Recurrent congenital cholesteatoma in autism spectrum disorder: A rare and complex case report and literature review

Autism spectrum disorder (ASD) is characterized by multifactorial etiology and high heritability but can be challenging to be diagnosed, especially in cases presenting subthreshold symptoms with no cognitive or language impairment, which may not be identified until adulthood but may occur in family members of subjects with ASD. This study explores the possible correlation between a genomic imbalance and clinical phenotypes in a family case of a proband with ASD, with subjects presenting full-blown or subthreshold ASD and/or mood disorders. Clinical assessments were carried out by means of the Structured Clinical Interview for DSM-5 (SCID-5) disorders, Autism Spectrum Quotient (AQ), Autism Diagnostic Interview–Revised (ADI-R), Autism Diagnostic Observation Schedule Module 2 (ADOS-2), and Adult Autism Subthreshold Spectrum (AdAS Spectrum). The genetic evaluation included array comparative genomic hybridization (array-CGH). The proband was diagnosed with ASD and bipolar disorder type I (BD-I), her twin brothers with ASD and intellectual disability (ID), and her father and sister with BD type II (BD-II) and autism traits. The proband, her father, twin brothers, and older sister showed a microduplication of 350 kb in 20q11.21. In contrast, the proband’s mother did not present the microduplication or any mental disorder. This study reports a microduplication that segregates with family members affected by ASD or autistic traits comorbid in some cases with bipolar disorder, and that has never been reported in healthy subjects. Among the genes harbored in this region, the TM9SF4 gene has been recently implicated in risk for ASD.

Amelioration of Aggression and Echolalia With Propranolol in Autism Spectrum Disorder

INTRODUCTION Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder that often presents before the child enters the educational system and is characterized by developmental deficits with impairments in three main areas [1] personal, [2] social, and [3] academic or occupational functioning. The neurodevelopmental disorders represent a group of conditions with an onset early in the developmental period. Sleep disorders are commonly reported by parents of children with an ASD diagnosis with between 50% to 80% of parents reporting sleep problems with their children. Problems can be categorized into dyssomnias (problems falling and/or remaining asleep) and parasomnias (abnormal and/or unnatural movements, behaviors, emotions, perceptions, and dreams).

Although the involvement of genetic abnormalities in autism spectrum disorders (ASD) is well-accepted, recent studies point to an equal contribution by environmental factors, particularly environmental toxicants. However, these toxicant-related studies in ASD have not been systematically reviewed to date. Therefore, we compiled publications investigating potential associations between environmental toxicants and ASD and arranged these publications into the following three categories: (a) studies examining estimated toxicant exposures in the environment during the preconceptional, gestational and early childhood periods; (b) studies investigating biomarkers of toxicants; and (c) studies examining potential genetic susceptibilities to toxicants. A literature search of nine electronic scientific databases through November 2013 was performed. In the first category examining ASD risk and estimated toxicant exposures in the environment, the majority of studies (34/37; 92%) reported an association. Most of these studies were retrospective case–control, ecological or prospective cohort studies, although a few had weaker study designs (for example, case reports or series). Toxicants implicated in ASD included pesticides, phthalates, polychlorinated biphenyls (PCBs), solvents, toxic waste sites, air pollutants and heavy metals, with the strongest evidence found for air pollutants and pesticides. Gestational exposure to methylmercury (through fish exposure, one study) and childhood exposure to pollutants in water supplies (two studies) were not found to be associated with ASD risk. In the second category of studies investigating biomarkers of toxicants and ASD, a large number was dedicated to examining heavy metals. Such studies demonstrated mixed findings, with only 19 of 40 (47%) case–control studies reporting higher concentrations of heavy metals in blood, urine, hair, brain or teeth of children with ASD compared with controls. Other biomarker studies reported that solvent, phthalate and pesticide levels were associated with ASD, whereas PCB studies were mixed. Seven studies reported a relationship between autism severity and heavy metal biomarkers, suggesting evidence of a dose–effect relationship. Overall, the evidence linking biomarkers of toxicants with ASD (the second category) was weaker compared with the evidence associating estimated exposures to toxicants in the environment and ASD risk (the first category) because many of the biomarker studies contained small sample sizes and the relationships between biomarkers and ASD were inconsistent across studies. Regarding the third category of studies investigating potential genetic susceptibilities to toxicants, 10 unique studies examined polymorphisms in genes associated with increased susceptibilities to toxicants, with 8 studies reporting that such polymorphisms were more common in ASD individuals (or their mothers, 1 study) compared with controls (one study examined multiple polymorphisms). Genes implicated in these studies included paraoxonase (PON1, three of five studies), glutathione S-transferase (GSTM1 and GSTP1, three of four studies), δ-aminolevulinic acid dehydratase (one study), SLC11A3 (one study) and the metal regulatory transcription factor 1 (one of two studies). Notably, many of the reviewed studies had significant limitations, including lack of replication, limited sample sizes, retrospective design, recall and publication biases, inadequate matching of cases and controls, and the use of nonstandard tools to diagnose ASD. The findings of this review suggest that the etiology of ASD may involve, at least in a subset of children, complex interactions between genetic factors and certain environmental toxicants that may act synergistically or in parallel during critical periods of neurodevelopment, in a manner that increases the likelihood of developing ASD. Because of the limitations of many of the reviewed studies, additional high-quality epidemiological studies concerning environmental toxicants and ASD are warranted to confirm and clarify many of these findings.

Evaluating Autism diagnosis agreement between primary care physicians/practitioners and experts through ECHO Autism STAT

Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are two frequently co-occurring neurodevelopmental conditions that share certain symptomatology, including social difficulties. This presents practitioners with challenging (differential) diagnostic considerations, particularly in clinically more complex cases with co-occurring ASD and ADHD. Therefore, the primary aim of the current study was to apply a data-driven machine learning approach (support vector machine) to determine whether and which items from the best-practice clinical instruments for diagnosing ASD (ADOS, ADI-R) would best differentiate between four groups of individuals referred to specialized ASD clinics (i.e., ASD, ADHD, ASD + ADHD, ND = no diagnosis). We found that a subset of five features from both ADOS (clinical observation) and ADI-R (parental interview) reliably differentiated between ASD groups (ASD & ASD + ADHD) and non-ASD groups (ADHD & ND), and these features corresponded to the social-communication but also restrictive and repetitive behavior domains. In conclusion, the results of the current study support the idea that detecting ASD in individuals with suspected signs of the diagnosis, including those with co-occurring ADHD, is possible with considerably fewer items relative to the original ADOS/2 and ADI-R algorithms (i.e., 92% item reduction) while preserving relatively high diagnostic accuracy. Clinical implications and study limitations are discussed.

IntroductionPsychotic disorders are significant comorbidities in young people with Autistic Spectrum Disorder (ASD). Evidence suggests that ASD & psychosis present with overlapping clinical features & cognitive symptoms leading to misdiagnosis (Trevisan et al. Front.Psych 2020;11:548). Clinicians encounter diagnostic dilemma during assessment of psychosis in adolescents with ASD.ObjectivesTo discuss the clinical challenges in the assessment & treatment of young people with ASD & comorbid psychosis.MethodsA case report of a young girl with ASD & comorbid psychotic illness.ResultsA young girl with ASD was admitted to CAMHS inpatient Unit with unusual beliefs & perceptual disturbances. She reported hearing the voice of ‘Hydrogis’ who was talking to her about his girlfriend. She made a voodoo doll & tried to set it on fire, as she believed that this would kill the girlfriend. She also heard voices of characters from a TV show, discussing her in third person. She absconded from home due to the distress associated. She attempted suicide by tying a ligature. She was seen responding to external stimuli, laughing incongruously & was thought disordered. Despite never being to USA, she spoke in American accent. She lacked insight & struggled to differentiate reality from fantasy. The aim of admission was to determine if the symptoms were part of ASD or a psychotic disorder. She had medication free assessment but continued to be very distressed. We commenced Aripiprazole which was optimised. She responded well to the treatment & was discharged to the care of Early Intervention in Psychosis team with partial remission of symptoms.ConclusionsHistorically psychotic illnesses & ASD were thought to be closely linked. Research suggest that they are two separate disorders with specific onset, progress, signs & symptoms. ASD might be misdiagnosed as psychosis as difficulties in communication may resemble thought disorder, ‘melt down’ may mimic catatonia & difficulties in recognising others’ intentions may mimic paranoia. Our patient was experiencing first episode psychosis in late adolescence. This age of onset is consistent with research findings. A study to differentiate between ASD & psychosis found that positive symptoms like hallucinations & delusions were suggestive of psychosis while odd emotional gestures, stereotyped speech & restricted interests indicated ASD. Our patient predominantly had positive symptoms of delusions, hallucinations & thought disorder, hence our diagnosis of psychotic episode. In some cases, it is difficult to differentiate childhood fantasies from delusional beliefs (Ribolsi et al. Front.Psych 2022;13:768586). Bleuler explains that children with ASD replace imperfect realities with imaginations & hallucinations but Michael Rutter claims that autistic children lack fantasy. There are varying views on this subject & this is the challenge we faced when treating this young person.Disclosure of InterestNone Declared

Introduction: Autism spectrum disorder (ASD) is a syndrome of social communication deficits and repetitive behaviors or restricted interests. While the impairments associated with ASD tend to deteriorate from childhood into adulthood, it is of critical importance that the syndrome is diagnosed at an early age. One means of facilitating this is through understanding how the brain of people with ASD develops from early childhood. Magnetic resonance imaging (MRI) is the method of choice for in vivo and non-invasive investigations of the morphology of the human brain, especially when the subjects are children. In this study, we conducted a systematic review of existing structural MRI studies that have investigated brain size in ASD children of up to 5 years old. Methods: In this study, we systematically reviewed published papers that describe research studies in which the brain size of ASD children has been examined. PubMed and Scopus databases were searched for all relevant original articles that described the use of MRI techniques to study ASD patients who were between 1 and 5 years old. To be included in the review, all studies needed to be cohort and case series that involved at least 10 patients. No time limitations were placed on the searched articles within the inclusion criteria. The exclusion criteria were non-English articles, case reports, and articles that described research involving subjects that were not within the qualifying age range of 1-5 years old.Result: After an initial screening process through which the title, abstracts, and full text of the articles were reviewed to confirm they met the inclusion criteria, a total of 10 relevant articles were studied in depth. All studies found that children with ASD who were within the selected age range had a larger brain size than children without ASD.Discussion: The findings of recent studies indicate that the vast majority of ASD patients exhibit an enlarged brain; however, the extent of the enlargement varies from study to study. As such, further studies are required to develop an understanding of the areas of the brain in which enlargement manifests in children with ASD before the age of five and to verify the significance of the prognostic value of MRI as a non-invasive diagnostic technique that can be employed to detect ASD in young children.Conclusion: Based on the extracted data, brain size was related to the emergence and presence of autism in children who were below school age. The use of MRI represents a functional and non-invasive method of confirming ASD in children who have an initial ASD diagnosis.

Introduction: Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by social interaction challenges, communication difficulties, and repetitive behaviors. While ASD lacks a cure, there is a growing interest in supplements, notably probiotics, for potential benefits. Probiotics are live microorganisms with health potential due to their role in the gut microbiome. Gut-brain axis is a bi-directional communication system that connects the gastrointestinal (GI) tract and the brain. Objective: This comprehensive review systematically searched scientific databases up to September 2023 to examine the use of supplements, particularly probiotics, in individuals with ASD. The review focused on addressing gut-related issues and improving behavior, speech, and overall well-being. Methods: A systematic search across databases such as PubMed, PsycINFO, and Cochrane library was conducted using keywords like "probiotics," "supplements," "ASD," "gut dysbiosis," and "therapeutic interventions." Studies meeting inclusion criteria, including clinical trials, observational studies, and case reports, were considered. Results: Several studies suggest that probiotics may improve behavior, brain activity, and eye contact in individuals with ASD by addressing gut dysbiosis. Lactobacillus reuteri and specific Bifidobacterium strains are recommended probiotics, but more research is needed to confirm their efficacy. This review also explores supplements like Vitamin B6, magnesium, Vitamin B12, Vitamin C, and Omega-3 fatty acids, which show potential in supporting speech and overall well-being in individuals with ASD. However, they are not a cure and should be used under professional guidance. The article also discusses supplements for adults with ASD, underlining the importance of consulting healthcare professionals before use and the necessity for further research to determine effectiveness and optimal dosages. Conclusion: Probiotics and supplements offer potential benefits for individuals with ASD, but they should be seen as complementary therapies rather than cures. A holistic approach, including medical supervision, therapy, and dietary considerations, is crucial for addressing the complex needs of individuals with ASD. Further research is necessary to uncover the precise mechanisms and therapeutic potential of these supplements in enhancing the lives of those with ASD. Categories: Neurology, Gastroenterology, Nutrition

Introduction: Autism spectrum disorder (ASD) is a neurodevelopmental disorder. The ADI-R and ADOS can be used to confirm ASD. These tools have not been tested in a non-sighted population.
 Through our clinical case, we highlight the clinical and therapeutic complexity of visually impaired children with ASD.
 Case report: A., 4 years and 7 months old, was admitted to the department for a diagnostic evaluation of a communication and language disorder concomitant with congenital blindness. At birth, bilateral anophthalmia was diagnosed. The complete pediatric evaluation was normal.
 After profound clinical observation, the diagnosis of ASD in comorbidity with congenital blindness was retained. The management was multidisciplinary.
 Discussion: ASD is the most clinically noted and scientifically studied disorder in visually impaired children. Specialists find difficulties in differentiating between the original developmental symptoms of visually impaired children and the symptoms relevant to ASD.
 Diagnostic investigation has been based on clinical observation. Several authors have demonstrated that careful observation can differentiate social interaction disorders caused by blindness from those of ASD.
 The treatment of children with ASD is essentially based on visual access to information, not adapted to ASD children with blindness.
 Conclusion: Blindness associated with ASD is a dual handicap. Validation of diagnostic instruments for ASD, developing appropriate therapeutic interventions for these patients are crucial.

Advances in genetics, molecular biology, and immunology over the past decades have significantly changed our understanding of the etiology and pathogenesis of autism spectrum disorders (ASD) in children. One of the key advances in this direction is the elucidation of the association of genetic deficiency of the folate cycle (GDFC) with ASD, evidence for which is based on the results of at least 5 meta-analyses of randomized controlled clinical trials and a number of additional controlled trials, the data of which have not yet been properly summarized. It has been established that GDFC leads to pathological biochemical changes in the child's body, which determine the development of encephalopathy with the clinical picture of ASD due to direct (metabolic) and indirect (immune-mediated) mechanisms, and immune-dependent pathways of cerebral damage are currently given a leading role in the pathogenesis of this mental disorder. Among the metabolic disorders induced by GDFC in the child's body, hyperhomocysteinemia, vitamin deficiencies, signs of mitochondrial dysfunction, and impaired nucleotide synthesis and DNA, protein, and lipid methylation processes are distinguished. These pathological biochemical changes lead to the development of persistent oxidative stress, as evidenced by the results of two systematic reviews and meta-analyses of randomized controlled clinical trials on this problem. The result of such disorders are the phenomena of neuro- and immunotoxicity, which underlie the above-mentioned direct and indirect mechanisms of neuronal damage in children with ASD. If we talk about immunotoxicity, it is currently established that in GDFC there is a disturbed development of the child's immune system with the formation of immune dysfunction and dysregulation, which, in turn, cause a phenomenon called a disturbed neuroimmune interface. It is believed that there are at least three main immune-mediated mechanisms of brain damage in GDFC, which can radically affect the development of associated encephalopathy with ASD symptoms. Neurotropic opportunistic and conditionally pathogenic infections, autoimmune reactions to neurons, myelin, glial cells of the cerebral hemispheres and cerebral vessels, systemic and associated intracerebral persistent aseptic inflammation mediated by existing immune dysregulation, constitute the indicated triad of key pathogenetic mechanisms of the development of ASD-forming encephalopathy in GDFC. Suppression or even eradication of these immune-dependent GDFC-induced pathways of CNS damage currently appears to be a promising prospect for effective treatment of ASD in children with GDFC. In particular, it is believed that the suppression of autoimmunity and neurons and myelin can significantly improve the mental functions of sick children. A number of clinical studies have already been conducted in this direction. In particular, clinical case reports and the results of small trials have shown the benefit of using glucocorticosteroids and some other anti-inflammatory agents in children with ASD, the mechanism of action of which is seen precisely in the implementation of anti-inflammatory action and suppression of anti-brain autoimmunity. At least 10 clinical studies have been conducted to test the immunomodulatory agent intravenous normal human immunoglobulin in ASD, which is believed to improve mental functions of patients by suppressing intracerebral inflammation and autoimmune reactions against brain autoantigens. Recently, infliximab, a monoclonal antibody against the tumor necrosis factor alpha molecule, has demonstrated efficacy in suppressing hyperactivity and hyperexcitability in children with ASD associated with GDFC in a controlled clinical trial. The prospect of developing new, more effective and safe methods of treating immune-mediated encephalopathy in children with ASD is an important task of modern neuroimmunology. Given that autoimmune reactions to CNS autoantigens in ASD are believed to be mainly mediated by autoantibodies rather than cellular autoimmune reactions, the monoclonal antibody to the CD20 molecule of B lymphocytes, rituximab, which has already undergone a number of successful trials in autoimmune diseases with a similar mechanism of development, seems promising for use in such children. Theoretically, by inducing B-cell depletion, rituximab can significantly suppress or even eliminate the production of autoantibodies to brain autoantigens in children with ASD, having a neuroprotective effect and thereby improving the mental status of patients. A dedicated clinical trial testing rituximab in children with ASD associated with GDFC and evidence of anti-brain humoral autoimmunity is needed.

Attention-Deficit/Hyperactivity Disorder (ADHD) and Autism Spectrum Disorder (ASD) are neurodevelopmental conditions which frequently co-occur. The Autism Diagnostic Observation Schedule (ADOS) is commonly used to aid with diagnostic assessment of ASD but was not originally designed for use in those with comorbid ADHD. Visual attention to social stimuli has been often studied in ASD using eye-tracking, to obtain quantitative indices of how attention is deployed to different parts of a social image/scene. As the ADOS includes tasks that rely on attending to and processing images of social scenes, these measures of visual attention could provide useful additional objective measurement alongside ADOS scores to enhance the characterisation of autistic symptoms in those with ADHD. Children with ASD, comorbid ASD and ADHD, ADHD and Neurotypical (NT) controls were recruited (n=84). Visual attention was measured using eye-tracking during free viewing of social scenes selected from the ADOS. The full ADOS was then administered. Stimulant medication was temporarily withdrawn during this assessment. Research diagnoses were based on the Development and Wellbeing Assessment (DAWBA), ADOS, Social Communication Questionnaire (SCQ, a measure of ASD severity) and Conners' Rating Scales (CRS-3, a measure of ADHD severity) following clinical consensus. Using factorial ANOVAs to model ADHD, Autism and their interaction, we found that fixation duration to faces was reduced in those with ASD (ASD and ASD+ADHD) compared to those without ASD (ADHD and NT). Reduced visual attention to faces in the whole sample was associated with Autism symptom severity (SCQ subscale scores) but not ADHD symptom severity (CRS-3 scores). Our findings provide preliminary evidence in support of implementing visual attention measurement during assessment of ASD in the context of comorbidity with ADHD. For example, if a child with ADHD was found to reduce attention to faces in ADOS pictures this may suggest additive difficulties on the autism spectrum. Replication across a larger sample would be informative. This work has future potential in the clinic to help with complex cases, including those with co-occurring ADHD and ASD.

To the Editors Our literature about catatonia, since the clinical designation of the condition in 1874, is drawn, with rare exception,1–4 from the scrutiny of hospitalized patients. Whether conclusions reached thereby represent catatonia in the world outside the hospital is almost untested, especially in adults. The current report is presented as a query of such conclusions in another population entirely, one of outpatients in a practice of general psychiatry. The record of every patient in the practice was surveyed; all evaluations were carried out by the author alone. Information about the means for diagnosis, the practice, and the community in which the latter is embedded is given in Supplemental Digital Content 1 (http://links.lww.com/JCP/A251). The total number of outpatients examined and observed during the study period is 298 (age, 16-89 y; mean and median, 46 y; 153 females and 145 males). Catatonia has been diagnosed at some time during the course of 8 (2.7%) of these: 4 men and 4 women aged 24 to 67 years at the time of diagnosis. In 2 instances, the diagnosis was made or suspected during the intake evaluation. In no patient had it been made earlier by another provider. In retrospect, it might have been made at intake in 2 of the patients but was not. In Table ​Table1,1, the characteristic features of catatonia are presented in 5 categories. The features were required to have had an onset, at that time to be new or considerably accentuated, to be considered catatonic. The diagnosis was difficult in only one instance, once it was considered, and here, a clear response to benzodiazepine was confirmatory. TABLE 1 Clinical Features Note the frequency with which catatonia is chronic (if the disorder is untreated or if benzodiazepine is not given coincidentally for another reason). In no patient for whom benzodiazepine was administered for catatonia was there a failure to respond, even if the features previously had waxed and waned chronically (benzodiazepine has been continued indefinitely in these patients, and a relapse that could not be relieved through dose adjustment did not occur in any of them); sometimes, considerable dose adjustment has been required (Case Report, Supplemental Digital Content 1 (http://links.lww.com/JCP/A251), and in 2 cases, the dose needed proved to be relatively high (lorazepam, total of 10 mg daily in 1 instance; diazepam, total of 30 mg daily in another). In the 2 patients with autism spectrum disorder (ASD) whose catatonia was of an acute pattern for whom benzodiazepine was tried and effective, the drug could be successfully tapered off some months later in 1 patient (severe environmental stress had been the triggering event for catatonia) and the other patient was lost to follow-up. Five of the 8 patients with catatonia are high school graduates (3 patients have an ASD). In 2 patients, the terminal degree is a bachelor’s degree (both patients have an ASD), and in 1 patient, it is a doctorate degree (the patient has an ASD); 1 is a graduate of a 2-year course in a community college. Four patients are employed; the fifth patient is a competent homemaker. The other 3 patients have mild or pronounced intellectual impairment (all patients have an ASD); none of the patients is employed gainfully enough for independent living. The most surprising finding within this report is the prevalence of ASD, or likely ASD, as the underlying or predisposing condition for catatonia: 6 of the 8 (Table ​(Table1).1). In none of the patients with ASD did catatonia emerge as a complication of depression. Autism spectrum disorder has been diagnosed or considered likely in 26 (9%) of the 298 patients in the practice, a diagnosis suspected before the patient entered the practice in only 3 patients. Catatonia has therefore complicated the course of 23% of these patients with ASD. A case report for 1 of the 8 patients, who has experienced both ASD and catatonia, is included in the Supplemental Digital Content 1 (http://links.lww.com/JCP/A251); it illustrates several of the observations previously described.

This comprehensive literature review summarizes reports on emergency department (ED) use by youth with autism spectrum disorder (ASD). We conducted a systematic search of the PubMed, PsycINFO, CINAHL, and EMBASE databases (1985-2016), limited to studies published in English. The following search terms were used: autism, autistic, Asperger, emergency department/room/physician/doctor/treatment/medicine, childhood developmental disorders (pervasive), and emergencies. Our search found 332 articles, of which 12 specifically addressed ED services in ASD youth. Abstracts or full text articles were reviewed for relevance. Case reports, review articles, and studies that reported on adults only or that included youth and adults but did not stratify results by age were excluded. Youth (aged 0-17 years) with ASD were up to 30 times more likely to present to the ED than youth without ASD. Individuals with ASD who visited the ED were older, more likely to have public insurance, and more likely to have nonurgent ED visits. For youth with ASD, up to 13% of visits were for behavioral or psychiatric problems, whereas for youth without ASD less than 2% were for psychiatric problems. ASD youth were more likely to present for externalizing problems or psychotic symptoms. Youth with ASD were also likely to have repeat visits to the ED and more likely to be admitted to a psychiatric unit or medical floor than youth without ASD. This review found significant gaps in the literature related to ED service use by youth with ASD. More research is needed to avoid unnecessary ED utilization and hospitalization, reduce medical costs, and improve outcome for youth with ASD.

The prevalence of traumatic dental injuries (TDI) in patients with autism spectrum disorders (ASD) remains unclear. Given these discrepancies, an updated review of the evidence on the risk of TDI in patients with ASD is essential. This systematic review and meta-analysis aimed to evaluate the prevalence of TDI in patients with ASD and compare it to that in neurotypical patients. This study protocol was registered on PROSPERO (CRD42024580127) and followed the Cochrane Handbook for Systematic Reviews of Interventions and PRISMA guidelines. A comprehensive search of four databases—MEDLINE/PubMed, Web of Science, Scopus, and Embase—was conducted for articles published up to August 2024. Moreover, the gray literature (ProQuest) and reference lists were screened. The inclusion criteria required participants with ASD to assess TDI across deciduous, mixed, and permanent dentition regardless of age. No restrictions were applied on TDI type, language, or publication date. Additionally, case reports, reviews, letters, and studies addressing other oral disorders without specific TDI data were excluded. A single-arm meta-analysis evaluated the cumulative proportion and 95% confidence interval (CI) of TDI in patients with ASD. Moreover, a comparative meta-analysis was performed to assess the risk of TDI between ASD and neurotypical patients, calculating the odds ratio (OR) with a 95% CI, and a p < 0.05 was deemed significant, using the R program. Quality assessment was performed using the National Heart, Lung, and Blood Institute tool, and the certainty of evidence was evaluated using GRADE. A total of 22 studies were included to determine the overall prevalence of TDI, of which 16 studies directly compared patients with ASD to neurotypical individuals. In total, 3817 participants were evaluated, including 2162 individuals with ASD and 1655 neurotypical patients. A single-arm meta-analysis estimated a TDI prevalence of 22% (Confidence Interval [CI]: 17–27%) among patients with ASD. A significant difference in the risk was observed between ASD and neurotypical patients (p = 0.003; Odds Ratio [OR]: 1.67; CI: 1.19–2.26). However, substantial heterogeneity was observed in this analysis. Although the majority of studies were rated as high quality, the certainty of the evidence was considered very low. Despite the limitations of this study, the findings suggest that patients with ASD are at a higher risk of developing TDI than the risk observed in neurotypical patients. Therefore, preventive educational initiatives are recommended to reduce the risk of TDI in this population.