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PubMed2006

Ontogeny of the adrenal response to (+)-methamphetamine in neonatal rats: the effect of prior drug exposure.

We examined the ontogeny of the corticosterone response to (+)-methamphetamine in neonatal rats. In experiment-1, animals were injected with 10 mg/kg of (+)-methamphetamine or saline and plasma corticosterone levels were examined in separate groups 30 or 105 min later on postnatal day (P) 1, 3, 5, 7, 9, 11, 13, 15, 17, or 19. The adrenal response to methamphetamine was best described by a U-shaped function with the nadir of corticosterone release occurring between P7 and P13. Experiment-2 was similar except that the effect of four consecutive days of exposure to (+)-methamphetamine (four times daily at 2 h intervals with 10 mg/kg) was assessed with a single final dose early on the fifth day (i.e. P1-5, 3-7, 5-9, 7-11, 9-13, 11-15, 13-17, 15-19). The 30 min corticosterone response after multiple methamphetamine doses was augmented compared to single exposures, with the exception of the two earliest dosing intervals ending on P5 and P7, where the responses were lower. In addition, at 105 min, the levels of corticosterone were attenuated relative to a single drug administration. With the exception of animals receiving methamphetamine from P15 to P19, thymus weights were unaffected. The data demonstrate that (+)-methamphetamine is a robust activator of corticosterone release in developing animals and this release is extensively modified by age and previous drug exposure.

Adrenal Glands↗

PubMed2006

Trends in production, trafficking, and consumption of methamphetamine and cocaine in Mexico.

Over the past decade, Mexico has experienced a significant increase in trafficking of cocaine and trafficking and production of methamphetamine. An estimated 70% of United States cocaine originating in South America passes through the Central America-Mexico corridor. Mexico-based groups are now believed to control 70%-90% of methamphetamine production and distribution in the United States. Increased availability of these drugs at reduced prices has led to a parallel rise in local drug consumption. Methamphetamine abuse is now the primary reason for seeking drug abuse treatment in a number of cities, primarily in northwestern Mexico. Although cocaine and methamphetamine use have been linked with the sex trade and high-risk behaviors, such as shooting gallery attendance and unprotected sex in other settings, comparatively little is known about the risk behaviors associated with use of these drugs in Mexico, especially for methamphetamines. We review historical aspects and current trends in cocaine and methamphetamine production, trafficking, and consumption in Mexico, with special emphasis on the border cities of Ciudad Juarez and Tijuana. Additionally, we discuss the potential public health consequences of cocaine use and the recent increase in methamphetamine use, especially in regards to the spread of bloodborne and other infections, in an effort to inform appropriate public health interventions.

Adolescent↗

PubMed2003

Crystal methamphetamine-associated cardiomyopathy: tip of the iceberg?

BACKGROUND: Crystal methamphetamine has become a drug of widespread use. Previous reports describe myocardial infarction, pulmonary edema, and aortic dissection related to methamphetamine use. Cardiomyopathy due to methamphetamine exposure has been rarely described. METHODS: We identified 1640 patients admitted in a 4-yr period with a primary or secondary diagnosis of cardiomyopathy. We excluded patients with known cause of cardiomyopathy other than substance abuse. We found 120 patients had a diagnosis of substance abuse, including 21 patients with methamphetamine use. We retrospectively reviewed the medical records of these 21 crystal methamphetamine users. RESULTS: Nineteen (84%) underwent echocardiography with consistent findings of dilated cardiomyopathy and global ventricular dysfunction. Of five who had a nuclear myocardial perfusion study, none had evidence of ischemia or infarct. Of six who underwent cardiac catheterization, only one had evidence of coronary stenosis. CONCLUSION: Methamphetamine use appears to produce cardiomyopathy in some users. The pathogenesis is probably similar to that of cocaine and catecholamine-induced cardiomyopathy. Cellular, animal, and clinical data support the link between methamphetamine exposure and myocardial pathology.

Adult↗

PubMed2005

Sexual behavior patterns of methamphetamine-using gay and bisexual men.

We assessed the sexual behaviors of 49 gay and bisexual methamphetamine users in New York City and the relationship between their use of the substance and their sexual practices as part of a larger investigation of the behavioral aspects of methamphetamine use. Participants were assessed on their use of methamphetamine and their sexual behaviors in conjunction with use of the substance. Participants reported equivalent rates of unprotected anal insertive and receptive behaviors when comparing their sexual acts while high on methamphetamine, high on other drugs, and sober. In addition, equivalent rates of "extreme" sex acts were found for 10 of the 12 behaviors examined while high on methamphetamine and while sober. While wefound few differences in terms of rates of sexual behaviors, our analysis revealed more frequent risky sexual behaviors among HIV positive men when compared with HIV negative men. Our results suggest that methamphetamine attracts a hypersexual risk-taking group of men who engage in unprotected sexual behaviors regardless of their methamphetamine use. Treatment implications are discussed.

Adult↗

PubMed2003

Why is parkinsonism not a feature of human methamphetamine users?

For more than 50 years, methamphetamine has been a widely used stimulant drug taken to maintain wakefulness and performance and, in high doses, to cause intense euphoria. Animal studies show that methamphetamine can cause short-term and even persistent depletion of brain levels of the neurotransmitter dopamine. However, the clinical features of Parkinson's disease, a dopamine deficiency disorder of the brain, do not appear to be characteristic of human methamphetamine users. We compared dopamine levels in autopsied brain tissue of chronic methamphetamine users with those in patients with Parkinson's disease and in a control group. Mean dopamine levels in the methamphetamine users were reduced more in the caudate (-61%) than in the putamen (-50%), a pattern opposite to that of Parkinson's disease. Some methamphetamine users had severely decreased dopamine levels, within the parkinsonian range, in the caudate (up to 97% dopamine loss) but not in the putamen. As the putamen and caudate subserve aspects of motor and cognitive function, respectively, our data suggest that methamphetamine users are not parkinsonian because dopamine levels are not sufficiently decreased in the motor component of the striatum. However, the near-total reduction in the caudate could explain reports of cognitive disturbances, sometimes disabling, in some drug users, and suggests that treatment with dopamine substitution medication (e.g. levodopa) during drug rehabilitation might be helpful.

Adolescent↗

PubMedDate not supplied

Retrospective analysis of some L-methamphetamine/L-amphetamine urine data.

A limited analysis is presented of data accumulated over about three years for specimens containing either nonracemic L-methamphetamine/L-amphetamine or racemic mixtures of the D and L stereoisomers. 55 data points for both nonracemic L-methamphetamine and racemic mixtures show that it is possible to report a specimen containing L-methamphetamine positive for illegal D-methamphetamine based on current guidelines unless chiral assays are performed on selected methamphetamine positives. Generation of only 45 racemic specimens from chiral analysis of about 5,000 urine methamphetamine positives demonstrates the overwhelming prevalence of nonracemic illegal D-methamphetamine in Southern California.

Amphetamine↗

PubMedDate not supplied

Detection and quantitation of amphetamine and methamphetamine: electron impact and chemical ionization with ammonia--comparative investigation on Shimadzu QP 5000 GC-MS system.

Gas chromatographic-mass spectrometric (GC-MS) analyses of amphetamine and methamphetamine with chemical ionization (CI) (NH3) and electron impact (EI) were compared after solid-phase extraction from urine. The optimal CI (NH3) conditions for amphetamines were selected; the CI mass spectra of amphetamine, methamphetamine, methylenedioxyamphetamine (MDA), methylenedioxymethamphetamine (MDMA), and methylenedioxyethylamphetamine (MDEA) were obtained. Amphetamine and methamphetamine were monitored as [M+H]+ ions in SIM mode. Under these conditions the GC-MS limits of detection and quantitation were determined for amphetamine (2.1 and 5.0 mg/L, respectively) and for methamphetamine (0.9 and 2.0 mg/L, respectively). The heptafluorobutanoyl (HFB) derivatives were used to increase the sensitivity of the GC-MS analysis of amphetamines. Under CI (NH3) conditions these compounds form mainly the cluster ions [M+NH4]+. For HFB-derivatives the limits of detection and quantitation for CI (NH3) were 95 and 170 micrograms/L, respectively, for amphetamine (m/z 349) and 90 and 160 micrograms/L, respectively, for methamphetamine (m/z 363). For EI they were 10 and 30 micrograms/L, respectively, for amphetamine (m/z 240) and 9 and 27 micrograms/L, respectively, for methamphetamine (m/z 254). The GC-MS-CI (NH3) technique was found to be suitable for confirmation of amphetamine and methamphetamine in urine samples in addition to the routine GC-MS-EI method.

Amphetamine↗

PubMed2004

Deposition characteristics of methamphetamine and amphetamine in fingernail clippings and hair sections.

Fingernail clippings collected from 97 consenting females, who admitted amphetamines and/or opiates use and are currently under treatment, were quantitatively analyzed for the presence of methamphetamine and amphetamine. Sixty-two subjects were found positive for methamphetamine/amphetamine. Paired nail-hair specimens were collected from 6 of these subjects for a 12-week period and analyzed to determine the duration of detectability and deposition characteristics of amphetamines in fingernails; whether data derived from the analysis of nail clippings and hair sections are reflective of drug use patterns; and whether there is a relationship between the analytical data derived from the paired nail-hair specimens. Typical sample pre-treatment procedures and GC-MS protocols were evaluated to establish the validity of various analytical parameters and to ensure that the resulting data can be properly interpreted. Major findings include 1. Methamphetamine was found in the nails of 62 subjects collected in Week 0. The distribution of methamphetamine concentrations (ng/mg) in these nail samples are range, 0.46-61.50; mean, 9.96; and standard deviation: 13.33. The corresponding data for amphetamine are < 0.20-5.42, 0.93, and 1.01, respectively. 2. Sectional analyses of hair samples collected from 6 subjects in Week 0 show methamphetamine concentrations peak at different distances from the root. 3. The concentrations of methamphetamine and amphetamine in nail clippings are generally lower than the first 1.5-cm section of hair samples collected at the same time from the same individual. 4. Amphetamine/ methamphetamine concentration ratios in nail clippings and hair samples are comparable. 5. Methamphetamine concentration in the nail clippings collected at Weeks 0, 4, 8, and 12 decreases in a pattern similar to that exhibited by the first 1.5-cm sections of the hair samples collected at the same time.

Adult↗

PubMed1996

Cardiac muscle lesions associated with chronic administration of methamphetamine in rats.

Cardiovascular complications associated with methamphetamine abuse have increasingly been reported. However, chronic cardiotoxicity of methamphetamine is not experimentally well documented. In this study, methamphetamine (1 mg/kg/day) was subcutaneously injected into 5-week-old male Wistar Kyoto rats (n = 30). Age- and sex-matched Wistar Kyoto rats served as controls (n = 30). After 14 and 56 days, hearts were examined by light and electron microscopy. Foci of myocytic degeneration and necrosis appeared in the sub-endocardial areas on day 14 of methamphetamine exposure. Myocytic degeneration and necrosis became more extensive on day 56. At this stage, myocytolysis, contraction bands, atrophied myocytes, and spotty fibrosis were patchily distributed throughout the myocardium in most of rats treated with methamphetamine. The accompanying ultrastructural features included marked degeneration of cardiac mitochondria with fractured and disrupted cristae, hypercontraction of myofibrils, and loss of myofilament. In contrast, cardiac myocyte lesions were not observed in control rats. These myocardial lesions in rats treated with methamphetamine for 56 days resemble the cardiomyopathy associated with methamphetamine abuse in humans.

Animals↗

PubMed1991

Clinical effects of daily methamphetamine administration.

This study investigated alterations in the disposition and pharmacodynamics of methamphetamine HCl after daily administration. Six male paid volunteers familiar with the use of amphetamines participated. Each subject was administered 10 mg of methamphetamine HCl as a slow-release preparation (Desoxyn Gradumets) at 9 a.m. for 13 consecutive days (days 2-14 of the study). On days 1 and 15 the subjects were challenged with 10 mg of oral deuterated methamphetamine HCl. Deuterated drug was used to differentiate plasma concentrations of challenge doses from those of daily doses. The heart rate, subjective perception of "high," and plasma concentrations of methamphetamine were examined on days 1 and 15. Repeated ANOVA measures indicate that a significant decrease in heart-rate acceleration in response to methamphetamine challenge occurred on day 15 [F(1,5) = 8.26, p less than or equal to 0.035]. However, no significant change in either the subjective ratings of "high" or the plasma concentrations of deuterated methamphetamine occurred. These findings indicate that the disposition of methamphetamine and its subjective effects were not altered by this period of daily exposure to a low dose of the drug. In contrast, tolerance to the heart-rate accelerating effect was observed.

Adult↗

PubMed1998

Inadvertent methamphetamine poisoning in pediatric patients.

With the increase in popularity of adult methamphetamine abuse in the state of Arizona, there has been an increase in the number of pediatric admissions from inadvertent methamphetamine poisoning. This report describes the signs and symptoms and the hospital course of pediatric patients inadvertently poisoned with methamphetamine. A nine-year retrospective chart review identified 18 pediatric patients poisoned only with methamphetamine. This review revealed that pediatric patients with methamphetamine poisoning commonly presented with the following signs and symptoms: tachycardia (18 patients), agitation (nine patients), inconsolable crying and irritability (six patients), and vomiting (six patients). The most common ancillary tests, excluding urine drug screens, used in formulating the diagnosis were computed tomography scans of the head (five patients) and lumbar punctures (three patients). Three patients received Centruroides sculpturatus antivenin intravenously. The most common complication of methamphetamine poisoning was rhabdomyolysis (two patients), and the average hospital stay for all patients was three days. This case series demonstrates that pediatric patients who ingest methamphetamine can present with signs and symptoms similar to those of an abdominal or neurologic pediatric emergency.

Adult↗

PubMed2004

Brain antioxidant systems in human methamphetamine users.

Animal data suggest that the widely abused psychostimulant methamphetamine can damage brain dopamine neurones by causing dopamine-dependent oxidative stress; however, the relevance to human methamphetamine users is unclear. We measured levels of key antioxidant defences [reduced (GSH) and oxidized (GSSG) glutathione, six major GSH system enzymes, copper-zinc superoxide dismutase (CuZnSOD), uric acid] that are often altered after exposure to oxidative stress, in autopsied brain of human methamphetamine users and matched controls. Changes in the total (n = 20) methamphetamine group were limited to the dopamine-rich caudate (the striatal subdivision with the most severe dopamine loss) in which only activity of CuZnSOD (+ 14%) and GSSG levels (+ 58%) were changed. In the six methamphetamine users with severe (- 72 to - 97%) caudate dopamine loss, caudate CuZnSOD activity (+ 20%) and uric acid levels (+ 63%) were increased with a trend for decreased (- 35%) GSH concentration. Our data suggest that brain levels of many antioxidant systems are preserved in methamphetamine users and that GSH depletion, commonly observed during severe oxidative stress, might occur only with severe dopamine loss. Increased CuZnSOD and uric acid might reflect compensatory responses to oxidative stress. Future studies are necessary to establish whether these changes are associated with oxidative brain damage in human methamphetamine users.

Adolescent↗

PubMed2006

Histological brain alterations following prenatal methamphetamine exposure in rats.

When pregnant women abuse methamphetamine, the foremost concern is the potential adverse effect of this substance on fetal development. Clinical studies in humans have found that exposure to methamphetamine during brain development can cause neurobehavioral abnormalities, such as aggressive behavior, learning problems, and poor social adaptation. In the present study, we examined the effects of prenatal methamphetamine exposure on brain development in rats. The first group of pregnant rats was administered methamphetamine at a dose of 5 mg/kg/day during gestational day (GD 10 to GD 20 [MA]. The second group of pregnant rats was injected with saline vehicle only [SAL]. On GD 21 their fetuses were removed and fetal brains were observed. We found various types of morphological damage in MA fetal brains, including microgyria, ectopia, and hemorrhage. In some cases, abnormal distribution of the leptomeninx, such as breach or accumulation, was observed in addition to these histological abnormalities. Therefore, we examined the expression of laminin, which is an important component of the pia mater, in the fetal brains. However, Western blot analysis revealed that there was no difference in expression amount of laminin in whole fetal brain between the MA and SAL groups. We concluded that methamphetamine use during pregnancy can cause histological brain alterations in fetuses. Morphological alterations of brain seen in the present study and previous human studies following prenatal exposure to methamphetamine might be related to the neurobehavioral abnormalities seen in patients who had been exposed to methamphetamine in utero.

Animals↗

PubMed1996

Neurochemical analysis of the psychotoxicity of methamphetamine and cocaine by microdialysis in the rat brain.

To examine the neurochemical mechanism underlying the development of psychotoxicity by methamphetamine and cocaine, the levels of dopamine, serotonin and their metabolites were determined by in vivo microdialysis in the brains of freely moving rats. Methamphetamine (0.5 mg/kg, s.c.) or cocaine (10 mg/kg, i.p.) was repeatedly administered for 8 to 21 experiment days, and after confirming the development of sensitization to the stimulating effect of the drugs on spontaneous motor activity, a microdialysis probe was implanted into the nucleus accumbens (N.Acc.) or striatum of the brain of the treated rats. Then, each test drug was readministered to the rats and dopamine and DOPAC or serotonin and 5-HIAA concentrations were determined. In the N.Acc. of untreated control rats, methamphetamine increased dopamine to about 4 times the preadministration value along with a decrease of DOPAC. Methamphetamine also increased serotonin to about twice the preadministration value along with no change in 5-HIAA. Cocaine increased dopamine to about 4 times along with a slight decrease in DOPAC. In the treated rats as compared with the untreated rats, the increasing effect of methamphetamine on dopamine in the N.Acc. was enhanced but that of cocaine was not. Also, the serotonin levels were lower than in the untreated rats and 5-HIAA was unchanged. In the striatum of untreated rats, methamphetamine increased dopamine to about 3 times the preadministration value along with a slight decrease in DOPAC. In the treated rats, the increasing effect of methamphetamine on dopamine in the striatum was enhanced, and the DOPAC level was higher than in the treated rats. The present study suggests that the dopamine level at the N.Acc. does not necessarily reflect the sensitization to spontaneous motor activity, and that enhancement of the motor activity does not seem to be the best model for psychotoxic manifestation.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2003

Involvement of adenosine A1 and A2A receptors in the adenosinergic modulation of the discriminative-stimulus effects of cocaine and methamphetamine in rats.

Adenosine, by acting on adenosine A1 and A2A receptors, is known to antagonistically modulate dopaminergic neurotransmission. We have recently reported that nonselective adenosine receptor antagonists (caffeine and 3,7-dimethyl-1-propargylxanthine) can partially substitute for the discriminative-stimulus effects of methamphetamine. In the present study, by using more selective compounds, we investigated the involvement of A1 and A2A receptors in the adenosinergic modulation of the discriminative-stimulus effects of both cocaine and methamphetamine. The effects of the A1 receptor agonist N6-cyclopentyladenosine (CPA; 0.01-0.1 mg/kg) and antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT; 1.3-23.7 mg/kg) and the A2A receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine hydrochloride (CGS 21680; 0.03-0.18 mg/kg) and antagonist 3-(3-hydroxypropyl)-8-(3-methoxystyryl)-7-methyl-1-propargylxanthin phosphate disodium salt (MSX-3; 1-56 mg/kg) were evaluated in rats trained to discriminate either 1 mg/kg methamphetamine or 10 mg/kg cocaine from saline under a fixed-ratio 10 schedule of food presentation. The A1 and A2A receptor antagonists (CPT and MSX-3) both produced high levels of drug-lever selection when substituted for either methamphetamine or cocaine and significantly shifted dose-response curves of both psychostimulants to the left. Unexpectedly, the A2A receptor agonist CGS 21680 also produced drug-appropriate responding (although at lower levels) when substituted for the cocaine-training stimulus, and both CGS 21680 and the A1 receptor agonist CPA significantly shifted the cocaine dose-response curve to the left. In contrast, both agonists did not produce significant levels of drug-lever selection when substituted for the methamphetamine-training stimulus and failed to shift the methamphetamine dose-response curve. Therefore, adenosine A1 and A2A receptors appear to play important but differential roles in the modulation of the discriminative-stimulus effects of methamphetamine and cocaine.

Adenosine↗

PubMed2002

Acute and chronic effects of methamphetamine on tele-methylhistamine levels in mouse brain: selective involvement of the D(2) and not D(3) receptor.

We have explored the role of endogenous dopamine in the control of histaminergic neuron activity in mouse brain regions evaluated by changes in tele-methylhistamine (t-MeHA) levels. In vitro, methamphetamine released [(3)H]noradrenaline but failed to release [(3)H]histamine from synaptosomes. In vivo, methamphetamine enhanced t-MeHA levels by about 2-fold with ED(50) values of approximately 1 mg/kg in caudate putamen, nucleus accumbens, cerebral cortex, and hypothalamus. This response selectively involved the D(2) and not the D(3) receptor as indicated by its blockade by haloperidol and by its persistence after administration of nafadotride, a D(3) receptor preferential ligand, or in (-/-) D(3) receptor-deficient mice. The t-MeHA response to methamphetamine was delayed compared with the locomotor-activating effect of this drug, suggesting that it is of compensatory nature. In agreement, ciproxifan, an inverse agonist known to enhance histamine neuron activity, decreased the hyperlocomotion induced by methamphetamine. Repeated methamphetamine administration resulted in the expected sensitization to the hyperlocomotor effect of the drug but did not modify either the ED(50) or the E(max) regarding t-MeHA levels. However, it resulted in an enhanced basal t-MeHA level (+30-40%), which was sustained for at least 11 days after withdrawal in hypothalamus, striatum, and cerebral cortex and suppressed by haloperidol. Hence, both the acute and chronic administration of methamphetamine enhance histamine neuron activity, presumably in a compensatory manner. Repeated methamphetamine administration also resulted in a modified balance in the opposite influences of dopamine and serotonin on histaminergic neurons as revealed by the enhanced response to haloperidol and abolished response to ketanserin, respectively.

Animals↗

PubMed2002

Mice with partial deficiency of c-Jun show attenuation of methamphetamine-induced neuronal apoptosis.

The regional distribution of c-Jun expression and of the number of apoptotic cells was compared in various brain areas after methamphetamine administration to mice. Our results showed that there was methamphetamine-induced overexpression of c-Jun in the cortex and striatum but not in the cerebellar cortex. There was an almost totally similar regional appearance of methamphetamine-induced apoptotic cells in the mouse brain; no apoptosis was present in the cerebellum. Additionally, in the neocortical area, more positive signals for c-Jun immunoreactivity were observed in the piriform cortex, an area that also showed more positive terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) signals than the frontal and parietal cortices. These observations suggested that c-Jun might be involved in methamphetamine-induced apoptosis. This idea was confirmed by using heterozygous c-Jun knockout mice that showed much less apoptosis than wild-type controls. In addition, we found that the majority of TUNEL-positive cells were also positive for c-Jun-like immunoreactivity in both genotypes. Moreover, methamphetamine-induced caspase-3 activity and PARP cleavage were also reduced in c-Jun heterozygous knockout mice. In contrast, methamphetamine-induced hyperthermia was essentially identical in the two genotypes. When taken together, our data support the hypothesis that c-Jun is involved in methamphetamine-induced apoptosis.

Animals↗

PubMed2005

Additive effects of HIV and chronic methamphetamine use on brain metabolite abnormalities.

OBJECTIVE: Proton magnetic resonance spectroscopy (1H-MRS) showed decreased neuronal marker N-acetylaspartate and increased glial marker myo-inositol in subjects with chronic methamphetamine use and in subjects infected with HIV. The authors sought to determine whether HIV and a history of chronic methamphetamine use might have additive or interactive effects on brain metabolite abnormalities. METHOD: 1H-MRS was performed in 68 HIV-positive subjects (24 with a history of chronic methamphetamine use with a lifetime exposure of a mean of 2,167 g [SD=2,788] and last use a mean of 4.9 months earlier [SD=6.0]; 44 with no history of drug abuse) and 75 HIV-negative subjects (36 with a history of chronic methamphetamine use with a lifetime exposure of a mean of 8,241 g [SD=16,850] and last use a mean of 6.3 months earlier [SD=7.8]; 39 with no history of drug abuse). Concentrations of N-acetylaspartate, creatine, choline, and myo-inositol were measured in the frontal cortex, frontal white matter, and basal ganglia. RESULTS: HIV-negative subjects with a history of chronic methamphetamine use showed lower concentrations of the neuronal marker N-acetylaspartate in the frontal white matter and basal ganglia and higher concentrations of choline compounds and the glial marker myo-inositol in the frontal cortex, relative to subjects with no history of drug abuse. HIV-positive status was associated with lower concentrations of N-acetylaspartate and creatine in the frontal cortex and higher concentrations of myo-inositol in the white matter, compared with HIV-negative status. Compared to the mean concentrations of metabolites in HIV-negative subjects with no history of drug abuse, the mean concentrations in subjects with HIV and chronic methamphetamine use showed additive effects on N-acetylaspartate in all three regions (-9% in the basal ganglia, -7% in the frontal white matter, and -6% in the frontal gray matter), on creatine in the basal ganglia (-7%), and on myo-inositol in the frontal white matter (+11%). CONCLUSIONS: The combined effects of HIV and chronic methamphetamine use were consistent with an additive model, suggesting additional neuronal injury and glial activation due to the comorbid conditions.

Adult↗