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Systematic Review

Botulinum Toxin in the Treatment of Hair and Scalp Disorders: Current Evidence and Clinical Applications

by
Sofia M. Perez
1,*,
Sarah A. AlSalman
1,2,
Betty Nguyen
1 and
Antonella Tosti
1
1
Dr Philip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA
2
Department of Dermatology, King Abdulaziz Medical City, Riyadh 22490, Saudi Arabia
*
Author to whom correspondence should be addressed.
Toxins 2025, 17(4), 163; https://doi.org/10.3390/toxins17040163
Submission received: 20 January 2025 / Revised: 17 March 2025 / Accepted: 20 March 2025 / Published: 25 March 2025
(This article belongs to the Special Issue Botulinum Toxins: New Uses in the Treatment of Diseases (2nd Edition))
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Abstract

:
Botulinum toxin (BoNT) is well-recognized throughout dermatology for its cosmetic indications and growing therapeutic value. Recent studies have trialed BoNT in the treatment of hair and scalp disorders, many of which lack long-term effective treatments and significantly impact quality of life. In this review, we summarize the current clinical literature on this topic to comprehensively evaluate the efficacy, safety, and clinical value of BoNT in treating hair and scalp conditions. A literature search on PubMed/MEDLINE and Scopus identified 40 articles reporting the use of 25–200 units of BoNT-A or B in 689 patients with hair loss (79.5%), scalp seborrheic dermatitis/hyperseborrhea (10%), craniofacial hyperhidrosis (9%), folliculitis decalvans/dissecting folliculitis (0.86%), scalp pain (0.43%), or linear scleroderma (0.29%). Most studies on BoNT therapy for androgenetic alopecia (AGA) reported mild or non-significant hair growth; however, considerable variability in outcome measures complicates the ability to draw definitive conclusions or justify the use of BoNT over established AGA therapies. BoNT-A and B showed consistent efficacy in treating craniofacial hyperhidrosis with minimal side effects. Additional scalp conditions may benefit from BoNT therapy, but the evidence is limited, and larger, controlled studies are needed to better understand BoNT’s clinical value in these conditions.
Keywords:
alopecia; hair loss; telogen effluvium; folliculitis decalvans; dissecting folliculitis; seborrheic dermatitis; hyperseborrhea; cutaneous piloleiomyomas; linear scleroderma; morphea; scalp pain; scalp dysthesia; trichodynia; hyperhidrosis; botox; neuromodulator; neurotoxin; onabotulinumtoxin; incobotulinumtoxin; abobotulinumtoxin; rimabotulinumtoxin; prabotulinumtoxin
Key Contribution: Randomized controlled studies demonstrate that Botulinum toxin A minimally promotes hair growth in patients with androgenetic alopecia; but results are not statistically significant. Botulinum toxin A and B both demonstrate significant efficacy in the treatment of craniofacial hyperhidrosis.

1. Introduction

Botulinum toxin (BoNT), derived from Clostridium botulinum, is well-known for its cosmetic use and therapeutic benefits in various neurological and dermatologic disorders. While numerous subtypes of C. botulinum toxins exist, denoted A through G, only subtypes A and B are available for clinical use [1]. Clinical formulations of BoNT-A and B including onabotulinumtoxin A, incobotulinumtoxin A, abobotulinumtoxin A, rimabotulinumtoxin B, and prabotulinumtoxin A differ slightly in their toxin concentration and are each approved by the United States Food and Drug Association (FDA) for various dermatologic indications [2]. The wide range of therapeutic benefits, including pain relief and anti-inflammatory effects, has driven the increased off-label use of BoNT in various dermatologic conditions including eczema, rosacea, idiopathic pruritus, keloidal scars, and hair disorders [2,3].
Hair disorders encompass a number of pathologies that differ in underlying cause and clinical manifestations. Androgenetic alopecia (AGA), also known as male or female pattern hair loss, is the most common hair loss disorder, affecting over 50% of men and 25% of women over the age of 50 [4]. Classically, AGA manifests as gradual thinning and eventual loss of terminal hairs across androgen-dependent regions of the scalp [4]. In genetically pre-disposed individuals, higher production of dihydrotestosterone (DHT) and consequent overactivation of hair follicle androgen receptors leads to follicular miniaturization through a progressive shortening of the anagen (growth) phase [5,6]. Standard treatments, such as minoxidil and finasteride, are aimed at prolonging the anagen phase through increased follicular blood flow and oxygen supply [7,8,9] and at decreasing DHT production by inhibiting 5-alpha-reductase, respectively [10,11]. Preliminary in vitro and animal studies have demonstrated the mechanistic potential of BoNT to similarly promote hair growth in AGA by increasing scalp blood flow, and oxygenation, and inhibiting DHT-induced miniaturization through antagonizing key cytokines like TGF-b1 [12,13,14]. However, its efficacy in clinical studies may not reflect these promising preclinical results.
While much of the recent literature has focused on AGA, BoNT’s role in other hair disorders including alopecia areata (AA), telogen effluvium (TE) and cephalalgia alopecia has also been explored [15,16]. A recent study of BoNT-A injections in mice models of wound healing demonstrated potent anti-inflammatory effects including decreased levels of pro-inflammatory M1 macrophages through BoNT-A inhibition of the JAK2/STAT1 pathway [17]; a signaling pathway targeted by novel biologic therapies in the treatment of AA [18,19]. BoNT’s potent inhibition of neurotransmitters like acetylcholine, substance P, and calcitonin gene-related peptide (CGRP) [20] may hypothetically improve the symptomatic treatment of hair and scalp conditions associated with scalp pain, dysthesia, or trichodynia [21,22].
Craniofacial hyperhidrosis is characterized by excessive sympathetic stimulation of eccrine gland sweat production localized to the face, head, or scalp [23]. OnabotulinumtoxinA, which is FDA-approved for the treatment of axillary hyperhidrosis, has preliminarily demonstrated promising therapeutic efficacy in craniofacial hyperhidrosis; however, it is not yet an FDA-approved clinical indication [24]. Notably, increased scalp sweating in a number of patients with inflammatory hair loss disorders suggests a potential association between increased sweating and scalp inflammation, where BoNT may additionally provide symptomatic benefit [25].
Recently, several studies have trialed the use BoNT in the management of hair and scalp conditions. In this article, we aim to comprehensively review the current clinical literature on this topic to present a critical evaluation on the efficacy, safety, cost-effectiveness, and clinical value of BoNT in the treatment of hair and scalp conditions.

2. Methods

We searched PubMed/MEDLINE and Scopus for articles published before November 2024 using the search terms “hair” OR “scalp” OR “alopecia” and their associated MESH terms, along with BoNT-related keywords, including all clinical formulations and brand names.
This review was registered on PROSPERO (ID: CRD42025641897). All resulting articles were uploaded into Covidence web-based software (Covidence systematic review software, Veritas Health Innovation, Melbourne, Australia, access date: 29 October 2024. https://www.covidence.org/) for removal of duplicates, screening, and full-text evaluation. Screening and review of articles was conducted according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines (Figure 1). Two researchers independently reviewed titles and abstracts to remove unrelated articles. Only articles that described patients with a diagnosed hair or scalp condition who received intradermal or intramuscular injections of BoNT as primary or adjuvant therapy were included. Articles were excluded if they were non-human studies, lacked full text (i.e., abstract only), or involved BoNT use for other clinical indications. Full-text review was conducted by two independent researchers and discrepancies were resolved by discussion and mutual agreement.

3. Results

3.1. Study Characteristics

Of the 949 articles yielded from our search, 40 articles (17 case reports, 10 randomized controlled trials, 9 clinical trials, 3 case reports/series, and 1 prospective cohort study) met inclusion criteria (Figure 1).
Included studies described 689 patients treated with 25–200 units (U) of BoNT-A or B for the following hair and scalp disorders: hair loss (79.5%, 548/698) (androgenetic alopecia [74.2%, 511/698], telogen effluvium [3.5%, 24/698], cephalalgia alopecia [0.43%, 3/698], alopecia areata [1%, 7/698], trichotillomania [0.14%, 1/698], filler-induced alopecia [0.14%, 1/698], radiotherapy-induced alopecia [0.14%, 1/698]), seborrheic dermatitis/hyperseborrhea (10%, 69/698), craniofacial hyperhidrosis (9%, 62/698), folliculitis decalvans/dissecting folliculitis (0.86%, 6/698), scalp pain (0.43%, 3/698), or linear scleroderma (0.29%, 2/698).
Formulations of BoNT used included onabotulinumtoxin A (Botox), Chinese botulinum toxin type A (Hengli), abobotulinumtoxin A (Dysport), prabotulinumtoxin A (Nabota), and rimabotulinumtoxin B (NeuroBloc).

3.2. Botulinum Toxin Efficacy

The efficacy of BoNT in the treatment of hair loss, craniofacial hyperhidrosis, and other scalp disorders are presented in Table 1, Table 2 and Table 3, respectively. Individual study details including BoNT dosage and injection protocol are also described.

3.3. Botulinum Toxin Safety

In all 40 included studies, reported adverse events due to BoNT-A injections included scalp irritation (12.5%), headache (1.5–31%), nausea (1.5%), and injection site reactions like pain, erythema, and edema in 3.1–4.7% of patients [33,35,59]. Reported adverse events due to BoNT-B injections included forehead stiffness (18–66.7%), eyebrow drooping (18%), headache (3%), nausea (33%), increased sweating (11–33%), dry mouth (3–33%), and injection site reactions like skin dryness and bruising (3–5%) [46,47].
In one randomized controlled trial of 29 patients with AGA, one patient reportedly developed a patch of AA on the occipital scalp 3 weeks following BoNT injections [31]. Treatment with topical corticosteroids resulted in prompt hair regrowth. The possibility that the patch was in reality caused by pressure alopecia due to excessive volume injection cannot be excluded.

4. Discussion

4.1. Hair Loss

The human hair cycle is a complex and tightly regulated process that oscillates between an active growth phase (anagen), apoptosis-driven regression phase (catagen), and resting (telogen) phase [63]. This cycle is highly influenced by a number of endogenous agents (e.g., oxygen, nutrients, hormones, neurotransmitters, cytokines) and exogenous stimuli (e.g., drug use, stress, and hair care practices) that if disrupted, can lead to a number of hair loss pathologies [63,64]. Given the complex nature of the hair growth cycle and hair disease pathogenesis, treatments are commonly aimed at a variety of regulatory components including follicular blood supply (minoxidil), hormonal influence (finasteride, dutasteride), inflammatory cytokine signaling (Janus kinase inhibitors, topical corticosteroids), and endogenous growth factors (platelet-rich plasma). Similarly, BoNT is also hypothesized to exhibit therapeutic efficacy in hair disease via its multifactorial influence on blood flow, local inflammation, and neurotransmitter activity (Figure 2) [12,65].
As a potent inhibitor of acetylcholine release, BoNT prevents muscle contraction which may reduce pressure on surrounding vasculature, increasing local blood flow [65,75]. BoNT’s ability to increase cutaneous blood supply [14,76,77] is hypothesized to promote hair growth by prolonging the anagen growth phase and by increasing follicular oxygen supply [12,65]. Both of these therapeutic functions are linked to underlying pathological processes in AGA: BoNT’s prolongation of the anagen phase may combat AGA-associated anagen shortening and BoNT’s increased hair follicle blood flow may improve scalp hypoxia in AGA [78,79,80].
Successful attenuation of cutaneous inflammation with BoNT has been demonstrated in animal studies [17,66,67] and supported with clinical evidence in the treatment of inflammatory skin conditions [81,82,83,84]. In mouse models of psoriasis, a one-time BoNT-A injection significantly decreased cutaneous infiltration of CD4+ lymphocytes [66]. In another study, BoNT-treated mice models of wound healing demonstrated inhibition of pro-inflammatory JAK2/STAT1 signaling and reduction in pro-inflammatory M1 macrophages [17]. These therapeutic functions are linked to underlying pathological processes in AGA and AA: BoNT’s suppression of CD4+ lymphocytes may antagonize their inflammatory activity in AGA [69,70] and BoNT’s inhibition of JAK/STAT signaling may block hair follicle immune privilege collapse in AA [68].
TGF-b is another pro-inflammatory cytokine that is influenced by BoNT-A. Dermal fibroblasts are a major source of TGF-b production which both perpetuates inflammation [85] and induces perifollicular fibrosis [86]. In vitro and in vivo studies have demonstrated an inhibitory effect of BoNT on both fibroblast proliferation [71] and expression of TGF-b [12]. These therapeutic functions are linked to underlying pathological processes in AGA and scarring alopecias: BoNT’s inhibition of fibroblast proliferation and TGF-b production may antagonize the DHT-induced upregulation of TGF-b and its subsequent pro-inflammatory signaling, fibrosis, and hair follicle miniaturization in AGA [86,87]. In scarring alopecia, BoNT’s inhibition of dermal fibroblast proliferation may attenuate peri- and intrafollicular fibrosis [88].
Hair follicles are richly innervated by both sensory and autonomic nerves [89,90]. While precise details of nerve-hair follicle interactions remain relatively unclear, hair loss pathologies associated with neurologic disorders or psychological stress [90] demonstrate the important influence of neurotransmitters and neuropeptides on the hair cycle [91,92]. Cephalalgia alopecia is a rare neurological condition characterized by recurrent burning or stabbing pain in a region of the scalp with colocalized hair loss [38]. Etiology likely involves repetitive activation of nociceptive C fibers resulting in headache/scalp pain and a large release of substance P (SP) and calcitonin gene-related peptide (CGRP) that triggers a perifollicular inflammatory response [72] and upsets the balance of trophic SP and CGRP levels necessary for normal hair growth [73,74]. BoNT’s ability to inhibit the release of SP and CGRP from nerve fiber terminals [20] therefore presents ideal therapeutic potential for both hair regrowth and temporary pain alleviation in cephalalgia alopecia [38,39].
Despite these encouraging mechanistic hypotheses from pre-clinical studies, the clinical role of BoNT in hair disorders is not as promising.
Clinical studies reporting BoNT in the management of AGA present variable evidence regarding its efficacy. While three studies reported a significant increase in hair growth after 2–5 sessions of BoNT-A [12,26,33], multiple randomized controlled trials demonstrated no significant difference from baseline [12,26,31,32,33,34,43], or when BoNT was used in combination with topical minoxidil and oral finasteride [32]. The reason for this discrepancy may be due to differences in BoNT dosage and evaluation methods used (Table 1). Studies demonstrating statistical significance tended to use higher total doses of BoNT (100–180 U) distributed across many regions of the scalp and over 2–6 sessions within 24–48 weeks, noting statistical significance only after a minimum of 2 sessions [12,26,33]. However, a recent randomized controlled trial similarly used 50 U of BoNT-A over 2 sessions separated by 12 weeks and reported no significant difference in hair growth from baseline or compared to placebo [43]. Notably, this trial used only a small 1 cm2 region of the scalp to inject BoNT and assess change in hair growth. Previous studies have employed less reliable methods to document BoNT efficacy including manual hair counts, global photographic assessment, and patient or physician-reported improvement [12,30,33,41,42].
In comparison to standard AGA therapies including topical minoxidil and oral finasteride, which have both demonstrated significant clinical efficacy in a number of randomized controlled trials [93,94,95,96]. BoNT seems to be a relatively low-evidence option for AGA management. One additional concern for clinical use of BoNT involves its significantly high cost ($600/100-unit vial, BOTOX®) compared to standard AGA treatment options (3-month supply 5% topical minoxidil: $47.99, 90-day supply 1 mg oral finasteride: $28.36) [97]. Recent literature has brought into question this practical aspect of BoNT use in AGA and calls for further evidence-based data in support of its superior efficacy in order to justify this cost discrepancy [97]. One way to optimize cost-effectiveness may be to use BoNT in combination with other “skin boosters” like platelet-rich plasma (PRP). Skin boosters are substances that stimulate collagen production and overall skin rejuvenation when injected into the dermis [98]. Many skin boosters including hyaluronic acid, poly-L-lactic acid, and PRP combat oxidative stress and skin aging, which may contribute to AGA [99]. However, PRP is currently the only skin booster with robust literature to confirm its evidence-based efficacy in AGA therapy [100,101] and future studies are needed to assess its synergistic effect when used with BoNT.

4.2. Craniofacial Hyperhidrosis

Similar to its mechanism in axillary hyperhidrosis, BoNT inhibits the release of acetylcholine, effectively blocking the excessive sympathetic stimulation of eccrine sweat glands [23]. The therapeutic efficacy of BoNT in treating craniofacial hyperhidrosis is consistently demonstrated with objective assessments (gravimetric analysis of sweat rate) and subjective measurements (DLQI, patient-reported improvement) throughout the 8 included studies [46,47,48,49,50,51,52,53]. Although no head-to-head comparison studies were found, the efficacy of BoNT-A seems to be relatively equitable to that of BoNT-B. Main clinical concerns include potential functional or cosmetic defects due to BoNT-induced facial muscle weakness [23]; however, eyebrow drooping was only reported in one of our included studies involving 7/38 (18%) of patients [47]. Forehead stiffness was the most common adverse event, reported by up to 67% of patients in one randomized controlled trial [46].

4.3. Other Scalp Conditions

While the use of BoNT in additional scalp conditions has been documented, evidence supporting its efficacy is variable and based solely on case reports and small observational studies. In contrast to the increasing evidence in support of BoNT for facial sebum production in acne treatment [102], we identified only two trials reporting BoNT for scalp sebum production [55,59]. Both studies reported a reduction in scalp sebum production with 50–100 U BoNT-A; however, this reduction was only statistically significant in one study [59].
The pathogenesis of folliculitis decalvans is still unclear and current treatment strategies including systemic antibiotics and steroids demonstrate limited efficacy in improving the disease severity or associated symptoms [103]. In the two studies we identified describing BoNT therapy for this condition, the therapeutic response was promising and resulted in decreased scalp secretions and even hair regrowth in 4 patients [56]. Notably, all patients were taking oral antibiotics during or shortly before initiation of BoNT therapy. A mechanistic explanation for this potential efficacy is lacking; however, it may involve BoNT’s inhibitory effect on fibroblasts and perifollicular fibrosis [88], or BoNT’s anti-inflammatory properties, since an excessive inflammatory response to scalp bacteria likely propagates this condition [104].
Scalp pain, dysthesia, or trichodynia can be caused by multiple hair, scalp, or systemic conditions [105]. Studies reporting BoNT for symptomatic management of scalp pain demonstrate promising efficacy, although effects are temporary and return of symptoms reportedly occurs within 3–4 months post-treatment [22,54,61]. Evidence is limited to case reports of scalp pain in the setting of cutaneous piloleiomyomas and idiopathic trichodynia or scalp dysthesia. It is unknown whether these therapeutic results are applicable to scalp pain of other etiologies.
Localized scleroderma involving the scalp may manifest as an atrophic, linear patch of alopecia termed linear scleroderma en coup de sabre [106]. Although rare, en coup de sabre morphea can be associated with neurologic symptoms, including migraines and trigeminal neuralgia [107]—both symptoms that have previously demonstrated a positive response to BoNT treatment [108,109]. BoNT’s ability to enhance blood flow may further contribute to its efficacy in this condition since one proposed mechanism behind en coup de sabre morphea involves aberrant vasoconstriction-induced skin and muscle atrophy [107]. In our study, we present two cases where BoNT provided cosmetic improvement to the frontotemporal patches of morphea [60,62]. While this treatment strategy is significantly limited by minimal evidence, it does provide a possibly favorable alternative to other cosmetic improvement options in en coup de sabre which typically involves invasive procedures like reconstructive surgery or fat grafting [107].

5. Conclusions

Many promising mechanistic hypotheses for the role of BoNT in the treatment of hair and scalp conditions have been presented in the literature; however, a thorough assessment of its clinical use is essential if BoNT hopes to be introduced as a standard treatment option for these conditions. In this review, we present the current clinical evidence of BoNT use in hair disorders, craniofacial hyperhidrosis, scalp hyperseborrhea, folliculitis decalvans, scalp pain, and linear scleroderma.
Evidence of BoNT in AGA has been presented in 6 clinical trials, 7 randomized controlled trials (RCTs), and 1 prospective cohort study with conflicting results and significant heterogeneity among BoNT dosage and evaluation methods. Based on three recent RCTs with robust sample sizes, BoNT-A does not significantly increase hair growth in AGA and is not a cost-effective treatment option. Future studies should include multicenter RCTs using established evaluation methods to assess short and long-term outcomes of BoNT in AGA, either alone or in combination with topical/oral minoxidil, anti-androgens, or skin boosters like PRP.
Evidence of BoNT in craniofacial hyperhidrosis has been presented in 2 clinical trials, 1 RCT, 4 case reports, and 2 case series demonstrating notable efficacy and little to no adverse events. Based on the 2 clinical trials and RCT, BoNT significantly decreases sweating of the face and scalp and should be considered an effective treatment for craniofacial hyperhidrosis. Future studies should include multicenter RCTs to evaluate the long-term efficacy and optimal dosing and injection frequency of BoNT treatment.
Evidence of BoNT in all other hair/scalp conditions (i.e., folliculitis decalvans, scalp pain, linear scleroderma) is weakly supported by evidence-based data and results should be interpreted with caution given their preliminary nature and need for further validation. Future studies should include larger cohorts and objective assessment of symptomatic and physical improvements with BoNT alone or in combination with other therapies.

Author Contributions

Conceptualization, A.T.; Article review and data extraction, S.M.P. and S.A.A.; Writing—original draft preparation, S.M.P., S.A.A. and B.N.; writing—review and editing, A.T. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

No new data were created or analyzed in this study.

Conflicts of Interest

AT is a consultant for DS Laboratories, Almirall, Thirty Madison, Eli Lilly, Bristol Myers Squibb, P&G, Pfizer, SUNpharma, and Myovant. The authors declare no conflict of interest.

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Figure 1. Flowchart of study identification according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.
Figure 1. Flowchart of study identification according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.
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Figure 2. Hypothesized mechanisms of botulinum toxin’s therapeutic effects in hair disease. Left: BoNT increases vascular supply and oxygenation to hair follicles by relaxing scalp musculature and reducing pressure on local vasculature [12,65]. Middle: BoNT decreases perifollicular infiltration of CD4+ T cells [66], mast cells [67], and M1 macrophages [17]—all classically found in the lymphocytic infiltrate of alopecia areata [68] and, to a lesser extent, androgenetic alopecia [69,70]. BoNT also antagonizes dermal fibroblast secretion of the pro-fibrotic and pro-inflammatory cytokine TGF-b [12,71]. Right: BoNT inhibits the release of SP and CGRP from dermal nerve fibers [20]. When overproduced, SP and CGRP may contribute to physical symptoms of scalp disease (i.e., scalp burning, itching, pain) or stress-induced hair loss [72,73,74]. BoNT: botulinum toxin, TNF: tumor necrosis factor, IL: interleukin, IFN: interferon, TGF: transforming growth factor, SP: substance P, CGRP: calcitonin gene-related peptide.
Figure 2. Hypothesized mechanisms of botulinum toxin’s therapeutic effects in hair disease. Left: BoNT increases vascular supply and oxygenation to hair follicles by relaxing scalp musculature and reducing pressure on local vasculature [12,65]. Middle: BoNT decreases perifollicular infiltration of CD4+ T cells [66], mast cells [67], and M1 macrophages [17]—all classically found in the lymphocytic infiltrate of alopecia areata [68] and, to a lesser extent, androgenetic alopecia [69,70]. BoNT also antagonizes dermal fibroblast secretion of the pro-fibrotic and pro-inflammatory cytokine TGF-b [12,71]. Right: BoNT inhibits the release of SP and CGRP from dermal nerve fibers [20]. When overproduced, SP and CGRP may contribute to physical symptoms of scalp disease (i.e., scalp burning, itching, pain) or stress-induced hair loss [72,73,74]. BoNT: botulinum toxin, TNF: tumor necrosis factor, IL: interleukin, IFN: interferon, TGF: transforming growth factor, SP: substance P, CGRP: calcitonin gene-related peptide.
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Table 1. Studies describing patients who received BoNT injections in the scalp for the treatment of hair loss conditions, organized in order of descending injection dose.
Table 1. Studies describing patients who received BoNT injections in the scalp for the treatment of hair loss conditions, organized in order of descending injection dose.
Title, Author and DateStudy Type# of PatientsHair/Scalp ConditionBoNT Type (Formulation)DoseResultsAdverse Events (AEs)
180 U BoNT
The effect of intradermal botulinum toxin on androgenetic alopecia and its possible mechanism
Shon et al., 2020 [12]		Clinical trial18AGAPrabotulinumtoxin A (Nabota®, Daewoong Pharmaceutical Co., Hwaseong, Gyeonggi Province, South Korea)Total dose: 180 U, 20 intradermal injection sites on entire scalpHair density assessment
Hair density (hairs/cm2)
Baseline: 129.61
12 weeks: 129.11
24 weeks:136.22
p = 0.803, comparison between baseline and week 12
p = 0.012, comparison between baseline and week 24		No AEs reported
150 U BoNT
Treatment of male pattern baldness with botulinum toxin: a pilot study
Freund et al., 2010 [26]		Clinical trial50AGAOnabotulinumtoxinA (BOTOX®, Allergan, Irvine, CA, USA)Total dose: 150 U, 30 intramuscular injection sites on entire scalpHair density assessment
Hair density (hairs/cm2)
Baseline: 234
48 weeks: 276
p = 0.001		No AEs reported
Treatment effects of intradermal botulinum toxin type A injection on alopecia areata
Cho et al., 2010 [27]		Clinical trial 7AAOnabotulinumtoxinA (BOTOX®, Allergan, Irvine, CA, USA)Total dose: 150 U, three intradermal injections in lesional AA patchesSubjective improvement assessment
Patient 1: Spontaneous hair regrowth after 2 months
Patient 2: No response
Patient 3: No response
Patient 4: No response
Patient 5: No response
Patient 6: No response
Patient 7: Aggravation and progression of disease severity		No AEs reported
Recent modalities in treatment of telogen effluvium: Comparative study
Khattab 2022 [28]		Randomized clinical trial12TEBoNT-A (REFINEX®, KC Pharmaceuticals, Pomona, CA, USA)Total dose: 150 U, intramuscular injection sites on entire scalpStatistically significant improvement in all hair parameters (increase in total hair count, terminal hairs, and multiple hair follicular units; decrease in vellus hairs and single follicular units) at 6 months post-treatmentNo AEs reported
Radiation-induced Alopecia Treated with Botulinum Toxin Type A Injection
Hyun et al., 2014 [29]		Case report1Radiation-induced alopeciaBotulax (Hugel Pharma, Seoul, Korea)Total dose: 150 U, 30 intradermal injection sites in alopecic regionSubjective clinical assessment
3 months post-treatment: Sparse vellus hairs observed
12 months post-treatment:
Improved hair density and thickness, some regrowth on the frontal scalp		No AEs reported
A Pilot Study to Evaluate Effectiveness of Botulinum Toxin in Treatment of Androgenetic Alopecia in Males
Singh et al., 2017 [30]		Clinical trial10AGABoNT-A (unspecified)Total dose: 150 U, 30 intramuscular injection sites on entire scalpClinical improvement assessment
Physician-rated assessment
Excellent: 8/10 (80%)
Fair: 1/10 (10%)
Poor: 1/10 (10%)		No AEs reported
100 U BoNT
Intradermal Injection in Balding Region Versus Intramuscular Injection in Surrounding Muscles: A Split-Scalp, Randomized Trial on BoNT for Androgenetic Alopecia
Li et al., 2024 [31]		Randomized controlled trial29AGAOnabotulinumtoxinA (BOTOX®, Allergan, Irvine, CA, USA)Total dose: 100 U, 16 intradermal or intramuscular injection sites on half the scalpIntradermal injections
Hair density (hairs/cm2):
Baseline—120.5
12 weeks—126.2
p = 0.217
Intramuscular injections
Hair density (hairs/cm2):
Baseline—118.3
12 weeks—136.1
p < 0.001		Alopecia areata: 1/29 (3.4%)
A study of combination unilateral subcutaneous botulinum toxin a treatment for androgenetic alopecia
Tian et al., 2022 [32]		Randomized controlled trial37AGAOnabotulinumtoxinA (BOTOX®, Allergan, Irvine, CA, USA)Total dose: 100 U, intradermal injections on half the scalpHair density assessment
Patients with increased hair density at 6 months
BoNT group: 29.31%
Placebo (NS): 12.88%		No AEs reported
Effectiveness and Safety of Botulinum Toxin Type A in the Treatment of Androgenetic Alopecia
Zhou et al., 2020 [33]		Randomized clinical trial63AGAOnabotulinumtoxinA (BOTOX®, Allergan, Irvine, CA, USA)Total dose: 100 U, 30 intradermal injections on entire scalp
33 patients used concomitant 1 mg finasteride		Hair density assessment-BoNT alone
Hair density (hairs/cm2)
Baseline: 180.57
6 months: 208.04
12 months: 218.26
p < 0.001, comparison between baseline and 12 months
Hair density assessment-BoNT + finasteride
Hair density (hairs/cm2)
Baseline: 178.21
6 months: 220.44
12 months: 234.01
p = 0.035, comparison between BoNT and BoNT + finasteride groups at 12 months (all other time points p > 0.05)		Headache: 1/63 (1.6%)
Injection site pain: 3/63 (4.8%)
Nausea: 1/63 (1.6%)
Efficacy of type A botulinum toxin treatment for androgenetic alopecia using ultrasound combined with trichoscopy
Li et al., 2024 [34]		Randomized clinical trial90AGABoNT-A (Lanzhou Institute of Biological Products Co., Ltd., Qilihe District, Lanzhou City, China)Total dose: 100 U, 20 intradermal injection sites on vertex and frontotemporal scalpHair density assessment
Hair count (hairs/1 cm2 pre-defined area)
Baseline—11
1 month—11
3 months—11		No AEs reported
Assessment of efficacy of different botulinum toxin A concentrations in the treatment of androgenetic alopecia assessed by dermoscopy
Seoudy et al., 2024 [35]		Randomized controlled trial32AGABoNT-A (unspecified)Total dose: 100 U, 15 intradermal injection sites on half the scalpDermoscopy assessment
Patients with hair shaft diversity, yellow dots, vellus hairs and/or peripilar sign
Baseline—6/32 (18.8%)
3 months—2/32 (6.2%)
6 months—2/32 (6.2%)
p < 0.001, between baseline and 6 months
Clinical assessment: Ludwig scale
Baseline—4/27 (14.8%) Grade 1; 6/27 (22.2%) Grade 2; 17/27 (63%) Grade 3
3 months—20/27 (74.1%) Grade 1; 7/27 (25.9%) Grade 2; 0.27 (0%) Grade 3
6 months—19/27 (70.4%) Grade 1; 7/27 (25.9%) Grade 2; 1/27 (3.7%) Grade 3
p = 0.009, comparison between 6 months and baseline
Clinical assessment: Norwood Hamilton scale
Baseline- 0/5 (0%) Grade 2; 2/5 (40%) Grade 3; 3/5 (60%) Grade 4
3 months- 7/5 (80%) Grade 2; 1/5 (20%) Grade 3; 0/5 (0%) Grade 4
6 months- 3/5 (60%) Grade 2; 2/5 (40%) Grade 3; 0/5 (0%) Grade 4
p < 0.001, comparison between 6 months and baseline		Scalp irritation: 4/32 (12.5%)
Headache: 10/32 (31.2%)
Injection site pain: 1/32 (3.1%)
Nausea: 1/32 (3.1%)
Efficacy and safety of botulinum toxin A in the treatment of female pattern hair loss
Hu et al., 2024 [36]		Clinical trial10AGABoNT-A (unspecified)Total dose: 100 U, 20 intradermal injection sites on half the scalpClinical improvement assessment
Change in severity after 3 months
Deterioration: 1/10 (10%)
No change: 6/10 (60%)
Mild improvement: 3/10 (30%)		No AEs reported
Assessing the efficacy and quality of Life improvements of botulinum toxin type a with topical minoxidil versus topical minoxidil in male androgenetic alopecia: a randomized controlled trial
Yu et al., 2024 [37]		Randomized controlled trial60AGABoNT-A (unspecified)Total dose: 100 U, 30 intradermal and intramuscular injection sites on entire scalp
Used with daily 5% topical minoxidil		Clinical improvement assessment
Average improvement (0 = no change, 3 = marked improvement)
2 months-post treatment: 0.96
4 months-post treatment: 2.06
p < 0.001, comparison between BTX group and placebo (5% minoxidil only) at 4 months		No AEs reported
Cephalalgia alopecia or nummular headache with trophic changes? A new case with prolonged follow-up
Irimia et al., 2013 [38]		Case report1CABoNT-A (unspecified)Total dose: 100 U, intramuscular injections surrounding alopecic patchSubjective improvement assessment
Baseline: 3 cm diameter alopecic patch
3 months post-treatment: complete resolution of patch		No AEs reported
Cephalalgic alopecia areata: a syndrome of neuralgiform head pain and hair loss responsive to botulinum A toxin injection
Cutrer et al., 2006 [39]		Case report1CABoNT-A (unspecified)Total dose: 100 U, intramuscular injections surrounding alopecic patchSubjective improvement assessment
Complete remission of head pain for 60 days and hair regrowth after 2nd BoNT session		No AEs reported
50 U BoNT
Hair-to-Hair Trichoscopy: An Objective Method to Assess Effectiveness of Botulinum Toxin in a Clinical Trial for Androgenetic Alopecia
Melo et al., 2023 [40]		Randomized clinical trial13AGAOnabotulinumtoxinA (BOTOX®, Allergan, Irvine, CA, USA)Total dose: 50 U, 10 intradermal or intramuscular injection sites on one 2 × 4 cm area on vertex and frontotemporal scalpTricholab® H2H-matching assessment
Average hair thickness
Baseline—0.056 mm
24 weeks post-treatment: 0.057 mm
Number of vellus hairs
Baseline—152
24 weeks post-treatment—148
Number of terminal hairs
Baseline—70
24 weeks post-treatment—82		No AEs reported
Efficacy of botulinum toxin A injection in the treatment of androgenic alopecia: A Comparative Controlled Study
Nassar et al., 2022 [41]		Randomized controlled trial62AGABoNT-A (unspecified)Total dose: 50 U, 30 intramuscular injection sites on entire scalpDermoscopy assessment
Patients with hair shaft diversity
Baseline—62/62 (100%)
6 months—50/62 (80.6%)
p < 0.001, between baseline and 6 months
Clinical assessment: Ludwig scale
Baseline—12% Grade 1; 36% Grade 2; 17/27 52% Grade 3
6 months—36% Grade 1; 44% Grade 2; 0% Grade 3
Clinical assessment: Norwood Hamilton scale
Baseline—50% Grade 3; 16.7% Grade 4, 33.3% Grade 5
6 months—16.7% Grade 1; 66.7% Grade 2; 16.7% Grade 3		No AEs reported
A small dose of botulinum toxin A is effective for treating androgenetic alopecia in Chinese patients
Zhang et al., 2019 [42]		Prospective interventional study24AGABoNT-A (unspecified)Total dose: 50 U, 30 intradermal injection sites on entire scalpClinical improvement assessment
3 months post-treatment:
Obvious hair regrowth—9/24 (37.5%)
No apparent hair regrowth—10/24 (41.6%)
Progressing hair loss—5/24 (20.8%)
6 months post-treatment:
Obvious hair regrowth—11/24 (45.8%)
No apparent hair regrowth—8/24 (33.3%)
Progressing hair loss—5/24 (20.8%)		No AEs reported
Efficacy of botulinum toxin in male androgenetic alopecia: A triple-blind, randomized clinical trial
Melo et al., 2024 [43]		Randomized controlled trial13AGABoNT-A (unspecified)Total dose: 50 U, 10 intradermal or intramuscular injection sites on one 2 × 4 cm area on vertex and frontotemporal scalpHair density assessment-vertex
Hair density (hairs/cm2)
Baseline—216.9
24 weeks—217.7
p = 0.408
Hair density assessment-frontotemporal
Hair density (hairs/cm2)
Baseline—216.0
24 weeks—218.8
p = 0.290		No AEs reported
45 U BoNT
Amelioration of trichotillomania with onabotulinumtoxinA for chronic migraine
Engel et al., 2023 [44]		Case report1TTMBoNT-A (unspecified)Total dose: 45 U, intradermal injections diffusely throughout scalp Patient-reported improvement
12 weeks-post treatment: reports no urges to pull hair
Subjective clinical assessment
12 weeks-post treatment: mild hair regrowth
1 year-post continual treatment: significant hair regrowth		No AEs reported
30 U BoNT
The combination of platelet-rich plasma with botulinum toxin A in the treatment of hyaluronic acid embolic cutaneous necrosis and alopecia
Guo et al., 2022 [45]		Case report1Filler-induced alopecia
(due to intravascular injection causing scalp necrosis)		BoNT-A (unspecified)Total dose: 30 U, intradermal injections in alopecic patch
Performed with PRP injections		Subjective clinical assessment
87 days after treatment: hair regrowth except for a 2 × 2 cm permanent cicatricial alopecia		No AEs reported
BoNT dosage not specified
Botulinum toxin treatment of cephalalgia alopecia increases substance P and calcitonin gene-related peptide-containing cutaneous nerves in scalp
Cutrer et al., 2010 [39]		Case report1CABoNT-A (unspecified)Total dose: not specified, intramuscular injections surrounding alopecic patchSubjective improvement assessment
Remission of scalp pain for about 6 weeks, with regrowth of hair. Subsequent treatments induced remissions lasting 4–12 weeks		No AEs reported
AA, alopecia areata; AE, adverse event; AGA, androgenetic alopecia; BoNT, botulinum toxin; NS, normal saline; PRP, platelet-rich-plasma; TE, telogen effluvium; TTM, trichotillomania. Underlined text = measurement method of BoNT efficacy.
Table 2. Studies describing patients who received BoNT injections in the scalp for the treatment of craniofacial hyperhidrosis, organized in order of descending injection dose.
Table 2. Studies describing patients who received BoNT injections in the scalp for the treatment of craniofacial hyperhidrosis, organized in order of descending injection dose.
Title, Author and DateStudy Type# of PatientsHair/Scalp ConditionBoNT Type (Formulation)DoseResultsAdverse Events (AEs)
2250 U BoNT
Postmenopausal craniofacial hyperhidrosis treated with botulinum toxin type B
Cabreus 2019 [46]		Randomized controlled trial8HHBoNT type B (NeuroBloc®; Eisai Europe, Hatfield, UK)Total dose: 2250 U, injected every 15 mm across the frontal, temporal, and occipital scalp, forehead, glabella, intraocular, and perioral areasDLQI Assessment
Placebo: 90% improvement from baseline
BoNT-B group: 18% decline from baseline
HDSS Assessment
Placebo average: 2.8
BoNT-B average: 1
Gravimetric Data (sweat rate) Assessment
Placebo average: 0.035 mg/min
BoNT-B average: 0.0012 mg/min		Forehead stiffness: 2/3 (66.7%)
Nausea during injection: 1/3 (33.3%)
Increased sweating from back: 1/3 (33.3%)
Dry mouth: 1/3 (33.3%)
250 U BoNT
Botulinum toxin B in the treatment of craniofacial hyperhidrosis
Karlqvist 2014 [47]		Clinical trial38HHRimabotulinumtoxinB (NeuroBloc®; Eisai Co., Ltd., Tokyo, Japan)Total dose: 250 U, injected every 15 mm across the frontal and occipital scalpDLQI assessment
Pre-treatment: 13.1 ± 1
Post-treatment: 5 ± 1
p < 0.001
Trans-epidermal water loss assessment
Pre-treatment: 52 ± 31 g/m2/h
Post-treatment: 18 ± 7 g/m2/h
p < 0.001
Gravimetric data (sweat rate) assessment
Pre-treatment: 0.07 ± 0.08 mg/min
Post-treatment: 0.02 ± 0.05 mg/min
p < 0.05
Clinical improvement assessment
Significant-complete reduction in sweating: 33/38 (87%)
Moderate reduction in sweating: 4/38 (10%) 		Forehead stiffness: 18%
Eyebrow drooping: 18%
Compensatory sweating: 11%
Local skin dryness: 5%
Dryness of the mouth: 3%
Local bruising: 3%
Worsening of migraine: 3%
A unique case of primary focal hyperhidrosis and treatment
Hannan 2022 [48]		Case report1HHAbobotulinumtoxinA (Dysport®; Galderma, Dallas, TX, USA)Total dose: 150 U, injected evenly into affected areasClinical improvement assessment
At the 3-month follow-up visit, patient reported decreased gustatory sweating		No AEs reported
100 U BoNT
Botulinum Toxin for the Treatment of Postmenopausal Craniofacial Hyperhidrosis
Patrick 2024 [49]		Case report1Craniofacial hyperhidrosis (HH)BoNT-A (unspecified)Total dose: 100 U, injected along the superior forehead and occipital hairlineClinical improvement assessment
Patient reported significant improvement in sweating and returned for four follow-up BTX sessions that were 11 months apart		No AEs reported
Effect of Botulinum Toxin in Stellate Ganglion for Craniofacial Hyperhidrosis: a Case Report
Park 2021 [50]		Case report1HHOnabotulinumtoxinA (BOTOX®; Allergan, Irvine, CA, USA)Total dose: 100 U, injected into bilateral stellate ganglionClinical improvement assessment
Sweating reduced at 6-month follow-up		No AEs reported
Postmenopausal craniofacial hyperhidrosis
Eustace 2018 [51]		Case series11HHBoNT-A (unspecified)Total dose: 100 U, injected into hairline and nape of neckClinical improvement assessment
64% (7/11) patients noticed complete remission of symptoms and 36% (4/11) had no improvement		No AEs reported
Hyperhidrosis of Face and Scalp: Repeated Successful Treatment with Botulinum Toxin Type A
Komericki 2012 [52]		Case report1HHOnabotulinumtoxinA (BOTOX™; Allergan, Irvine, CA, USA)Total dose: 100 U, 30 injection points across the upper forehead and scalpClinical improvement assessment
Sweating completely stopped after treatments		No AEs reported
BoNT dosage not specified
Craniofacial Hyperhidrosis in Post-Menopausal Women
Alsharqi 2012 [53]		Case series2HHBoNT-A (unspecified)Total dose: not specified, BoNT-A injected into hyperhidrotic areas on face and scalpClinical improvement assessment
“Patient showed good response”		No AEs reported
AE, adverse event; BoNT, botulinum toxin; Dermatology Life Quality Index, DLQI; HDSS, Hyperhidrosis disease severity score. Underlined text = measurement method of BoNT efficacy.
Table 3. Studies describing patients who received BoNT injections in the scalp for the treatment of other scalp conditions, organized in order of descending injection dose.
Table 3. Studies describing patients who received BoNT injections in the scalp for the treatment of other scalp conditions, organized in order of descending injection dose.
Title, Author and DateStudy Type# of PatientsHair/scalp ConditionBoNT Type (Formulation)DoseResultsAdverse Events (AEs)
200 U BoNT
Botulinum Toxin Type A- Treatment of a Patient with Multiple Cutaneous Piloleiomyomas
Sifaki et al., 2008 [54]		Case report1Scalp pain (etiology: cutaneous piloleiomyomas)BoNT-A (unspecified)Total dose: 200 U, 10–20 intralesional injectionsSymptom severity assessment
Patient-reported in a 0–10 range (0 = no pain, 10 = most severe pain)
Baseline: 10/10
4 days post-BoNT: 2/10		No AEs reported
150 U BoNT
Evaluation of the effect of botulinum toxin injection in aggravating or improving seborrheic dermatitis symptoms: A prospective, single-arm clinical trial
Bazargan et al., 2023 [55]		Clinical trial20Seborrheic dermatitisBoNT-A (MASPORT®, MasoonDarou Pharmaceutical Company, Karaj, Alborz Province, Iran)Total dose: 150 U, intradermal injections in the scalp hairlineExtent of scalp involvement
Rated on a scale 1–5 (1 = less than 10%, 2 = 11–30%, 3 = 31–50%, 4: 51–70%, 5: more than 70%)
Baseline: 2.10 ± 1.02
1 month-post BTX-A: 1.15 ± 1.23
(p > 0.05)
Seborrheic dermatitis severity
Patient-reported symptom severity on a scale 0–3 (0 = symptom not present, 3 = symptom is at most severe condition)
Baseline:
Skin erythema: 0.25 ± 0.44
Skin sebum: 1.35 ± 1.04
Scaling: 1.60 ± 0.68
1 month-post BTX-A:
Skin erythema: 0.15 ± 0.37
Skin sebum: 1.25 ± 1.16
Scaling: 1.40 ± 0.68
(p = 0.528, overall severity score compared to baseline)		No AEs reported
Folliculitis Responds to Botulinum Toxin: Is It Possible?
Tamura et al., 2007 [56]		Case series4Folliculitis decalvans (biopsy-confirmed)OnabotulinumtoxinA (BOTOX®, Allergan, Irvine, CA, USA)Total dose: 60–150 U, 2.5 U injected in intralesional and perilesional locationsPatient 1: 80 U BoNT-A total
Reduced secretion 30 days after injection
Signs of hair growth 30 days after injection
Patient 2: 60 U BoNT-A total
Reduced secretion
Discrete, diffuse, and slow hair growth
Patient 3: 150 U BoNT-A total
Reduced secretion 30 days after injection
Signs of hair growth 30 days after injection
Patient 4: 100 U BoNT-A total
Reduced secretion 6 months after injection. No significant hair growth		No AEs reported
100 U BoNT
Botulinum toxin A as an alternative treatment for folliculitis decalvans
Neri et al., 2023 [57]		Case report1Folliculitis decalvans (biopsy-confirmed)BoNT-A (unspecified)Total dose: 100 U, intralesional injections Clinical assessment
Improvement in inflammatory lesions and elimination of scalp itch within “a few days”
Full remission of the disorder within 4 months of first BoNT-A session
Condition remained stable with no relapses for the following 5-year follow up period		No AEs reported
Therapeutic effect of botulinum toxin A on folliculitis dissecans of the scalp
Neri et al., 2024 [58]		Case report1Dissecting folliculitis of the scalp (biopsy-confirmed)OnabotulinumtoxinA (BOTOX®, Allergan, Irvine, CA, USA)Total dose: 100 U, injected intradermally outlining the infection sites2 weeks post-BoNT: resolution of scalp pain
8 weeks post-BoNT: resolution of abscesses and swelling with significant increase in hair density over infection sites		No AEs reported
Successful Treatment of Refractory Trichodynia With Onabotulinumtoxin-A
Alhomida et al., 2024 [22]		Case report1Trichodynia (unknown etiology)OnabotulinumtoxinA (BOTOX®, Allergan, Irvine, CA, USA)Total dose: 100 U, intradermal injections throughout the scalpSymptom severity assessment
Patient-reported in a 0–10 range (0 = no pain, 10 = most severe pain)
Baseline: 10/10
One-month post-BoNT: 0/10
Six-weeks post-BoNT: 6/10
Three-months post-BoNT: 10/10		No AEs reported
25–50 U BoNT
Intradermal Botulinum Toxin A Injection for Scalp Sebum Secretion Regulation: A Multicenter, Randomized, Double-Blinded, Placebo-Controlled, Prospective Study in Chinese Subjects
Li et al., 2023 [59]		Randomized controlled trial49Scalp hyperseborrheaChinese BoNT-A (Hengli®, Lanzhou Institute of Biology, Lanzhou, China)Total dose: 50–65 U, 25 intradermal injection sites throughout the scalpIntradermal BoNT-A treatment significantly reduced the scalp sebum secretion at 24-, 48-, and 72-h post-shampooing at the 1- and 3-month follow-up (p < 0.05)scalp tightness dizziness insomnia itchiness folliculitis hematoma
tinnitus
(% of patients affected not specified)
Parry-Romberg Syndrome Vasculopathy and Its Treatment with Botulinum Toxin
Borodic et al., 2014 [60]		Case report1Linear scleroderma/En coup de sabre morpheaBoNT-A (unspecified)Total dose: 50 U, 6 injections along the forehead and frontotemporal scalpClinical improvement assessment
After first BoNT injection: “dramatic improvement in pain”
After second BoNT injection: “dramatic relief of pain, hair loss, and improvement of memory”		No AEs reported
Botulinum Toxin for Scalp Dysthesia
Phan et al., 2022 [61]		Case report1Scalp dysthesia (unknown etiology)BoNT-A (unspecified)Total dose: 40 U, 20 intradermal injections across half the scalpSymptom severity assessment
Patient-reported in a 0–10 range (0 = no pain, 10 = most severe pain)
Baseline: 4/10
8 weeks post-BoNT: 2/10
16 weeks post-BoNT: 4/10		No AEs reported
Improvement of “En Coup de Sabre” Morphea and Associated Headaches with Botulinum Toxin Injections
Rimoin et al., 2016 [62]		Case report1Linear scleroderma/En coup de sabre morpheaBoNT-A (unspecified)Total dose: 25 U, 10 intralesional and perilesional injections Cosmetic appearance assessment
Physician-reported based on pigmentation and sclerotic changes in a 0–10 range (1 = least severe, 10 = most severe)
Baseline: 10/10
4 months post-BoNT: 4/10
6 months post-BoNT: 4/10
9 months post-BoNT: 3/10
12 months post-BoNT: 3/10		No AEs reported
AA, alopecia areata; AE, adverse event; AGA, androgenetic alopecia; BoNT, botulinum toxin; NS, normal saline; PRP, platelet-rich-plasma; TE, telogen effluvium; TTM, trichotillomania; VAS, visual analogue scale. Underlined text= measurement method of BoNT efficacy.
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Perez, S.M.; AlSalman, S.A.; Nguyen, B.; Tosti, A. Botulinum Toxin in the Treatment of Hair and Scalp Disorders: Current Evidence and Clinical Applications. Toxins 2025, 17, 163. https://doi.org/10.3390/toxins17040163

AMA Style

Perez SM, AlSalman SA, Nguyen B, Tosti A. Botulinum Toxin in the Treatment of Hair and Scalp Disorders: Current Evidence and Clinical Applications. Toxins. 2025; 17(4):163. https://doi.org/10.3390/toxins17040163

Chicago/Turabian Style

Perez, Sofia M., Sarah A. AlSalman, Betty Nguyen, and Antonella Tosti. 2025. "Botulinum Toxin in the Treatment of Hair and Scalp Disorders: Current Evidence and Clinical Applications" Toxins 17, no. 4: 163. https://doi.org/10.3390/toxins17040163

APA Style

Perez, S. M., AlSalman, S. A., Nguyen, B., & Tosti, A. (2025). Botulinum Toxin in the Treatment of Hair and Scalp Disorders: Current Evidence and Clinical Applications. Toxins, 17(4), 163. https://doi.org/10.3390/toxins17040163

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