Disease relevance of Ritalin

• Reversible hemiplegia after presumed intracarotid injection of Ritalin [1].
• Methylphenidate-induced cardiac arrhythmias [2].
• Tics following methylphenidate administration. A report of 20 cases [3].
• Cerebral arteritis and oral methylphenidate [4].
• The results indicate that specific measures, including behavioral response to methylphenidate, presence of tardive dyskinesia, and, under specific pharmacologic conditions, tardive dyskinesia, blink-rate, and pulse-rate responses to methylphenidate, are associated with time and propensity to relapse following neuroleptic withdrawal [5].

Psychiatry related information on Ritalin

• Daily treatment with methylphenidate significantly changed the T2 relaxation times in the putamen of children with attention-deficit/hyperactivity disorder, although the magnitude and direction of the effect was strongly dependent on the child's unmedicated activity state [6].
• Methylphenidate in hyperkinetic children: differences in dose effects on learning and social behavior [7].
• However, therapeutic administration of stimulants such as methylphenidate (MPH) in children with attention deficit hyperactivity disorder reportedly reduces the risk of substance abuse [8].
• There was no evidence that methylphenidate altered the severity of tic disorder, but it may have a weak effect on the frequency of motor (increase) and vocal (decrease) tics [9].
• Methylphenidate effects in learning disabilities. Psychometric changes [10].

High impact information on Ritalin

• T2 relaxation time measures in thalamus did not differ significantly between groups, and were not affected by methylphenidate [6].
• OBJECTIVE: To deal with public and professional concern regarding possible overprescription of attention-deficit/hyperactivity disorder (ADHD) medications, particularly methylphenidate, by reviewing issues related to the diagnosis, optimal treatment, and actual care of ADHD patients and of evidence of patient misuse of ADHD medications [11].
• DATA SOURCES: Literature review using a National Library of Medicine database search for 1975 through March 1997 on the terms attention deficit disorder with hyperactivity, methylphenidate, stimulants, and stimulant abuse and dependence [11].
• Oxygen consumption did not change (P = .40), but heart rate (P = .001) and blood pressure (P = .003) increased significantly with methylphenidate therapy [12].
• Heart rate, blood pressure, and oxygen consumption were measured in 27 hyperactive children during rest, exercise, and recovery, once taking placebo and again taking methylphenidate hydrochloride [12].

Chemical compound and disease context of Ritalin

• A transient psychotic exacerbation was induced with an infusion of the psychotomimetic methylphenidate hydrochloride (0.5 mg/kg of body weight over a 60-second period) [13].
• Pemoline, methylphenidate, and placebo in children with minimal brain dysfunction [14].
• These results provide evidence for the potential brain targets of modafinil, which differ from those of amphetamine or methylphenidate, and suggest that modafinil induces wakefulness by mechanisms distinct from those of the two stimulants [15].
• We have examined the effects of methylphenidate (MPD), an inhibitor of DAT, administered alone or with levodopa, on parkinsonism measured with tapping and walking speeds, dyskinesia, subjective effects, and vital signs [16].
• In normal animals, amphetamine and methylphenidate increase extracellular levels of dopamine, leading to an enhancement of locomotor activity [17].

Biological context of Ritalin

• Is methylphenidate like cocaine? Studies on their pharmacokinetics and distribution in the human brain [18].
• BACKGROUND: The purposes of this study were to investigate the pharmacokinetics of methylphenidate hydrochloride (Ritalin) in the human brain, to compare them with those of cocaine, and to evaluate whether cocaine and methylphenidate compete for the same binding sites [18].
• The authors investigated the effect of the stimulant drug methylphenidate (given intravenously) on sexual desire as a possible contributing factor to risky sexual behavior associated with the contraction of HIV [19].
• METHOD: T(2) relaxometry was used to indirectly assess blood volume in the cerebellum (hemispheres and midline vermis) of 10 boys with ADHD who were administered placebo or one of three different doses of methylphenidate continuously for 1 week [20].
• Enhancement of plasticity under methylphenidate and tacrine was associated with an increase in corticomotoneuronal excitability of the prime mover of the practice, as measured by the motor evoked potential amplitude, but with a decrease under cabergoline [21].

Anatomical context of Ritalin

• In contrast, addicts showed an increased response to methylphenidate in the thalamus (a region that conveys sensory input to the cortex) [22].
• Administration of either amphetamine or methylphenidate evoked Fos-like immunoreactivity in a large number of neurons in the striatum and whole cortex, especially in the caudate nucleus and mediofrontal cortex, which are known to be dopaminergic targets [15].
• That is, when subjects expected to receive methylphenidate but received placebo there were significant increases in ventral cingulate gyrus (BA 25) and nucleus accumbens (regions involved with emotional reactivity and reward) [23].
• Methylphenidate-induced changes in the right orbitofrontal cortex and right striatum were associated with craving, and those in the prefrontal cortex were associated with mood [24].
• Methylphenidate significantly increased "relative" (region relative to the whole brain) metabolism in the cerebellum and decreased it in the basal ganglia [25].

Associations of Ritalin with other chemical compounds

• METHODS: We used positron emission tomography to measure the temporal and spatial distribution of carbon 11 (11C)-labeled methylphenidate [18].
• A double-blind study using the protooncogene c-fos as experimental marker in the cat was, therefore, carried out to identify the potential target neurons of modafinil and compare them with those for amphetamine and methylphenidate [15].
• The 22 children with attention deficit hyperactivity disorder were treated with methylphenidate, and they were further divided into methylphenidate responders (n = 18) and nonresponders (n = 4). beta-Phenylethylamine levels significantly increased after methylphenidate therapy in responders, whereas they did not increase in nonresponders [26].
• Functional connectivity of caudate nucleus was modulated specifically by dopaminergic drugs, with opposing effects of sulpiride and methylphenidate [27].
• PET study examining pharmacokinetics, detection and likeability, and dopamine transporter receptor occupancy of short- and long-acting oral methylphenidate [28].

Gene context of Ritalin

• Stimulant drugs (eg, methylphenidate) are effective in the treatment of ADHD and inhibit the dopamine transporter [29].
• Three studies by three different groups have reported decreased DAT binding after methylphenidate treatment [30].
• cAMP and extracellular signal-regulated kinase signaling in response to d-amphetamine and methylphenidate in the prefrontal cortex in vivo: role of beta 1-adrenoceptors [31].
• Blockade of dopamine or N-methyl-d-aspartate (NMDA) receptors or serotonin depletion had no effect on d-amphetamine-induced GluR1 phosphorylation. d-amphetamine but not methylphenidate increased ERK phosphorylation [31].
• Six adults phenotyped as either extensive (N = 4) or poor (N = 2) metabolizers for cytochrome P450 (CYP) 2D6 were given a 10-mg oral dose of methylphenidate (MPH) on two separate occasions with and without quinidine, a potent CYP2D6 inhibitor [32].

Analytical, diagnostic and therapeutic context of Ritalin

• A double-blind, methylphenidate-placebo cross-over design was used within the hyperactive group [33].
• Clinical trials. Planned Ritalin trial for tots heads into uncharted waters [34].
• CONCLUSION: We speculate that because the experience of the high is associated with the fast uptake of cocaine and methylphenidate in the brain, the slow clearance of methylphenidate from the brain may serve as a limiting factor in promoting its frequent self-administration [18].
• Functional MRI revealed differences between children with Attention Deficit Hyperactivity Disorder (ADHD) and healthy controls in their frontal-striatal function and its modulation by methylphenidate during response inhibition [35].
• Oral administration of methylphenidate hydrochloride (Ritalin) increased resting Fg values in awake narcoleptics, particularly in BSC regions, but attentuated Fg increases during sleep onset [36].

References