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Methamphetamine

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This article is about the free base and salts of Methamphetamine. For the socio-cultural aspects of Methamphetamine and other substituted amphetamines, see History and culture of amphetamines.

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Methamphetamine
Clinical data
Other namesN-methylamphetamine
License data
Dependence
liability		Very high
Routes of
administration		Medical: Oral
Recreational: Oral, Intravenous, Insufflation, Inhalation, Suppository
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability62.7% oral; 79% nasal; 90.3% smoked; 99% rectally; 100% IV
MetabolismHepatic: CYP2D6[2] and FMO[3]
Elimination half-life9–12 hours[1]
ExcretionRenal
Identifiers
  • N-methyl-1-phenylpropan-2-amine
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.007.882 Edit this at Wikidata
Chemical and physical data
FormulaC10H15N
Molar mass149.2337 g/mol g·mol−1
3D model (JSmol)
Melting point3 °C (37 °F) [4]
Boiling point212 °C (414 °F) [5] at 760 MM HG
  • N(C(Cc1ccccc1)C)C
  • InChI=1S/C10H15N/c1-9(11-2)8-10-6-4-3-5-7-10/h3-7,9,11H,8H2,1-2H3 checkY
  • Key:MYWUZJCMWCOHBA-UHFFFAOYSA-N checkY
  (verify)

Methamphetamine[note 1] ( /ˌmɛθæmˈfɛtəmiːn/; contracted from N-methyl-alpha-methylphenethylamine) is a neurotoxin and potent psychostimulant of the phenethylamine and amphetamine classes that is used to treat attention deficit hyperactivity disorder (ADHD) and obesity.[9][10][11] Methamphetamine exists as two enantiomers, dextrorotary and levorotary.[note 2] Dextromethamphetamine is a stronger CNS stimulant than levomethamphetamine; however, both are addictive and produce the same toxicity symptoms at high doses. Although rarely prescribed due to the potential risks, methamphetamine hydrochloride is approved by the United States Food and Drug Administration (USFDA) under the trade name Desoxyn. Recreationally, methamphetamine is used as an aphrodisiac, euphoriant, and stimulant, allowing some users to engage in sexual activity continuously for several days straight.[12][13]

Illicitly, methamphetamine may be sold either as pure dextromethamphetamine or in an equal parts mixture of the enantiomers, i.e., 50% levomethamphetamine and 50% dextromethamphetamine. Both dextromethamphetamine and racemic methamphetamine are schedule II controlled substances in the United States, and similarly the production, distribution, sale, and possession of methamphetamine is restricted or illegal in many other countries due to its placement in schedule II of the United Nations Convention on Psychotropic Substances treaty. In contrast, levomethamphetamine is an over-the-counter drug in the United States.[12][14]

In low doses, methamphetamine can cause euphoria and increase alertness, concentration, and energy in fatigued individuals. At higher doses, it can induce methamphetamine psychosis, rhabdomyolysis and cerebral hemorrhage. Methamphetamine is known to have a high potential for abuse and addiction. Recreational use of methamphetamine may result in methamphetamine psychosis or lead to post-withdrawal syndrome, a withdrawal syndrome that can persist for months beyond the typical withdrawal period. Unlike amphetamine and cocaine, methamphetamine is neurotoxic to humans, damaging both dopamine and serotonin neurons in the central nervous system (CNS). Entirely opposite to the long-term use of amphetamine, there is significant evidence that methamphetamine causes brain damage from long-term use in humans; this damage includes severe adverse changes in brain structure and function, such as marked reductions in gray matter volume in several brain regions and adverse changes in markers of metabolic integrity.[9][10][12][15]

Uses

Medical

In the United States, methamphetamine hydrochloride, under the trade name Desoxyn, has been approved by the USFDA for treating ADHD and exogenous obesity (obesity originating from factors outside of the patient's control) in both adults and children;[12] however, the USFDA also indicates that the limited therapeutic usefulness of methamphetamine should be weighed against the inherent risks associated with its use.[12] In the United States, methamphetamine's levorotary form is available in some over-the-counter nasal decongestant products, such as Vicks Vapoinhaler.[note 3]

As methamphetamine is associated with a high potential for misuse, the drug is regulated under the Controlled Substances Act and is listed under Schedule II in the United States.[12] Methamphetamine hydrochloride dispensed in the United States is required to include the following black box warning:[12]

Methamphetamine has a high potential for abuse and should be tried only in weight reduction programs where alternative therapy has been ineffective. Administration of Methamphetamine for prolonged periods may lead to drug dependence. The drug should be prescribed or dispensed sparingly. Misuse may cause sudden death and serious cardiovascular adverse events.

Recreational

See also: Party and play and the Recreational routes of methamphetamine administration

Methamphetamine is often used recreationally for its effects as a potent aphrodisiac, euphoriant, and stimulant.[18] According to a National Geographic TV documentary on methamphetamine, "an entire subculture known as party and play is based around methamphetamine use."[18] Gay men belonging to this subculture will typically meet up through internet dating sites and have sex.[18] Due to its strong stimulant and aphrodisiac effects and inhibitory effect on ejaculation, with repeated use, these sexual encounters will sometimes occur continuously for several days.[18] The crash following the use of methamphetamine in this manner is very often severe, with marked hypersomnia.[18]

Desoxyn tablet
Desoxyn tablets – pharmaceutical methamphetamine hydrochloride
Crystal meth
Crystal meth – illicit methamphetamine hydrochloride

Contraindications

Methamphetamine is contraindicated in individuals with a history of drug abuse, heart disease, or severe agitation or anxiety, or in individuals currently experiencing arteriosclerosis, glaucoma, hyperthyroidism, or severe hypertension.[12] The USFDA states that individuals who have experienced hypersensitivity reactions to other stimulants in the past or are currently taking monoamine oxidase inhibitors should not take methamphetamine.[12] The USFDA also advises individuals with bipolar disorder, depression, elevated blood pressure, liver or kidney problems, mania, psychosis, Raynaud's phenomenon, seizures, thyroid problems, tics, or Tourette syndrome to monitor their symptoms while taking methamphetamine.[12] Due to the potential for stunted growth, the USFDA advises monitoring the height and weight of growing children and adolescents during treatment.[12]

Side effects

Physical

The physical effects of methamphetamine can include anorexia, hyperactivity, dilated pupils, flushed skin, excessive sweating, increased movement, dry mouth and bruxism (leading to "meth mouth"), headache, irregular heartbeat (usually as accelerated heartbeat or slowed heartbeat), rapid breathing, high blood pressure, low blood pressure, high body temperature, diarrhea, constipation, blurred vision, dizziness, twitching, numbness, tremors, dry skin, acne, and pallor.[12][19] Methamphetamine that is present in a mother's bloodstream can pass through the placenta to a fetus and is or be secreted into breast milk.[20] Infants born to methamphetamine-abusing mothers were found to have a significantly smaller gestational age-adjusted head circumference and birth weight measurements.[20] Methamphetamine exposure was also associated with neonatal withdrawal symptoms of agitation, vomiting and tachypnea.[20] This withdrawal syndrome is relatively mild and only requires medical intervention in approximately 4% of cases.[21]

Meth mouth

Main article: Meth mouth

Methamphetamine users and addicts may lose their teeth abnormally quickly, regardless of the route of administration, from a condition informally known as meth mouth.[22] The condition is generally most severe in users who inject the drug, rather than those who smoke, ingest or inhale it.[22] According to the American Dental Association, meth mouth "is probably caused by a combination of drug-induced psychological and physiological changes resulting in xerostomia (dry mouth), extended periods of poor oral hygiene, frequent consumption of high-calorie, carbonated beverages and bruxism (teeth grinding and clenching)."[22][23]

Psychological

The psychological effects of methamphetamine can include euphoria, dysphoria, changes in libido, alertness, apprehension, concentration, decreased sense of fatigue, insomnia or wakefulness, self-confidence, sociability, irritability, restlessness, grandiosity and repetitive and obsessive behaviors.[12][19][24] Methamphetamine use also has a high association with anxiety, depression, methamphetamine psychosis, suicide, and violent behaviors.[25] Methamphetamine also has a very high addiction risk.[12]

Neurotoxicity

Unlike cocaine and amphetamine, methamphetamine is directly neurotoxic to midbrain dopamine neurons.[9] Moreover, methamphetamine abuse is associated with an increased risk of Parkinson's disease due to excessive pre-synaptic dopamine autoxidation, a mechanism of neurotoxicity.[15][26][27][28] Similar to the neurotoxic effects on the dopamine system, methamphetamine can also result in neurotoxicity to serotonergic neurons.[10] It has been demonstrated that a high core temperature is correlated with an increase in the neurotoxic effects of methamphetamine.[29] As a result of methamphetamine-induced neurotoxicity to dopaminergic neurons, chronic use may also lead to post acute withdrawals which persist beyond the withdrawal period for months, and even up to a year.[15]

Sexually transmitted infection

Gay men who use methamphetamine appear more likely to have unprotected sex than those who do not use such drugs.[30] Methamphetamine use was found to be related to higher frequencies of unprotected sexual intercourse in both HIV-positive and unknown casual partners, an association more pronounced in HIV-positive participants.[31] These findings suggest that methamphetamine use and engagement in unprotected anal intercourse are co-occurring risk behaviors, behaviors that potentially heighten the risk of HIV transmission among gay and bisexual men.[31] Methamphetamine use allows users of both sexes to engage in prolonged sexual activity, which may cause genital sores and abrasions as well as priapism in men.[12][32] Methamphetamine may also cause sores and abrasions in the mouth via bruxism, increasing the risk of sexually transmitted infection.[12][32]

Besides the sexual transmission of HIV, it may also be transmitted between users who share a common needle.[33] The level of needle sharing among methamphetamine users is similar to that among other drug injection users.[33]

Dependence, addiction, and withdrawal

See also: Amphetamine dependence

Tolerance is expected to develop with regular methamphetamine use and, when abused, this tolerance develops rapidly.[34][35]

A Cochrane Collaboration review on amphetamine and methamphetamine dependence and abuse indicates that the current evidence on effective treatments is extremely limited.[36] While the review indicated that Fluoxetine[note 4] and Imipramine[note 5] have some limited benefits in treating abuse and addiction, it concluded, "no treatment has been demonstrated to be effective for the treatment of [methamphetamine] dependence and abuse."[36]

According to another Cochrane Collaboration review on withdrawal in highly dependent amphetamine and methamphetamine abusers, "when chronic heavy users abruptly discontinue [methamphetamine] use, many report a time-limited withdrawal syndrome that occurs within 24 hours of their last dose."[37] This review noted that withdrawal symptoms in chronic, high-dose users are frequent, occurring in up to 87.6% of cases, and persist for three to four weeks with a marked "crash" phase occurring during the first week.[37] Methamphetamine withdrawal symptoms can include anxiety, drug craving, dysphoric mood, fatigue, increased appetite, increased movement or decreased movement, lack of motivation, sleeplessness or sleepiness, and vivid or lucid dreams.[37] The review suggested that withdrawal symptoms are associated with the degree of dependence (i.e., the extent of abuse).[37] The mental depression associated with methamphetamine withdrawal lasts longer and is more severe than that of cocaine withdrawal.[21]

Overdose

A methamphetamine overdose may result in a wide range of symptoms.[12] A moderate overdose of methamphetamine may induce symptoms such as: arrhythmia, confusion, dysuria, hypertension or hypotension, hyperthermia, hyperreflexia, myalgia, severe agitation, tachypnea, tremor, urinary hesitancy, and urinary retention.[19] An extremely large overdose may produce symptoms such as adrenergic storm, methamphetamine psychosis, anuria, cardiogenic shock, cerebral hemorrhage, circulatory collapse, hyperpyrexia, pulmonary hypertension, renal failure, rhabdomyolysis, serotonin syndrome, and a form of stereotypy ("tweaking").[Refnote 1] A methamphetamine overdose will likely also result in mild brain damage due to dopaminergic and serotonergic neurotoxicity.[9][10] Death from fatal methamphetamine poisoning is typically preceded by convulsions and coma.[12]

Emergency treatment

The USFDA states[note 6] that acute methamphetamine intoxication is largely managed by treating the symptoms and includes gastric evacuation, administration of activated charcoal, and sedation.[12] There is inadequate evidence on the usefulness of hemodialysis or peritoneal dialysis in cases of methamphetamine intoxication.[12] Forced acid diuresis (e.g., with vitamin C) will increase methamphetamine excretion, but increases the risk of renal failure in the presence of myoglobinuria.[12] Intravenous (IV) phentolamine may be useful for acute cases of severe hypertension if the condition complicates methamphetamine overdose.[12] Often, blood pressure drops gradually following sufficient sedation.[12] Chlorpromazine may be useful in decreasing the sympathomimetic and CNS effects of a methamphetamine overdose.[12]

Psychosis

Template:Main section

Abuse of methamphetamine can result in a stimulant psychosis which may present with a variety of symptoms (e.g. paranoia, hallucinations, delusions).[41] A Cochrane Collaboration review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely.[41][42] The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.[41] Methamphetamine psychosis may also develop occasionally as a treatment-emergent side effect.[43]

Interactions

Methamphetamine is metabolized by the liver enzyme CYP2D6, so CYP2D6 inhibitors (e.g., selective serotonin reuptake inhibitors (SSRIs)) will prolong the elimination half-life of methamphetamine.[2] Methmphetamine also interacts with monoamine oxidase inhibitors (MAOIs), since both MAOIs and methamphetamine increase plasma catecholamines; therefore, concurrent use of both is dangerous.[12] Methamphetamine may decrease the effects of sedatives and depressants and increase the effects of stimulants and antidepressants as well.[12] Methamphetamine may counteract the effects of antihypertensives and antipsychotics due to its effects on the cardiovascular system and cognition respectively.[12] The pH of gastrointestinal content and urine affects the absorption and excretion of methamphetamine.[12] Specifically, acidic substances will reduce the absorption of methamphetamine and increase urinary excretion, while alkaline substances do the opposite.[12] Due to the effect pH has on absorption, proton pump inhibitors, which reduce gastric acid, are known to interact with methamphetamine.[12]

Pharmacology

An image of methamphetamine pharmacodynamics
This illustration depicts the normal operation of the dopaminergic terminal to the left, and the dopaminergic terminal in presence of methamphetamine to the right. Methamphetamine reverses the action of the dopamine transporter (DAT) by activating TAAR1 (not shown). TAAR1 activation also causes some of the dopamine transporters to move into the presynaptic neuron and cease transport (not shown). At VMAT2 (labeled VMAT), methamphetamine causes dopamine efflux (release).

Pharmacodynamics

Like amphetamine, methamphetamine has been identified as a potent full agonist of trace amine-associated receptor 1 (TAAR1), a G protein-coupled receptor (GPCR) that regulates brain catecholamine systems.[44][45] Activation of TAAR1, via adenylyl cyclase, increases cyclic adenosine monophosphate (cAMP) production and either completely inhibits or reverses the transport direction of the dopamine transporter (DAT), norepinephrine transporter (NET), and serotonin transporter (SERT).[44][46] When methamphetamine binds to TAAR1, it triggers transporter phosphorylation via protein kinase A (PKA) and protein kinase C (PKC) signaling, ultimately resulting in the internalization or reverse function of monoamine transporters.[44][47] Other transporters that methamphetamine is known to inhibit are vesicular monoamine transporter 1 (VMAT1), vesicular monoamine transporter 2 (VMAT2), SLC22A3, and SLC22A5.[48] SLC22A3 is an extraneuronal monoamine transporter that is present in astrocytes and SLC22A5 is a high-affinity carnitine transporter.[45][49] When methamphetamine interacts with VMAT2, it induces a release of monoamines from the synaptic vesicles (vesicles that stores monoamines) into the cytosol (intracellular fluid) of the presynaptic neuron.[50]

Methamphetamine is also an agonist of the alpha-2 adrenergic receptors and inhibits vesicular monoamine transporter 1 (VMAT1), monoamine oxidase B (MAO-B), and monoamine oxidase A (MAO-A).[45] Methamphetamine is known to inhibit the CYP2D6 liver enzyme as well.[2] Dextromethamphetamine is a stronger psychostimulant, but levomethamphetamine has a longer half-life and is CNS-active with weaker effects (approximately one-tenth) on striatal dopamine and shorter perceived effects.[51][52][53] At high doses, both enantiomers of methamphetamine can induce stereotypy and psychosis,[52] but levomethamphetamine is less desired by drug abusers because of its weaker pharmacodynamic profile.[53]

Although all of the mechanisms are not fully understood, methamphetamine is a known neurotoxin in both lab animals and humans.[54][55] Beyond neurotoxicity, magnetic resonance imaging studies on human methamphetamine addicts and abusers indicate adverse neuroplastic changes, such as significant abnormalities in various brain structures.[10] In particular, methamphetamine appears to cause white matter hyperintensity and hypertrophy, marked shrinkage of hippocampi, and a reduction in gray matter in the cingulate cortex, limbic cortex, and paralimbic cortex.[10] Moreover, there are adverse changes in various metabolic markers of metabolic integrity or synthesis in methamphetamine abusers, such as reductions in N-acetylaspartate and creatine as well as elevated choline and myoinositol levels.[10]

Comparison to amphetamine pharmacodynamics

Both amphetamine and methamphetamine are potent central nervous system stimulants with a few biomolecular targets and affected transporters in common; however, there are important pharmacodynamic differences between the two compounds.[Refnote 2] Both compounds are potent trace amine-associated receptor 1 (TAAR1) agonists (causing non-competitive inhibition of DAT, NET, and SERT) and inhibitors of VMAT2, SLC22A3, and SLC22A5.[Refnote 3] However, methamphetamine appears to bind at a different site at VMAT2 than amphetamine.[59] Methamphetamine also inhibits VMAT1, has agonist activity at all alpha-2 adrenergic receptor subtypes, and is a neurotoxin in humans, whereas there is no evidence of amphetamine neurotoxicity in humans.[9][10][45] Amphetamine is an agonist of cocaine and amphetamine regulated transcript (CART), a psychostimulant neuropeptide with neurogenerative and neuroprotective effects in vitro;[57][58] in contrast, the limited available research on the association between methamphetamine and CART in humans suggests methamphetamine has no significant effects on the neuropeptide.[45][60]

In contrast to the adverse neuroplastic effects evident in methamphetamine addicts and abusers, long-term use of amphetamine or methylphenidate at therapeutic doses appears to produce beneficial changes in brain function and structure, such as normalization of the right caudate nucleus.[61][62]

Pharmacokinetics

Following oral administration, methamphetamine is well-absorbed into the bloodstream, with peak plasma methamphetamine concentrations achieved in approximately 3.13 to 6.3 hours post ingestion.[11] Methamphetamine is also well absorbed following inhalation and following intranasal administration.[1] Due to the high lipophilicity of methamphetamine, it can readily move through the blood brain barrier faster than other stimulants, where it is more resistant to against degradation by monoamine oxidase (MAO).[1][11] The amphetamine metabolite peaks at 10 to 24 hours.[1] It is excreted by the kidneys, with the rate of excretion into the urine heavily influenced by urinary pH.[11][12] When taken orally, 30–54% of the dose is excreted in urine as methamphetamine and 10–23% as amphetamine.[11] Following IV doses, about 45% is excreted as methamphetamine and 7% as amphetamine.[11] The half-life of methamphetamine is variable with a mean value of between 5 and 12 hours.[1][11]

Methamphetamine is metabolized in the liver by CYP2D6[2] and Flavin-containing monooxygenase[3] with the main metabolites being amphetamine and 4-hydroxymethamphetamine; other minor metabolites include: 4-hydroxyamfetamine, 4-hydroxynorephedrine, 4-hydroxyphenylacetone, benzoic acid, hippuric acid, norephedrine, and phenylacetone, the metabolites of amphetamine.[11][63][64][65] Among these metabolites, the active sympathomimetics are amphetamine, 4‑hydroxyamphetamine,[66] 4‑hydroxynorephedrine,[67] and norephedrine.[68]

The main metabolic pathways involve aromatic para-hydroxylation, aliphatic alpha- and beta-hydroxylation, N-oxidation, N-dealkylation, and deamination.[63][64] The known metabolic pathways include:[11][63][65]

Metabolic pathways of methamphetamine
Graphic of several routes of methamphetamine metabolism
The image above contains clickable links
The primary metabolites of methamphetamine are amphetamine and 4-hydroxymethamphetamine.[11]

Detection in biological fluids

Methamphetamine and amphetamine are often measured in urine or blood as part of a drug test for sports, employment, poisoning diagnostics, and forensics.[69][70][71][72] Chiral techniques may be employed to help distinguish the source the drug to determine whether it was obtained illicitly or legally via prescription or prodrug.[73] Chiral separation is needed to assess the possible contribution of levomethamphetamine (e.g., Vicks Vapoinhaler) toward a positive test result.[73][74][75] Dietary zinc supplements can mask the presence of methamphetamine and other drugs in urine.[76]

Physical and chemical properties

Pure shards of methamphetamine hydrochloride, also known as crystal meth

Methamphetamine is a chiral compound with two enantiomers, dextromethamphetamine and levomethamphetamine. At room temperature, the free base of methamphetamine is a clear and colorless liquid with an odor characteristic of geranium leaves.[5] It is soluble in diethyl ether and ethanol as well as miscible with chloroform.[5] In contrast, the methampetamine hydrochloride salt is odorless with a bitter taste and occurs as a white crystal or white crystalline powder.[5] Methamphetamine hydrochloride has a melting point between 170 to 175 °C (338 to 347 °F) and occurs as white crystals or a white crystalline powder.[5] The hydrochloride salt is also freely soluble in alcohol and water.[5]

Synthesis

Racemic methamphetamine may be prepared starting from phenylacetone by either the Leuckart[77] or reductive amination methods.[78] In the Leuckart reaction, one equivalent of phenylacetone is reacted with two equivalents of N-methylformamide to produce the formyl amide of methamphetamine plus carbon dioxide and methylamine as side products.[78] In this reaction, an iminium cation is formed as an intermediate which is reduced by the second equivalent of N-methylformamide.[78] The intermediate formyl amide is then hydrolyzed under acidic aqueous conditions to yield methamphetamine as the final product.[78] Alternatively phenylacetone can be reacted with methylamine under reducing conditions to yield methamphetamine.[78]

Methamphetamine synthesis
Diagram of methamphetamine synthesis by reductive amination
Method of methamphetamine synthesis of methamphetamine via reductive amination
Diagram of methamphetamine synthesis by Leuckart reaction
Methods of methamphetamine synthesis via the Leuckart reaction

History, society, and culture

Main article: History and culture of substituted amphetamines

Amphetamine, discovered before methamphetamine, first synthesized in 1887 in Germany by Romanian chemist Lazăr Edeleanu who named it phenylisopropylamine.[79][80] Three decades later, in 1919, methamphetamine hydrochloride was synthesized by pharmacologist Akira Ogata via reduction of ephedrine using red phosphorus and iodine.[81] During World War II, methamphetamine was used extensively by the Axis forces for its stimulant effects.[80][82] Obetrol, patented by Obetrol Pharmaceuticals in the 1950s and indicated for treatment of obesity, was one of the first brands of pharmaceutical methamphetamine products.[83] Due to the psychological and stimulant effects of methamphetamine, Obetrol became a popular diet pill in America in the 1950s and 1960s.[83] Eventually, as the addictive properties of the drug became known, governments began to strictly regulate the production and distribution of methamphetamine.[80] For example, during the early 1970s in the United States, methamphetamine became a schedule II controlled substance under the Controlled Substances Act.[84] Currently, methamphetamine is sold under the trade name Desoxyn, trademarked by the Danish pharmaceutical company Lundbeck.[85] As of January 2013, the Desoxyn trademark had been sold to Italian pharmaceutical company Recordati.[86]

Main article: Legal status of methamphetamine

The production, distribution, sale, and possession of methamphetamine is restricted or illegal in many jurisdictions.[14] Methamphetamine has been placed in Schedule II of the United Nations Convention on Psychotropic Substances treaty.[14]

See also

Notes

  1. ^ Synonyms and alternate spellings include: metamfetamine (International Nonproprietary Name (INN)), N-methylamphetamine, desoxyephedrine, Syndrox, and Desoxyn.[6][7] Common slang terms for methamphetamine include: speed, meth, crystal, crystal meth, glass, shards, ice, and tic.[8]
  2. ^ Enantiomers are molecules that are mirror images of one another; they are structurally identical, but of the opposite orientation.
  3. ^ The active ingredient in Vicks Vapoinhaler is listed as Levmetamfetamine, the INN of Levomethamphetamine.[16][17]
  4. ^ During short-term treatment, Fluoxetine may decrease drug craving.[36]
  5. ^ During "medium-term treatment," Imipramine may extend the duration of adherence to addiction treatment.[36]
  6. ^ They advise individuals experiencing a methamphetamine overdose to first consult with a Certified Poison Control Center on treatment for up-to-date information, advice, and guidance.[12]

Reference notes

  1. ^ [12][19][24][38][39][40]
  2. ^ [45][48][56][57][58]
  3. ^ [44][48][50][56]

References

  1. ^ a b c d e Schep LJ, Slaughter RJ, Beasley DM (August 2010). "The clinical toxicology of metamfetamine". Clinical Toxicology (Philadelphia, Pa.). 48 (7): 675–94. doi:10.3109/15563650.2010.516752. ISSN 1556–3650. PMID 20849327. {{cite journal}}: Check |issn= value (help)CS1 maint: multiple names: authors list (link)
  2. ^ a b c d "Methamphetamine". DrugBank. University of Alberta. 8 February 2013. Retrieved 31 December 2013. {{cite web}}: |section= ignored (help)
  3. ^ a b Krueger SK, Williams DE (2005). "Mammalian flavin-containing monooxygenases: structure/function, genetic polymorphisms and role in drug metabolism". Pharmacol. Ther. 106 (3): 357–387. doi:10.1016/j.pharmthera.2005.01.001. PMC 1828602. PMID 15922018. {{cite journal}}: Unknown parameter |month= ignored (help)
  4. ^ "Methmphetamine". Chemspider. Retrieved 3 January 2013. {{cite web}}: |section= ignored (help)
  5. ^ a b c d e f "Methamphetamine". PubChem Compound. National Center for Biotechnology Information. Retrieved 31 December 2013. {{cite web}}: |section= ignored (help)
  6. ^ "Methamphetamine". Drug profiles. European Monitoring Centre for Drugs and Drug Addiction (EMCDDA). 16 August 2010. Retrieved 1 September 2011.
  7. ^ "Methamphetamine". DrugBank. University of Alberta. 8 February 2013. Retrieved 31 December 2013. {{cite web}}: |section= ignored (help)
  8. ^ "Meth Slang Names". MethhelpOnline. Retrieved 1 January 2014.
  9. ^ a b c d e Malenka RC, Nestler EJ, Hyman SE (2009). "15". In Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 370. ISBN 9780071481274. Unlike cocaine and amphetamine, methamphetamine is directly toxic to midbrain dopamine neurons.{{cite book}}: CS1 maint: multiple names: authors list (link)
  10. ^ a b c d e f g h Krasnova IN, Cadet JL (2009). "Methamphetamine toxicity and messengers of death". Brain Res Rev. 60 (2): 379–407. doi:10.1016/j.brainresrev.2009.03.002. PMC 2731235. PMID 19328213. 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) ...
    Neuropsychological studies have detected deficits in attention, working memory, and decision-making in chronic METH addicts …
    There is compelling evidence that the negative neuropsychiatric consequences of METH abuse are due, at least in part, to drug-induced neuropathological changes in the brains of these METH-exposed individuals …
    Structural magnetic resonance imaging (MRI) studies in METH addicts have revealed substantial morphological changes in their brains. These include loss of gray matter in the cingulate, limbic and paralimbic cortices, significant shrinkage of hippocampi, and hypertrophy of white matter (Thompson et al., 2004). In addition, the brains of METH abusers show evidence of hyperintensities in white matter (Bae et al., 2006; Ernst et al., 2000), decreases in the neuronal marker, N-acetylaspartate (Ernst et al., 2000; Sung et al., 2007), reductions in a marker of metabolic integrity, creatine (Sekine et al., 2002) and increases in a marker of glial activation, myoinositol (Chang et al., 2002; Ernst et al., 2000; Sung et al., 2007; Yen et al., 1994). Elevated choline levels, which are indicative of increased cellular membrane synthesis and turnover are also evident in the frontal gray matter of METH abusers (Ernst et al., 2000; Salo et al., 2007; Taylor et al., 2007).     {{cite journal}}: Unknown parameter |month= ignored (help)
  11. ^ a b c d e f g h i j "Methamphetamine". DrugBank. University of Alberta. 8 February 2013. Retrieved 31 December 2013. {{cite web}}: |section= ignored (help)
  12. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag "Desoxyn Prescribing Information" (PDF). United States Food and Drug Administration. 2013. Retrieved 31 December 2013. {{cite web}}: Unknown parameter |month= ignored (help)
  13. ^ Castle L, Aubert RE, Verbrugge RR, Khalid M, Epstein RS (2007). "Trends in medication treatment for ADHD". J Atten Disord. 10 (4): 335–42. doi:10.1177/1087054707299597. PMID 17449832. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  14. ^ a b c "List of psychotropic substances under international control" (PDF). International Narcotics Control Board. Archived from the original (PDF) on 2005-09-07. Retrieved 2010-05-10. Cite error: The named reference "incb" was defined multiple times with different content (see the help page).
  15. ^ a b c Cruickshank CC, Dyer KR (2009). "A review of the clinical pharmacology of methamphetamine". Addiction. 104 (7): 1085–99. doi:10.1111/j.1360-0443.2009.02564.x. PMID 19426289. {{cite journal}}: Unknown parameter |month= ignored (help)
  16. ^ "Vicks Vapoinhaler". Vicks. Retrieved 2 January 2014. {{cite web}}: |section= ignored (help)
  17. ^ "Levomethamphetamine". Pubchem Compound. National Center for Biotechnology Information. Retrieved 2 January 2014. {{cite web}}: |section= ignored (help)
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    The prevalence of this withdrawal syndrome is extremely common (Cantwell 1998; Gossop 1982) with 87.6% of 647 individuals with amphetamine dependence reporting six or more signs of amphetamine withdrawal listed in the DSM when the drug is not available (Schuckit 1999) ... Withdrawal symptoms typically present within 24 hours of the last use of amphetamine, with a withdrawal syndrome involving two general phases that can last 3 weeks or more. The first phase of this syndrome is the initial "crash" that resolves within about a week (Gossop 1982;McGregor 2005) ...    {{cite journal}}: CS1 maint: multiple names: authors list (link)
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