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Drivers with ADHD are far more likely to be involved in crashes, to be at fault in crashes,to be in severe crashes, and to be killed in crashes. The more severe the ADHD symptoms, the higher the risk. Moreover, ADHD is often accompanied by comorbid conditions such as oppositional-defiant disorder, depression, and anxiety that further increase the risk.

What can be done to reduce this risk? A group of experts has offered the following consensus recommendations:

·   Use stimulant medications. While there is no reliable evidence on whether non-stimulant medications are of any benefit for driving, there is solid evidence that stimulant medications are effective in reducing risk. But there is also a rebound effect in many individuals after the medication wears off, in which performance actually becomes worse than if had been prior to medication. It is therefore important to time the taking of medication so that its period of effectiveness corresponds with driving times. If one has to drive right after waking up, it makes sense to take a rapid acting form. The same holds for late night driving that may require a quick boost.

·   Use a stick shift vehicle wherever possible. Stick shifts make drivers pay closer attention than automatic transmissions. The benefits in alertness are most notable in city traffic. But using a stick shift is far less beneficial in highway driving, where shifting is less frequent.

·  Avoid cruise control. Highways can be monotonous, making drivers more prone to boredom and distraction. That is even more true for those with ADHD, so it is best to keep cruise control turned off.

·   Avoid alcohol. Drinking and driving is a bad idea for everyone, but, once again, it's even worse for those with ADHD. Parents should consider a no-questions-asked policy of either picking up their teenager anytime and anywhere, or setting up an account with a ride-sharing service.·   Place the smartphone out of reach and hearing. Cell phone use is as about as likely to impair as alcohol. Hands-free devices only reduce this risk moderately, because they continue to distract. Texting can be deadly. Sending a short text or emoticon can be the equivalent of driving 100 yards with one's eyes closed. Either turn on Do Not Disturb mode, or, for even greater effectiveness, place the smart phone in the trunk.

·   Make use of automotive performance monitors. These can keep track of maximum speeds and sudden acceleration and braking, to verify that a teenager is not engaging in risky behaviors.

·   Take advantage of graduated driver's licensing laws wherever available. These laws forbid the presence of peers in the vehicle for the first several (for example, six) months of driving. Parents can extend that period for teenagers with ADHD, or set it as a condition in states that lack such laws.

·  Encourage practicing after obtaining a learner's permit. Teenagers with ADHD generally require more practice than those without. A pre-drive checklist can be a good place to start. For example:check the gas, check the mirrors, make sure the view through the windows is unobstructed, put cell phone in Do Not Disturb mode and place it out of reach, put on seat belt, scan for obstacles.

·   Consider outsourcing. Look for a driving school with a professional to teach good driving skills and habits.

Experts do not agree on whether to delay licensing for those with ADHD. On the one hand, teenagers with ADHD are 3-4 years behind in the development of brain areas responsible for executive functions that help control impulses and better guide behavior. Delaying licensing can reduce risk by about 20 percent. On the other hand, teens with ADHD are more likely to drive without a license, and no one wants to encourage that, however inadvertently. Moreover, graduated driver's licensing laws only have legal effect on teens who get their licenses at the customary age.

A cohort study looked at over five million adults, and over 850,000 children between the ages of five and eleven, who received care at Kaiser Permanente Northern California during the ten-year period from the beginning of 2007 through the end of 2016. At any given time, KPNC serves roughly four million persons. It is representative of the population of the region, except for the highest and lowest income strata.

Among adults rates of ADHD diagnosis rose from 0.43% to 0.96%. Among children the diagnosis rates rose from 2.96% to 3.74%, ending up almost four times as high as for adults.

Non-Hispanic whites had the highest adult rates throughout, increasing from 0.67% in 2007 to 1.42% in 2016. American Indian or Alaska Native (AIAN) had the second highest rates, rising from 0.56% to 1.14%. Blacks and Hispanics had roughly comparable rates of diagnosis, the former rising from 0.22% to 0.69%, the latter from 0.25% to 0.65%. The lowest rates were among Asians (rising from 0.11% to 0.35%) and Native Hawaiian or other Pacific Islanders (increasing from 0.11% to 0.39%).

Odds of diagnosis dropped steeply with age among adults. Relative to 18-24-year-olds, 25-34-year-olds were 1/6th less likely to be diagnosed with ADHD, 35-44-year-olds 1/3rd less likely, 45-54-year-olds less than half as likely, 55-64-year-olds less than a quarter as likely, and those over 65 about a twentieth as likely. This is consistent with other studies reporting and age dependent decline in the diagnosis.

Adults with the highest levels of education were twice as likely to be diagnosed as those with the lowest levels. But variations in median household income had almost no effect. Women were marginally less likely to be diagnosed than men.

ADHD is associated with some other psychiatric disorders. Compared with normally developing adults, and adjusted for confounders, those with ADHD were five times as likely to have an eating disorder, over four times as likely to be diagnosed with bipolar disorder or depression, more than twice as likely to suffer from anxiety, but only slightly more likely to abuse drugs or alcohol.

The authors speculate that rising rates of diagnosis could reflect increasing recognition of ADHD in adults by physicians and other clinicians as well as growing public awareness of ADHD during the decade under study. Turning to the strong differences among ethnicities, they note, Racial/ethnic differences could also reflect differential rates of treatment seeking or access to care. Racial/ethnic background is known to play an important role in opinions on mental health services, health care utilization, and physician preferences. In addition, rates of diagnosis- seeking to obtain stimulant medication for nonmedical use may be more common among white vs nonwhite patients. They conclude, greater consideration must be placed on cultural influences on health care seeking and delivery, along with an increased understanding of the various social, psychological, and biological differences among races/ethnicities as well as culturally sensitive approaches to identify and treat ADHD in the total population.

But the main take home message of this work is that most cases of ADHD in adults are not being diagnosed by clinicians. We know from population studies, worldwide, that about three percent of adults suffer from the disorder. This study found that less than 1 percent are diagnosed by their doctors. Clearly, more education is needed to teach clinicians how to identify, diagnose and treat ADHD in adults.

Sleep disorders are one of the most commonly self-reported comorbidities of adults with ADHD, affecting 50 to 70 percent of them. A team of British researchers set out to see whether this association could be further confirmed with objective sleep measures, using cognitive function tests and electroencephalography (EEG).

Measured as theta/beta ratio, EEG slowing is a widely used indicator in ADHD research. While it occurs normally in non-ADHD adults at the conclusion of a day, during the day it signals excessive sleepiness, whether from obstructive sleep apnea or from neurodegenerative and neurodevelopmental disorders. Coffee reverses EEG slowing, as do ADHD stimulant medications.

Study participants were either on stable treatment with ADHD medication (stimulant or non-stimulant medication), or on no medication. Participants had to refrain from taking any stimulant medications for at least 48 hours prior to taking the tests. Persons with IQ below 80 or with recurrent depression or undergoing a depressive episode were excluded.

The team administered a cognitive function test, The Sustained Attention to Response Task (SART). Observers rated on-task sleepiness using videos from the cognitive testing sessions. They wired participants for EEG monitoring.

Observer-rated sleepiness was found to be moderately higher in the ADHD group than in controls. Although sleep quality was slightly lower in the sleepy group than in the ADHD group, and symptom severity slightly greater in the ADHD group than the sleepy group, neither difference was statistically significant, indicating extensive overlap.

Omission errors in the SART were strongly correlated with sleepiness level, and the strength of this correlation was independent of ADHD symptom severity. EEG slowing in all regions of the brain was more than 50 percent higher in the ADHD group than in the control group and was highest in the frontal cortex.

Treating the sleepy group as a third group, EEG slowing was highest for the ADHD group, followed closely by the sleepy group, and more distantly by the neurotypical group. The gaps between the ADHD and sleepy groups on the one hand, and the neurotypical group on the other, were both large and statistically significant, whereas the gap between the ADHD and sleepy groups was not. EEG slowing was both a significant predictor of ADHD and of ADHD symptom severity.

The authors concluded, These findings indicate that the cognitive performance deficits routinely attributed to ADHD  are largely due to on-task sleepiness and not exclusively due to ADHD symptom severity. We would like to propose a simple working hypothesis that daytime sleepiness plays a major role in cognitive functioning of adults with ADHD. As adults with ADHD are more severely sleep deprived compared to neurotypical control subjects and are more vulnerable to sleep deprivation, in various neurocognitive tasks they should manifest larger sleepiness-related reductions in cognitive performance. One clear testable prediction of the working hypothesis would be that carefully controlling for sleepiness, time of day and/or individual circadian rhythms, would result in substantial reduction in the neurocognitive deficits in replications of classic ADHD studies.

ADHD continues to be a significant and difficult challenge in the collegiate world. The symptoms of the disorder directly impact a person's ability to manage the demands of college. Matriculating students are expected to rapidly obtain and deploy many self-management skills. Increased academic expectations demand a greater capacity for sustained attention. And the evolving social milieu can tax the emotional regulation and social cognition of those with ADHD.

Having seen our patients struggle, the Association for Collegiate Psychiatry decided to submit a workshop for presentation at the 2019 APA meeting in San Francisco. While developing the presentation we discovered a wealth of recent young adult follow-up data from longitudinal studies.1 Without exception, the study's findings reflected a significant decrease in functional outcomes across multiple domains of adult life. Further, we discovered that the new work coming from the TRAC observational study of college students has found troublesome rates of psychiatric comorbidity after the first year.

This epidemiologic evidence supports devoting resources to the care of this cohort. But it appears that this has not penetrated the world of campus mental health treatment. At present, most post-secondary schools (to our knowledge, data is quite limited) lean toward policies that make it difficult for students with ADHD to be diagnosed or treated on campus. One obstacle is requiring evidence of a childhood diagnosis, which many children with high-IQ compensated ADHD may not have received. Another can be the demand for expensive and comprehensive neuropsychological testing even though the diagnostic value of that testing remains unclear.3 Some student health centers ask students to obtain prescriptions from the treaters they saw prior to coming to campus, even if those prescribers are out of state. Though these policies may be deployed in an effort to decrease the diversion of stimulant medication, such hurdles may be difficult for the 18-year-old ADHD student to navigate. The result is that many students with this predictably destructive condition go untreated.

The good news is this subject interests the collegiate community. Among other things, our APA workshop was selected to be the APA's Member's Course of the Month for January 2020.

Much work remains in developing and deploying diagnostic policies and treatment strategies that colleges and universities feel comfortable supporting. We mentioned the APSARD community during the workshop as a resource for professionals interested in ADHD. And we hope the wider ADHD research and treatment communities will join us in focusing our energy on this underserved and sometimes maligned group of students who need our help.

ADHD is far more prevalent among persons with AUD (roughly 20 percent) than it is in the general population. The most accurate way of identifying ADHD is through structured clinical interviews. Given that this is not feasible in routine clinical settings, ADHD self-report scales offer a less reliable but much less resource-intensive alternative. Could the latter be calibrated in a way that would yield diagnoses that better correspond with the former?

A German team compared the outcomes of both methods on 404 adults undergoing residential treatment for AUD. All were abstinent while undergoing evaluations. First, to obtain reliable ADHD diagnoses, each underwent the Diagnostic Interview for ADHD in Adults, DIVA. If DIVA indicated probable ADHD, two expert clinicians conducted successive follow-up interviews. ADHD was only diagnosed when both experts concurred with the DIVA outcome.

Participants were then asked to use two adult ADHD self-report scales, the six-item Adult ADHD Self Report Scale v1.1 (ASRS) and the 30-item Conners’ Adult ADHD Rating Scale (CAARS-S-SR). The outcomes were then compared with the expert interview diagnoses.

Using established cut-off values for the ASRS, less than two-thirds of patients known to have ADHD were scored as having ADHD by the test. In other words, there was a very high rate of false negatives. Lowering the cut-off to a sum score ≥ 11 resulted in a correct diagnosis of more than seven out of eight. But the rate of false positives soared to almost two in five.  Similarly, the CAARS-S-SR had its greatest sensitivity (ability to accurately identify those with ADHD) at the lowest threshold of ≥ 60, but at a similarly high cost in false positives (more than a third).

The authors found it was impossible to come anywhere near the precision of the expert clinical interviews. Nevertheless, they judged the best compromise to be to use the lowest thresholds on both tests and then require positive determinations from both. That led to successfully diagnosing more than three out of four individuals known to have ADHD, with a false positive rate of just over one in five.

Using this combination of the two self-reporting questionnaires with lower thresholds, they suggest, could substantially reduce the under-diagnosis of ADHD in alcohol-dependent patients.

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The ENIGMA-ADHD Working Group published their second large study on the brains of people with ADHD in the American Journal of Psychiatry this month. In this second study, the focus was on the cerebral cortex, which is the outer layer of the brain.

ADHD symptoms include inattention and/or hyperactivity and acting impulsively. The disorder affects more than one in 20 (5.3%) children, and two-thirds of those diagnosed continue to experience symptoms as adults.

In this study, researchers found subtle differences in the brain’s outer layer - the cortex - when they combined brain imaging data on almost 4,000 participants from 37 research groups worldwide. The differences were only significant for children and did not hold for adolescents or adults. The childhood effects were most prominent and widespread for the surface area of the cortex. More focal changes were found in the thickness of the cortex. All differences were subtle and detected only at a group level, and thus these brain images cannot be used to diagnose ADHD or guide its treatment.

These subtle differences in the brain’s cortex were not limited to people with the clinical diagnosis of ADHD: they were also present - in a less marked form - in youth with some ADHD symptoms. This second finding results from a collaboration between the ENIGMA-ADHD Working Group and the Generation-R study from Rotterdam, which has brain images on 2700 children aged 9-11 years from the general population. The researchers found more symptoms of inattention to be associated with a decrease in cortical surface area. Furthermore, siblings of those with ADHD showed changes to their cortical surface area that resembled their affected sibling. This suggests that familial factors such as genetics or shared environment may play a role in brain cortical characteristics.

This is the largest study to date to look at the cortex of people with ADHD. It included 2246 people with a diagnosis of ADHD and 1713 people without, aged between four and 63 years old. This is the second study published by the ENIGMA-ADHD Working Group; the first examined structures that are deep in the brain. The ADHD Working Group is one of over 50 working groups of the ENIGMA Consortium, in which international researchers pull together to understand the brain alterations associated with different disorders and the role of genetic and environmental factors in those alterations.

The authors say the findings could help improve understanding of the disorder. ‘We identify cortical differences that are consistently associated with ADHD by combining data from many different research groups internationally. We find that the differences extend beyond narrowly-defined clinical diagnoses and are seen, in a less marked manner, in those with some ADHD symptoms and in unaffected siblings of people with ADHD. This finding supports the idea that the symptoms underlying ADHD may be a continuous trait in the population, which has already been reported by other behavioral and genetic studies.’. In the future, the ADHD Working Group hopes to look at additional key features in the brain- such as the structural connections between brain areas – and to increase the representation of adults affected by ADHD, in whom limited research has been performed to date. 

See: https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.2019.18091033

Sleep disorders are one of the most commonly self-reported comorbidities of adults with ADHD, affecting 50 to 70 percent of them. A team of British researchers set out to see whether this association could be further confirmed with objective sleep measures, using cognitive function tests and electroencephalography (EEG).

Measured as theta/beta ratio, EEG slowing is a widely used indicator in ADHD research. While it occurs normally in non-ADHD adults at the conclusion of a day, during the day it signals excessive sleepiness, whether from obstructive sleep apnea or neurodegenerative and neurodevelopmental disorders. Coffee reverses EEG slowing, as do ADHD stimulant medications.

Study participants were either on stable treatment with ADHD medication (stimulant or non-stimulant medication) or on no medication. Participants had to refrain from taking any stimulant medications for at least 48 hours prior to taking the tests. Persons with IQ below 80 or with recurrent depression or undergoing a depressive episode were excluded.

The team administered a cognitive function test, The Sustained Attention to Response Task (SART). Observers rated on-task sleepiness using videos from the cognitive testing sessions. They wired participants for EEG monitoring.

Observer-rated sleepiness was found to be moderately higher in the ADHD group than in controls. Although sleep quality was slightly lower in the sleepy group than in the ADHD group, and symptom severity slightly greater in the ADHD group than the sleepy group, neither difference was statistically significant, indicating extensive overlap.

Omission errors in the SART were strongly correlated with sleepiness level, and the strength of this correlation was independent of ADHD symptom severity. EEG slowing in all regions of the brain was more than 50 percent higher in the ADHD group than in the control group and was highest in the frontal cortex.

Treating the sleepy group as a third group, EEG slowing was highest for the ADHD group, followed closely by the sleepy group, and more distantly by the neurotypical group. The gaps between the ADHD and sleepy groups on the one hand, and the neurotypical group on the other, were both large and statistically significant, whereas the gap between the ADHD and sleepy groups was not. EEG slowing was both a significant predictor of ADHD and of ADHD symptom severity.

The authors concluded, These findings indicate that the cognitive performance deficits routinely attributed to ADHD are largely due to on-task sleepiness and not exclusively due to ADHD symptom severity.  we would like to propose a simple working hypothesis that daytime sleepiness plays a major role in cognitive functioning of adults with ADHD. As adults with ADHD are more severely sleep deprived compared to neurotypical control subjects and are more vulnerable to sleep deprivation, in various neurocognitive tasks they should manifest larger sleepiness-related reductions in cognitive performance. One clear testable prediction of the working hypothesis would be that carefully controlling for sleepiness, time of day, and/or individual circadian rhythms would result in a substantial reduction in the neurocognitive deficits in replications of classic ADHD studies.