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The issue of ‘sensitization' to adverse effects following repeated low to moderate doses of stimulants is a critical issue in the treatment of attention deficit hyperactivity disorders (ADHD) in children as well as adolescents and adults. Is there sensitization to drug reinforcement or potential for psychosis? The suggested dose range for methylphenidate and dextroamphetamine dosing in most children is 0.3– 2.0 mg/kg daily and slightly lower doses for adolescents and adults. The dose for dextroamphetamine is cited as being approximately half that for methylphenidate (226). Even without considering the rodent to man correction, 0.25–1.0 mg/kg/day is clearly within the dose range quoted in most paradigms of locomotion sensitization in experimental animals. Studies in adolescents generally indicate that the stimulants are efficacious and safe in the treatment of ADHD (226). There are no reported differences in the incidence of substance abuse in medicated vs. unmedicated adolescents (90); this is based on a review of eight outcome studies comprising 580 adolescents previously treated with stimulants for six months to five years. Looney (135) suggested that adequate treatment of ADHD children and adolescents with stimulants may indeed have a protective effect against the development of substance abuse. There have been no systematic studies on the risk for development of substance abuse in ADHD adults treated with stimulants, and such a study would have difficulties based on the high comorbidity of adult ADHD and stimulant abuse.

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Methamphetamine toxicity is inhibited by a variety of drug treatments, including: 1) DA synthesis inhibitor alpha-methyl-para-tyrosine; 2) DA receptor antagonists; 3) NMDA receptor antagonists, e.g., MK-801; 4) DA and serotonergic reuptake inhibitors protecting against DA and serotonin toxicity respectively (195). Even though most studies have found that serotonergic and DA reuptake inhibitors specifically protect these two sites, certain reuptake blockers (such as benztropine) do not (195). On the other hand, mazindol, a non-specific blocker, protects against both DA and serotonergic neurotoxicity. Ali et al. (1994) have further demonstrated in mice that a major factor for neurotoxicity is hyperthermia which is highly correlated with the degree of long-term DA depletion (21). Furthermore, haloperidol, diazepam and MK-801, all of which can reduce methamphetamine-induced hyperthermia, protect rats against DA depletion (4). They also demonstrated that reducing the ambient temperature (4°C) reduced neurotoxicity to the same levels found when phenobarbital, diazepam and MK-801 were present to protect the cell. Tolerance to methamphetamine induced by increasing doses also reduces the hyperthermic response and as well protects against neurotoxicity (89, 188).

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One of the hallmarks of amphetamine-induced neurotoxicity is the loss of DA uptake sites in the striatum and accumbens. These studies of transporters after chronic amphetamine have reported decreases in the range of 30–40% (158). Recently, Silvia et al. (198) addressed the functional significance of changes in transporters on amphetamine's behavioral effects. After seven days of infusion of transporter RNA antisense ODN into the SN/VTA nuclei, mazindol binding was reduced 32% in the caudate. Administration of 2 mg/kg of amphetamine at this time resulted in robust contralateral turning (an increase of 400%); in contrast, 10 mg/kg of cocaine induced no changes in the turning response. The lack of turning response to cocaine after transporter reduction contrasts with the substantial cocaine-induced contralateral turning after unilateral SN/VTA D ODN to reduce D autoreceptors in the striatum (199). Thus, the amphetamine-induced loss of DA uptake sites could have two consequences: 1) a protective mechanism reducing further neurotoxicity, and 2) reverse tolerance to subsequent amphetamine administration, perhaps resulting in adverse symptoms such as paranoid psychosis (see also the discussion on neurotoxicity in the habenular interpeduncular track and its possible relationship to augmentation amphetamine-induced adverse effects).

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In this category, AAS and AAS prohormones are the most widely known. They work by enhancing protein synthesis and decreasing the breakdown of muscle. The net effect is to allow an increase in muscle size and strength, along with a quicker recovery after workouts. Hence, these substances are effective, but their use can come at a very high cost. If used during adolescence, they can cause premature closure of the growth plates and a decrease in final adult height. Other common side effects include cardiovascular disease, blood clots, stroke and an increased risk of suicide.

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Parkinson's disease represents a hypodopaminergic syndrome with cognitive-neuromotor effects that resemble some of the more marginal effects of stimulant withdrawal. The latter effects may be characterized by a hypodopaminergic state. One of the more remarkable changes in Parkinsonism is the loss of executive function, which refers to a group of cognitive skills involved in the initiation, planning, and monitoring of goal-directed behaviors (132). These functions include the ability to: 1) establish and maintain set, shift from one set to another, formulate concepts and reason abstractly; 2) use feedback to monitor behavior, program sequential motor activities; 3) develop strategies to learn and copy complex figures; and 4) exert emotional self-control and maintain socially appropriate behaviors (144). Tests such as the Wisconsin Card Sorting Test (WCST), a task of concept formation and set shifting ability are impaired in Parkinsonism even when psychomotor speed is factored out (144). The executive functions revolving around verbal capacity are not consistently impaired. Visuospatial skills have been the most frequently reported cognitive disturbance (26). Such studies have found that Parkinson patients exhibited deficits in visual analysis and synthesis (e.g., imbedded figure task, visual discrimination and matching and pattern completion, constructional praxis) even when the speed component was eliminated (144). Even patients in the early stages of Parkinsonism, before treatment is initiated, have psychomotor slowing, loss of cognitive flexibility and mild reductions in learning and recall (128). If the case can be made that the stimulant withdrawal hypodopaminergic state results in similar mild defects, these changes in the executive functions of monitoring behavior, executing plans, etc. could contribute to the lack of therapeutic engagement and accomplishment noted with many of these patients.

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The use of stimulant compounds has a long history. Chinese native physicians have been using the drug Ma-huang for more than 5000 years. In 1887, Nagai found the active agent in Ma-huang to be ephedrine. Amphetamine proper was first synthesized in 1887 by Edeleau as part of a systematicprogram to manufacture aliphatic amines. Early investigations of the properties of amphetamine focused on the peripheral effects and found that amphetamine was a sympathomimetic agent with bronchodilator properties. Oddly, the central nervous system actions were not reported until approximately 1933, and this was closely followed by the first reports of amphetamine abuse. Amphetamines produce feelings of euphoria and relief from fatigue, may improve performance on some simple tasks, increase activity levels, and produce anorexia. The abuse liability of the amphetamines is thought to be primarily related to their euphorigenic effects which leads to high-dose use and the final stage—compulsive abuse. The following sections discuss the basic and clinical research regarding the licit and illicit use of amphetamines and related stimulants.