This study sought to characterize neuropsychological functioning in MJ-using adolescents and emerging adults (ages 18–26) and to investigate whether gender moderated these effects. Data were collected from 59 teens and emerging adults including MJ users (n = 23, 56% female) and controls (n = 35, 50% female) aged 18–26 (M = 21 years). Exclusionary criteria included independent Axis I disorders (besides SUD), and medical and neurologic disorders. After controlling for reading ability, gender, subclinical depressive symptoms, body mass index, and alcohol and other drug use, increased MJ use was associated with slower psychomotor speed/sequencing ability (p < .01), less efficient sustained attention (p < .05), and increased cognitive inhibition errors (p < .03). Gender significantly moderated the effects of MJ on psychomotor speed/sequencing ability (p < .003) in that males had a more robust negative relationship. The current study demonstrated that MJ exposure was associated with poorer psychomotor speed, sustained attention and cognitive inhibition in a dose-dependent manner in young adults, findings that are consistent with other samples of adolescent MJ users. Male MJ users demonstrated greater cognitive slowing than females. Future studies need to examine the neural substrates underlying with these cognitive deficits and whether cognitive rehabilitation or exercise interventions may serve as a viable treatments of cognitive deficits in emerging adult MJ users. (JINS, 2012, 18, 1–11)

In adults, studies examining the long-lasting cognitive effects of marijuana use demonstrate subtle deficits in attention, executive function, and memory. Because neuromaturation continues through adolescence, these results cannot necessarily generalize to adolescent marijuana users. The goal of this study was to examine neuropsychological functioning in abstinent marijuana using and demographically similar control adolescents. Data were collected from 65 adolescent marijuana users (n = 31, 26% females) and controls (n = 34, 26% females) 16–18 years of age. Extensive exclusionary criteria included independent psychiatric, medical, and neurologic disorders. Neuropsychological assessments were conducted after > 23 days of monitored abstinence. After controlling for lifetime alcohol use and depressive symptoms, adolescent marijuana users demonstrated slower psychomotor speed (p < .05), and poorer complex attention (p < .04), story memory (p < .04), and planning and sequencing ability (p < .001) compared with controls. Post hoc analysis revealed that the number of lifetime marijuana use episodes was associated with poorer cognitive function, even after controlling for lifetime alcohol use. The general pattern of results suggested that, even after a month of monitored abstinence, adolescent marijuana users demonstrate subtle neuropsychological deficits compared with nonusers. It is possible that frequent marijuana use during adolescence may negatively influence neuromaturation and cognitive development. (JINS, 2007, 13, 807–820.)

Ecstasy (MDMA) is a popular drug that can act as a selective serotonin neurotoxin in several species. The goal of the present study was to examine the relationship between ecstasy exposure and cognitive functioning after controlling for other drug use and demographic variables. Furthermore, we assessed whether gender was a moderator of the relationship between cognitive functioning and ecstasy use. Data were collected from 31 men and 34 women with a wide range of ecstasy use (17 marijuana users with no ecstasy use and 48 ecstasy users ranging from low to heavy use). Participants were interviewed and administered a battery of neuropsychological tests. The primary finding was that ecstasy exposure was significantly related to poorer verbal learning and memory ability in a dose-dependent manner, while no such relationship was observed between ecstasy exposure and executive functioning or attentional ability. Gender was found to significantly moderate the relationship between ecstasy consumption and design fluency. These results suggest primary memory dysfunction among abstinent recreational ecstasy users. This finding is consistent with reports of hippocampal vulnerability, particularly among heavy users. (JINS, 2005, 11, 753–765.)

Both HIV infection and methamphetamine dependence can be associated with brain dysfunction. Little is known, however, about the cognitive effects of concurrent HIV infection and methamphetamine dependence. The present study included 200 participants in 4 groups: HIV infected/methamphetamine dependent (HIV+/METH+), HIV negative/methamphetamine dependent (HIV−/METH+), HIV infected/methamphetamine nondependent (HIV+/METH−), and HIV negative/methamphetamine nondependent (HIV−/METH−). Study groups were comparable for age, education, and ethnicity, although the HIV−/METH− group had significantly more females. A comprehensive, demographically corrected neuropsychological battery was administered yielding a global performance score and scores for seven neurobehavioral domains. Rates of neuropsychological impairment were determined by cutoff scores derived from performances of a separate control group and validated with larger samples of HIV+ and HIV− participants from an independent cohort. Rates of global neuropsychological impairment were higher in the HIV+/METH+ (58%), HIV−/METH+ (40%) and HIV+/METH− (38%) groups compared to the HIV−/METH− (18%) group. Nonparametric analyses revealed a significant monotonic trend for global cognitive status across groups, with least impairment in the control group and highest prevalence of impairment in the group with concurrent HIV infection and methamphetamine dependence. The results indicate that HIV infection and methamphetamine dependence are each associated with neuropsychological deficits, and suggest that these factors in combination are associated with additive deleterious cognitive effects. This additivity may reflect common pathways to neural injury involving both cytotoxic and apoptotic mechanisms. (JINS, 2004, 10, 1–14.)Note: Dr. Erin D. Bigler served as action editor during the course of this review.

The aim of this prospective study was to examine skin reactivity to four vasomotor agents and to determine whether non-eosinophilic rhinitis patients differ from patients with eosinophilic rhinitis. Nasal cytology enabled us to classify 74 rhinitis patients into a non-eosinophilic (n = 63) and an eosinophilic group (n = 11). Skin reactivity to intradermal tests with papaverine, metacholine, histamine and compound 48/80 was measured. No significant difference for papaverine, metacholine, histamine and compound 48/80, singly, was found between the non-eosinophilic and eosinophilic group. The frequency of the total pathological skin reactivity to vasomotor agents, singly and in combinations, was greater in the eosinophilic (91 per cent) then in the non-eosinophilic group (78 per cent) but intergroup difference was not significant. These findings suggest that pathologic skin reactivity to vasomotor agents is a feature of non-eosinophilic as well as eosinophilic non-allergic rhinitis patients and indicate that no difference is noticed in the skin reactivity between these groups.

Background and objective To investigate whether the administration of ketamine before induction with propofol produces a smaller decrease in arterial pressure.

Methods Twenty-two patients were assigned to one of two groups to receive either propofol with ketamine (n = 11) or propofol alone (n = 11, control). Anaesthesia was induced with 2 mg kg−1 propofol and 0.5 mg kg−1 ketamine or 2 mg kg−1 propofol alone. Ketamine was administered 1 min prior to induction with propofol. Immediately after induction with propofol, vecuronium (0.15 mg kg−1) was administered. Four minutes after administration of vecuronium, tracheal intubation was performed. Anaesthesia was maintained using sevoflurane (0.5%) in 66% nitrous oxide until 3 min after intubation. Systolic, diastolic and mean arterial pressure and heart rate were recorded on arrival, directly before induction with propofol, prior to tracheal intubation, immediately after intubation and at 3 min after intubation.

Results and conclusions Administration of ketamine before induction with propofol preserved haemodynamic stability compared with induction with propofol alone.

Parental dependence on illicit drugs is a growing concern across a number of disciplines. It has implications that are at once medical, political, social, and psychological. In recent years, researchers from the U.S.A. (Austin & Prendergast, 1991; Deren, 1986; Johnson, 1991) and the U.K. (Burns, O'Driscoll, & Wason, 1996) have called for greater attention to be paid to social and psychological, rather than solely physical, effects of parental drug use on children. In Ireland, against the backdrop of an intractable and escalating intravenous opiate problem, the issue of how children are affected by parental drug dependence is emerging as a new social and clinical concern. A recent government report, for example, recognises that children of drug users may be in need of clinical interventions and special care arrangements (Rabitte, 1996). But what form should such services take? Are these children at greater risk than other children from similar socioeconomic backgrounds for experiencing social and psychological problems? Is the nurturing environment provided to children whose parents are dependent on illicit drugs less adequate than that provided to children whose parents do not use drugs? At present research does not provide conclusive answers to these questions. Research that focuses on the effects of postnatal parental drug use on children's social and psychological well-being is strikingly scarce, with the majority of child-oriented research concentrating instead on the effects of prenatal exposure to drugs. The small amount of research that has been conducted on the caregiving environments of children of drug users has produced largely inconclusive findings.

The aims of the present paper are to review and analyse existing research on the social environments provided to children of drug users, and on the developmental outcomes for this group. A further aim is to provide pointers to gaps and shortcomings that need to be addressed in future research. The focus is on parental addiction to “hard drugs”, namely opiates (primarily heroin and methadone) and cocaine. Studies dealing exclusively with the impact on children of prenatal exposure to drugs and of parental alcohol use are excluded, as are studies of a primary addiction to amphetamines and other illicit substances, although it is recognised that these are frequently used in addition to opiates and cocaine.