Methylphenidate (MPH) is widely used to treat attention-deficit/hyperactivity disorder (ADHD) in children and adolescents. However, concerns persist about its potential to induce psychotic symptoms, including hallucinations. This study aimed to evaluate the association between MPH exposure and psychotic symptoms in children and adolescents using VigiBase®, the World Health Organization global pharmacovigilance database. We conducted a retrospective, observational study using disproportionality analysis on reports from children and adolescents (5-17 years) exposed to MPH and other ADHD drugs (amitriptyline, atomoxetine, clomipramine, clonidine, desipramine, guanfacine, and nortriptyline). Multivariate logistic regression was used to calculate adjusted reporting odds ratios (aRORs) of psychotic symptoms in MPH-exposed children and adolescents. Among 1,992 cases of psychotic symptoms, 1,232 were MPH-associated, with 51.7% classified as serious; significant disproportionalities were observed for the overall age range (aROR = 1.27; 95% confidence intervals [CI]: 1.15-1.40) and the 5-11 (children) age group (aROR = 1.35; 95%CI: 1.19-1.53). Of 1,250 hallucination cases, 809 were MPH-associated, with 59.2% serious; significant disproportionalities were found for the entire age range (aROR = 1.35; 95% CI: 1.19-1.52) and the children age group (aROR = 1.43; 95% CI: 1.23-1.67). The most common type of hallucination was visual (43.2%). MPH discontinuation or dose reduction led to a significantly higher rate of symptom abatement (88.6% of cases) compared to those without these measures (12.0%) (p < .001). These results suggest that MPH exposure in children is associated with an increased probability of serious psychotic symptoms, including hallucinations, which typically resolve with discontinuation or dose reduction. Further research is needed to better understand the MPH-induced psychotic symptoms.

Methylphenidate (MPD) is a widely prescribed psychostimulant used to treat behavioral disorders such as attention deficit hyperactivity disorder (ADHD), as well as for cognitive and memory enhancement across all age groups. In addition, MPD is often used—and abused—recreationally by adolescents, adults, and older individuals. The increasing use of MPD among healthy individuals has raised concerns regarding its potential neurological and behavioral consequences, including dependence and abuse. This study examines the behavioral and neuronal effects of MPD by simultaneously recording neural activity from three key monoaminergic brain regions—the locus coeruleus (LC), dorsal raphe nucleus (DR), and ventral tegmental area (VTA)—in freely behaving adolescent and adult rats. Recording electrodes were implanted in these regions, and both behavior and neural activity were recorded using a wireless telemetry system over ten consecutive days. Rats from each age group were assigned to one of the following five experimental groups: time control, saline control, or one of three MPD treatment groups receiving acute and repeated (chronic) doses of 0.6, 2.5, or 10.0 mg/kg. MPD was administered daily from experimental recording (ER) days 1 to 6 (ER1–6), followed by a three-day washout period (ER7–9), and a rechallenge with saline and MPD on ER10. A total of 2,679 neurons were recorded from 311 adolescent and adult male rats. The results revealed significant age- and brain region-dependent differences in both behavioral and neuronal responses to MPD. These findings emphasize the importance of considering both age and specific brain regions when evaluating the effects of psychostimulants. The data suggests that MPD differentially affects the noradrenergic, serotonergic, and dopaminergic systems in adolescents and adults. Furthermore, repeated MPD exposure produced dependency-like behavioral and neuronal patterns in both age groups, underscoring the need for caution in its therapeutic and non-therapeutic use.

ABSTRACT Background: Cocaine’s psychoactive effects arise primarily from dopamine transporter (DAT) inhibition. Prior trials suggest methylphenidate, a DAT inhibitor with pharmacologic overlap with cocaine, may reduce cocaine use, but real-world data are limited. Objectives: To evaluate whether methylphenidate exposure is associated with reduced likelihood of subsequent positive cocaine screens among veterans treated within the VA healthcare system. Methods: This retrospective cohort study used the Veterans Affairs Informatics and Computing Infrastructure (VINCI) to identify 109,608 patients with a positive cocaine screen. Among these patients 109,105 (103,535 male) had no methylphenidate exposure and 503 (458 male) were prescribed methylphenidate. Patients with methylphenidate were compared to unexposed patients and to an active comparator, bupropion. Baseline covariates included age, sex, ADHD, psychiatric and substance use disorders and comorbidities. Propensity score matching balanced groups and logistic regression models with generalized estimating equations estimated adjusted odds ratios (ORs) for a positive cocaine screen during one-year follow-up. Results: After matching, methylphenidate exposure was associated with lower odds of a follow-up positive cocaine screen compared with no exposure (OR = 0.71, 95% CI 0.51–0.98) and with bupropion (OR = 0.60, 95% CI 0.41–0.87). Conclusion: In this large real-world cohort of US veterans, methylphenidate exposure was significantly associated with a lower likelihood of subsequent cocaine detection. These results suggest that methylphenidate is a viable pharmacologic candidate for addressing cocaine use disorder, demonstrating superior outcomes in this population when compared to no exposure or the use of bupropion.

As attention-deficit/hyperactivity disorder (ADHD) is commonly diagnosed in childhood, methylphenidate (MPH) is the most widely prescribed treatment. Although effective for symptom management, concerns remain about an association with growth and body composition. To investigate the associations of the prevalence of ADHD and MPH use in childhood with body mass index (BMI) and height at adulthood (aged 20 to 25 years). In this nationwide retrospective cohort study, data of children aged 6 to 11 years and adolescents aged 12 to 19 years with newly diagnosed ADHD from the Korean National Health Insurance Service were included between January 2008 and December 2013. Exact matched controls of children and adolescents without ADHD were also included. Their cumulative medication exposure over a 4-year period was assessed, and their height and weight during adulthood were subsequently evaluated from January 2018 to December 2022. Data extraction and statistical analyses were conducted from November 2024 to May 2025. Diagnosis with ADHD and MPH prescriptions (cumulative days of MPH use, <1 year or 1 to 4 years, within 4 years after the diagnosis). The primary outcomes were BMI (calculated as weight in kilograms divided by height in meters squared) and height (in centimeters) at adulthood, assessed as continuous variables (crude mean [SD] and adjusted mean [95% CI]) and binary outcomes (adjusted odds ratio [AOR] [95% CI]). Measures for being overweight and obese were a BMI of 25 or more for males and 23 or more for females; measures for having short stature were a mean (SD) less than 174.4 [5.5] cm for males and less than 161.8 [5.3] cm for females. In this cohort study of 34 850 youths (n = 12 866 prepubertal children aged 6-11 years; mean [SD] age, 9.3 [1.4] years; 9329 males [72.5%]; and n = 21 984 adolescents aged 12-19 years; mean [SD] age, 14.5 [1.8] years; 14 633 males [66.6%]), prepubertal children with ADHD compared with those without ADHD had a higher adjusted mean BMI (24.3 [95% CI, 24.2-24.4 vs 23.3 [95% CI, 23.2-23.4]; P < .001) but not a significantly shorter height (167.8 cm [95% CI, 167.7-167.9 cm] vs 167.9 cm [95% CI, 167.8-168.0 cm]; P = .10) at adulthood. Those with ADHD who received MPH therapy compared with participants without ADHD had greater odds of a BMI classified as overweight and obese (AOR, 1.60 [95% CI, 1.51-1.71]; P < .001) and short stature (AOR, 1.08 [95% CI, 1.02-1.15]; P = .01) at adulthood. In this cohort study, patients with ADHD, particularly those treated with MPH, had a higher BMI and shorter height at adulthood than individuals without ADHD. Although the observed height difference was clinically small in both sexes and age groups, the findings suggest that long-term MPH exposure may be associated with growth and body composition, highlighting the need for regular monitoring of growth.

Chronic methylphenidate abuse: Effects on behaviour, redox homeostasis, and cholinergic system.

Psychostimulants have been recommended as first-line therapy for attention-deficit/hyperactivity disorder (ADHD), and safety concerns related to cardiovascular events in psychostimulant users have attracted increasing attention. However, evidence remains limited regarding the cardiovascular risks associated with methylphenidate use in children and adolescents who have heart disease or a family history of cardiovascular conditions. We conducted a self-controlled case series (SCCS) study using Taiwan's nationwide insurance database (2004-2021), which links data from births registered in the National Health Insurance system. A total of 2,493 individuals with ADHD, at least one methylphenidate prescription, and incident cardiovascular disease (CVD) were enrolled. A stratified Cox regression model adjusted for time-varying confounders was used to estimate the relative risks (RRs) of arrhythmias, ischaemic heart disease, and cerebrovascular disease during methylphenidate exposure compared with those during unexposed periods. Effect modification by congenital heart disease and family history of CVD was also assessed. We found a significantly increased risk of arrhythmias during both the exposed period (RR: 1.41, 95% CI (Confidence Interval): 1.21-1.63) and the pre-exposed period (RR: 1.50, 95% CI: 1.15-1.96). No significant association was observed between methylphenidate use and the risk of ischaemic heart disease (RR: 0.86, 95% CI: 0.49-1.50) or cerebrovascular disease (RR: 0.79, 95% CI: 0.45-1.39). A family history of CVD did not affect cardiovascular risk. However, individuals with congenital heart diseases had an elevated risk of arrhythmias during the pre-exposed period (RR: 3.19, 95% CI: 1.47-6.94) but not during the exposed period. These findings suggest that methylphenidate use is not significantly associated with ischaemic heart disease or cerebrovascular events in ADHD youth, even those with a family history of CVD or congenital heart diseases. The relationship between methylphenidate and the increased risk of arrhythmias during both the exposed and pre-exposed periods needs further investigation.

Methylphenidate (Ritalin) induces neuroinflammation. Besides, antioxidant properties of Tribulus terrestris (Tt) are approved biochemically. This study aimed to assess the protective effects of Tt on fetal neuroinflammation caused by maternal Methylphenidate exposure. Methylphenidate was prepared in two high (50 mg/kg) and low (10 mg/kg) doses and Tt extract (100 mg/kg) was also obtained for treatment. 36 adult female Wistar rats were categorized into six groups and were enrolled for mating. Pregnant rats were treated with Tt (orally) and followed by Methylphenidate exposure (orally) for 21 days. On day 22, maternal serum sample (assessment of GPx, MDA, TAC, IL-1, and IL-10) and fetal tissue samples (brain staining of H&E, LFB, and Nissl, morphometry, and anti-inflammatory genes expression of TNF-α and IL-1β) were collected. Finally, data were analyzed by SPSS v.16 (p-value < 0.05). Phytochemically, Tt was found to be highly rich in antioxidant agents. Maternal exposure to Methylphenidate caused high oxidative stress levels (GPx and MDA) and low TAC in blood serum (p < 0.05). In this regard, following Tt administration, maternal oxidative stress was decreased (p < 0.05) to physiological status. Following maternal Methylphenidate exposure, the size of embryos and anti-inflammatory gene expression were decreased (p < 0.05); besides, vast neuroinflammation and neural cell apoptosis were detected, histologically. In these groups, treatment with Tt caused an acceleration in fetus sizes and anti-inflammatory gene expression, along with a decrease in neuro-inflammation were approved (p < 0.05). Maternal Methylphenidate exposure in higher doses induces embryo abortion. While in lower doses, teratogenic effects were approved. Tt can potentially cause physiological embryogenesis with mothers exposed to Methylphenidate.

The increasing use of Methylphenidate (MPD) among adolescents and adults raises important concerns regarding its developmental and long-term neurophysiological effects. This study examined behavioral and neuronal responses in the Locus Coeruleus (LC)—a critical hub for Norepinephrine (NE) signaling—following administration of various MPD doses in adolescent and adult rats. Four experimental groups were used for each age cohort: saline, 0.6, 2.5, and 10.0 mg/kg MPD. Animals received six consecutive daily MPD injections from Experimental Days (ED) 1 to 6, followed by a threeday washout period and a single rechallenge dose on ED10. A total of 174 adolescent and 157 adult rats were used for concurrent behavioral assessments, while LC neuronal activity was recorded from 409 and 461 neurons, respectively. Significant age-dependent differences emerged in both acute and chronic responses to MPD. As the MPD dose increased, a greater number of rats and LC neurons exhibited altered activity. Notably, some animals displayed behavioral and neuronal sensitization at all MPD doses, whereas others exhibited tolerance. These effects varied significantly between age and MPD groups in both magnitude and incidence. Furthermore, Baseline (BL) LC activity following the six-day MPD regimen and after the washout period (ED10) was markedly altered, particularly in adolescents, indicating withdrawal-related changes. These shifts in BL activity from ED1 to ED10 indicate the presence of withdrawal behavior. This study highlights clear age-dependent differences in response to chronic MPD exposure. The observed patterns of sensitization, tolerance, and withdrawal serve as potential experimental biomarkers for drug dependence, emphasizing the clinical relevance of these findings. Importantly, the results underscore the value of combining electrophysiological and behavioral analyses and reaffirm the central role of the LC and NE signaling in mediating MPD’s effects, with distinct implications for adolescent and adult populations

Age-dependent effects of cumulative methylphenidate exposure on brain structure and symptom amelioration in youth with ADHD: A longitudinal MRI study.

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder that is widely observed from childhood to adulthood and is treated with methylphenidate (MPH) as a first-line treatment. However, recent findings indicate that the paternal environment preceding conception may influence offspring health, potentially affecting subsequent generations. Moreover, we previously reported that MPH administration to sires reduced anxiety-related behaviors and induced memory impairments in the F1 generation. Therefore, in the present study, we investigated the effects of MPH exposure to sires on development, behavior, and brain gene expression in the F2 generation to extend our previous findings and examine the range of transgenerational effects. Although MPH exposure did not affect the number of births or survival rates, the body weight of mice in the MPH group was significantly lower than those in the control group. Additionally, motor development showed transient delays in early development but normalized by the age of weaning. Behavioral analysis further revealed a pronounced reduction in anxiety-like behaviors in the MPH group, particularly in female mice, with no effect on learning or memory. Finally, transcriptome analysis of the female cortex predicted the activation of neuroplasticity-related pathways, including the S100 family and CREB signaling. Notably, MPH was not administered to male F1 mice whose fathers had been administered MPH. Therefore, the ova of females mated with F1 males were not exposed to MPH. Nevertheless, the confirmation of behavioral abnormalities in the F2 generation strongly suggests that these abnormalities may have been induced by epigenetic changes in germ cells.

The effects of methylphenidate, a stimulant often prescribed for the treatment of attention-deficit/hyperactivity disorder (ADHD), on the development of central nervous system oxygen toxicity (COT) have not been experimentally evaluated. The records of all pure-oxygen-rebreather divers evaluated at our institution from 1975-2022 were assessed. Cases of COT were defined as a new onset of tinnitus, tunnel vision, myoclonus, headache, nausea, loss of consciousness, or seizures resolving within 15 minutes from breathing normobaric air, and matched 4:1 with similar controls. Any medications issued to the diver in the preceding three months, including methylphenidate, were recorded. In the animal arm of this study, male mice were exposed to increasing doses of methylphenidate orally, with subsequent exposure to hyperbaric O₂ until clinically evident seizures were recorded. Seventy-five cases of COT were identified in divers, occurring at a median of 80 (range 2-240) minutes after dive initiation at a median depth of 5 m (2-13). Hypercarbia was documented in 11 (14.7%) cases. Prescription of methylphenidate in the preceding three months was not associated with increased risk (OR 0.72, 95% CI 0.16-3.32) of COT. In mice, increasing methylphenidate exposure dose was associated with significantly longer mean COT latency time being 877 s (95% CI 711-1,043) with doses of 0 mg·kg⁻¹; 1,312 s (95% CI 850-1,773) when given 0.75 mg·kg⁻¹; and 1,500 s (95% CI 988-2,012) with 5 mg·kg⁻¹ (F = 4.635, P = 0.014). Observational human data did not demonstrate an association between methylphenidate and an increased risk of COT. Methylphenidate exposure in mice prolongs COT latency and may have protective effects against COT.

Methylphenidate (MPD) remains a cornerstone pharmacological intervention for managing ADHD, yet its increasing usage among ordinary youth and adults outside clinical contexts necessitates a thorough investigation into its developmental effects. This study seeks to simultaneously investigate the behavioral and neuronal changes within the dorsal raphe (DR) nucleus, a center of serotonergic neurons in the mammalian brain, before and after the administration of varying doses of acute and chronic MPD in freely behaving young and adult rats implanted with DR recording electrodes. Wireless neuronal and behavioral recording systems were used over 10 consecutive experimental days. Eight groups were examined: saline, 0.6, 2.5, and 10.0 mg/kg MPD for both young and adult rats. Six daily MPD injections were administered on experimental days 1 to 6, followed by a three-day washout period and MPD re-administration on experimental day 10 (ED10). The analysis of neuronal activity recorded from 504 DR neurons (DRNs) in young rats and 356 DRNs in adult rats reveals significant age-dependent differences in acute and chronic MPD responses. This study emphasizes the importance of aligning electrophysiological evaluations with behavioral outcomes following extended MPD exposure, elucidating the critical role of DRNs and serotonin signaling in modulating MPD responses and delineating age-specific variations in young versus adult rat models.

Effects of methylphenidate on mitochondrial dynamics and bioenergetics in the prefrontal cortex of juvenile rats are sex-dependent

A total of 3102 neurons were recorded before and following acute and chronic methylphenidate (MPD) administration. Acute MPD exposure elicits mainly increases in neuronal and behavioral activity in dose-response characteristics. The response to chronic MPD exposure, as compared to acute 0.6, 2.5, or 10.0 mg/kg MPD administration, elicits electrophysiological and behavioral sensitization in some animals and electrophysiological and behavioral tolerance in others when the neuronal recording evaluations were performed based on the animals' behavioral responses, or amount of locomotor activity, to chronic MPD exposure. The majority of neurons recorded from those expressing behavioral sensitization responded to chronic MPD with further increases in firing rate as compared to the initial MPD responses. The majority of neurons recorded from animals expressing behavioral tolerance responded to chronic MPD with decreases in their firing rate as compared to the initial MPD exposures. Each of the six brain areas studied-the ventral tegmental area, locus coeruleus, dorsal raphe, nucleus accumbens, prefrontal cortex, and caudate nucleus (VTA, LC, DR, NAc, PFC, and CN)-responds significantly (p < 0.001) differently to MPD, suggesting that each one of the above brain areas exhibits different roles in the response to MPD. Moreover, this study demonstrates that it is essential to evaluate neuronal activity responses to psychostimulants based on the animals' behavioral responses to acute and chronic effects of the drug from several brain areas simultaneously to obtain accurate information on each area's role in response to the drug.

Use of medications for attention-deficit/hyperactivity disorder (ADHD) during pregnancy is increasing in the US. Whether exposure to these medications in utero impacts the risk of neurodevelopmental disorders in children is uncertain. To evaluate the association of childhood neurodevelopmental disorders with in utero exposure to stimulant medications for ADHD. This cohort study included health care utilization data from publicly insured (Medicaid data from 2000 to 2018) and commercially insured (MarketScan Commercial Claims Database data from 2003 to 2020) pregnant individuals aged 12 to 55 years in the US with enrollment from 3 months prior to pregnancy through 1 month after delivery, linked to children. Children were monitored from birth until outcome diagnosis, disenrollment, death, or end of the study (December 2018 for Medicaid and December 2020 for MarketScan). Dispensing of amphetamine/dextroamphetamine or methylphenidate in the second half of pregnancy. Autism spectrum disorder, ADHD, and a composite of any neurodevelopmental disorder were defined using validated algorithms. Hazard ratios were estimated comparing amphetamine/dextroamphetamine and methylphenidate to no exposure. The publicly insured cohort included 2 496 771 stimulant-unexposed, 4693 amphetamine/dextroamphetamine-exposed, and 786 methylphenidate-exposed pregnancies with a mean (SD) age of 25.2 (6.0) years. The commercially insured cohort included 1 773 501 stimulant-unexposed, 2372 amphetamine/dextroamphetamine-exposed, and 337 methylphenidate-exposed pregnancies with a mean (SD) age of 31.6 (4.6) years. In unadjusted analyses, amphetamine/dextroamphetamine and methylphenidate exposure were associated with a 2- to 3-fold increased risk of the neurodevelopmental outcomes considered. After adjustment for measured confounders, amphetamine/dextroamphetamine exposure was not associated with any outcome (autism spectrum disorder: hazard ratio [HR], 0.80; 95% CI, 0.56-1.14]; ADHD: HR, 1.07; 95% CI, 0.89-1.28; any neurodevelopmental disorder: HR, 0.91; 95% CI, 0.81-1.28). Methylphenidate exposure was associated with an increased risk of ADHD (HR, 1.43; 95% CI, 1.12-1.82]) but not other outcomes after adjustment (autism spectrum disorder: HR, 1.06; 95% CI, 0.62-1.81; any neurodevelopmental disorder: HR, 1.15; 95% CI, 0.97-1.36). The association between methylphenidate and ADHD did not persist in sensitivity analyses with stricter control for confounding by maternal ADHD. The findings in this study suggest that amphetamine/dextroamphetamine and methylphenidate exposure in utero are not likely to meaningfully increase the risk of childhood neurodevelopmental disorders.

Currently, methylphenidate (MPD) is one of the most commonly prescribed psychostimulants for management and treatment of attention deficit hyperactivity disorder (ADHD). A rise in the consumption of MPD by “ordinary” youth and adults prompted concern regarding the ontogeny effects of acute and chronic MPD exposure. The objective of this study is to concomitantly record behavioral and neuronal activity from the dorsal raphe (DR) nucleus, a major source of serotonergic innervation in the mammalian brain before and following different doses of acute and chronic administration of MPD in freely behaving adolescent (young) and adult rats previously implanted with electrodes in the DR. A wireless recording system over 10 consecutive experimental days was used. Four experimental groups were used: saline, 0.6, 2.5, and 10.0 mg/kg MPD for young and similar groups for adult rats. Animals received one daily MPD injection on experimental days 1-6, followed by three washout days, and then drug rechallenge on experimental day 10 (ED10). 860 DR units were recorded, 356 from adult rats and 504 from young rats. The study provides experimental evidence that the responses to acute and chronic MPD were significantly different between the two age groups. Moreover, the study implies that it is essential to evaluate the electrophysiological responses to a drug based on the animal’s behavioral response to chronic drug exposure and that the DR and serotonin signaling has a significant role in the response to MPD as well as a different role in young as compared to adult rats.

Objective: To investigate the association between atomoxetine or methylphenidate use and arrhythmia, heart failure (HF), stroke, and myocardial infarction (MI) in attention-deficit/hyperactivity disorder (ADHD) patients mainly focused on the people of working age. Methods: In a self-controlled case series study using a Japanese claims database, we identified events of arrhythmia, HF, stroke, and MI among 15,472 atomoxetine new users and 12,059 methylphenidate new users. Adjusted incidence rate ratios (aIRRs) of outcome events were estimated using multivariable conditional Poisson regression. Results: An increased risk of arrhythmia was observed during the first 7 days after the initial atomoxetine exposure (aIRR 6.22, 95% CI [1.90, 20.35]) and in the subsequent exposure (3.23, [1.58, 6.64]). No association was found between methylphenidate exposure and arrhythmia, nor between atomoxetine or methylphenidate exposure and HF. The limited number of stroke and MI cases prevented thorough analysis. Conclusions: Clinicians should consider monitoring for arrhythmia after patients initiating or re-initiating atomoxetine.

Methylphenidate exposure in juvenile period elicits locomotion changes and anxiolytic-like behavior in adulthood: Evidence using zebrafish as a translational model

Introduction: Given the increasing adult use of amphetamine and methylphenidate and their high misuse potential, we examined suspected suicide attempts and other intentional misuse and medical outcomes and their associations with co-used other substances among amphetamine and methylphenidate exposure cases aged 50+. Methods: Using the 2015–2021 U.S. National Poison Data System (N = 7701 amphetamine and/or methylphenidate cases), we fit two generalized linear models for a Poisson distribution with a log link function, with suspected suicide attempt versus intentional misuse and major medical effect/death versus other outcomes as the dependent variables. Results: Of all amphetamine/methylphenidate exposure cases, suspected suicide attempts and intentional misuse were 28.4% and 13.2%, respectively. Benzodiazepine use was associated with a higher likelihood, but any illicit drug use was associated with a lower likelihood of suspected suicide attempts compared to intentional misuse. The type of stimulant involved (amphetamine or methylphenidate) was not significant. The co-use of antidepressants (IRR = 1.43, 95% CI = 1.16–1.76), prescription opioids (IRR = 1.48, 95% CI = 1.21–1.81), drugs for cardiovascular disease (IRR = 1.51, 95% CI = 1.20–1.90), antipsychotics (IRR = 1.26, 95% CI = 1.02–1.55), or illicit drugs (IRR = 2.40, 95% CI = 1.82–3.15) was associated with a higher likelihood of major effect/death. Conclusions: Suspected suicide attempts or intentional misuse accounted for more than 40% of amphetamine or methylphenidate exposure cases aged 50+. The higher likelihood of major effect/death in cases involving antidepressants, antipsychotics, and cardiovascular disease drugs also suggests the confounding effects of comorbid mental and physical health problems. Careful monitoring of those who were prescribed amphetamine or methylphenidate and use other substances is needed.

Effects of methylphenidate on femoral bone growth in male rats.