Prevalence, Phenotypic Correlates and Predictive Factors of Catatonia in Adolescents With Autism Spectrum Disorder

ABSTRACT

Background

Catatonia, a psychomotor syndrome increasingly recognized in individuals with autism spectrum disorder (ASD), remains frequently underdiagnosed due to symptom overlap, particularly in adolescent populations where data remain limited. This study aimed to determine the prevalence, clinical correlates and predictive factors of catatonia in adolescents with ASD, focusing on sociodemographic, behavioural and affective characteristics.

Methods

A total of 107 adolescents aged 12–20 years with ASD were evaluated at a tertiary child and adolescent psychiatry outpatient clinic. The diagnosis of catatonia was established using DSM‐5 criteria and the Bush–Francis Catatonia Rating Scale (BFCRS). ASD severity, repetitive behaviours and internalizing symptoms were assessed using the Global Assessment Scale, the Autism Behaviour Checklist (ABC), the Repetitive Behaviour Scale–Revised (RBS‐R) and the Revised Child Anxiety and Depression Scale–Parent version (RCADS‐P). Group comparisons, correlation analyses and binary logistic regression were performed.

Results

Catatonia was identified in 21.5% of participants. The most frequent symptoms were stereotypy (73.8%), impulsivity (37.4%), echolalia (36.4%), verbigeration (30.8%) and agitation/excitement (30.8%). Female sex, greater ASD severity, depressive symptoms and separation anxiety were significantly associated with catatonia. The catatonia group demonstrated higher scores on the ABC‐Relationship Building, RBS‐R‐Stereotyped Behaviour and RCADS‐P‐Depression subscales. Logistic regression revealed that female gender and clinically significant separation anxiety symptoms were independent predictors of catatonia (Nagelkerke R ² = 0.26, p < 0.001).

Conclusions

These findings highlight the importance of targeted screening for catatonia in ASD populations, particularly in females and individuals with co‐occurring separation anxiety symptoms. Early recognition and intervention may mitigate functional deterioration and improve clinical outcomes.

1. Introduction

Autism spectrum disorder (ASD) is a neurodevelopmental disorder with onset in early developmental periods characterized by persistent impairments in social communication and interaction, alongside restricted and repetitive patterns of behaviour, interests or activities (American Psychiatric Association [APA] ²⁰¹³).

Catatonia is a psychomotor syndrome characterized by a range of motor abnormalities (e.g., stereotypy, posturing, catalepsy, waxy flexibility, akinesia and stupor), affective symptoms (e.g., fear, aggression, anxiety, flat affect, affective instability and impulsivity) and cognitive‐behavioural disturbances (e.g., mutism, negativism, echolalia, echopraxia, grimacing, mannerisms and ritualistic behaviours) (Fink and Taylor 2006; Fink et al. ²⁰⁰⁶; Hirjak et al. ²⁰²⁴). Although recognized as a distinct diagnostic entity in contemporary classification systems, catatonia remains frequently underdiagnosed, particularly in neurodevelopmental conditions such as ASD (Taylor and Fink 2003; Ghaziuddin et al. ²⁰¹²). It is estimated to affect approximately 7%–35% of adolescents and young adults with ASD (Wing and Shah 2000; Breen and Hare ²⁰¹⁷; Yurumez et al. ²⁰²⁴). Researchers suggest that the wide variation may be due to the lack of empirically based diagnostic criteria, (Breen and Hare 2017) as well as the clinical heterogeneity and symptom overlap between ASD and catatonia (Wing and Shah 2000; Fink et al. ²⁰⁰⁶; Moore et al. ²⁰²²). Recent research has increasingly focused on the symptomatic overlap between catatonia and ASD (Wing and Shah 2000; Ghaziuddin et al. ²⁰¹²; Vaquerizo‐Serrano et al. ²⁰²²; Trelles et al. ²⁰²⁶). Common features, including social indifference, mannerisms and echolalia, are often present in both conditions (Mahgoub et al. 2025). This overlap poses challenges for the accurate diagnosis of catatonia in individuals with ASD (Ghaziuddin et al. 2012; Breen and Hare ²⁰¹⁷; Vaquerizo‐Serrano et al. ²⁰²²; Yurumez et al. ²⁰²⁴; Trelles et al. ²⁰²⁶).

Individuals with ASD may exhibit a marked deterioration in motor functioning, which may be mistaken for catatonia or may represent an emerging catatonic episode. However, the presence of stereotypies, echolalia, mannerisms or other repetitive behaviours alone should not be considered sufficient evidence of catatonia, as these features may represent stable manifestations of ASD (Ghaziuddin et al. 2012; Breen and Hare ²⁰¹⁷; Munoz et al. ²⁰²⁵). Instead, catatonia is more appropriately suspected when there is a noticeable change from the individual's developmental baseline, including the new onset, substantial worsening or qualitative alteration of motor and behavioural symptoms accompanied by functional decline (Wing and Shah 2000; Ghaziuddin et al. ²⁰¹²; Hauptman et al. ²⁰²³). In this context, stereotypies and self‐injurious behaviours that become significantly more frequent, severe or disruptive than previously observed may represent manifestations of an emerging catatonic process rather than merely an exacerbation of core ASD symptoms (Wing and Shah 2000; Ghaziuddin et al. ²⁰¹²). Moreover, given the high prevalence of depressive and anxiety disorders in individuals with ASD, these comorbid conditions may further contribute to the overlap between ASD and catatonia, highlighting the need for thorough and accurate assessment (Vaquerizo‐Serrano et al. ²⁰²²; Yurumez et al. ²⁰²⁴; Munoz et al. ²⁰²⁵; Öksüzoğlu et al. ²⁰²⁵).

Given these diagnostic challenges, early screening and accurate differentiation of catatonia from baseline ASD manifestations are of critical importance (Breen and Hare 2017; Yurumez et al. ²⁰²⁴; Munoz et al. ²⁰²⁵). Recent efforts to improve the early identification of catatonia have led to the development of the Catatonia Quick Screen, a brief screening instrument designed to facilitate the rapid and systematic identification of catatonic symptoms across paediatric and adult populations (Luccarelli et al. 2025).

Early identification is particularly important because catatonia is a potentially treatable condition. Emerging evidence supports the use of pharmacological interventions, particularly benzodiazepines, for symptom management, whereas electroconvulsive therapy remains an effective treatment option for severe, persistent or treatment‐resistant cases of catatonia in individuals with ASD and other neurodevelopmental disorders (Smith et al. 2025; Wachtel et al. ²⁰²⁴).

Importantly, three clinically related but conceptually distinct phenomena must be differentiated in adolescents with ASD: (i) core ASD‐related motor and repetitive behaviours (e.g., stereotypies, mannerisms, echolalia), which are typically longstanding and developmentally stable; (ii) catatonia as a discrete psychomotor syndrome characterized by the emergence or marked worsening of motor, behavioural and affective symptoms that exceed baseline autistic features and meet standardized diagnostic criteria; and (iii) deterioration in baseline functioning, reflected by a subacute or progressive decline in previously acquired skills or adaptive capacities. Failure to distinguish these entities may lead to overestimation of catatonia prevalence or misattribution of autistic behaviours to catatonic processes (Wing and Shah 2000; Ghaziuddin et al. ²⁰¹²; Breen and Hare ²⁰¹⁷; Vaquerizo‐Serrano et al. ²⁰²²). Careful longitudinal assessment is therefore essential to distinguish catatonia from baseline autistic characteristics and to ensure an accurate diagnosis.

Despite growing recognition of catatonia in ASD and recent efforts to synthesize the existing evidence (Trelles et al. 2026), important gaps remain in the literature. In particular, there is limited systematic evidence focusing specifically on adolescents with ASD; integrating standardized catatonia assessments with detailed evaluation of sociodemographic factors, ASD severity, repetitive behaviours and internalizing symptoms; and examining potential clinical predictors beyond motor manifestations. In light of these gaps, the present study aimed to investigate the occurrence and clinical features of catatonia in adolescents with ASD, with a particular emphasis on sociodemographic variables, ASD symptom severity, co‐occurring psychiatric and medical conditions and potential predictors of catatonia within this population. The specific objectives were (1) to determine the prevalence of catatonia in a clinical sample of adolescents with ASD; (2) to examine the sociodemographic and clinical correlates associated with the presence of catatonia; and (3) to identify significant predictors of catatonia in this population. This study extends existing literature by focusing specifically on an adolescent clinical ASD population, applying both DSM‐5 criteria and the Bush–Francis Catatonia Rating Scale (Bush et al. 1996), one of the most widely used and validated clinical assessment tools for catatonia, to enhance diagnostic specificity, and examining affective correlates alongside core autistic features. By integrating functional impairment, behavioural dimensions and internalizing symptoms, the present work provides a more comprehensive characterization of catatonia in ASD during adolescence.

2. Methods

2.1. Participants and Procedure

The study sample comprised adolescents aged 12–20 years who had a diagnosis of ASD and were receiving continuous care at the Child and Adolescent Psychiatry Outpatient Clinic of a tertiary healthcare facility in Ankara, Türkiye, from December 2023 to January 2025. This recruitment period was selected based on feasibility and outpatient clinic availability, corresponding to a continuous interval during which standardized catatonia screening, including routine application of the BFCRS, was systematically implemented in the clinic and complete clinical data were consistently recorded.

Participants were recruited consecutively during routine outpatient visits throughout the study period. All adolescents meeting DSM‐5 criteria for ASD and within the specified age range were approached for participation. Of those invited, 25 families declined participation primarily due to time constraints or lack of interest. Exclusion criteria included an acute medical illness, known neurological disorders (e.g., epilepsy with uncontrolled seizures or neurodegenerative disease) or severe sensory impairments that could interfere with clinical assessment. A total of 15 adolescents were excluded based on these criteria prior to enrollment. Psychiatric comorbidities were not grounds for exclusion, as these were considered intrinsic to the clinical characterization of the sample and were systematically recorded. Accordingly, the final sample consisted of 107 participants.

A psychiatric examination based on DSM‐5 criteria was administered to adolescents referred to our outpatient clinic. The patients aged 12–20 years who received a diagnosis of ASD based on DSM‐5 criteria were invited to participate. Prior to enrollment, all participating adolescents and their parents were thoroughly informed about the study's objectives and procedures, and inclusion was limited to those adolescents and parents who provided voluntary consent to participate.

The research protocol was approved by the hospital's local ethics committee (ethics approval number: İ03‐181‐23), and the study was conducted in accordance with the Declaration of Helsinki (1975, revised 2013). Written informed consent from adolescents and their parents was secured before the psychiatric assessments and completion of study measures. Verbal consent was witnessed and formally recorded. Due to ethical considerations, the data underpinning the findings of this study are not publicly accessible; however, they may be made available by the corresponding author upon a justified request. The participants' sociodemographic characteristics of the were obtained from their parents using a Sociodemographic Data Form developed by the authors and administered during the initial psychiatric evaluation. The diagnosis of catatonia was determined by consensus of at least two experienced child and adolescent psychiatrists, following a comprehensive assessment protocol that included direct clinical evaluation, application of DSM‐5 diagnostic criteria and standardized measurement using the Bush–Francis Catatonia Rating Scale. Functional impairment related to ASD was evaluated using the Global Assessment Scale. Subsequently, the Autism Behaviour Checklist, the Repetitive Behaviour Scale–Revised and the Revised Child Anxiety and Depression Scale–Parent version were administered to the parents. The average duration of the clinical examination for each participant was approximately 45 min, whereas completion of parent‐reported forms required an additional 15 min, for a total of approximately 1 h.

2.2. Measures

The Sociodemographic Data Form (SDF) encompasses information on participants' age, gender, medical history and family characteristics. Socio‐economic status (SES) was categorized as low (≤ 22), medium (23–44) or high (≥ 45) based on the Hollingshead‐Redlich Scale (Hollingshead and Redlich 2007). Additional clinical information—including age at initial ASD diagnosis, previous psychiatric comorbidities and intelligence quotient level—was documented using the SDF.

The DSM‐5 criteria were used to confirm the diagnosis of catatonia, which requires the presence of three or more of the following symptoms: stupor, catalepsy, waxy flexibility, mutism, negativism, posturing, mannerism, stereotypy, agitation, grimacing, echolalia and echopraxia (APA ²⁰¹³). The ASD and psychiatric comorbidities were also diagnosed according to DSM‐5 criteria.

The Bush–Francis Catatonia Rating Scale (BFCRS) is a widely used clinical tool for the assessment, diagnosis and monitoring of catatonia (Bush et al. 1996). The screening score is derived from the sum of the initial 14 items, whereas the severity score is calculated by summing the severity ratings of all 23 items. The presence of four or more screening symptoms confers the highest diagnostic confidence, whereas three or more symptoms constitute a positive screening. The validation and reliability study demonstrated that the Turkish version of the scale exhibited excellent internal consistency, with a Cronbach's alpha coefficient of 0.90 (Erdoğan et al. 2022). In the current study, the BFCRS was employed to assess catatonia in the ASD sample. Catatonia was operationalized as meeting DSM‐5 diagnostic criteria in conjunction with a positive BFCRS screening score (≥ 4 items). For descriptive purposes, individual BFCRS items were additionally mapped onto the psychomotor framework proposed by Walther et al. (2019), which was originally derived from analyses of catatonic signs assessed using standardized catatonia rating scales. Symptoms were categorized as increased psychomotor activity (agitation/excitement, impulsivity and combativeness), decreased psychomotor activity (stupor, ambitendency, staring, negativism, mutism and withdrawal) and abnormal psychomotor activity (grimacing, stereotypy, mannerism, posturing, perseveration, echolalia, echopraxia, verbigeration, automatic obedience, waxy flexibility, catalepsy, rigidity, gegenhalten, mitgehen and grasp reflex). Symptom frequencies were subsequently examined within each domain to facilitate clinical interpretation.

The Global Assessment Scale (GAS) is a clinician‐rated instrument designed to evaluate an individual's overall functioning over a specified time frame, ranging from psychiatric disorder to optimal health (Endicott et al. 1976). The GAS yields scores ranging from 0 to 100, with higher scores reflecting greater levels of overall functioning. According to the classification by Köhler et al., scores between 61 and 100 indicate good functioning, scores between 31 and 60 reflect moderate functioning, and scores below 30 signify poor functioning (Köhler et al. 2016). In the present study, the GAS was utilized to assess functional impairment associated with ASD.

The Autism Behaviour Checklist (ABC), developed by Krug et al., is used for the assessment and screening of autism (Krug et al. 1988). The ABC consists of 57 items divided into five subscales: sensory (9 items), relationship building (12 items), body and object use (12 items), language skills (13 items) and social and self‐help skills (11 items). Upon evaluation, children receive scores ranging from 0 to 159, with higher scores indicating more severe problems. The Turkish validity and reliability study reported a Cronbach's alpha coefficient and split‐half reliability of 0.92 for the total score (Irmak et al. 2007). In the present study, the ABC was utilized to assess ASD‐related symptomatology and to investigate its association with catatonia.

The Repetitive Behaviour Scale–Revised (RBS‐R) was developed to assess the presence and severity of repetitive behaviours. The RBS‐R comprises six subscales: stereotyped behaviour, self‐injurious behaviour, compulsive behaviour, routine behaviour, sameness behaviour and restricted behaviour. This parent report instrument is composed of 43 items, each rated on a 4‐point Likert scale, with higher scores indicating greater severity of repetitive behaviours (Bodfish et al. 2000). The Turkish version of the RBS‐R demonstrated acceptable validity and reliability, with internal consistency coefficients ranging from 0.73 to 0.94 (Akcamus et al. 2019). Several domains assessed by the ABC and RBS‐R, including stereotyped movements, repetitive behaviours and self‐injurious behaviours, may overlap phenomenologically with the behavioural manifestations commonly observed in catatonia.

The Revised Child Anxiety and Depression Scale–Parent version (RCADS‐P) is a 47‐item questionnaire rated by parents, designed to assess symptoms of anxiety and depression in children and adolescents (Chorpita et al. 2000). Items are rated on a 4‐point Likert scale (0 = never, 1 = sometimes, 2 = often, 3 = always), with higher scores reflecting greater symptom severity. The RCADS‐P comprises six subscales—Separation Anxiety Disorder (SAD), Social Phobia (SoP), Generalized Anxiety Disorder (GAD), Obsessive‐Compulsive Disorder (OCD), Panic Disorder (PD) and Major Depressive Disorder (MDD)—in addition to an Anxiety Total Score (sum of the five anxiety subscales) and a Total Internalizing Score (sum of all six subscales). The Turkish version of the RCADS‐P demonstrated strong reliability and validity, with Cronbach's alpha and test–retest coefficients ranging from 0.76 to 0.95 across subscales (Gormez et al. 2017). In the current study, the scale was used to measure the severity of internalizing symptoms, including depression and anxiety, in participants.

2.3. Statistical Analysis

IBM SPSS (Statistical Package for Social Sciences) 23.0 was used for statistical analyses of the sociodemographic and clinical characteristics of the participants. Descriptive data were presented as frequencies and percentages for categorical variables and as medians (interquartile ranges) or means (standard deviations), as appropriate, for continuous variables. Variable classification as categorical or continuous was based on the measurement level and distributional properties. Prior to comparative analyses, the Shapiro–Wilk test was used to assess the normality of continuous data distributions. Continuous variables were analysed using the Mann–Whitney U test due to non‐normal distributions, whereas categorical variables were analysed using chi‐square or Fisher's exact tests based on expected cell counts. Effect sizes (r) were calculated for Mann–Whitney U tests to facilitate interpretation of the magnitude of group differences. Spearman's correlation coefficients were used to examine associations between scale scores. A binary logistic regression model was conducted to identify independent factors associated with catatonia. Multicollinearity was assessed prior to regression analysis. All statistical tests were two‐tailed, with a threshold for statistical significance set at α = 0.05.

3. Results

3.1. Sociodemographic and Clinical Characteristics of the Sample

Among the 107 adolescents with ASD, 21 (19.6%) were female, and 86 (80.4%) were male. The mean age was 14.13 ± 1.95 years. Among the whole sample, 27 (25.2%) participants had a documented family history of psychopathology. Of these participants, 6 participants reported psychiatric disorders among second‐degree relatives, whereas 21 reported such a history among parents and siblings. The reported psychopathologies included anxiety disorders in parents; specific learning disorder (SLD), attention‐deficit/hyperactivity disorder (ADHD), ASD and obsessive‐compulsive disorder (OCD); and tic disorders in siblings.

The sample included adolescents with ASD who had typical intellectual functioning (n = 19, 17.8%) and adolescents with intellectual disability (ID) at mild, moderate and severe levels. The ASD severity, assessed using the GAS, was classified into mild, moderate and severe categories. When the clinical characteristics of the participants were examined, psychiatric comorbidity was detected in 95 (11.2%) of them, and the presence of at least two psychiatric comorbidities was present in 40 cases (37.4%). ID was diagnosed in 98 cases (82.2%); ADHD in 60 cases (56%); language and speech disorder in 10 cases (9.4%); and anxiety disorder in 7 cases (6.5%). Table 1 presents a detailed overview of the sociodemographic and clinical characteristics of the participants.

TABLE 1.

Sociodemographic and clinical characteristics of participants.

Sociodemographic variables	Participants (n = 107) mean ± SD (Min–Max)/n (%)
Gender, n (%)
Female	21 (19.6)
Male	86 (80.4)
Child age (years)	14.13 ± 1.95 (11–20)
Mothers' age (years)	43.58 ± 5.04 (32–60)
Mothers' educational level
Less than high school	44 (41.1)
High school	41 (38.3)
Bachelor's degree or higher	22 (20.6)
Mothers' employment status
Employed	27 (25.2)
Unemployed	80 (74.8)
Fathers' age (years)	47.17 ± 6.15 (37–73)
Fathers' educational level
Less than high school	33 (30.8)
High school	43 (40.2)
Bachelor's degree or higher	31 (29)
Fathers' employment status
Employed	95 (88.8)
Unemployed	9 (8.4)
Ex	3 (2.8)
Number of siblings	1.16 ± 0.78 (0–4)
Socio‐economic status, n (%)
Low	32 (29.9)
Medium	49 (45.8)
High	26 (24.3)
Familial psychopathology
Absent	80 (74.8)
Present	27 (25.2)

Clinical variables
Age of first ASD diagnosis	3.47 ± 2.17 (1–16)
Psychiatric comorbidity
Absent	12 (11.2)
Present	95 (88.8)
Intellectual quotient level, n (%)
Normal or higher	19 (17.8)
Mild–moderate intellectual disability	74 (69.2)
Severe intellectual disability	14 (13.0)
Autism spectrum disorder severity
Mild	35 (32.7)
Moderate	54 (50.5)
Severe	18 (16.8)

Abbreviations: Max, maximum; Min, minimum; SD, standard deviation.

3.2. Prevalence and Clinical Correlates of Catatonia

When assessed concurrently using both the BFCRS and DSM‐5 criteria, catatonia was identified in 21.5% of the participants (n = 23). The distribution of catatonic symptoms according to the psychomotor framework proposed by Walther et al. (2019) is presented in Figure 1. Abnormal psychomotor manifestations constituted the predominant symptom domain, with stereotypy (73.8%) emerging as the most frequently observed symptom, followed by echolalia (36.4%) and verbigeration (30.8%). Within the increased psychomotor activity domain, impulsivity (37.4%) and agitation/excitement (30.8%) were the most prevalent symptoms. Among decreased psychomotor manifestations, staring (20.6%) and negativism (14.0%) were the most frequently observed symptoms. Overall, abnormal psychomotor symptoms were substantially more common than increased or decreased psychomotor activity symptoms.

FIGURE 1.

Distribution of catatonic symptoms according to psychomotor activity domains. Symptoms were categorized into increased psychomotor activity, abnormal psychomotor activity and decreased psychomotor activity based on the psychomotor framework proposed by Walther et al. (2019). Values represent the percentage of participants exhibiting each symptom.

Two groups, consisting of participants with catatonia (n = 23) and without catatonia (n = 84), were compared with respect to sociodemographic variables. While comparing sociodemographic variables between two groups, a chi‐square test of independence revealed a statistically significant association between gender and catatonia status. Females were more frequently represented in the catatonia (+) group compared to the catatonia (−) group [χ²(1) = 4.27, p = 0.039]. A statistically significant association was observed between the presence of catatonia and ASD severity as determined by GAS. However, no significant relationship was found between IQ levels (normal, mild–moderate and severe) and the presence of catatonia [Fisher's exact test, χ²(2) = 0.46, p = 0.93; 3 (13%) normal, 17 (73.9%) mild–moderate and 3 (13%) severe]. Similarly, there is no significant relationship between SES (low, medium and high) and the presence of catatonia [chi‐squared test, χ²(2) = 2.01, p = 0.36; 5 low (15.6%), 10 medium (20.4%) and 8 high (30.8%)]. Detailed comparisons of sociodemographic and clinical variables were presented in Table 2.

TABLE 2.

Comparisons of sociodemographic and clinical characteristics across the catatonia (+) and catatonia (−) groups.

Sociodemographic variables	Catatonia + (n = 23) Mdn (IQR)/n (%)	Catatonia − (n = 84) Mdn (IQR)/n (%)	χ2/U	p
Sex a
Female	8 (34.8%)	13 (15.5)	4.27	0.039*
Male	15 (65.2%)	71 (81.5)
Participants' age (years) b	13 (12–15)	14 (13–16)	785	0.164
Age of first ASD diagnosis (years) b	3 (2.12–3.37)	3 (2.12–4)	624.5	0.210
Psychiatric comorbidity c
Yes	22 (95.7)	72 (85.7)	1.67	0.291
No	1 (4.3)	12 (14.3)
ASD severity a
Mild	2 (8.7)	33 (39.3)	7.68	0.006*
Moderate–severe	21 (91.3)	51 (60.7)
IQ level c
Normal or higher	3 (13)	16 (19)
Mild–moderate	17 (74)	57 (67.9)	0.46	0.934
Severe	3 (13)	11 (13.1)
Mothers' age (years) b	42 (39–45)	43 (40–47)	751.00	0.118
Fathers' age (years) b	46 (42–51)	46 (43–50)	892.00	0.824
Number of siblings	1 (1–2)	1 (1–1)	945.00	0.857
SES a , n (%)
Low	5 (21.7)	27 (32.1)
Medium	10 (43.5)	39 (46.4)	2.01	0.366
High	8 (34.8)	18 (21.4)
Familial psychopathology a , n (%)
None	16 (69.6)	65 (77.4)	0.60	0.439
Either parents or siblings	7 (30.4)	19 (22.6)

Note: Frequencies are reported as numbers and percentages in parentheses; and medians are shown with inter‐quartile range in parentheses.

Abbreviations: IQ, intelligence quotient; IQR, interquartile range; Mdn, median; SES, socio‐economic status.

^a Chi‐squared test.

^b Mann–Whitney U test.

^c Fisher's exact test.

^* p < 0.05.

^** p < 0.01.

^*** p < 0.001.

In the comparative analysis of psychiatric scale scores between the two groups, the catatonia (+) group demonstrated significantly higher scores on the ABC/Relationship building, RCADS‐P/MDD and RBS‐R/SMM subscales. Comparisons of all scale scores, including their respective subscales, are detailed in Table 3.

TABLE 3.

Comparisons of scale scores across the catatonia (+) and catatonia (−) groups.

Psychiatric measures	Catatonia + (n = 23)	Catatonia − (n = 84)	Z/U	p	r
	Mdn (IQR)	Mdn (IQR)
ABC
Sensory	4 (3–12)	4 (0–7)	−1.83/727	0.067	0.177
Relationship Building	17 (11–22)	11 (5–17.75)	−2.81/596	0.005**	0.272
Body and Object Use	11 (7–16)	10 (4–15.75)	−0.68/876.5	0.496	0.066
Language Behaviours	11 (6–18)	10 (6.25–16)	−0.46/906	0.649	0.044
Social and Self‐Help	7 (5–13)	8 (5–11)	−0.27/962.5	0.979	0.026
Total Score	49 (33–85)	46.5 (30–61.5)	−1.34/789	0.179	0.130
RCADS‐P
GAD	41 (39–51)	45 (40–57)	−1.06/816.5	0.289	0.102
SAD	66 (47–78)	55 (47–64)	−0.90/838	0.370	0.087
PD	51 (41–67)	47 (41–58)	−0.58/879	0.561	0.056
OCD	52 (43–65)	52 (45–63)	−0.37/906.5	0.712	0.036
SoP	39 (37–46)	40 (33–50)	−0.41/901.5	0.684	0.040
MDD	60 (48–69)	49 (41–58)	−2.26/660	0.024*	0.218
Total Anxiety	50 (39–64)	47 (39–59)	−0.35/909.5	0.730	0.034
Total Internalizing	53 (42–65)	46 (40–59)	−0.85/844	0.397	0.082
RBS‐R
SMM	5 (2–7)	3 (1–6)	−2.00/705.5	0.047*	0.193
SIB	2 (1–4)	1 (0–3)	−1.01/835.5	0.311	0.098
CB	3 (1–6)	4 (1–7)	−0.95/842	0.344	0.092
RB	2 (0–6)	4 (2–7)	−1.43/779	0.154	0.138
SB	5 (2–14)	7 (3–12)	−0.56/893	0.579	0.054
RI	2 (0–4)	3 (0.25–5)	−0.92/846	0.356	0.089
Total score	20 (13–40)	23 (12.25–36.5)	−0.27/931	0.791	0.026

Note: Effect sizes were calculated as r. Mann–Whitney U test.

Abbreviations: ABC, Autism Behaviour Checklist; CB, compulsive behaviour; GAD, generalized anxiety disorder; IQR, interquartile range; MDD, major depressive disorder; Mdn, median; OCD, obsessive‐compulsive disorder; PD, panic disorder; RB, routine behaviour; RBS‐R, Repetitive Behaviour Scale–Revised; RCADS‐P, Revised Children's Anxiety and Depression Scale–Parent version; RI, restricted interest; SAD, separation anxiety disorder; SB, sameness behaviour; SIB, self‐injurious Behaviour; SMM, stereotyped motor movements; SoP, social phobia.

^* p < 0.05.

^** p < 0.01.

^*** p < 0.001.

3.3. Correlations of Psychiatric Scale Scores in Participants

Associations between the subscale and total scores of the ABC and RBS‐R and those of the RCADS‐P were analysed using Pearson's correlation coefficients. Significant correlations were observed between almost all subscales of the RBS‐R and the ABC, with effect sizes in the moderate range. Furthermore, a comparison of the RCADS‐P subscales with ABC scores revealed significant moderate correlations between the SAD subscale and the ABC scores, as well as mild correlations between ABC scores and both total anxiety and internalizing symptoms. Comprehensive correlation analyses between the scales are detailed in Table 4.

TABLE 4.

Correlations between Autism Behaviour Checklist and Repetitive Behaviour Scale–Revised and Revised Children's Anxiety and Depression Scale–Parent version subscales.

ABC subscales	Sensory	Relationship building	Body and object use	Language	ABC‐Social and Self‐Help
	r/p	r/p	r/p	r/p	r/p
RBS‐R/SMM	0.32 *** /< 0.001	0.41 *** /< 0.001	0.57 *** /< 0.001	0.180/0.063	0.36 *** /< 0.001
RBS‐R/SIB	0.25/0.798	0.17/0.085	0.33 *** /< 0.001	0.06/0.530	0.24 * /0.015
RBS‐R/CB	0.19 * /0.051	0.22 * /0.022	0.31 ** /0.001	0.27 ** /0.005	0.29 ** /0.002
RBS‐R/RB	0.11/0.271	0.06/0.537	0.26 ** /0.006	0.19 * /0.049	0.29 ** /0.002
RBS‐R/SB	0.18/0.070	0.14/0.140	0.29 ** /0.002	0.30 ** /0.002	0.33 *** /< 0.001
RBS‐R/RI	0.09/0.311	0.07/0.498	0.32 *** /< 0.001	0.16/0.101	0.24 * /0.013
RCADS‐P
GAD	−0.07/0.484	−0.18/0.065	−0.04/0.666	0.12/0.222	0.11/0.282
SAD	0.18/0.070	0.11/0.244	0.32 *** /< 0.001	0.30 ** /0.002	0.26 ** /0.006
PD	0.05/0.595	−0.14/0.153	0.06/0.540	0.04/0.674	0.14/0.157
OCD	−0.08/0.388	−0.13/0.199	−0.01/0.944	0.19/0.053	−0.14/0.145
SoP	−0.07/0.487	−0.23/0.018	−0.15/0.132	0.01/0.919	0.16/0.092
MDD	−0.01/0.915	0.03/0.793	0.09/0.373	0.09/0.378	0.19/0.055
Total Anxiety	−0.01/0.943	−0.14/0.152	0.02/0.811	0.15/0.118	0.20 * /0.037
Total Internalizing	−0.01/0.922	−0.11/0.250	0.04/0.678	0.13/0.198	0.21 * /0.030

Note: Pearson's correlation test. Bold values indicate significant results.

Abbreviations: ABC, Autism Behaviour Checklist; CB, compulsive behaviour; GAD, generalized anxiety disorder; MDD, major depressive disorder; OCD, obsessive‐compulsive disorder; PD, panic disorder; RB, routine behaviour; RBS‐R, Repetitive Behaviour Scale–Revised; RCADS‐P, Revised Children's Anxiety and Depression Scale–Parent version; RI, restricted interest; SAD, separation anxiety disorder; SB, sameness behaviour; SIB, self‐injurious behaviour; SMM, stereotyped motor movements; SoP, social phobia.

^* p < 0.05.

^** p < 0.01.

^*** p < 0.001.

3.4. Predictors of Catatonia Among Adolescents With ASD

To further determine factors that might be associated with the presence of catatonia evaluated by BFCRS and DSM‐5, binary logistic regression was carried out in the whole sample. After univariate analyses, sex, family type (nuclear, extended and single parent), fathers' educational level (below high school, high school, college degree and higher), mothers' age, ASD severity (mild, moderate and severe evaluated using GAS), RCADS‐P/SAD categoric variable (normal and clinic) ABC‐relating and RBS‐SMM subscale scores were included in the regression model (p < 0.05).

The overall model was statistically significant, indicating that the set of predictors reliably distinguished between individuals with and without catatonia [χ²(5) = 19.65, p < 0.001]. The model explained approximately 26% (Nagelkerke R ²) of the presence of catatonia. The Hosmer–Lemeshow test yielded a non‐significant result, χ²(8) = 11.28, p = 0.186, suggesting good model fit. Among the predictors, female sex and the clinical level of separation anxiety symptoms were significantly associated with the presence of catatonia (see Table 5).

TABLE 5.

Logistic regression analysis for prediction of catatonia among participants.

	B	SE	p	OR (95% CI)
Sex	1.221	0.594	0.040*	3.39 (1.06–10.86)
ASD severity	0.431	0.445	0.333	1.54 (0.64–3.68)
RCADS‐P/SAD	1.205	0.552	0.029*	3.34 (1.13–9.84)
ABC‐relationship building	0.092	0.041	0.026*	1.09 (1.01–1.19)
RBS‐R/SMM	−0.042	0.093	0.651	0.96 (0.79–1.15)

Note: Dependent variable: Presence of catatonia.

Abbreviations: ABC, Autism Behaviour Checklist; ASD, autism spectrum disorder; CI, confidence interval; OR, odds ratio; RBS‐R, Repetitive Behaviour Scale–Revised; RCADS‐P, Revised Children's Anxiety and Depression Scale–Parent Version; SAD, separation anxiety disorder; SE, standard error; SMM, stereotyped motor movements.

^* p < 0.05.

^** p < 0.01.

^*** p < 0.001.

4. Discussion

In this clinically referred sample of adolescents with ASD, (i) we identified a high rate of catatonia (21.5%) using both DSM‐5 and BFCRS. (ii) In the catatonia (+) group, the prevalence of females was higher. The prevalence of catatonia was higher among adolescents with clinically determined greater ASD severity. (iii) The catatonia (+) group exhibited significantly higher levels of symptoms on the ABC/Relationship building subscale, higher stereotypic behaviours as measured by the RBS‐R and higher depressive symptoms on the RCADS‐P scale, compared to the catatonia (−) group. (iv) Female gender and the presence of clinically significant separation anxiety symptoms were identified as significant predictors of catatonia in adolescents with ASD. These findings underscore the multidimensional clinical profile of catatonia in ASD and provide a framework for the interpretation of the results discussed below.

Initially, in the current study, the prevalence of catatonia among adolescents with ASD was determined to be approximately 21.5%. Although this finding aligns with rates reported in certain previous studies (Breen and Hare 2017), it is important to acknowledge the potential influence of referral bias due to the clinical nature of the sample. Nevertheless, the prevalence of catatonia among individuals with ASD has been reported to vary considerably across studies. A recent meta‐analysis reported that 10.4% of individuals with ASD have catatonia (Vaquerizo‐Serrano et al. ²⁰²²), and similarly, a study conducted in Turkey diagnosed catatonia in 10.7% of adolescents and adults with ASD (Öksüzoğlu et al. 2025). In contrast, previous research identified a prevalence rate of up to 35% among adolescents diagnosed with ASD (Yurumez et al. 2024). A major challenge moving forward will be the refinement and validation of catatonia diagnosis in individuals with ASD, given the heterogeneity of clinical presentations and substantial symptom overlap with other conditions (Ghaziuddin et al. 2012; Breen and Hare ²⁰¹⁷; Moore et al. ²⁰²²). Therefore, incorporating standardized assessment scales and consistent case reporting may enhance the comparability of findings across studies and contribute to a clearer understanding of the course and characteristics of catatonia within the ASD population (Breen and Hare 2017; Öksüzoğlu et al. ²⁰²⁵).

ASD is a neurodevelopmental condition that typically manifests in early childhood, whereas catatonia is more commonly diagnosed based on motor and behavioural symptoms observed during adolescence and adulthood (Wing and Shah 2000). Nevertheless, there is a significant overlap in the symptomatology of these conditions. Consistent with the psychomotor framework proposed by Walther et al. (2019), catatonic symptoms observed in our sample were distributed across increased, abnormal and decreased psychomotor activity domains. Abnormal psychomotor manifestations constituted the predominant symptom domain, with stereotypy emerging as the most frequent symptom, followed by echolalia and verbigeration. Increased psychomotor activity was primarily characterized by impulsivity and agitation/excitement, whereas staring and negativism were the most frequently observed symptoms of decreased psychomotor activity. These findings suggest that catatonia in adolescents with ASD may present predominantly as abnormal motor and behavioural phenomena rather than through classical stuporous presentations alone. Importantly, many of these manifestations overlap with core ASD characteristics, including stereotyped behaviours, atypical communication patterns and motor abnormalities, which may contribute to diagnostic uncertainty and delayed recognition of catatonia in clinical practice.

Several studies have demonstrated no statistically significant association between gender and the incidence of catatonia, indicating that catatonia diagnosis is independent of gender (Wing and Shah 2000; Breen and Hare ²⁰¹⁷; Öksüzoğlu et al. ²⁰²⁵). However, other investigations have reported a higher prevalence of catatonia in male populations (Wachtel 2019; Vaquerizo‐Serrano et al. ²⁰²²). On the other hand, it has been previously announced that in non‐ASD adult samples, some disorder‐specific catatonia presentations (e.g., depression) show female predominance (Dell'Osso et al. ²⁰²³). Concurrently, in our study, we observed an increased likelihood of catatonia among females and identified female gender as a significant predictor of its occurrence. A primary explanation for this finding is that females with ASD often engage in social masking, which may conceal core symptoms but increase internal distress and the expression of motor and affective symptoms like catatonia (Lai et al. 2015; Hull et al. ²⁰¹⁷). Masking may make social deficits less apparent, but motor symptoms can become more pronounced or harder to compensate for (Dean et al. 2017). Secondly, internalizing disorders, such as anxiety and depression, are more prevalent in females with ASD and are known to increase the risk of catatonia (Joshi et al. 2010). The affective dysregulation associated with these conditions may precipitate or exacerbate catatonic symptoms (Fink and Taylor 2006). Furthermore, many diagnostic tools and rating scales have been normed predominantly on male populations, which can result in under‐recognition of ASD and associated symptoms in females (Mandy et al. 2012). Consequently, catatonic symptoms in females may appear more salient or severe, leading to higher detection rates. Lastly, gender‐specific social expectations may affect symptom expression and caregiver reporting. Families and clinicians might be more vigilant about motor and affective symptoms in females, increasing the likelihood of identifying catatonia (Kreiser and White 2014). Future research should focus on improving the identification of catatonia in females with ASD by examining sex‐specific clinical presentations and patterns of symptom progression. Longitudinal studies evaluating changes from a developmental baseline may help clarify whether catatonic symptoms emerge differently in females and whether current diagnostic approaches adequately capture these presentations. Research exploring caregiver and clinician recognition of catatonic symptoms, as well as validating catatonia assessment tools in female ASD populations, may improve diagnostic sensitivity and reduce the risk of under‐recognition in this group.

In our study, the presence of catatonia was associated with lower GAS scores, reflecting poorer overall functioning. This aligns with previous findings indicating that individuals with catatonia are typically older and exhibit diminished global functioning (Ghaziuddin et al. 2012; Yurumez et al. ²⁰²⁴). Similarly, it has been pronounced that catatonia should be considered as a differential diagnosis in individuals with ASD who demonstrate a marked decline in previously stable functioning (Breen and Hare 2017). In this regard, an exacerbation of core autistic symptoms accompanied by functional deterioration may be indicative of an underlying catatonic process.

In the present study, no statistically significant differences in age were identified among participants with and without catatonia. However, prior studies encompassing broader age ranges, including both adolescents and adults, have consistently reported an association between increasing age and greater severity or more distinct presentation of catatonic symptoms (Vaquerizo‐Serrano et al. ²⁰²²). The absence of such a finding in our study may reflect the restricted age range of the sample (12–20 years) and the exclusion of adult participants, which likely reduced the variability necessary to detect age‐related effects.

Our findings indicate a higher prevalence of depressive symptoms in the catatonia (+) ASD group. This may reflect a greater comorbidity of depression among individuals with catatonia (Unal et al. 2013; Hasan et al. ²⁰²⁵), or the symptoms and signs might, in fact, originate from both conditions, and a causal relationship between them might not be established (Breen and Hare 2017). For example, the high correlation observed between catatonia and depression may be attributable to shared symptomatic features, particularly social withdrawal (Zingela et al. 2022). Indeed, supporting literature confirms that depression, characterized by symptoms such as psychomotor retardation, social withdrawal and poor oral intake, may contribute to the development of catatonic features (Beach et al. 2024). Although the directionality of the relationship between depression and catatonia remains unclear, the greater prevalence of depressive symptoms in individuals presenting with catatonia may suggest the presence of underlying depressive pathology potentially leading to underdiagnosis during routine clinical assessments and may be underdiagnosed (Mazzone et al. 2014). In this context, it is essential that clinicians obtain comprehensive, multi‐informant feedback from parents and the wider social network to enhance diagnostic accuracy.

Our research findings demonstrated associations among catatonia, stereotypic behaviours, depressive symptoms and social relating abilities. Consistent with previous studies, existing evidence also indicates an association between catatonia and depressive symptoms, as well as restrictive and repetitive behaviours; however, a causal relationship has not yet been established (Breen and Hare 2017). However, these findings should be interpreted cautiously, as several behaviours captured by the ABC and RBS‐R may overlap with manifestations of catatonia itself. In particular, stereotyped motor movements, repetitive behaviours, motor abnormalities and self‐injurious behaviours may contribute to elevated scores independent of core ASD symptom severity. Therefore, higher scores observed in the catatonia group may reflect both greater neurodevelopmental impairment and the shared phenomenology between ASD‐related behaviours and catatonic symptoms. Similarly, several BFCRS items, including stereotypy, mannerisms, echolalia, posturing and grimacing, may overlap with core ASD features. Consequently, BFCRS scores may be partially influenced by baseline autistic symptomatology, which underscores the importance of evaluating symptom change relative to the individual's developmental baseline when diagnosing catatonia in ASD. These results underscore the complex interplay between behavioural and affective symptoms in individuals with ASD and highlight the need for further research to clarify the mechanisms underlying catatonia in this population.

Although previous studies have reported a tendency towards higher rates of catatonia among individuals with ID, the absence of a significant association between IQ level and catatonia in our sample was not entirely unexpected, as these differences have generally been modest and often failed to reach statistical significance (Wing and Shah 2000; Ghaziuddin et al. ²⁰¹²). Nevertheless, the high prevalence of ID in our overall sample (82.2%) is noteworthy and consistent with recent literature. In a systematic review, Vaquerizo‐Serrano et al. (2022) highlighted that catatonia in ASD is frequently reported in individuals with co‐occurring ID. Similarly, Smith et al. (2025), in a longitudinal study of autistic individuals with catatonia, specifically examined a cohort with ID, emphasizing the substantial overlap between these clinical conditions. Therefore, the high proportion of ID observed in our sample likely reflects the tertiary care nature of our recruitment setting and may partly explain the relatively high prevalence of catatonia identified in the present study. Overall, our findings remain broadly consistent with the existing literature, suggesting that intellectual functioning alone may not be a reliable determinant of catatonia risk in individuals with ASD. The prevalence of medical comorbidities was also comparable between individuals with and without catatonia (Wing and Shah 2000). Similarly, neither IQ level nor the presence of medical comorbidities was significantly associated with catatonia in the present sample. Although ID was not statistically associated with catatonia in our sample, the high proportion of participants with ID may limit the generalizability of prevalence estimates and clinical correlates to higher‐functioning ASD populations. Moreover, reduced communicative abilities in individuals with ID may increase reliance on observable motor and behavioural signs, potentially influencing the detection of catatonic features. Future studies including broader community‐based samples with a wider range of cognitive functioning are needed to clarify the role of ID in the presentation and identification of catatonia in ASD (Wing and Shah 2000; Dhossche et al. ²⁰¹²; Ghaziuddin et al. ²⁰¹²; Breen and Hare ²⁰¹⁷; Vaquerizo‐Serrano et al. ²⁰²²).

Previous research has reported that adolescents and adults with ASD and comorbid catatonia exhibit significantly higher rates of psychiatric comorbidities, particularly depression, anxiety and OCD (Breen and Hare 2017; Zingela et al. ²⁰²²; Öksüzoğlu et al. ²⁰²⁵). Although catatonia was more prevalent among participants with psychiatric comorbidities in the present study, this difference did not reach statistical significance. Nonetheless, the catatonia (+) group demonstrated higher levels of depressive symptoms and a greater prevalence of clinically significant separation anxiety symptoms compared with their catatonia (−) counterparts based on the parent‐report measures. The findings imply that enhancing clinicians' awareness and promoting a more refined clinical perspective could facilitate earlier identification of internalizing disorders, given the challenges individuals with ASD face in identifying and expressing emotional states and anxiety‐related issues during childhood and the overlapping clinical characteristics of autism, depression and anxiety.

In our study, clinically significant separation anxiety emerged as an important clinical correlate of catatonia. Previous research has consistently demonstrated a strong association between catatonia and anxiety symptoms in the ASD sample (Vaquerizo‐Serrano et al. ²⁰²²; Hasan et al. ²⁰²⁵). Alternatively, catatonia may present with prominent anxiety symptoms as part of its clinical manifestation (Northoff 2002; Fink and Taylor ²⁰⁰⁶; Zingela et al. ²⁰²²). Given that anxiety, fear and panic have been identified as psychological correlates of catatonia (Moskowitz 2004; Shorter and Fink ²⁰¹⁸; Zingela et al. ²⁰²²), it is plausible that such symptoms may have been reflected as separation anxiety features among ASD individuals, particularly in parent‐report assessments.

In 1949, Mahler described autism as ‘symbiotic infantile psychosis’ in children who appeared to make desperate efforts to avoid the overwhelming anxiety associated with separation (Mahler 1952). In fact, the association between ASD and SAD may, in part, be attributed to the characteristically reduced interest in social and affective relationships often observed in individuals with ASD (Pini et al. 2025). From this perspective, some ASD‐related characteristics, particularly those involving social engagement and dependence on familiar caregivers, may overlap with constructs measured by parent‐report instruments as separation anxiety.

Nevertheless, this interpretation does not preclude the presence of genuine anxiety symptoms. Indeed, recent studies suggest that individuals with ASD may be at increased risk of developing clinically significant separation anxiety due to heightened reliance on familiar caregiving environments, intolerance of uncertainty and increased need for predictability (Chan et al. 2023; Keshavarz and Esmaeilpour ²⁰²⁵). Therefore, the observed association between separation anxiety symptoms and catatonia may reflect both measurement overlap and true affective vulnerability within the ASD population. Furthermore, heightened sensory sensitivity may intensify the anxiety experienced during separation and social interactions, prompting individuals to seek consistency and predictability in their environment as a means of coping (Keshavarz and Esmaeilpour 2025). The reciprocal nature of this association implies that anxiety‐related problems can amplify catatonic manifestations, highlighting the importance of individualized treatment approaches that consider both the fundamental aspects of ASD and the associated psychiatric comorbidities (Wing and Shah 2000; Dhossche et al. ²⁰¹²).

Importantly, our findings extend prior work by demonstrating that separation anxiety emerged as an independent predictor of catatonia after accounting for core autistic features and other affective symptoms. Although previous studies have primarily focused on motor deterioration or general emotional dysregulation, the present results suggest a specific role for attachment‐related anxiety in the clinical expression of catatonia during adolescence. This novel observation highlights the potential relevance of separation anxiety as a clinically accessible marker for early identification and risk stratification and underscores the importance of incorporating affective dimensions into routine assessment of adolescents with ASD (Ghaziuddin et al. 2012; Breen and Hare ²⁰¹⁷; Vaquerizo‐Serrano et al. ²⁰²²).

5. Strengths and Limitations

This study has several notable strengths. It is one of the few investigations examining catatonia in adolescents with ASD using a large, clinically well‐characterized sample from a tertiary care setting. The combined use of DSM‐5 criteria and the BFCRS provided a rigorous and standardized approach to diagnosis, enhancing reliability and enhanced reliability. Multiple validated instruments were employed to assess ASD severity, repetitive behaviours and internalizing symptoms, providing a comprehensive clinical profile. The inclusion of detailed sociodemographic and family variables enabled the identification of contextual factors, such as family structure and parental education, that are rarely addressed in catatonia research. Finally, the multivariate regression analysis helped to distinguish independent predictors from simple associations, adding to the robustness and clinical relevance of the findings.

Despite its strengths, the present study is subject to certain limitations that warrant consideration. First, the cross‐sectional design limits causal inference between catatonia and associated factors. Second, the sample was recruited from a single tertiary care centre, potentially introducing referral bias and limiting generalizability to community populations. Third, reliance on parent‐reported measures of anxiety and depressive symptoms may be subject to informant bias, particularly in adolescents with communication difficulties. Additionally, the interpretation of RCADS‐P scores in adolescents with ASD and ID warrants caution. Certain items assessing internalizing symptoms, particularly those related to social withdrawal, avoidance or reduced social engagement, may overlap with core features of neurodevelopmental conditions rather than reflecting anxiety or depressive psychopathology alone. Consequently, some RCADS‐P scores may be influenced by baseline ASD‐related characteristics, potentially affecting the specificity of parent‐reported internalizing symptom measures in this population. Fourth, autism severity was evaluated using the GAS rather than autism‐specific standardized instruments validated for adolescents (e.g., Childhood Autism Rating Scale or Autism Diagnostic Observation Schedule), and this may have limited the precision of the severity assessment. Additionally, the omission of neurobiological assessments restricts conclusions about the underlying mechanisms of catatonia in ASD. Furthermore, clinically relevant variables such as IQ, psychiatric comorbidities and SES were not included in the logistic regression model due to the limited sample size and potential multicollinearity with other predictors. Although the regression analysis identifies significant associations, these factors may nonetheless influence the presence of catatonia and should be considered in future studies with larger samples.

Future research should include larger, multicentre samples with longitudinal follow‐up to clarify temporal relationships and causal mechanisms. Incorporating multi‐informant and clinician‐administered psychiatric assessments, as well as neurobiological and neuroimaging approaches, may further elucidate the pathophysiology of catatonia in ASD. Intervention trials targeting modifiable risk factors, such as anxiety, may also help inform prevention and management strategies.

6. Conclusions

Catatonia is a relatively common yet frequently under‐recognized condition among adolescents with ASD, characterized by distinct sociodemographic and clinical correlates. Clinicians should therefore carefully consider catatonia when evaluating skill regression or behavioural deterioration in this population. Female gender and separation anxiety symptoms emerged as key factors associated with catatonia, underscoring the need for gender‐sensitive and affect‐informed assessment approaches. Routine screening for catatonia in adolescents with ASD—particularly in those presenting with heightened anxiety or functional decline—may facilitate earlier detection. These findings support the integration of targeted affective screening alongside systematic monitoring of functional change relative to the developmental baseline within routine ASD follow‐up. Future longitudinal studies are warranted to clarify the developmental course of catatonia and the interplay between affective symptoms, autistic characteristics and functional decline in adolescents with ASD.

Funding

The authors have nothing to report.

Ethics Statement

Written informed consent was obtained from all participants and their parents or legal guardians prior to enrollment in the study. Participants and their caregivers were provided with detailed information regarding the study objectives, procedures, potential risks and benefits and were informed of their right to withdraw from the study at any time without any consequences. Participation was entirely voluntary. All procedures involving human participants were conducted in accordance with the ethical standards of the institutional and/or national research committee and with the principles of the Declaration of Helsinki. Ethics approval was obtained from the local ethics committee of the hospital (Ethics approval number: İ03‐181‐23).

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The data supporting these findings are not publicly accessible due to ethical restrictions but can be obtained upon reasonable request from the corresponding author.