Clinical Profile and Plasma Vitamin B6 Levels in Children with Tourette Syndrome: A Case-control Study

Abstract

Background:

Tourette syndrome (TS) is a childhood-onset neuropsychiatric disorder characterized by recurrent motor and vocal tics. Histaminergic dysregulation in the brain has been proposed as a mechanism underlying TS. Vitamin B6, a key cofactor in histamine metabolism, may therefore play a contributory role in its pathophysiology.

Methods:

This was an observational, unmatched case–control study in which clinical features of 25 children diagnosed with TS were assessed using the Yale Global Tic Severity Scale. Plasma vitamin B6 levels were measured using enzyme-linked immunosorbent assay (ELISA) and compared with those of a control group.

Results:

Most participants were males, and 16% had comorbid attention deficit hyperactivity disorder (ADHD) or obsessive–compulsive disorder (OCD). The most common motor tics were eye blinking, shoulder shrugging, head jerking, and orofacial movements. Frequent vocal tics included throat clearing and sniffing. Coprolalia was observed in four children. The median plasma vitamin B6 level in the TS group was 25.01 ng/mL, which was significantly lower than the 36.33 ng/mL in the control group (Mann–Whitney U = 225, p = .03). The rank-biserial correlation indicated a moderate effect size (r = 0.35).

Conclusions:

TS in children predominantly affects males and is commonly associated with ADHD and OCD. Coprolalia—a clinically distressing symptom—was present only in a small subgroup. The lower plasma vitamin B6 levels observed in children with TS suggest a possible role for vitamin B6 in disease pathogenesis, potentially through its involvement in histaminergic and GABAergic neurotransmission and in modulating neuroinflammatory processes.

Keywords

Coprolalia histidine decarboxylase (HDC) gene histamine Tourette syndrome vitamin B6

Key Messages:

Question: What are the demographic characteristics, tic phenotypes, and plasma vitamin B6 levels in children with Tourette syndrome (TS)?

Findings: TS in children mainly affects boys with often co-occurring attention deficit hyperactivity disorder (ADHD) and obsessive–compulsive disorder (OCD), characterized by motor and vocal tics, with rare coprolalia, and possible contribution from low plasma vitamin B6.

Meaning: Frequent co-occurrence of ADHD and OCD indicates TS is part of a broader neurodevelopmental spectrum and suggests that vitamin B6 deficiency might be a modifiable risk factor.

Tourette syndrome (TS) is characterized by multiple brief, stereotypical nonrhythmic movements and vocalizations called tics that last at least a year. The prevalence is around 0.3%–1% worldwide.¹ It is seen more in males with attention deficit hyperactivity disorder (ADHD), obsessive–compulsive disorder (OCD), learning difficulties, and disruptive behavior, being the common comorbidities. Common motor tics include eye blinking, facial grimacing, nose twitching, and movements of the jaw, neck, and shoulders. Motor tics usually appear between 4 and 6 years, several years before the onset of vocal tics, which usually begin between 8 and 12 years. With increasing age, motor tics may evolve into more elaborate movements (e.g., purposeful movements or lewd gestures), and vocal tics often develop into repeating words (echolalia), phrases (palilalia), or obscene words (coprolalia). Tics have a waxing and waning character with approximately 50% of children achieving remission by 15 years.²

TS is associated with dysregulation of dopaminergic signaling within the basal ganglia and frontostriatal pathways.² Increased activity in the striatum and heightened compensatory activity of the left prefrontal cortex and subthalamic nucleus have been observed in patients with TS.³ Postmortem analysis of the striatal transcriptome showed increased inflammatory response in microglia.⁴ TS is normally treated by using dopamine blockers such as risperidone, haloperidol, or pimozide.²

In addition to dopamine, histamine dysregulation has been implicated in the pathophysiology of TS.⁵ In a family with a high incidence of TS, a nonsense mutation in the histidine decarboxylase (HDC) gene was identified (W317X).⁶ The HDC gene is essential to convert histidine to histamine. Reduced histamine levels dysregulate dopamine activity, thereby contributing to the development of TS.⁵ The HDC W317X mutation is rare and has not been identified outside of the index family. Other disruptions in the histamine pathway that reduce histamine levels may prove causative in TS pathophysiology. We hypothesize that vitamin B6, through its role as a cofactor of the HDC enzyme, plays a role in histamine regulation and, thereby, TS. This hypothesis has a potential translational significance in the management of TS. Though antipsychotics improve the symptoms of TS, their side effects limit long-term use. A nutritional supplement containing vitamin B6 may be beneficial in a subset of patients. The study had the following objectives: (a) To characterize the clinical features of children with TS, and (b) to compare plasma vitamin B6 levels in children with TS and those of a control population.

Methods

The Institutional Ethics Committee approved the study. Written informed consent was obtained from the participants and parents. Assent was obtained from participants under 18 years of age. Written informed consent was obtained from the control population as well. Data collection began in June 2022 and ended in December 2024. This manuscript was prepared in accordance with the Strengthening the Reporting of Observational Studies in Epidemiology guidelines for case–control studies (see Supplementary Table).⁷ The study included 25 individuals diagnosed with TS and 29 healthy individuals. Since TS in children is relatively uncommon, the sample size was determined based on feasibility and the number of eligible children attending the outpatient services during the study duration. Given limited prior data on vitamin B6 levels in this population, a formal a priori power calculation was not performed. The effect size (rank-biserial correlation) was calculated to aid the interpretation of the results.

Inclusion Criteria

Twenty-five children aged 5–18 years with TS, as per Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition criteria, were included in the study.⁸ The children were recruited from the outpatient services of a tertiary care child psychiatry department. The Yale Global Tic Severity Scale was used to assess the severity and phenomenology of tics.⁹

Individuals with psychiatric disorders resulting from organic causes and substance abuse, intellectual disability, neurological, and neurodevelopmental disorders were excluded from the study.

An unrelated non-psychiatric healthy control group (age >20 years; n = 29) with no personal and family history of psychiatric disorders was recruited from the public. Controls were older adults; age- and sex-matching were not feasible due to logistical constraints. No multivariable analyses were performed to adjust for potential confounding factors such as age and sex, due to the small sample size and the non-overlapping age distribution between cases and controls. Therefore, the analysis was limited to unadjusted group comparisons. This limitation was taken into account when interpreting the biochemical findings.

Sample collection: 10 mL of venous blood from the subjects was collected in an Ethylenediaminetetraacetic Acid (EDTA) Vacutainer for biochemical and molecular studies. Plasma and peripheral blood mononuclear cells were separated and stored at −80°C in a deep freezer for further analysis. All plasma samples were protected from direct light throughout processing and storage to prevent analyte photodegradation. Plasma vitamin B6 levels were measured in 24 patients, as one blood sample was unavailable for analysis.

Biochemical Analysis

Vitamin B6 levels were measured in plasma samples from individuals (TS and controls) using an enzyme-linked immunosorbent assay (ELISA) according to the manufacturer’s protocol (GENLISA Human Vitamin B6 ELISA, KBH1539; Krishgen Biosystems, India).

Statistical Analysis

Statistical analysis was done using JASP 0.18.3.¹⁰ Quantitative variables were expressed as median (interquartile range) or mean ± standard deviation, as appropriate. The normality of data distribution was assessed using the Shapiro–Wilk test. Due to non-normal data distribution, comparisons between the two study groups were performed using the Mann–Whitney U test (two-tailed). A p value < .05 was considered statistically significant. Sensitivity analysis was performed by repeating the primary analysis after excluding extreme plasma vitamin B6 values (below the fifth percentile and above the 95th percentile) to assess the robustness of the findings.

Results

There were 25 cases of TS, with a mean age of 11 years. Eighty-four percent of the cases were males. Sixteen percent of the cases had ADHD or OCD as a comorbid diagnosis. Thirty-two percent of the cases had a family history of TS, while 20% had a family history of OCD. Two children had a specific learning disorder (SLD) (Table 1).

Table 1.

Clinical Characteristics of Children with Tourette Syndrome (N = 25).

Characteristics	n (%)
Male	21 (84.0)
Female	4 (16.0)
Comorbid ADHD	4 (16.0)
Comorbid OCD	4 (16.0)
Family history of OCD	5 (20.0)
Family history of TS	8 (32.0)
SLD	2 (8.0)

ADHD: Attention deficit hyperactivity disorder, OCD: Obsessive–compulsive disorder, SLD: Specific learning disorder.

The most common motor tics were eye blinking, shoulder shrugging, head jerking, and mouth movements. Common vocal tics included throat clearing, sniffing, uttering syllables, and breathing tics. Coprolalia was seen in four children (Table 2). Among the children with comorbid OCD, checking, washing, and symmetry were the predominant symptoms.

Table 2.

Phenomenology of Tics in Children with Tourette Syndrome (N = 25).

Tic Type	N (%)
Eye blinking	19 (76.0)
Head jerk	14 (56.0)
Shoulder shrugs	12 (48.0)
Mouth movements	10 (40.0)
Throat clearing	9 (36.0)
Nose movements	8 (32.0)
Hand movements	7 (28.0)
Leg/toe movements	7 (28.0)
Facial grimace	6 (24.0)
Arm movements	6 (24.0)
Sniffing	5 (20.0)
Syllable utterance	4 (16.0)
Gulping	4 (16.0)
Atypical breathing tics	4 (16.0)
Coprolalia	4 (16.0)
Palilalia	3 (12.0)
Speech atypicality	3 (12.0)
Dystonic postures	2 (8.0)
Bending	2 (8.0)
Coughing	2 (8.0)
Snorting	2 (8.0)
Whistling	2 (8.0)
Humming	2 (8.0)
Burping	2 (8.0)
Hand gestures	2 (8.0)
Animal noises	2 (8.0)
Echolalia	2 (8.0)
Blocking	2 (8.0)
Writing tics	1 (4.0)
Hiccups	1 (4.0)
Word utterance	1 (4.0)
Copropraxia	1 (4.0)
Self-abusive behavior	1 (4.0)
Paroxysms of tics	1 (4.0)
Disinhibited behavior	1 (4.0)

*More than one tic type could be present in a single participant; therefore, percentages do not total 100%.

The mean age of females and males in this study was similar. No female participants had comorbid ADHD, OCD, or SLD. A single female had copropraxia and disinhibited behavior. Complex tics were observed in eight males and one female. These differences between females and males were not statistically significant. Coprolalia was seen only in males. Among the males with coprolalia, two exhibited comorbid OCD, and two presented with ADHD. Two children had a family history of TS, while none had a family history of OCD. The median vitamin B6 levels in this subgroup did not differ significantly from those of other children with TS.

The control group had a mean age of 24 years and consisted of 22 females and seven males. The median vitamin B6 level in the TS group was 25.01 ng/mL, compared with 36.33 ng/mL in the control group. This difference was statistically significant (Mann–Whitney U = 225, p = .03). The difference in plasma vitamin B6 levels between children with TS and controls remained statistically significant after exclusion of extreme values. The rank-biserial correlation indicated a moderate effect size (r = 0.35) (Table 3).

Table 3.

Plasma Vitamin B6 Concentrations in Tourette Syndrome (Case) and Controls.

N	Case	Control
N	24	29
Mean age (years)	10.9	24.6
Male	20	7
Female	4	22
Median B6 level in ng/mL (Interquartile range)	25.01 (26.75)	36.33 (14.28)
Mann–Whitney U	225
p value	.03

Discussion

This study assessed the clinical features of TS in children under 18 years and compared their vitamin B6 levels with those of normal controls. Common motor tics in our study group were eye blinking, shoulder shrugging, and head jerking, while common phonic tics were throat clearing and sniffing. Complex tics, such as complex hand movements, were less frequent. Similar patterns have been reported in previous studies.¹¹

Studies have shown that TS is one of the most heritable non-Mendelian neuropsychiatric disorders, with population-based heritability estimated to be 0.77. Rare, high-impact variants in genes involved in chromatin regulation and synaptic development, such as ASH1L, have been shown to confer susceptibility to TS, supporting a neurodevelopmental model with substantial genetic heterogeneity.¹² Analyses of familial transmission patterns indicate that obsessive–compulsive disorder and TS share common genetic risk factors.² About one-third of patients had a family history of TS. In contrast, another one-fifth had a family history of OCD.

The study found that 16% of children with TS had comorbid OCD and ADHD, with these comorbidities occurring exclusively in males. Two males also displayed an SLD. These findings align with global research, which shows that ADHD, OCD, learning difficulties, and disruptive behavior are the common comorbidities in TS.¹³

The OCD in TS showed predominance of sexual, religious, aggressive, or symmetry obsessions.¹⁴ Symmetry obsessions were found in our group of patients in line with previous studies.

The TS is more prevalent in males with earlier onset and a higher chance of ADHD and disruptive behavior. In contrast, females are less likely to develop TS, have a later age of onset, and have more complex tics. They have less chance of comorbid ADHD but are more predisposed to comorbid OCD and mood symptoms. They also have a lower remission rate with increasing age. Eighty-four percent of our cases were males with a mean age of 11 years.¹⁵ The mean age was similar for females and males in our study, differing from previous reports.

Complex tics were observed in eight males and one female. This difference was not statistically significant. A study found that, aside from ADHD, the frequency distribution and complexity of tics were similar in both genders. But in those below 18 years, earlier onset and complex tics were more common in males.¹⁶ Hyperandrogenism is postulated as the cause for the increased prevalence of TS in males. Sex specific neuroanatomic differences in the brain are less frequently reported in women with TS.¹⁶ Case reports show worsening of tics in men treated with androgenic steroids.¹⁷ Flutamide and finasteride, which are androgen blockers, showed improvement of tics in men.^18,19 All these points relate to the role of androgens in the causation of tics.

Coprolalia is a complex, socially inappropriate vocal tic where patients utter obscene words, while in copropraxia, patients show obscene gestures. Coprolalia and copropraxia are together called the copro phenomenon.²⁰ The prevalence of coprolalia varies from 8% to 33% of patients with TS in various studies.²¹ Coprolalia is more than four times as common as copropraxia, and both are common in males. The copro phenomenon is associated with tic severity, aggression, self-injurious behavior, greater brain dysfunction, and poor quality of life.²⁰ In our study, coprolalia was observed in 16% of the patients, all being males. Two had a family history of TS. None had a family history of OCD. Two patients had comorbid ADHD, while two had OCD. Their mean age of vitamin B6 onset did not differ from that of the remaining patients. Copropraxia was recorded in one female.

We found that the median vitamin B6 level in patients was lower than that in the control group, with a medium effect size. Whether this small amount is a causal factor in TS pathogenesis remains to be evaluated. Vitamin B6 is involved in multiple biochemical pathways relevant to this disorder.

Tics occur due to increased dopamine levels in the striatum.² This increased dopamine may occur due to multiple pathways, with altered histaminergic metabolism being one. This is corroborated by studies showing altered signaling through H1 and H2 receptors in TS.⁵ A case–control study of copy number variation analysis showed enrichment of genes within histamine and Gamma-Aminobutyric Acid (GABA) receptor pathways.²² Moreover, both H2 and H3 receptors are highly abundant in the human and rodent striatum and cortex—regions that have been implicated in the pathophysiology of TS.²³ In a subset of patients with a mutation in the HDC gene, reduced histamine levels increased striatal dopamine and resulted in tics.²⁴ Vitamin B6 is a cofactor for the HDC enzyme.²⁵ Other than a mutation in the enzyme, reduced B6 may impair the HDC enzyme activity, reduce histamine, and thus increase striatal dopamine. This provides a biologically plausible mechanism by which lower vitamin B6 levels could contribute to TS pathophysiology through the histamine pathway.

But impaired histamine metabolism is found only in a subset of TS. A genome-wide association study failed to identify any common polymorphisms with genome-wide statistical significance.²⁶ In a post-mortem study, the transcriptome of the caudate and putamen of nine patients was assessed. They found a decrease in nitric oxide synthase–positive interneurons, reduced voltage-gated potassium channels in parvalbumin interneurons, and reduced GABA signaling genes.⁴ Vitamin B6 is a cofactor of glutamate decarboxylase, which synthesizes GABA.²⁵ Thus, other than histamine, reduced B6 may decrease GABA, thereby increasing the risk for TS.

In addition to its roles in histamine and GABA synthesis, the immunoregulatory effects of B6 may also contribute to TS pathogenesis. Genome-wide association studies have identified variants in Fms-Like Tyrosine Kinase 3 (FLT3), a key regulator of innate immune signaling, as being associated with TS.²⁷ Post-mortem transcriptomic analyses of the striatum have demonstrated an increased microglial inflammatory response.⁴ Vitamin B6 suppresses pro-inflammatory signaling pathways in activated microglia, including TLR4/NF-κB and TREM-1/DAP12–NLRP3–caspase-1–IL1β cascades, and reduces the production of reactive oxygen species, IL-6, and Tumor Necrosis Factor-alpha (TNF-α).^28,29 Together, these mechanisms suggest that vitamin B6 may mitigate genetically and transcriptionally driven neuroinflammatory processes implicated in TS. Supporting his hypothesis, a clinical trial in children with TS demonstrated a significant reduction in tics with vitamin B6 and magnesium supplements.³⁰

This study is among the few in India to characterize the clinical profile of children with TS and plasma vitamin B6 levels.

Limitation

The study is limited by a small sample size and differences in age and sex distribution between cases and controls, which may introduce residual confounding. In addition, plasma vitamin B6 levels may not accurately reflect central nervous system availability and the underlying neurobiological mechanisms relevant to TS.

Conclusions

Our study shows that TS in children is more common in males, with comorbid ADHD and OCD. Coprolalia, which causes significant distress to the patients, was found in a small subgroup. Plasma vitamin B6 levels were lower in this group, which may contribute to the disease pathogenesis. Future studies should use a larger sample size and include age- and sex-matched controls to reduce confounding. Measuring B6 levels in Cerebrospinal Fluid (CSF) and identifying neuroinflammation using imaging would help clarify the causal role of B6 in the pathophysiology of this disorder. Experiments using human microglial cell lines that integrate transcriptomics and proteomics will help identify novel biomarkers. Well-designed clinical trials with B6 supplementation will help in understanding its translational and therapeutic potential.

Supplemental Material

Supplemental material for this article is available online.

Footnotes

Acknowledgements

The authors acknowledge institutional infrastructure support.

Reporting Guideline

STROBE

Appropriate Permissions from the Concerned Authorities

Nil.

Data Sharing Statements

Deidentified individual participant data (including data dictionaries) will be made available, in addition to study protocols, the statistical analysis plan, and the informed consent form. The data will be made available upon publication to researchers who provide a methodologically sound proposal to achieve the goals of the approved proposal. Proposals should be submitted to rajith@imhans.ac.in.

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Declaration Regarding the Use of Generative AI

No part of this article was written or generated by a generative AI tool. The authors take full responsibility for the accuracy, integrity, and originality of the published article.

Ethical Approval

Name of the Institutional Ethics Committee/Independent Review Board: Institutional Ethics Committee, Government Medical College, Kozhikode.

Approval Ref. No.: GMCKKD/RP/2022/IEC-42

Date: March 25, 2022

Funding

The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: State Board for Medical Research, Government of Kerala.

Informed Consent/Assent

For participants who were minors at the time of participation, written informed consent for publication was obtained from their parent(s) or legally authorized representative(s), and assent was obtained from the minor participants where appropriate and in accordance with institutional and ethical guidelines. For adult control participants, written informed consent for publication was obtained directly from the participants themselves.

Prior Presentations

None.

PROSPERO/CTRI Details

NA.

Registration

Trial registry name: NA (observational case– control study)

URL: NA

Registration number: NA

Simultaneous Submission to Another Journal or Resource

A preprint version of this manuscript has been posted on medRxiv (https://www.medrxiv.org/content/10.64898/2026.01.14.26343936v1).

Status of Your Study (for Study Protocol)

NA.

Citation Diversity Statement

The authors made efforts to ensure that the reference list reflects diversity in terms of gender, geography, and scientific perspectives relevant to the field. Citations were selected primarily on scientific relevance and quality.

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