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PubMed2004

An open-label pilot study of methylphenidate in the treatment of cocaine dependent patients with adult attention deficit/hyperactivity disorder.

A multi-site, open-label study of methylphenidate for treating patients with comorbid diagnoses of attention deficit/hyperactivity disorder and cocaine dependence was performed. Forty-one participants, who met DSM-IV criteria for adult attention deficit/hyperactivity disorder and cocaine dependence, were enrolled into this ten week outpatient study. The targeted total daily dose of methylphenidate was 60 mg (20 mg TID). Participants received individual substance abuse therapy throughout the trial. Safety measures included adverse events, vital signs, and electrocardiograms. Methylphenidate's efficacy was assessed by both objective and subjective measures. Seventy percent of the participants completed final study measures. Safety measures indicated that methylphenidate was well tolerated by the participants. Subjective efficacy measures suggested that participants evidenced improvement in both cocaine dependence and adult attention deficit/hyperactivity disorder symptoms. Quantitative benzoylecgonine indicated that only those participants categorized as being compliant showed improvement. A double-blind, placebo-controlled study of methylphenidate for this population may be warranted.

Adult↗
PubMedDate not supplied

Potential interactions of methylphenidate and atomoxetine with dextromethorphan.

OBJECTIVE: To examine the potential for drug-drug interactions to influence drug metabolism between the attention-deficit/hyperactivity disorder (ADHD) dl-methylphenidate and atomoxetine with dextromethorphan, a probe for interactions involving cytochrome P450 (CYP) 2D6 isoenzyme. DESIGN: In vitro and ex vivo analysis of changes in metabolism of study drugs. SETTING: Laboratory. PATIENTS: Not applicable. INTERVENTIONS: Pooled human liver microsomal fractions prepared at CEDRA Corporation (now CellzDirect, Austin, Tex.) by the standard differential centrifugation method (lot 821-1). Human liver microsomes were pooled from 15 donors. Recombinant CYP 2D6-containing microsomes (Supersomes; lots 20 and 24 BD Gentest; Woburn, Mass.) were prepared from a baculovirus-infected insect cell line that expressed only the human CYP 2D6 isoform. Dextromethorphan, with and without effector, was incubated with pooled human liver and recombinant CYP 2D6-containing microsomes. Atomoxetine and dl-methylphenidate were tested at 0.1x, 1x, and 10x their reported therapeutic concentrations. Paroxetine, a known inhibitor of CYP 2D6, was used as a reference agent, and quinidine was used as a positive control inhibitor of CYP 2D6. MAIN OUTCOME MEASURES: Changes in substrate metabolism indicative of CYP 2D6-mediated interactions. RESULTS: Atomoxetine and paroxetine inhibited the formation of dextrorphan by about 50% in human liver microsomes and by more than 80% in recombinant microsomes; the profiles of atomoxetine and the known 2D6 inhibitor paroxetine were similar. High concentrations of dextromethorphan reversed the inhibition of its metabolism, indicating a competitive mechanism of the interaction. Conversely, dextromethorphan and dextrorphan only modestly inhibited atomoxetine and paroxetine metabolism. dl-Methylphenidate did not inhibit dextrorphan formation in either microsome preparation, and dl-methylphenidate metabolism was unaffected by dextromethorphan or dextrorphan. CONCLUSION: These results demonstrate the potential for in vivo interactions between dextromethorphan and atomoxetine in patients with ADHD. However, they do not support the plausibility of an in vivo interaction between dextromethorphan and dl-methylphenidate.

Adrenergic Uptake Inhibitors↗
PubMed2005

Use of methylphenidate in traumatic brain injury.

OBJECTIVE: To review literature regarding the effectiveness of methylphenidate in the management of the cognitive and behavioral changes observed following traumatic brain injury (TBI). DATA SOURCES: A literature search was conducted using the following databases: MEDLINE (1966-June 2004); Cochrane Central Register of Controlled Trials, fourth quarter 2004 (1988-June 2004); and International Pharmaceutical Abstracts (1970-June 2004). Methylphenidate and brain injury were the key search terms used. Limits were set to include clinical trial publications, human subjects, and English language. DATA SYNTHESIS: Ten clinical trials evaluating the efficacy and safety of methylphenidate in pediatric and adult patients with TBI are reviewed. Improvements in different aspects of cognition and behavior were evaluated before, during, and after treatment with methylphenidate. The results demonstrated that methylphenidate is likely to improve memory, attention, concentration, and mental processing, but its effects on behavior have not been determined. CONCLUSIONS: Larger, double-blind, placebo-controlled studies are needed to determine optimal doses, during which phase of recovery to begin treatment, length of treatment, and long-term effects for patients with mild, moderate, and severe TBI.

Brain Injuries↗
PubMed2005

Activation of orbital and medial prefrontal cortex by methylphenidate in cocaine-addicted subjects but not in controls: relevance to addiction.

Drugs of abuse are rewarding to addicted and nonaddicted subjects, but they trigger craving and compulsive intake only in addicted subjects. Here, we used positron emission tomography (PET) and [18F] deoxyglucose to compare the brain metabolic responses (marker of brain function) of cocaine-addicted subjects (n = 21) and controls (n = 15) to identify brain regions that are uniquely activated in addicted subjects by intravenous methylphenidate (a drug that cocaine-addicted subjects report to be similar to cocaine). In parallel, we also measured the changes in dopamine (DA) induced by intravenous methylphenidate (using PET and [11C] raclopride) in the striatum and in the thalamus. Metabolic responses between groups differed significantly only in the right medial orbital prefrontal cortex [Brodmann's area (BA) 25 and medial BA 11], where methylphenidate increased metabolism in addicted subjects but decreased metabolism in controls. These changes were associated in all subjects with increased "desire for methylphenidate" and in the addicted subjects with "cocaine craving." In addicted subjects, increases in BA 25 were also associated with mood elevation. Methylphenidate-induced increases in metabolism in the medial orbital prefrontal cortex were associated with its increase of DA in the thalamus but not in the striatum. These findings provide evidence that enhanced sensitivity of BA 25 (region involved with emotional reactivity) and BA 11 (region involved with salience attribution and motivation) in cocaine-addicted subjects may underlie the strong emotional response to the drug and the intense desire to procure it that results in craving and compulsive drug intake. It also suggests that the mesothalamic DA pathway may contribute to these processes.

Adult↗
PubMed2006

Relative benefits of stimulant therapy with OROS methylphenidate versus mixed amphetamine salts extended release in improving the driving performance of adolescent drivers with attention-deficit/hyperactivity disorder.

OBJECTIVE: Automobile accidents are the leading cause of death among adolescents, and collisions are 2 to 4 times more likely to occur among adolescents with attention-deficit/hyperactivity disorder. Studies have demonstrated that stimulants improve driving performance. This study compared 2 long-acting stimulant medications during daytime and evening driving evaluations. METHODS: Adolescent drivers with attention-deficit/hyperactivity disorder were compared on a driving simulator after taking 72 mg of OROS methylphenidate, 30 mg of mixed amphetamine salts extended release, or placebo in a randomized, double-blind, placebo-controlled, crossover study design. During laboratory testing, adolescents drove a driving simulator at 5:00 pm, 8:00 pm, and 11:00 pm. Driving performance was rated by adolescents and investigators. RESULTS: The study included 35 adolescent drivers with attention-deficit/hyperactivity disorder (19 boys/16 girls). The mean age was 17.8 years. The overall Impaired Driving Score demonstrated that OROS methylphenidate led to better driving performance compared with placebo and mixed amphetamine salts extended release, whereas mixed amphetamine salts extended release demonstrated no statistical improvement over placebo. Specifically, relative to placebo, OROS methylphenidate resulted in less time driving off the road, fewer instances of speeding, less erratic speed control, more time executing left turns, and less inappropriate use of brakes. OROS methylphenidate and mixed amphetamine salts extended release worked equally well for male and female adolescents and equally as well with teenagers who have combined and inattentive subtypes of attention-deficit/hyperactivity disorder. CONCLUSIONS: This study validates the use of stimulants to improve driving performance in adolescents with attention-deficit/hyperactivity disorder. In the study, OROS methylphenidate promoted significantly improved driving performance compared with placebo and mixed amphetamine salts extended release.

Accidents, Traffic↗
PubMed2004

Polymorphisms of the dopamine transporter gene: influence on response to methylphenidate in attention deficit-hyperactivity disorder.

Attention deficit-hyperactivity disorder (ADHD) is a very common and heterogeneous childhood-onset psychiatric disorder, affecting between 3% and 5% of school age children worldwide. Although the neurobiology of ADHD is not completely understood, imbalances in both dopaminergic and noradrenergic systems have been implicated in the origin and persistence of core symptoms, which include inattention, hyperactivity, and impulsivity. The role of a genetic component in its etiology is strongly supported by genetic studies, and several investigations have suggested that the dopamine transporter gene (DAT1; SLC6A3 locus) may be a small-effect susceptibility gene for ADHD. Stimulant medication has a well-documented efficacy in reducing ADHD symptoms. Methylphenidate, the most prescribed stimulant, seems to act mainly by inhibiting the dopamine transporter protein and dopamine reuptake. In fact, its effect is probably related to an increase in extracellular levels of dopamine, especially in brain regions enriched in this protein (i.e. striatum). It is also important to note that dopamine transporter densities seem to be particularly elevated in the brain of ADHD patients, decreasing after treatment with methylphenidate. Altogether, these observations suggest that the dopamine transporter does play a major role in ADHD. Among the several polymorphisms already described in the SLC6A3 locus, a 40 bp variable number of tandem repeats (VNTR) polymorphism has been extensively investigated in association studies with ADHD. Although there are some negative results, the findings from these reports indicate the allele with ten copies of the 40 bp sequence (10-repeat allele) as the risk allele for ADHD. Some investigations have suggested that this polymorphism can be implicated in dopamine transporter gene expression in vitro and dopamine transporter density in vivo, even though it is located in a non-coding region of the SLC6A3 locus. Despite all these data, few studies have addressed the relationship between genetic markers (specifically the VNTR) at the SLC6A3 locus and response to methylphenidate in ADHD patients. A significant effect of the 40 bp VNTR on response to methylphenidate has been detected in most of these reports. However, the findings are inconsistent regarding both the allele (or genotype) involved and the direction of this influence (better or worse response). Thus, further investigations are required to determine if genetic variation due to the VNTR in the dopamine transporter gene is able to predict different levels of clinical response and palatability to methylphenidate in patients with ADHD, and how this information would be useful in clinical practice.

Attention Deficit Disorder with Hyperactivity↗
PubMed2005

Effects of methylphenidate on quantitative EEG of boys with attention-deficit hyperactivity disorder in continuous performance test.

The purpose of this study was to investigate the effects of methylphenidate, a psychostimulant, on quantitative electroencephalography (QEEG) during the continuous performance test (CPT) in boys with attention-deficit hyperactivity disorder (ADHD). The QEEG was obtained from 20 boys with ADHD. The amplitudes of 4 bands (alpha, beta, delta, and theta) in the QEEG, as well as the theta /beta ratio, before and after the administration of methylphenidate were compared during both the resting and CPT states. Methylphenidate induced a significant increase of alpha activities in both the right and left frontal and occipital areas, an increase of beta activities in almost all areas except for the temporal region, a decrease of theta activities in both the occipital and right temporo-parietal areas, a mild decrease of delta activities in the occipito-parietal areas, and an increase of the theta/beta ratio in the right frontal and parieto-occipital, and left temporal areas during the CPT state. No significant QEEG changes were induced by the administration of methylphenidate in the resting state. These data suggest that methylphenidate has greater electrophysiological influences on the cerebral topographical activities during the performance of attentional tasks, as compared to the resting state, in boys with ADHD.

Attention Deficit Disorder with Hyperactivity↗
PubMed2003

Methylphenidate treatment for attention-deficit/hyperactivity disorder in children and adolescents with velocardiofacial syndrome: an open-label study.

BACKGROUND: Velocardiofacial syndrome (VCFS) is a common microdeletion syndrome associated with psychiatric morbidity and developmental disabilities. Although attention-deficit/hyperactivity disorder (ADHD) is the most common psychiatric problem associated with VCFS, there are no reports on methylphenidate treatment in this patient population. Indeed, clinicians have commonly avoided the use of methylphenidate in children with VCFS because of concerns about ineffectiveness or psychotic exacerbation. METHOD: Forty subjects of mean +/- SD age 11.0 +/- 5.0 years with VCFS were assessed for DSM-IV diagnoses using the Schedule for Affective Disorders and Schizophrenia for School-Aged Children, Present and Lifetime Version, and its extended ADHD module (K-SADS-P-ADHD). Those found to have comorbid ADHD were treated with methylphenidate, 0.3 mg/kg once daily. Treatment efficacy was evaluated after 4 weeks with the K-SADS-P-ADHD, the Conners' Abbreviated Teacher Questionnaire, and the Conners' Continuous Performance Test. Side effects were evaluated with a modified version of the Barkley Side Effects Rating Scale. RESULTS: Of the 18 subjects (45%) diagnosed with ADHD, 12 agreed to participate in the study. Their ADHD symptoms, both behavioral and cognitive, improved significantly with treatment. None of the patients showed clinical worsening or psychotic symptoms. Side effects were usually mild and did not warrant discontinuation of methylphenidate. The most common side effects were anorexia and depressive-like symptoms. CONCLUSION: This open-label study indicates that methylphenidate is effective and safe in patients with VCFS. Therefore, its current limited use in this population seems to be unjustified. Larger, controlled clinical and pharmacogenetic studies are needed to confirm these findings.

Adolescent↗
PubMed2003

Combined treatment with methylphenidate and citalopram for accelerated response in the elderly: an open trial.

BACKGROUND: Accelerated antidepressant treatment response may be particularly beneficial for older patients, yet there are few data to inform clinical practice. We evaluated the potential of methylphenidate to accelerate antidepressant response to citalopram and the safety and tolerability of the combined treatment in patients with geriatric major depressive disorder. METHOD: We studied 11 elderly outpatients aged 70 years and older who were diagnosed with DSM-IV major depressive disorder in a 10-week, open-label, structured trial (July 2001-July 2002). Methylphenidate was tapered and discontinued during weeks 9 and 10. Response was defined as a Hamilton Rating Scale for Depression (HAM-D) score of less than 10. The daily dose of citalopram ranged between 20 and 40 mg, and the daily dose of methylphenidate ranged between 5 and 20 mg. RESULTS: Nine patients completed the study. Six patients met criteria for accelerated response (HAM-D score < 10 and Clinical Global Impressions-Improvement scale score of 1 or 2 by treatment day 14), and 2 more patients responded by week 3. One patient was a nonresponder. The mean (SD) citalopram dose for all subjects was 27.5 (10.3) mg and the mean (SD) methylphenidate dose was 12.2 (4.9) mg. The observed side effects were mild to moderate in severity and included sedation, nausea, anxiety, polyuria, dry mouth, and hypersalivation. CONCLUSION: Methylphenidate augmentation of citalopram may be a safe and viable strategy for accelerating antidepressant response in elderly depressed patients. The results of this open-label trial need to be confirmed in a placebo-controlled trial.

Aged↗
PubMed1999

The activations of calcium/calmodulin-dependent protein kinase II in hippocampus and nucleus accumbens of rats after methylphenidate injection.

Attention-deficit hyperactivity disorder (ADHD) is characterized by a history of impulsivity, hyperkinesis, short attention span, and poor peer relations. Treatment of ADHD with stimulants, such as methylphenidate, reduces motor activity and improves performance of tasks requiring attention, learning, and memory. The ADHD children may have a central neurophysiological disturbance involving catecholamine metabolism. However, the ADHD children may have deviation in the reticular system, which causes them difficulty in sensory integration and eventually disturbs their attention span. In addition, a recent study reports that methylphenidate enhances motivational strength of the ADHD children. Therefore, ADHD pathology may not be as simple as just an "uninhibitory" locomotor activity; several systems must have been affected. The present research aimed to clarify each specific component of behavior, and to trace the possible neural substrate involved. Male Wistar rats of three different ages were used to distinguish the biological maturation effect on the locomotor activity. The methylphenidate-injected rats showed significantly higher activity times (AT) compared to the controls at 8 and 12 weeks old. The in-vitro kinase assay results show that CaM-kinase II in the hippocampus and nucleus accumbens of methylphenidate-injected rats had significantly higher calcium independent activity compared to the controls at 12 weeks old. Furthermore, the percentage of calcium independent CaM-kinase II activity in the nucleus accumbens was directly correlated with AT. This suggests that the underlying mechanism of the effect of methylphenidate might be via CaM-kinase II activation in nucleus accumbens.

Animals↗
PubMed2000

Methylphenidate enhances working memory by modulating discrete frontal and parietal lobe regions in the human brain.

The indirect catecholamine agonist methylphenidate (Ritalin) is the drug treatment of choice in attention deficit/hyperactivity disorder (AD/HD), one of the most common behavioral disorders of childhood (DSM-IV), although symptoms may persist into adulthood. Methylphenidate can enhance cognitive performance in adults and children diagnosed with AD/HD (Kempton et al., 1999; Riordan et al., 1999) and also in normal human volunteers on tasks sensitive to frontal lobe damage, including aspects of spatial working memory (SWM) performance (Elliott et al., 1997). The present study investigated changes in regional cerebral blood flow (rCBF) induced by methylphenidate during performance of a self-ordered SWM task to define the neuroanatomical loci of the beneficial effect of the drug. The results show that the methylphenidate-induced improvements in working memory performance occur with task-related reductions in rCBF in the dorsolateral prefrontal cortex and posterior parietal cortex. The beneficial effects of methylphenidate on working memory were greatest in the subjects with lower baseline working memory capacity. This is to our knowledge the first demonstration of a localization of a drug-induced improvement in SWM performance in humans and has relevance for understanding the treatment of AD/HD.

Adrenergic Uptake Inhibitors↗
PubMed2001

Locomotor effects of acute and repeated threshold doses of amphetamine and methylphenidate: relative roles of dopamine and norepinephrine.

The prescribed use of methylphenidate (Ritalin) in the treatment of attention deficit hyperactivity disorder has risen dramatically in recent years. The relative roles of dopamine, norepinephrine, and serotonin in the therapeutic action of these drugs was assessed by comparing the responses of extracellular nucleus accumbens dopamine and serotonin and hippocampus norepinephrine to the acute administration of low methylphenidate and amphetamine doses. The comparative neurochemical profiles in response to methylphenidate and amphetamine suggest that the norepinephrine effects may play an important role in the therapeutic effects of low doses of psychostimulants. In addition, to assess possible long-term consequences of prolonged exposure to this drug, we examined whether changes in the locomotor response occurred with repeated administration of these stimulant doses. Threshold doses of methylphenidate (0.5-1.0 mg/kg) or amphetamine (0.1-0.25 mg/kg) were administered twice daily, and then animals were tested in response to 2.5 mg/kg methylphenidate or 0.5 mg/kg amphetamine. Our results provide evidence that low-dose stimulant administration can result in the development of behavioral sensitization, which is evident in the subsequent behavioral response to the drug. The relevance of these data to the therapeutic uses of these drugs is discussed within the context of the many variables that can affect the behavioral and neurochemical responses to stimulants.

Amphetamine↗
PubMed1975

A choice procedure for drug reinforcers: cocaine and methylphenidate in the rhesus monkey.

A choice procedure was developed to compare the reinforcing efficacy of drug solutions delivered via intravenous catheters to rhesus monkeys. Choices were arranged between doses of cocaine or methylphenidate and saline, different doses of the same drug and doses of both drugs. In each session, monkeys were allowed to self-inject one solution five times in the presence of a stimulus. Thirty minutes after the fifth injection, a second solution could be self-injected five times in the presence of a different stimulus. Thirty minutes later, choice trials began in which both stimuli were present and monkeys could choose one of the two solutions. Rate of responding decreased with increases in dose for both cocaine (0.05-1.5 mg/kg) and methylphenidate (0.075-0.7 mg/kg). Response rates maintained by cocaine were 2 to 3 times higher than those maintained by methylphenidate. Drug was always chosen over saline. Higher doses of cocaine were preferred to lower doses except when both were above 0.5 mg/kg, when no preference was shown. Higher doses of methylphenidate were preferred over low doses, but compared to cocaine, a greater absolute difference between dose magnitude was required to demonstrate preference. When equal doses of cocaine and methylphenidate were compared, no preference was shown. On other comparisons between the drugs, the higher dose was generally preferred regardless of the drug. The reinforcing efficacy of drugs must be considered not only in terms of response rate maintained or reinforcement schedule but also with reference to concurrently available drugs.

Animals↗
PubMed2001

Methylphenidate use for attention deficit hyperactivity disorder in northern Israel--a controversial issue.

BACKGROUND: The prevalence of attention deficit hyperactivity disorder and its pharmacologic treatment have increased dramatically in the past decade in the United States and Britain. We examined the use of methylphenidate hydrochloride for the treatment of ADHD in children in northern Israel. METHODS: We evaluated all prescriptions for methylphenidate filled in 1999 for children aged 5-18 years residing in northern Israel who were insured by Clalit Health Services, a health maintenance organization that covers approximately 70% of the population. RESULTS: Methylphenidate was prescribed to 1.45% of the children in northern Israel in 1999, an increase of 20% in the overall prevalence of methylphenidate use since 1992. Eighty-two percent were boys. The rate of prescription varied widely by type of settlement, from 0.2% in Arab cities and towns to 5.7% in kibbutzim. Primary care physicians wrote 78% of all the prescriptions. CONCLUSIONS: The increase in methylphenidate use was much smaller in northern Israel than in most other developed regions and countries. More efforts at diagnosis and treatment of attention deficit disorders may need to be directed at Arab populations and those with inadequate medical services.

Adolescent↗
PubMed1991

Social acceptability of methylphenidate and behavior modification for treating attention deficit hyperactivity disorder.

The social acceptability of methylphenidate, behavior modification, and methylphenidate plus behavior modification was evaluated. Fifty mothers of children with attention deficit hyperactivity disorder (ADHD) and 50 control mothers, along with 21 children with ADHD and 20 control children, read a case vignette of an 8-year-old boy with ADHD and descriptions of the three treatment conditions. Subjects then rated the acceptability of each treatment. The mothers of children with ADHD were reassessed 3.5 months later, after experience with interventions for their children. Both ADHD and control families rated behavior modification as the most acceptable, methylphenidate as least acceptable, and the combined condition intermediate between the other two. At follow-up, there was a significant improvement in the acceptability of methylphenidate and the combined condition. The increased acceptability of methylphenidate at follow-up was related to increases in parents' knowledge about ADHD but not to the significant improvements that occurred in the children's hyperactive behavior.

Adult↗
PubMed1987

[Attention in hyperkinetic children: a signal detection analysis of the effect of methylphenidate].

The effects of methylphenidate on sustained attention were investigated in a placebo-controlled double-blind trial with 20 hyperactive boys of normal intelligence with minimal brain dysfunction (MBD). Using signal detection theory methylphenidate significantly increased sensitivity (d) and did not change response bias (beta), independent of the dosage (5 to 20 mg/d). Responders and nonresponders to methylphenidate were differentiated by signal detection analysis: responders improved primarily in sensitivity, whereas nonresponders changed response bias. No response difference was found in physiological and biochemical measures (catecholamines), showing a general activation caused by methylphenidate. It is discussed that methylphenidate is improving information processing and arousal modulation in responders and is raising unspecific activation in nonresponders.

Attention↗
PubMedDate not supplied

Hyperresponsiveness to methylphenidate in rats following prenatal ethanol exposure.

Rats exposed in utero to ethanol are hyperresponsive to methylphenidate when tested as neonates or adults. Long-Evans rats were maintained on liquid diets containing either ethanol or maltose-dextrin (35% of total calories) or on lab chow and water throughout pregnancy. Male offspring, who were raised by foster mothers maintained on lab chow and water throughout pregnancy and lactation, were used in two experiments to examine the effects of methylphenidate on activity. In Experiment 1, a time-sampling procedure revealed that methylphenidate (0, 1, 2 & 4 mg/kg) increases the frequency of ambulation in young (26-38 day old) ethanol-treated offspring more than in control offspring. In Experiment 2, an open-field procedure revealed that methylphenidate (0, 2, 4, 6 & 8 mg/kg) produces greater increases in number of squares covered and the total duration of ambulation during 5-min tests in adult (100-184 day old) offspring treated prenatally with ethanol than in control offspring. Both studies revealed that the hyperactivation effect increases with increased doses of methylphenidate.

Animals↗
PubMedDate not supplied

The effect of methylphenidate on overactivity in rats prenatally exposed to alcohol.

Pregnant Long-Evans rats were provided with isocaloric liquid diets containing either ethanol or sucrose, or a standard lab chow diet. Male offspring were utilized to test the effectiveness of methylphenidate in mitigating the overactivity associated with prenatal alcohol exposure. In two experiments, 19 day old rat pups from each prenatal condition were injected with methylphenidate and placed in an open-field. Subjects in the first experiment were injected with 0, 0.5 or 1.0 mg/kg methylphenidate and tested for 5 minutes on each of 3 consecutive days. Drug doses in the second experiment were 0, 2.0 or 8.6 mg/kg and subjects were tested over four days. No evidence was obtained in either experiment that methylphenidate reduced the overactivity of the alcohol-exposed offspring. In fact, in the second experiment, pups exposed to alcohol in utero appeared more sensitive to the stimulating effects of methylphenidate than controls.

Animals↗