Edward E. Herschaft, DDS, MA

Disclosures

October 03, 2011

Methamphetamine Use and Addiction

Methamphetamine (MA) is a schedule 2 central nervous system stimulant, which in low doses has been US Food and Drug Administration approved for use in the treatment of narcolepsy and attention-deficit/hyperactivity disorder. Among illicit drug users, it is commonly known as meth, speed,chalk, ice, crystal, tina, fire, glass, or crank.[1,2] Recreational users of the drug take it by smoking, snorting, injection, and oral or rectal routes.[3] This highly addictive, relatively inexpensive, and easily manufactured cousin of amphetamine has become the nonmedical drug of choice for many recreational stimulant drug abusers throughout the United States.

The National Survey on Drug Use and Health reported that approximately 21.8 million American adults (8.7%) used illicit drugs in 2009.[4] This represents a 9% increase over the 2008 rate, the highest rate since 2001. The number of nonmedical users of stimulants also increased from 904,000 (0.4%) in 2008 to 1.3 million (0.5%) in 2009, credited to an increase in the number of MA users from 314,000 (0.1%) to 502,000 (0.2%). This increase was considered statistically significant (P < .05).

MA produces its agonistic effect on dopamine and other monoamines (norepinephrine and serotonin) by blocking the function of dopamine transporter, the protein responsible for removing dopamine from neural synapses. This reverses the direction of flow in neural synapses and floods these sites with the neurotransmitter. Thus, the concentration of dopamine in synaptic gaps increases along with dopaminergic signaling.[5] An alternative mechanism that causes retention of dopamine in neural synapses is exemplified by cocaine, a dopamine reuptake inhibitor. This drug class prevents clearing of dopamine from synaptic gaps.[6] Because dopamine plays an important role in essential regulatory functions of the central nervous system, including mood, motor control, motivation, emotion, neuroendocrine regulation, cognition, and the reward system of the brain, increased extracellular concentrations of dopamine can alter these functions.[7]

Clinical manifestations of MA abuse include a variety of neurologic, psychogenic, and motor-related signs and symptoms, the most evident of which are loss of appetite, hyperactivity, restlessness, headache, rapid heart rate, arrhythmias, hypertension, increased respiration rate, sweating, constipation, twitching, insomnia, numbness,[8,9] psychosomatic disorders, paranoia, and psychosis. These may persist for more than 6 months after MA use and are often resistant to traditional treatment.[10]

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