Zolpidem is a short-acting imidazopyridine hypnotic that is an agonist at the gamma-aminobutyric acid A type (GABAA) receptor. It has been suggested that it acts selectively on alpha1 subunit-containing GABAA benzodiazepine (BZ1) receptors presenting (contrary to classic benzodiazepines) low or no affinity for other subtypes. Therefore, it has been proposed that it lacks the benzodiazepines-like side-effects, having minimal abuse and dependence potential. Nevertheless, there is a considerable number of zolpidem dependence case reports in the literature. We present eight cases of zolpidem abuse and dependence without criminal record, without history of substance abuse (except for one alcohol abuser), with minor psychiatric disorders, who took zolpidem after physicians prescription in order to deal with their insomnia. However, they became zolpidem abusers not craving its sedative, but its anxiolytic and stimulating action, which helped them to cope with everyday activities. It is possible that, in the high doses that our patients used, zolpidem abandons its selectivity for BZ1 receptors and demonstrates all the actions of classic benzodiazepines. Molecular biology, via possible mutations on GABA receptors, may provide some answers as to why our eight patients (who did not differ much from the thousands of insomniacs who use zolpidem) and other zolpidem abusers, raised the dose progressively, and sought something from the drug other than hypnotic action.
CPAP therapy improves QoL and lessens depressive symptoms in our group of well-treated OSA patients. However, physical activity and energy expenditure did not present statistically significant improvement in the same group of OSA patients.
BackgroundGABAergic anticonvulsants have been recommended for the treatment of alcohol dependence and the prevention of relapse. Several studies have demonstrated topiramate's efficacy in improving drinking behaviour and maintaining abstinence. The objective of the present open-label controlled study was to assess efficacy and tolerability of low-dose topiramate as adjunctive treatment in alcohol dependence during the immediate post-detoxification period and during a 16-week follow-up period after alcohol withdrawal.MethodsFollowing a 7-10 day inpatient alcohol detoxification protocol, 90 patients were assigned to receive either topiramate (up to 75 mg per day) in addition to psychotherapeutic treatment (n = 30) or psychotherapy alone (n = 60). Symptoms of depression and anxiety, as well as craving, were monitored for 4-6 weeks immediately following detoxification on an inpatient basis. Thereafter, both groups were followed as outpatients at a weekly basis for another 4 months in order to monitor their course and abstinence from alcohol.ResultsA marked improvement in depressive (p < 0.01), anxiety (p < 0.01), and obsessive-compulsive drinking symptoms (p < 0.01) was observed over the consecutive assessments in both study groups. However, individuals on topiramate fared better than controls (p < 0.01) during inpatient treatment. Moreover, during the 4-month follow up period, relapse rate was lower among patients who received topiramate (66.7%) compared to those who received no adjunctive treatment (85.5%), (p = 0.043). Time to relapse in the topiramate augmentation group was significantly longer compared to the control group (log rank test, p = 0.008). Thus, median duration of abstinence was 4 weeks for the non-medicated group whereas it reached 10 weeks for the topiramate group. No serious side effects of topiramate were recorded throughout the study.ConclusionsLow-dose topiramate as an adjunct to psychotherapeutic treatment is well tolerated and effective in reducing alcohol craving, as well as symptoms of depression and anxiety, present during the early phase of alcohol withdrawal. Furthermore, topiramate considerably helps to abstain from drinking during the first 16-week post-detoxification period.
The aim of this study was to evaluate the effect of obstructive sleep apnea syndrome on the cognitive performance of young and middle-aged patients. Patients were divided into two groups, one consisting of 30 patients less than 50 years of age and the other consisting of 28 patients 50 years and over. Normal subjects were similarly divided into two groups, composed of 17 younger and 24 older controls. Patients and controls were examined with all-night polysomnography and subsequently underwent cognitive testing via attention-alertness tests. Comparing young to middle-aged patients, there were statistically significant differences in cognitive performance, especially in attention tests. Younger patients' cognitive performance was similar to their age-matched controls, while middle-aged patients showed cognitive decline in comparison with their age-matched controls. Although we studied only two age groups using 50 years of age as a cut-off, we could demonstrate that cognitive deterioration of untreated sleep apnea patients is age dependent, and several factors may contribute to this effect including brain hypoxia, sleep fragmentation, or comorbidities. Aging patients with sleep apnea demonstrate cognitive decline, while younger patients with the same disease severity are (somehow) able to compensate for this effect.
BackgroundPatients suffering from several neurologic disorders may bear the “stigma” of their disease, being disqualified from full social acceptance. Although stigma is considered to be present in Multiple Sclerosis (MS), the factors that influence its levels are ambiguous. Aim of our study was to examine, for the first time in the literature, the basic determinants of stigma in a Hellenic MS-patients cohort, as well as how stigma affects their Quality-of-Life (QoL) profiles.MethodsThree hundred forty two patients were recruited in this study. Data collected concerned sociodemographic and disease-related variables, mental illness assessment, Multiple-Sclerosis-QoL-54 (MSQoL-54) and Stigma-Scale-for-Chronic-Illness-24 (SSCI-24) questionnaires. Potential determinants were evaluated with univariate statistical analyses for their contribution to total, internalized (inner-self derived) and externalized (society derived) stigma. Important findings were further evaluated on hierarchical regression models.ResultsDisability levels were found to be the most powerful predictor in all stigma categories, followed by the presence of mental illness. Working and caregiving status were also ascertained as determinants of internalized stigma. Stigma levels displayed strong negative correlation with all composites of MSQoL-54.ConclusionsStigma is present in the social environment of MS patients and was confirmed as a barrier (according to the International Classification of Functioning, Disability and Health), with detrimental effects on their QoL levels and functioning performances. Disability and mental illness were shown as the principal determinants of stigma, while financial characteristics were not as equally involved. Further validation of these results in other MS populations may provide safer conclusions, towards more efficacious patient-centered care outcomes.
The P600 component of event-related potentials, believed to be generated by anterior cingulate gyrus and basal ganglia, is considered as an index of aspects of second-pass parsing processes of information processing, having much in common with working memory (WM) systems. Moreover, dysfunction of these brain structures as well as WM deficits have been implicated in the pathophysiology of opioid addicts. The present study is focused on P600 elicited during a WM test in twenty heroin addicts with prolonged abstinence compared with an equal number of healthy controls. The results showed significantly prolonged latencies at right hemisphere, specifically at Fp2 abduction. Moreover, memory performance of patients did not differ from that of normal controls. These findings may indicate that abstinent heroin addicts manifest abnormal aspects of second-pass parsing processes as are reflected by the P600 latencies, elicited during a WM test. Additionally, the P600 might serve as a valuable investigative tool for a more comprehensive understanding of the neurobiological substrate of drug abuse.
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