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Stimulant use disorder is a type of substance use disorder where the use of stimulants caused clinically significant impairment or distress. It is defined in the DSM-5 as "the continued use of amphetamine -type substances, cocaine , or other stimulants leading to clinically significant impairment or distress, from mild to severe". [ 1 ]
919.3 Blister of other multiple and unspecified sites infected; 919.4 Insect bite nonvenomous of other multiple and unspecified sites without infection; 919.5 Insect bite nonvenomous of other multiple and unspecified sites infected; 919.6 Superficial foreign body of other multiple and unspecified sites without major open wound and without infection
Oxilofrine, also known as 4,β-dihydroxy-N-methyl-α-methylphenethylamine or as 4,β-dihydroxy-N-methylamphetamine, is a substituted phenethylamine and amphetamine derivative.
Cocaine is a powerful stimulant known to make users feel energetic, cheerful, talkative, etc. In time, negative side effects include increased body temperature, irregular or rapid heart rate, high blood pressure, increased risk of heart attacks, strokes and even sudden death from cardiac arrest.
Amphetamine-type stimulants in general are sympathomimetic amine that stimulates the central nervous system, also proven to cause insomnia, arousal, and reduced hunger. Due to its physiological and psychological effects, ATS has been used to suppress appetite, improve cognitive performance, as well as treating ADHD, depression, and narcolepsy.
Addiction is a serious risk with heavy recreational amphetamine use, but is unlikely to occur from long-term medical use at therapeutic doses; [123] [124] [65] in fact, lifetime stimulant therapy for ADHD that begins during childhood reduces the risk of developing substance use disorders as an adult. [41]
Methylhexanamine (also known as methylhexamine, 1,3-dimethylamylamine, 1,3-DMAA, dimethylamylamine, and DMAA; trade names Forthane and Geranamine) is an indirect sympathomimetic drug invented and developed by Eli Lilly and Company and marketed as an inhaled nasal decongestant from 1948 until it was voluntarily withdrawn from the market in the 1980s.
[179] [180] [181] Some evidence suggests the possibility that opioid use disorders occur due to genetic or other chemical mechanisms that may be difficult to identify or change, such as dysregulation of brain circuitry involving reward and volition. But the exact mechanisms involved are unclear, leading to debate over the influence of biology ...