Effects of High-Potency Cannabis on Psychomotor Performance in Frequent Cannabis Users.

Background: Recently increased access to cannabis products in the United States has been associated with increased rates of driving after cannabis use. Although numerous studies indicate that cannabis impairs psychomotor and neurocognitive functions that can affect driving ability, the determination of cannabis-impaired driving risk is complicated by the extent to which frequent cannabis users develop tolerance to THC's subjective, cognitive, and psychomotor effects, and by the fact that there is no validated behavioral or biological marker of recent cannabis use or cannabis-related impairment. This study examined the psychomotor impairment-related effects experienced by frequent cannabis users in Colorado after naturalistic consumption of smoked cannabis, both immediately and 1 h postuse. Results were then validated in a smaller replication sample from Washington state. Methods: In the primary Colorado study, participants (n=70) used the DRUID® mobile app, a brief measure of psychomotor and cognitive domains that are sensitive to the effects of cannabis. First, participants used DRUID to establish a sober baseline impairment score. During a second appointment, they used DRUID at three time points: preuse, immediately after acutely using cannabis, and 1 h postuse. In the Washington replication sample, participants (n=39) used DRUID before acute cannabis consumption and then every half hour for 2.5 h. Results: In both studies, peak DRUID impairment effects were seen immediately after cannabis use, with recovery of performance at 1 h postuse. Specifically, significant quadratic effects of time emerged for both studies (Colorado study: (ß=-0.935, SE=0.204, p<0.001); Washington study: ß=3.0299, SE=1.3085, p<0.01). Domain-specific effects were tested in the larger Colorado study and were observed for reaction time within a complex divided attention task and a postural-stability balance task. Conclusions: These findings demonstrate that psychomotor impairment emerges immediately after acute cannabis use even in regular users, but decreases significantly 1 h postuse. These results underscore the potential utility of the DRUID app for assessing acute cannabis-related psychomotor impairment. Further research is needed to explore whether the DRUID app and/or the specific psychomotor functions it assesses might serve as a tool for measuring cannabis-related driving impairment. Clinical trials registration number for the Colorado Study: NCT03522103.

Intoxication by a synthetic cannabinoid (JWH-018) causes cognitive and psychomotor impairment in recreational cannabis users.

BACKGROUND: Smoking mixtures containing synthetic cannabinoids (SCs) have become very popular over the last years but pose a serious risk for public health. Limited knowledge is, however, available regarding the acute effects of SCs on cognition and psychomotor performance. Earlier we demonstrated signs of impairment in healthy volunteers after administering one of the first SCs, JWH-018, even though subjective intoxication was low. In the current study, we aimed to investigate the acute effects of JWH-018 on several cognitive and psychomotor tasks in participants who are demonstrating representative levels of acute intoxication. METHODS: 24 healthy cannabis-experienced participants took part in this placebo-controlled, cross-over study. Participants inhaled the vapor of 75 µg JWH-018/kg body weight and were given a booster dose if needed to induce a minimum level of subjective high. They were subsequently monitored for 4 h, during which psychomotor and cognitive performance, vital signs, and subjective experience were measured, and serum concentrations were determined. RESULTS: Maximum subjective high (average 64%) was reached 30 min after administration of JWH-018, while the maximum blood concentration was shown after 5 min (8 ng/mL). JWH-018 impaired motor coordination (CTT), attention (DAT and SST), memory (SMT), it lowered speed-accuracy efficiency (MFFT) and slowed down response speed (DAT). CONCLUSION: In accordance with our previous studies, we demonstrated acute psychomotor and cognitive effects of a relatively low dose of JWH-018.

Combined HIV-1 Tat and oxycodone activate the hypothalamic-pituitary-adrenal and -gonadal axes and promote psychomotor, affective, and cognitive dysfunction in female mice.

The majority of HIV+ patients present with neuroendocrine dysfunction and ~50% experience co-morbid neurological symptoms including motor, affective, and cognitive dysfunction, collectively termed neuroHIV. In preclinical models, the neurotoxic HIV-1 regulatory protein, trans-activator of transcription (Tat), promotes neuroHIV pathology that can be exacerbated by opioids. We and others find gonadal steroids, estradiol (E2) or progesterone (P4), to rescue Tat-mediated pathology. However, the combined effects of Tat and opioids on neuroendocrine function and the subsequent ameliorative capacity of gonadal steroids are unknown. We found that conditional HIV-1 Tat expression in naturally-cycling transgenic mice dose-dependently potentiated oxycodone-mediated psychomotor behavior. Tat increased depression-like behavior in a tail-suspension test among proestrous mice, but decreased it among diestrous mice (who already demonstrated greater depression-like behavior); oxycodone reversed these effects. Combined Tat and oxycodone produced apparent behavioral disinhibition of anxiety-like responding which was greater on diestrus than on proestrus. These mice made more central entries in an open field, but spent less time there and demonstrated greater circulating corticosterone. Tat increased the E2:P4 ratio of circulating steroids on diestrus and acute oxycodone attenuated this effect, but repeated oxycodone exacerbated it. Corticotropin-releasing factor was increased by Tat expression, acute oxycodone exposure, and was greater on diestrus compared to proestrus. In human neuroblastoma cells, Tat exerted neurotoxicity that was ameliorated by E2 (1 or 10 nM) or P4 (100, but not 10 nM) independent of oxycodone. Oxycodone decreased gene expression of estrogen and κ-opioid receptors. Thus, neuroendocrine function may be an important target for HIV-1 Tat/opioid interactions.

Neuroprotective effect of resveratrol on rotenone-treated C57BL/6 mice.

The aim of the present study was to investigate whether resveratrol could reduce nigral iron levels to prevent the degeneration of dopaminergic neurons in the substantia nigra (SN) of C57BL/6 mice induced by rotenone. Parkinson's disease (PD) is an age-related neurodegenerative disorder; elevated iron levels in the SN participate in neuronal death in PD. Resveratrol is a kind of polyphenolic compounds and possess antioxidant, anticancer, and anti-inflammatory biological functions. Although many research groups have investigated the neuroprotective effects of resveratrol against PD, the precise mechanisms underlying its beneficial effects on dopaminergic neuron are poorly defined. In this study, rotenone-treated mice were used to examine neuroprotective roles of resveratrol in PD. Sixty-four adult C57BL/6 mice were divided into four groups: vehicle control mice, rotenone mice, resveratrol-treated rotenone mice, resveratrol mice. In the present study, we found that chronic administration of rotenone significantly induced motor coordination impairment and increased iron levels and dopaminergic neuron loss in SN in mice. Resveratrol administration significantly protected mice from rotenone-induced motor coordination impairment, elevated iron levels, and dopaminergic neuronal loss. Our results show that resveratrol can elicit neuroprotective effects on rotenone-induced parkinsonism through reducing nigral iron levels.

Neurobehavioural Toxicity of Iron Oxide Nanoparticles in Mice.

Iron oxide nanoparticles (Fe2O3-NPs) are widely used in various biomedical applications, extremely in neurotheranostics. Simultaneously, Fe2O3-NP usage is of alarming concern, as its exposure to living systems causes deleterious effects due to its redox potential. However, study on the neurobehavioural impacts of Fe2O3-NPs is very limited. In this regard, adult male mice were intraperitoneally administered with Fe2O3-NPs (25 and 50 mg/kg body weight) once a week for 4 weeks. A significant change in locomotor behaviour and spatial memory was observed in Fe2O3-NP-treated animals. Damages to blood-brain barrier permeability by Fe2O3-NPs and their accumulation in brain regions were evidenced by Evan's blue staining, iron estimation and Prussian blue staining. Elevated nitric oxide, acetylcholinesterase, lactate dehydrogenase leakage and demyelination were observed in the Fe2O3-NP-exposed brain tissues. Imbalanced levels of ROS generation and antioxidant defence mechanism (superoxide dismutase and catalase) cause damages to lipids, proteins and DNA. PARP and cleaved caspase 3 expression levels were found to be increased in the Fe2O3-NP-exposed brain regions which confirms DNA damage and apoptosis. Thus, repeated Fe2O3-NP exposure causes neurobehavioural impairments by nanoparticle accumulation, oxidative stress and apoptosis in the mouse brain.

Neonatal exposure to benzo[a]pyrene induces oxidative stress causing altered hippocampal cytomorphometry and behavior during early adolescence period of male Wistar rats.

Environmental neurotoxicants like benzo[a]pyrene (B[a]P) have been well documented regarding their potential to induce oxidative stress. However, neonatal exposure to B[a]P and its subsequent effect on anti-oxidant defence system and hippocampal cytomorphometry leading to behavioral changes have not been fully elucidated. We investigated the effect of acute exposure of B[a]P on five days old male Wistar pups administered with single dose of B[a]P (0.2 µg/kg BW) through intracisternal mode. Control group was administered with vehicle i.e., DMSO and a separate group of rats without any treatment was taken as naive group. Behavioral analysis showed anxiolytic-like behavior with significant increase in time spent in open arm in elevated plus maze. Further, significant reduction in fall off time during rotarod test showing B[a]P induced locomotor hyperactivity and impaired motor co-ordination in adolescent rats. B[a]P induced behavioral changes were further associated with altered anti-oxidant defence system involving significant reduction in the total ATPase, Na(+) K(+) ATPase, Mg(2+) ATPase, GR and GPx activity with a significant elevation in the activity of catalase and GST as compared to naive and control groups. Cytomorphometry of hippocampus showed that the number of neurons and glia in B[a]P treated group were significantly reduced as compared to naive and control. Subsequent observation showed that the area and perimeter of hippocampus, hippocampal neurons and neuronal nucleus were significantly reduced in B[a]P treated group as compared to naive and control. The findings of the present study suggest that the alteration in hippocampal cytomorphometry and neuronal population associated with impaired antioxidant signaling and mood in B[a]P treated group could be an outcome of neuromorphological alteration leading to pyknotic cell death or impaired differential migration of neurons during early postnatal brain development.

Impact of anti-tumor necrosis factor alpha antibodies administered to pregnant women with inflammatory bowel disease on long-term outcome of exposed children.

BACKGROUND: Prenatal exposure to anti-tumor necrosis factor α (TNF-α) antibodies seems to be safe for fetal development. Data on long-term outcome of exposed children are missing. Our aim was to assess long-term postnatal development of children exposed to anti-TNF-α during pregnancy. METHODS: Consecutive children aged ≥ 12 months exposed to anti-TNFs prenatally for maternal inflammatory bowel disease in 3 centers in the Czech Republic were enrolled. Data on psychomotor development, infections, antibiotics, vaccination, and allergy were retrospectively obtained from mothers, treating pediatricians, and children's vaccination cards. Furthermore, standardized laboratory tests on humoral and cellular immunity were performed. RESULTS: Twenty-five children exposed to biologicals were included (median age, 34 mo; range, 14-70 mo). All children had normal growth, and all but 1 had normal psychomotor development. Majority (80%) experienced at least 1 infection (mainly respiratory), and 60% of infants received antibiotics, 32% of those within the first year of life. Vaccination was undertaken according to vaccination protocol to 23 infants (92%). Fifteen children also had tuberculosis vaccination without serious complication. Immunological investigation was performed with 17 children (68%). Cellular immunity was normal in all infants, and 7 children had mild decrease in IgA and/or IgG immunoglobulins without clinical significance. All children had a detectable serologic response to vaccination. CONCLUSIONS: Exposure to anti-TNF-α antibodies seems to be safe for growth and psychomotor development of children, although clinical significance of relatively high frequency of infections and antibiotic use among infants remains questionable because of the lack of a control group. Continuous follow-up of exposed children is absolutely warranted.

Low to moderate alcohol intake during pregnancy and risk of psychomotor deficits.

BACKGROUND: To examine the effects of low to moderate alcohol consumption during pregnancy on child motor function at age 5. METHODS: A prospective follow-up study of 685 women and their children sampled from the Danish National Birth Cohort based on maternal alcohol consumption during pregnancy. At 5 years of age, the children were tested with the "Movement Assessment Battery for Children" (MABC). Parental education, maternal IQ, prenatal maternal smoking, the child's age at testing, and gender of child were considered core confounders, while the full model also controlled for prenatal maternal binge drinking episodes, age, maternal prepregnancy body mass index, parity, home environment, postnatal parental smoking, health status, and indicators for hearing and vision impairment. RESULTS: There were no systematic or significant differences in motor function between children of mothers reporting low to moderate levels of average alcohol consumption during pregnancy and children of mothers who abstained. CONCLUSIONS: In this study, we found no systematic association between low to moderate maternal alcohol intake during pregnancy and child motor function at age 5.

Effect of the p38 MAPK inhibitor SB-239063 on Lipopolysaccharide-induced psychomotor retardation and peripheral biomarker alterations in rats.

Lipopolysaccharide (LPS) administration in rats induces a characteristic syndrome termed 'sickness behavior', including profound changes on locomotor activity and circulating stress and inflammatory mediators. The aim of the present investigation was to evaluate whether the behavioral and the peripheral biomarker responses induced by LPS could be modified by acute treatment with the p38 mitogen-activated protein kinase inhibitor SB-239063. Male Sprague-Dawley rats were treated orally either with vehicle or SB-239063 (3, 10 and 30 mg/kg) 1h before an intraperitoneal injection of either saline or LPS 125 µg/kg. Two hours after LPS injection, rats were placed in a novel open field arena for locomotion assessment during both the light and dark periods. Inflammation and stress mediators were evaluated in plasma 2, 3, 5 or 14 h into the dark phase. Pre-treatment with SB-239063 significantly reversed the locomotor deficits induced by LPS injection. Interleukin (IL)-1ß, IL-6, IL-10, Granulocyte-Macrophage-Colony Stimulating Factor, Interferon-γ, and C-reactive-protein levels were increased significantly by LPS, but not when LPS was preceded by SB-239063 treatment. LPS significantly decreased growth-hormone and Prolactin, and this effect was attenuated by SB-239063. Tumor Necrosis Factor-α, Adrenocorticotropic Hormone and Corticosterone levels were significantly higher in LPS-treated rats and were not normalized by SB-239063. Thus, we demonstrate that acute treatment with SB-239063 may have ameliorating effects in early changes of LPS-induced sickness behavior and alteration in the peripheral cytokines/hormones. As such, our procedure may offer an opportunity to test the activity of novel anti-inflammatory compounds on specific symptoms of sickness associated with neuroimmune dysfunctions.

Impairment due to cannabis and ethanol: clinical signs and additive effects.

AIMS: Studies have shown that the impairing effects of Delta-9-tetrahydrocannabinol (THC) are dose-related. Cannabis intake increases the risk of traffic accidents. The purpose of this study was to see how different clinical tests and observations were related to blood THC concentrations and to determine whether the combined influence of THC and ethanol was different from either drug alone. DESIGN: A retrospective cross-sectional forensic database study. SETTING: Drivers apprehended by the police suspected of driving under the influence of alcohol and other drugs. PARTICIPANTS: We investigated 589 cases positive for THC only. In addition, 894 cases with THC and ethanol were included. A comparison was made with 3480 drivers with only ethanol in their blood and 79 drivers who tested negative. MEASUREMENTS: Data were analytical results of blood samples and the 27 clinical tests and observations included in the Norwegian clinical test for impairment (CTI). FINDINGS: No relationship was found between blood THC concentration and most of the CTI tests. Blood THC concentration was, however, related to conjunctival injection, pupil dilation and reaction to light and to the overall risk of being judged impaired. When THC and ethanol were detected together the risk of being judged impaired was increased markedly. CONCLUSIONS: This study demonstrates that cannabis impairs driving ability in a concentration-related manner. The effect is smaller than for ethanol. The effect of ethanol and cannabis taken simultaneously is additive. Conjunctival injection, dilated pupils and slow pupil reaction are among the few signs to reveal THC influence.

[Neurodevelopmental disorders in response to hormonally active environmental pollutants]. / Zaburzenia neurorozwojowe w kontekscie obecnych w srodowisku substancji hormonalnie czynnych.

BACKGROUND: In recent years, the major concern has been focused on persistent organic pollutants (POPs), which are present in ecosphere in increasing concentrations, especially since 1950s. Among of these pollutants are dioxins and polychlorinated biphenyls (PCBs) released during vast burning and plastics processing, as well as pesticides which were industrial chemicals intensively produced for many years. RESULTS: In last decade, dioxins together with PCBs and pesticides have been classified as endocrine disrupting chemicals, because they are able to alter hormone-dependent processes and disrupt functioning of endocrine glands, e.g. thyroid and gonads. Furthermore, these pollutants have been included in neural disrupting chemicals due to their ability of altering neural transmission and formation of neural networks. Since POPs may persist in the environment for dozens of years, an exposure to these organic pollutants creates a serious issue for environmental toxicologists. POP intoxication creates severe clinical problems, which became evident in dramatic circumstances, e.g. Yusho incident in Japan, Yu-Cheng incident in Tajwan, Michigan Lake poisoning. Clinical problems have been recognized as disruption of thyroid and gonadal functions, immunodeficiency as well as psychomotor deficits and increased occurrence of hormone-dependent cancers. Thus, knowledge on POP effects on human nervous system has been related mainly to toxic effects of these organic pollutants. Little is known, however, about the action of very low, so called background, doses of POPs and their effects on hormonal homeostasis in developing brain. It is of particular importance, because doses which are low for adults might become toxic for fetuses, infants or children. Recently, the public concern has been focused on POP effects on brain function, concomitantly with the increase in neuropsychiatric disorders, including autism, attention deficit and hyperactivity disorder (ADHD) as well as learning disabilities. Although some of epidemiological data are controversial, most of them point to adverse effects of prenatal exposure to polychlorinated biphenyls (PCBs) and polycyclic aromatic hydrocarbons (PAH) on cognitive function and, in general, mental development of infants and children. Studies on prenatal exposure to pesticides demonstrated increased incidence of autism and ADHD as well as deficits in psychomotor and visio-spatial skills, which were observed in infants and 8 years old children, respectively. Psychomotor deficits were also indicated in 6 months old infants exposed prenatally to polychlorinated dibenzo-p-dioxin (PCDD) and in 1-6 year old children affected prenatally by polybrominated difenyl ethers (PBDE). Recent data also demonstrate the strong correlation between exposure to bisphenol A at early pregnancy and increased locomotor activity and aggressiveness of children. CONCLUSIONS: Our knowledge on POP effects on human nervous system seems rather extensive, but is related mainly to toxic effects of these organic pollutants. Little is known, however, about the action of very low doses of POPs and their effects on hormonal homeostasis in developing brain. Therefore, the role of scientists and clinicians is to recognize the mechanisms of POP action, especially in respect to prenatal and early postnatal period when the nervous system develops and is particularly sensitive to hormonally active chemicals present in the environment.

[Isotretinoin embryopathy. Report of one case]. / Embriopatía por isotretinoína: Un daño evitable.

Retinoic acid is a widely used drug in the treatment of cystic acne. It has teratogenic effects that depend on the gestational period in which it is used. We report a seven months old female whose mother was exposed to retinoic acid in both pre-gestational and gestational periods. She had a retardation of psychomotor development and a brain MRI showed frontal atrophy and a malformation of the posterior fossa. We discuss the mechanisms of the teratogenic effects of retinoic acid.

Embriopatía por isotretinoína: Un daño evitable / Isotretinoin embryophaty: Report of one case

Retinoic acid is a widely used drug in the treatment of cystic acné. It has teratogenic effects that depend on the gestational period in which it is used. We report a seven months of female whose mother was exposed to retinoic acid in both pregestational and gestational periods. She had a retardation of psychomotor development and a brain MRI showed frontal atrophy and a malformation of the posterior fossa. We discuss the mechanisms ofthe teratogenic effeets of retinoic acid.

Local adverse effects of amalgam restorations.

Amalgam has been used for the restoration of teeth for well over 100 years, and is the most successful of the direct restorative materials with respect to longevity. Despite the increasing use of tooth-coloured materials, with advantages of aesthetics and adhesion, amalgam is one of the most widely used dental restorative materials. One of the principal disadvantages of amalgam, apart from aesthetics, is that it may have adverse biological effects, both locally and systemically. Locally, it can cause an erythematous lesion on the adjacent oral soft tissues (tongue and buccal mucosa), and systemically free mercury in the amalgam may give rise to a hypersensitivity reaction. The purpose of this paper is to review the literature concerning the local adverse reactions to dental amalgam. The focus will be on the reactions of the oral mucosa, and brief consideration will be given to laboratory cytotoxicity of dental amalgam and its components, and to the 'amalgam tattoo'.

A randomised placebo-controlled trial of the effects of midazolam premedication on children's postoperative cognition.

This randomised, placebo-controlled study assessed the effects of midazolam premedication on children's postoperative cognition and physical morbidity. In all, 179 children aged 5-10 years were randomly assigned to receive buccal midazolam (0.2 mg x kg(-1)) or placebo before sevoflurane-nitrous oxide anaesthesia for multiple dental extractions. They performed tests of choice reaction time, attention, psychomotor co-ordination and memory pre-operatively (baseline), before discharge and at 48 h. The reaction time of both groups was significantly slower before discharge compared to baseline, with the midazolam group being significantly slower than placebo. Psychomotor co-ordination was also significantly impaired postoperatively after midazolam. Performance on both tests had recovered to baseline by 48 h. Midazolam was also associated with significant anterograde amnesia, both postoperatively and at 48 h, for information presented in the interval between premedication and surgery. The results show significant short-term impairment of children's cognitive function and amnesia enduring for 48 h after low-dose midazolam premedication.

Developmental delays and locomotor activity in the C57BL6/J mouse following neonatal exposure to the fully-brominated PBDE, decabromodiphenyl ether.

After several decades of commercial use, the flame retardant chemicals polybrominated diphenyl ethers (PBDEs) and their metabolites have become pervasive environmental contaminants with a global distribution. PBDEs have entered the food chain and increasing levels can be detected in the human body. Decabrominated diphenyl ether (decaBDE) is currently the most widely used of the PBDEs in the United States. Despite its widespread use, little is known about the health effects of decaBDE. The current study examined the effects of neonatal exposure to decaBDE in the inbred C57BL6/J mouse. Neonatal male and female mice were exposed to a daily oral dose of 0, 6, or 20 mg/kg decaBDE from postnatal day 2 to 15. Three groups of endpoints were examined: the ontogeny of sensorimotor responses and serum thyroxine levels in immature animals, and locomotor activity in adult animals. In immature animals, 20 mg/kg/day produced developmental delays in the acquisition of the palpebral reflex. At this age, exposed males also showed a dose-related reduction of serum thyroxine levels. As adults, decaBDE exposure altered the normal sex- and age-specific characteristics of spontaneous locomotor activity. The most striking effect was an increase of activity during the first 1.5 h of the 2 h assessment in males exposed to 20 mg/kg/day decaBDE. These effects suggest that decaBDE is a developmental neurotoxicant that can produce long-term behavioral changes following a discrete period of neonatal exposure.

Adverse effects of opioids on the central nervous systems of palliative care patients.

Opioids, defined as drugs that stimulate opioid receptors, are primarily used in the treatment of moderate to severe pain. They induce central nervous system (CNS) adverse effects which can be divided into three groups. The first group includes effects that lower the level of consciousness-sedation, drowsiness and sleep disturbance. The second group affects the thinking process and the ability to react-cognitive impairment, psychomotor impairment, delirium, hallucinations, dreams and nightmares. The third group is of the direct toxic effects of opioids on neurons and includes myoclonus (perhaps), hyperalgesia and tolerance. This review addresses the incidence, possible mechanisms, and treatment of each of these groups of opioid-induced adverse effects.

Facial motion analysis of acid burn victims--development of a new facial motion impairment index.

OBJECTIVES: Evaluation of facial movement is necessary for the assessment of motor deficits and planning reconstructive surgery in facial burns. Clinicians recognise the need for an accurate and reproducible method of functional assessment. We propose a new facial functional impairment index (FFII) for assessing facial motor dysfunction due to severe burn injury and provide inter/intra-patient comparison for documenting rehabilitation. METHODS: The maximal static response assay (MSRA) was used to compare facial movement in 20 acid burn victims with 20 control subjects. Data compiled from 12 soft tissue landmarks was used to quantify rest and dynamic asymmetry, anatomic and non-anatomic motion and calculate the FMII. The Katz score, Nottingham index and number of affected aesthetic units provided insight into FFII efficacy. RESULTS: Patients with greater aesthetic disfigurement demonstrated significantly poorer anatomic function (c=0.62; p=0.03) as well as larger global facial functional impairment (c=0.52; p=0.08). CONCLUSION: Acid burns caused severe asymmetry and functional impairment. The FFII is a composite score of global function based on a reproducible method of data collection and it differentiated between acid burn victims and provided objective comparative measures. Software automation, integration of video and 3D data, appropriate graphical and pictorial depiction of variables and measurements, and further research into the accuracy of FFII as a marker of clinical recovery and assessment of function in facial burns, will enhance future clinical applications and potentially aid surgical reconstruction.

Neuropsychological dysfunction related to earlier occupational exposure to mercury vapor.

We assessed the neuropsychological test performances of 26 patients (mean age = 41.5 +/- 6.1 years; mean years of education = 9.8 +/- 1.8; 20 males) diagnosed with chronic occupational mercurialism who were former workers at a fluorescent lamp factory. They had been exposed to elemental mercury for an average of 10.2 +/- 3.8 years and had been away from this work for 6 +/- 4.7 years. Mean urinary mercury concentrations 1 year after cessation of work were 1.8 +/- 0.9 microg/g creatinine. Twenty control subjects matched for age, gender, and education (18 males) were used for comparison. Neuropsychological assessment included attention, inhibitory control, verbal and visual memory, verbal fluency, manual dexterity, visual-spatial function, executive function, and semantic knowledge tests. The Beck Depression Inventory and the State and Trait Inventory were used to assess depression and anxiety symptoms, respectively. The raw score for the group exposed to mercury indicated slower information processing speed, inferior performance in psychomotor speed, verbal spontaneous recall memory, and manual dexterity of the dominant hand and non-dominant hand (P < 0.05). In addition, the patients showed increased depression and anxiety symptoms (P < 0.001). A statistically significant correlation (Pearson) was demonstrable between mean urinary mercury and anxiety trait (r = 0.75, P = 0.03). The neuropsychological performances of the former workers suggest that occupational exposure to elemental mercury has long-term effects on information processing and psychomotor function, with increased depression and anxiety also possibly reflecting the psychosocial context.