|The structural formula of methamphetamine|
Signs of amphetamine intoxication manifest themselves in euphoria, hypersexuality, tachycardia, diaphoresis, and intensifications of the train of thought, speech, and movement. Over time, neurodegenerative changes become apparent in the form of altered behavior, reduced cognitive functions, and signs of neurological damage, such as a decrease in the levels of dopamine transporters (DAT) and serotonin transporters (SERT) in the brain. Amphetamine use within teenagers can have lasting effects on their brain, in particular the prefrontal cortex. Amphetamine use is rising among students due to the ability to easily access prescribed stimulants like Adderall. Also, in case of chronic use, vegetative disorders soon occur such as bouts of sweating, trouble sleeping, tremor, ataxia and diarrhea; the degradation of the personality takes place relatively slowly. Tolerance is expected to develop with regular substituted amphetamine use. When substituted amphetamines are used, drug tolerance develops rapidly. Amphetamine dependence has shown to have the highest remission rate compared to cannabis, cocaine, and opiods. Severe withdrawal associated with dependence from recreational substituted amphetamine use can be difficult for a user to cope with. Long-term use of certain substituted amphetamines, particularly methamphetamine, can reduce dopamine activity in the brain.
For amphetamine dependent individuals, psychotherapy is currently the best treatment option as no pharmacological treatment has been approved. Another treatment option for amphetamine dependence is aversion therapy based on classical conditioning module; this will combine the amphetamine with a negative thing or opposite stimulus. Treatment for amphetamines is growing at extremely high rates around the world. Psychostimulants that increase dopamine and mimic the effects of substituted amphetamines, but with lower abuse liability, could theoretically be used as replacement therapy in amphetamine dependence. However, the few studies that used amphetamine, bupropion, methylphenidate, and modafinil as a replacement therapy did not result in less methamphetamine use or craving.
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Pharmacologic treatment for psychostimulant addiction is generally unsatisfactory. As previously discussed, cessation of cocaine use and the use of other psychostimulants in dependent individuals does not produce a physical withdrawal syndrome but may produce dysphoria, anhedonia, and an intense desire to reinitiate drug use.
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Neuroimaging studies have revealed that METH can indeed cause neurodegenerative changes in the brains of human addicts (Aron and Paulus, 2007; Chang et al., 2007). These abnormalities include persistent decreases in the levels of dopamine transporters (DAT) in the orbitofrontal cortex, dorsolateral prefrontal cortex, and the caudate-putamen (McCann et al., 1998, 2008; Sekine et al., 2003; Volkow et al., 2001a, 2001c). The density of serotonin transporters (5-HTT) is also decreased in the midbrain, caudate, putamen, hypothalamus, thalamus, the orbitofrontal, temporal, and cingulate cortices of METH-dependent individuals (Sekine et al., 2006).
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Unlike cocaine and amphetamine, methamphetamine is directly toxic to midbrain dopamine neurons.
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+ Media related to Amphetamine dependence at Wikimedia Commons