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Overview of Methamphetamine

Pharmacology

*Clinical Aspects of Methamphetamine

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*Introduction:.Methamphetamine, which was developed in 1893, is a synthetic

stimulant that affects regions of the central nervous system and other major organ systems.

Street names: Crystal; tina; speed; crank; ice; meth

Classification: Major central nervous system (CNS) stimulant (An amphetamine analog)Other stimulants: cocaine; caffeine; nicotine; methylphenidate; dextroamphetamine)Schedule II drug: High potential for abuse

.The primary reason for the growth of methamphetamine use was the wide availability of pseudoephedrine, the primary precursor of methamphetamine, which is contained in many over-the-counter cold medications including Sudafed,Nyquil,and Claritin-D.

.Methamphetamine was manufactured and distributed by small mom-and-pop type “kitchen chemists,” as well as larger syndicates and drug cartels. dr.farahzadi

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-Neurologically: Dopamine Triggers the release of large amounts of dopamine, a neurotransmitter, which causes an “energizing” euphoria; releases lesser amounts of seratonin Inhibits the reuptake of synaptic dopamine

-Dopamine affects a region of the brain that controls pleasure

-Dopamine is involved in reward behavior, leading to continued use of the substance that is subjectively experienced as pleasurable

-While all stimulants release some dopamine, crystal meth releases much larger amounts :

-Cocaine releases 400% more dopamine-Crystal meth releases almost 1500% more dopamine

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*Neurobiological Impact of Methamphetamine:

-once methamphetamine has been ingested, profound changes occur in the structure and chemistry of the brain:

Methamphetamine blocks the reuptake of released dopamine in the synaptic clefts, resulting in increased levels of dopamine in the synapse of neurons in the nucleus accumbens and other areas of the mesolimbic region of the brain.

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-Methamphetamine is extremely powerful and addictive central nervous system stimulant, that also affects the cardiovascular system.

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-Methamphetamine use also results in a significant loss of dopamine transporters (used as markers of the dopamine terminal), which is associated with slower motor function and decreased memory, attention, and cognitive functioning, such as .inhibitory control.

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-The chronic and long-term use of methamphetamine results in lower levels of dopamine receptors that are associated with increased dependency, i.e., loss of control and compulsive drug use.

-In chronic methamphetamine abusers, there are structural changes including greater cortical volume and changes in the hippocampus that relate to cognitive deficit . Increased striatal volume and decreased striatal metabolism have been found and postulated to be a function of increased water content or as result of inflammation.

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-Furthermore, methamphetamine increases cytoplasmic concentration of dopamine, which promotes oxidation products that are toxic to the nerve terminals .

The neurotoxicity of methamphetamine is further accentuated by its prolonged half-life and, therefore, long duration of action.

-Other findings include reduced concentrations of the neuronal marker

N-acetyl asparate and total creatine in the basal ganglia, and the striatum has been shown to be considerably affected by methamphetamine use, with lower levels of dopamine transporters and lessened dopamine receptor availability , indicating compromises that manifest in cortical regions that control executive function.

-In brief, the research has documented abnormalities in cortical and limbic systems, deficits in dopaminergic and serotonergic neurotransmitter systems, deficits in gray matter, and variations in glucose metabolism compared with nonusers of methamphetamine

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.Changes in glucose metabolism have been shown to be associated with severity of psychiatric symptoms.

Imaging studies of methamphetamine-abusing individuals have also revealed greater activity in the amygdala and less activity in the infralimbic cortex among methamphetamine abusers than in non-using individuals, as well as changes in glial cell proliferation or metabolism and in neural integrity

-After protracted abstinence, methamphetamine abusers showed increased metabolism in the thalamus, similar to controls, whereas recently abstinent methamphetamine abusers had lower metabolism in both the striatum and thalamus.

Furthermore, after methamphetamine cessation and recovery over time, there appears to be some

improvement in dopamine transport function . for example, found that serotonin transporter

density generally decreased as the years of methamphetamine use increased and serotonin transporter density was correlated inversely with aggression scale scores.

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