The BART scores increased significantly with abstinence , whereas the IGT scores did not change during abstinence. Self-reported total and motor impulsivity decreased significantly with abstinence and the non-planning score tended to decrease . The following changes were observed when restricting our longitudinal analysis to only those 17 PSU with baseline and follow-up data: general intelligence, executive function, working memory , visuospatial skills , global cognition , and processing speed . The 19 PSU not studied longitudinally differed from our abstinent PSU restudied on lifetime years of cocaine use . PSU not restudied performed significantly worse at baseline than abstinent PSU on cognitive efficiency, processing speed, and visuospatial learning . Furthermore, they did not differ significantly on years of education, AMNART, tobacco use severity, and proportions of smokers or family members with problem drinking, or the proportion of individuals taking a prescribed psychoactive medication.In PSU, more lifetime years drinking correlated with worse performance on domains of cognitive efficiency, executive function, intelligence, processing speed, visuospatial skills, and global cognition . More cocaine consumed per month over lifetime correlated with worse performance on executive function and greater attentional impulsivity . More marijuana consumed per month over lifetime correlated with worse performance on fine motor skills and tended to correlate with higher BIS-11 motor impulsivity ; in addition, more marijuana use in the year preceding the study correlated with higher non-planning and total impulsivity. Earlier onset age of marijuana use correlated with higher non-planning impulsivity and worse visuospatial learning . Interestingly, more lifetime years of amphetamine use correlated with better performance on fine motor skills, executive function, visuospatial skills, and global cognition . Similar to the associations found in PSU, more lifetime years drinking in AUD correlated with worse performance on cognitive efficiency, visuospatial skills, cannabis grow equipment and global cognition , and worse performance on visuospatial memory correlated with greater monthly alcohol consumption averaged over the year preceding assessment and over lifetime . In addition, longer duration of alcohol use in AUD was related to worse auditory-verbal learning and memory .
Our primary aim was to compare neurocognitive functioning and inhibitory control in onemonth-abstinent PSU and AUD. Poly substance users at one month of abstinence showed decrements on a wide range of neurocognitive and inhibitory control measures compared to normed measures. The decrements in neurocognition ranged in magnitude from 0.2 to 1.4 standard deviation units below a zscore of zero, with deficits >1 standard deviation below the mean observed for visuospatial memory and visuospatial learning. In comparisons to AUD, PSU performed significantly worse on measures assessing auditory-verbal memory, and tended to perform worse on measures of auditory-verbal learning and general intelligence. Chronic cigarette smoking status did not significantly moderate cross-sectional neurocognitive group differences at baseline. In addition, PSU exhibited worse decision-making and higher self-reported impulsivity than AUD , signaling potentially greater risk of relapse for PSU than AUD . Being on a prescribed psychoactive medication related to higher self-reported impulsivity in PSU. For both PSU and AUD, more lifetime years drinking were associated with worse performance on global cognition, cognitive efficiency, general intelligence, and visuospatial skills. Within PSU only, greater substance use quantities related to worse performance on executive function and fine motor skills, as well as to higher self-reported impulsivity. Neurocognitive deficits in AUD have been described extensively. However, corresponding reports in PSU are rare and very few studies compared PSU to AUD during early abstinence on such a wide range of neurocognitive and inhibitory control measures as administered here . To our knowledge, no previous reports have specifically shown PSU to perform worse than AUD on domains of auditory-verbal learning and general intelligence at one month of abstinence. Our studies confirmed previous findings of worse auditory-verbal memory and inhibitory control in individuals with a comorbid alcohol and stimulant use disorder compared to those with an AUD, and findings of no differences between the groups on measures of cognitive efficiency .
Some of the cross-sectional neurocognitive and inhibitory control deficits described in this PSU cohort are associated with previously described morphometric abnormalities in primarily prefrontal brain regions of a subsample of this PSU cohort with neuroimaging data . Our neurocognitive findings also further complement studies in subsamples of this PSU cohort that exhibit prefrontal cortical deficits measured by magnetic resonance spectroscopy and cortical blood flow . Our secondary aim was to explore if PSU demonstrate improvements on neurocognitive functioning and inhibitory control measures between one and four months of abstinence from all substances except tobacco. Polysubstance users showed significant improvements on the majority of cognitive domains assessed here, particularly cognitive efficiency, executive function, working memory, self-reported impulsivity, but an unexpected increase in risk-taking behavior . By contrast, no significant changes were observed for learning and memory domains, which were also worst at baseline, resulting in deficits in visuospatial learning and visuospatial memory at four months of abstinence of more than 0.9 standard deviation units below a z-score of zero. There were also indications for significant time-by-smoking status interactions for visuospatial memory and fine motor skills, however these analyses have to be interpreted with caution and considered very preliminary, considering the small sample sizes of smoking and nonsmoking PSU at followup. Nevertheless, the demonstrations of cognitive recovery in abstinent PSU, and potential effects of smoking status on such recovery, are consistent with our observations of corresponding recovery in abstinent AUD . The 19 PSU not studied at follow-up differed significantly from abstinent PSU at baseline onseveral important variables: they had more years of cocaine use over lifetime, and performed worse on cognitive efficiency, processing speed, and visuospatial learning. As such, these differences should be tested as potential predictors of relapse in future larger studies. Several factors limit the generalizability of our findings. Our cross-sectional sample size was modest and therefore our longitudinal sample of abstinent PSU was small; as not uncommon in clinical samples, about half of our PSU cohort relapsed between baseline and follow-up, a rate comparable to what has been reported elsewhere . This made us focus our longitudinal results reporting on the main effects of time and to de-emphasize the reporting of time-by-smoking status interactions. Larger studies are needed to examine the potential effects of smoking status and gender on neurocognitive recovery during abstinence from substances. The study sample was drawn from treatment centers of the Veterans Affairs system in the San Francisco Bay Area and a community based healthcare provider,vertical grow system and the ethnic breakdown of the study groups was different.
Therefore, our sample may not be entirely representative of community-based substance use populations in general. Although preliminary, the within subject statistics are meaningful as they are more informative for assessing change over time than larger cross-sectional studies at various durations of abstinence. In addition, premorbid biological factors and other behavioral factors not assessed in this study may have influenced cross-sectional and longitudinal outcome measures. Nonetheless, our study is important and of clinical relevance in that it describes deficits in neurocognition and inhibitory control of detoxified PSU that are different from those in AUD, and that appear to recover during abstinence from substances, potentially as a function of smoking status. Our cross-sectional and longitudinal findings are valuable for improving current substance use rehabilitation programs. The higher impulsivity and reduced cognitive abilities of PSU compared to AUD, likely the result of long-term comorbid substance use, and the lack of improvements in learning and memory during abstinence indicate a potentially reduced ability of PSU to acquire new cognitive skills necessary for remediating maladaptive behavioral patterns that impede successful recovery. As such, PSU may require a post-detox treatment approach that accounts for these specific deficits relative to AUD. Our results show that PSU able to maintain abstinence for 4 months had less total lifetime years of cocaine use and performed better on cognitive efficiency, processing speed and visuospatial learning than those PSU not restudied ; these variables may therefore be valuable for predicting future abstinence or relapse in PSU. Additionally, and if confirmed in larger studies, our preliminary results on differential neurocognitive change in smoking and nonsmoking PSU may inform a treatment design that addresses the specific needs of these subgroups within this largely understudied population of substance users. Potentially, concurrent treatment of cigarette smoking in treatment-seeking PSU may also help improve long-term substance use outcomes, just as recently proposed for treatment seeking individuals with AUD.
Finally, our findings on neurocognitive improvement in PSU imply that cognitive deficits are to some extent a consequence of long-term substance use , which have the potential for remediation with abstinence. This information is of clinical relevance and of psychoeducational value for treatment providers and treatment-seeking PSU alike. Patients with obstructive sleep apnea experience apneic and hypopneic events that, when untreated, have detrimental cardiovascular and neurocognitive consequences. Under normal conditions, blood pressure and heart rate decrease during non–rapid eye movement sleep and increase commensurately upon waking. This is attributed to a decrease in sympathetic nervous system activation and a subsequent increase in cardiac vagal tone during sleep . The transient episodes of hypoxemia and hypercapnia caused by apneas or hypopneas, as well as arousals, result in an increase in cardiac output and heart rate that leads to sympathetically induced peripheral vasoconstriction that causes a marked increase in blood pressure. The result of this chronic sympathetic excitation and inflammation does not resolve upon waking, and over time, together with the loss of the normal nocturnal blood pressure dip, it can lead to pathophysiologic changes such as impaired vascular function and stiffness . This impairment in the untreated patient with moderate to severe OSA has been found to increase the risk of both acute coronary syndrome and sudden cardiac death . The increased sympathetic nervous activity, inflammation, and oxidative stress seen in OSA can lead to hypertension. The prevalence of hypertension in moderate to severe OSA ranges between 13% and 60%, and OSA is considered the most common cause of secondary hypertension . Arrhythmias can be common in patients with OSA, and the prevalence of atrial fibrillation is higher in these patients than in patients without OSA. In fact, severe sleep disordered breathing is associated with twofold to fourfold higher odds of having complex arrhythmias. In addition, untreated OSA has been associated with higher rates of failure to maintain sinus rhythm after cardio version or ablation therapy . Inflammation, atrial fibrillation, and atherosclerosis are all associated with OSA and overlap with risk factors for cerebrovascular disease. OSA may be frequently diagnosed after stroke, and it can be difficult to determine whether the condition is causal or resultant. Evidence suggests that OSA is associated with an increased risk of stroke in elderly patients, and untreated OSA after stroke increases mortality risk during 10-year follow-up . Another disease state affected by sleep apnea is heart failure. Both OSA and central sleep apnea are common in patients with acute and chronic systolic and diastolic heart failure.However, screening for sleep disordered breathing can be difficult because patients with OSA and heart failure often do not report excessive daytime sleepiness. This absent symptom raises challenges in diagnosis and treatment adherence for OSA . Untreated OSA can affect many cognitive domains, including learning, memory, attention, and executive functioning. Data suggest that OSA is linked with cognitive impairment and may advance cognitive decline or dementia . In addition, intermittent hypoxemia and sleep fragmentation have been linked to structural changes in the brain that may be responsible for cognitive impairment . Given the increased prevalence of obesity and the common nature of diagnoses such as hypertension, coronary artery disease, atrial fibrillation, heart failure, and neurocognitive impairment, healthcare providers should be cognizant of the hazards of untreated OSA .Substance use, misuse, and dependence contribute immensely to the global burden of disease. Their harms extend far beyond their corrosive effects on health, safety, and well being and additionally include those associated with healthcare expenditures, productivity losses, criminal justice involvement, and other negative effects on social welfare. The incidence and harms of substance use, misuse, and dependence involve multilevel explanatory factors.