodynia, and a single term does not measure up to this circumstance, it may be wiser to describe the condition depending on the type of scalp sensation and its specific disease association. Further studies are warranted into the neural/endothelial/follicular interactions both in hair growth and shedding and the psychosomatic diseases of the hair and scalp.

Askin et al.’s [1] recent publication on “Presence of Trichodynia Symptoms in Hair Diseases and Related Factors” in one of the recent issues of Skin Appendage Disorders drew our attention to the definition of trichodynia and problems in the nomenclature of the symptomatic scalp. Rebora et al. [2] are to be credited for originally proposing the term trichodynia for a condition of scalp tenderness that is usually related to the complaint of hair loss. Probably the first case published in 1946 was a woman with alopecia associated with amenorrhea [3]. Its best description before Rebora et al. [2] dates back to 1960, when Sulzberger et al. [4] reported it on the occasion of an apparent increase in incidence of unexplained diffuse alopecia in women.

While Rebora et al. [2] reported a frequency of 34.2% in females with hair loss, others reported a frequency of 22.1% [5] and 17%, specifically in 20% of women and in 9% of men [6]. In the so far largest number of patients (n = 403) studied, Willimann and Trüeb [6] assessed the correlation of trichodynia with the patient gender, cause relationships, and activity of hair loss. Trichodynia proved to be a feature of both telogen effluvium (TE) and androgenetic alopecia (AGA), and there was no correlation between presence of trichodynia, degree or type of hair thinning, and quantifiable hair loss. In fact, the results of Sulzberger et al.’s [4] questionnaire-based study did not allow a discrimination between the types of underlying hair loss, specifically between Ludwig-type female AGA and diffuse alopecia, since the former was originally labeled as such starting only in 1977 [7]. Eventually, Rushton et al. [8, 9] characterized diffuse hair loss in women to be a diffuse androgen-dependent type of alopecia in the majority of cases. Later studies on trichodynia have not provided any further relevant insights. One study confirmed trichodynia to be a common symptom of either TE or AGA, often coexisting with psychopathologic comorbidities, such as depression, anxiety, or obsessive personality disorder [10].

Finally, Askin et al. [1] found the highest frequency of trichodynia in scarring alopecia. However, by definition, trichodynia is to be differentiated from a symptomatic scalp due to a specific dermatologic condition of the scalp, such as the inflammatory scarring alopecias, and this leads us to the ultimate question on terminology.

Medical terminology is frequently composed of a prefix and a suffix. The suffix -dynia from Ancient Greek οδύνη (“sorrow, grief, anguish, and unhappiness”) forms medical terms relating to pain, while the prefix trich- stems from θρίξ (“hair”). Another suffix used for pain is -algia. There does not exist any consensus on the difference between the use of the two, though -dynia is not used as commonly as -algia. Nevertheless, in medical terminology, there exist 52 words ending with -dynia, with the prefix mostly denoting the anatomic location of the discomfort. Allodynia is defined as pain resulting from a stimulus that does not normally provoke pain. Therefore, trichodynia could also be called scalp allodynia, since the pain is elicited by the touching or brushing of the hair, as opposed to scalp dysesthesia, which refers to symptoms localized to the scalp skin. Other authors have proposed yet another condition that may be related to trichodynia: trichoknesis, where the patient experiences a sensation of itch instead of pain that is elicited through the touching of the hair [11].

Hoss and Segal [12] reported women with pain and/or itching of the scalp without objective physical findings and proposed the term scalp dysesthesia. The majority benefited from low-dose antidepressant therapy [12] and were interpreted to suffer from underlying psychiatric disorders, specifically depression, anxiety, or somatoform disorder.

Patients suffering from chronic cutaneous sensory disorder in the absence of any somatic finding are either afflicted by a diagnosable underlying psychiatric disorder, such as depression or anxiety, or are labeled to be suffering from somatoform pain disorder. The somatoform disorders involve varied clinical patterns of complaints, including the skin and hair, that are based on a unifying emotional disorder. Typically, patients repeatedly present with physical symptoms in combination with a stubborn demand for medical attention, while repeated medical examinations fail to reveal any somatic pathology. In dermatology, Cotterill [13] proposed to call the condition dermatologic nondisease. Among patients with dermatologic nondisease are also patients with imaginary hair loss who are persuaded that they are going bald without any evidence of hair loss. These patients may also suffer of trichodynia, which then represents a somatoform pain disorder.

Differential diagnosis may be demanding, since psychological problems frequently overlap with hair loss. Patients suffering from alopecia show lower self-confidence, higher depression scores, greater introversion, and higher grades of neuroticisms than their peers [14].

While there has been some discussion whether trichodynia may be caused by a mild perifollicular scalp inflammation [15], histopathologic studies have failed to demonstrate follicular inflammation in either TE or trichodynia. In fact, Whiting [16] found follicular microinflammation to be a distinguishing feature of AGA as opposed to TE and even to be a predictive value for response to treatment [17]. However, the follicular microinflammation in AGA is usually asymptomatic. Only in case of clinically manifest inflammation and fibrosis in fibrosing alopecia in a pattern distribution [18] or in central centrifugal cicatricial alopecia [19], patients may complain of a symptomatic scalp. Rebora [20] proposed existence of an inflammatory or autoimmune type of TE on the basis of the observation of associated trichodynia, autoimmune phenomena, and response to corticosteroid treatment.

In the absence of histopathological evidence of follicular inflammation in TE, we understand this condition to represent what Rebora et al. [21] have originally coined alopecia areata (AA) incognita, basically an identical condition to a subtype of AA with diffuse hair loss in women, as originally reported by Braun-Falco and Zaun [22]. Presence of AA-typical trichoscopic features and occasionally associated autoimmune phenomena are clues to the diagnosis, which may be confirmed by histopathology and/or response with complete hair regrowth to systemic corticosteroids. Ultimately, Moftah et al. [23] demonstrated expression of UL16-binding protein-3 in AA incognita as a marker for AA. Therefore, there is no reason beyond doubt to make a distinction between diffuse AA and AA incognita based only on acuity and severity of the condition [24].

In summary, until proven otherwise, the term inflammatory TE should be reserved for TE resulting from inflammatory conditions of the scalp with shedding of telogen hairs, such as severe seborrheic dermatitis, acute allergic contact dermatitis from exposure to para-phenylenediamine in hair coloring agents [25], erythroderma of psoriasis or lymphoma, or interface dermatitis from lupus erythematosus or dermatomyositis, exempting diffuse AA which has its own designation. In these cases, we are again dealing with a symptomatic scalp and not with trichodynia.

Miscellaneous conditions reported in association with scalp dysesthesia have been cervical spine disease [26, 27], vitamin B12 deficiency [28], exposition to radiofrequency waves from mobile phone use [29], and more recently stress-related poor sleep in the context of the current pandemic [30]. So far, postinfectious effluvium has been observed in association with the novel viral pandemic coronavirus disease 2019, with the type (dystrophic anagen effluvium or TE) and amount of hair shedding depending on the clinical severity of disease and associated fever [31]. A symptomatic scalp has been found to be a possible, but unspecific, feature. Whether coronavirus disease 2019 primarily infects human hair follicle dermal papilla cells like in dengue hemorrhagic fever [32] has as yet not been elucidated.

Should we eventually narrow down the definition of trichodynia to a condition of primary scalp discomfort elicited through the manipulation of the hair and by exclusion of a specific dermatologic condition, ultimately, the studies of Ericson et al. [33] may be of particular interest for a better understanding. Ericson et al.’s [33] landmark investigations into trichodynia uncovered expression of neuropeptide substance P (NPSP) in the scalp. NPSP is involved in nociception and neurogenic inflammation and exerts a potent vasodilatory effect. Though only a minority of patients with trichodynia showed telangiectasia of the scalp (Fig. 1) in the study of Willimann and Trüeb [5], this finding significantly correlated with presence of trichodynia. Other trichoscopic findings in scalp dysesthesia, such as evidence of broken hair, are unspecific features resulting from scratching or rubbing of the scalp [34].

Fig. 1.

Scalp telangiectasia in a patient with trichodynia (dermoscopic finding).

Fig. 1.

Scalp telangiectasia in a patient with trichodynia (dermoscopic finding).

Close modal

By virtue of the bidirectional effects of NPSP and other neuropeptides on the neuroendocrine and immune systems, these may represent the missing link between the central nervous system and the skin according to the psychosomatic theory of the somatic representations of unsolved emotional conflicts. At the first level, the psychosomatic response represents the physiological body reaction to emotional shifts. At the second level, the individual becomes aware of the respective bodily sensations, such as scalp dysesthesia, which are essentially of functional nature at this time point, and begins to analyze them, while becoming anxious that they may be associated with some serious medical condition, such as hair loss. Finally, at the third level, psychiatry and internal somatic medicine meet. When the underlying emotional distress is prolonged, the body loses its elasticity, no longer being able to cope, and finally protests in terms of the psychosomatic organ lesion. Meanwhile, it has been hypothesized that an organ is vulnerable to psychosomatic ailments when several etiologic factors are operable. These include emotional factors, specific correlations between the emotional drive and the target organ, and a constitutional vulnerability of the target organ [35]. NPSP may well represent a key player in the interaction between the central nervous system and the skin immune and microvascular system. Such mechanisms would explain the noxious effects not only of external stimuli (mechanical, thermal, and chemical) but also of emotional distress on cutaneous nociception.

Accordingly, Arck et al. [36] demonstrated that injection of NPSP in nonstressed animals could mimic the stress-induced changes at the level of the hair follicles in mice and that these changes could be abrogated by selective NPSP inhibition in stressed animals, further corroborating a brain-hair follicle axis. A lesser occurrence of trichodynia in males may be explained by gender-related differences in pain perception, in as much as pain perception in relation to anxiety scores has been found to be more pronounced in females [37]. Finally, trichodynia tends to affect the centroparietal scalp area, surprisingly since the threshold for pain in this area is higher than the rest of the scalp, which is why it is also the preferred site of hair plucking in trichotillomania [38] and by the Jain [39].

Since we have begun to understand more on the diverse specific etiologies of the symptomatic scalp, one term may not measure up to this circumstance. Therefore, it may be wiser to describe the condition depending on the type of the scalp sensation and its specific disease association. Or else, the attending physician risks to come to an immature end of his diagnostic assessments, while the patient risks to stigmatize himself with suffering of a specific condition called trichodynia. Others have also stressed that a detailed evaluation for making a specific diagnosis is warranted in patients with scalp dysesthesia [40].

So far, the therapeutic choices for trichodynia have pragmatically included nonirritating shampoos [41], topical antipruritic or anesthetic agents, capsaicin, tricyclic antidepressants, gabapentin, and pregabalin with variable results. Patients need to be reassured that trichodynia does not reflect hair loss activity, which may ease their anxiety, and the attending physician must remain aware that trichodynia often coexists with psychopathologic issues. Most importantly, topical overtreatment is to be avoided, specifically with corticosteroids.

Ultimately, treatment with botulinum toxin (BTX) seems a rational approach, since BTX decreases the mechanical sensitivity of nociceptors and inhibits neurogenic vasodilation through inhibition of sensory neuropeptide release [42]. BTX has shown to be effective in the treatment of chronic daily headache, with presence of scalp allodynia representing a predictor of response to treatment with BTX [43].

In summary, unless a condition is unambiguously defined, further investigations into its origins and management may remain obscured. Further studies are warranted into the neural/endothelial/follicular interactions both in hair growth and shedding and the psychosomatic diseases of the hair and scalp under the clinical presentation of trichodynia.

The authors report no conflicts of interest.

The authors did not receive any funding.

Professors Trüeb, Piraccini, and Reis Gavazzoni Dias take responsibility for the integrity of the data and the accuracy of the data analysis. Drafting of the manuscript: Trüeb, Starace, Piraccini, Dutra, and Gavazzoni. Critical revision of the manuscript for important intellectual content: Trüeb, Piraccini, and Gavazzoni.

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