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The relationship between substance misuse and acquired brain injury (ABI) is well documented. Studies examining traumatic brain injury (TBI) model systems data revealed that more than 50% of patients treated for TBI were intoxicated at the time of injury.

 Alcohol misuse is also a risk factor for stroke. Chronic alcohol misuse has been associated with heart arrhythmias, blood clotting disorders, hypertension, and diabetes, all of which are risk factors for stroke.

Opioids and illicit “street drugs” have also been linked to ABI. Nonfatal opioid overdose is associated with anoxic and hypoxic brain injuries due to the depressive effect of opioids on the respiratory system.

 Use of illicit stimulant drugs (eg, cocaine, methamphetamine, etc) can elevate heart rate and blood pressure to dangerous levels and have been associated with hemorrhagic stroke.

It is important for clinicians to understand the relationship between substance misuse and acquired brain injury, and to accurately diagnose and treat these cooccurring conditions, as a substantial number of individuals with ABI return to risky levels of alcohol and/or drug consumption within the first few years after injury.

 Individuals who continue to misuse substances following discharge from rehabilitation are at higher risk for reinjury, development of mood disorders, increased mortality, and decreased life satisfaction.

A thorough clinical interview can provide a subjective measure of both the extent and the impact of substance misuse. Evidence demonstrates that using motivational interviewing techniques (eg, asking open-ended questions, reflective listening, and eliciting the patient’s thoughts about change) can help obtain information, build rapport, and begin the process of behavior change.

 Gauging a patient’s readiness for change can also guide treatment planning and selection of appropriate interventions in order to meet the patient where they are in the change process.

Standardized assessments provide an objective measure of substance use/misuse. Instruments that have been used successfully with the ABI population include the CAGE Assessment

 and the Alcohol Use Disorders Identification Test (AUDIT)

 for alcohol use, and the Alcohol, Smoking, and Substance-Use Involvement Screening Test (ASSIST)

 and the Substance Abuse Subtle Screening Inventory (SASSI)

Several treatment interventions for cooccurring ABI and substance misuse have been proposed and evaluated. Brief treatment including screening, patient education, and brief interventions may slow the resumption of future alcohol use.

 Other best practices for the treatment of substance use disorders in the ABI population include patient and family education, incentives to encourage treatment attendance and retention, use of motivational interviewing techniques, and interventions to support adaptive coping and adjustment.

Patient and family education with information about the negative effects of continued substance misuse—particularly suppression of cognitive recovery, increased risk for seizures, potential interactive effects of alcohol and prescribed medications, and increased risk for sustaining a second TBI—have been shown to be beneficial in reducing resumption of substance use.

 Some studies suggest that providing firm recommendations regarding abstinence, at least for the first full year following injury, can also impact substance misuse following rehabilitation.

 has suggested tailoring substance misuse treatment and modifying any written materials to account for cognitive and linguistic deficits stemming from brain injury (eg, attention, memory, information processing speed, etc). Additionally, Corrigan

 has recommended a 4-quadrant model that describes the various settings where individuals with ABI can receive treatment, as well as the best treatment based on the severity of the brain injury and severity of substance misuse.

Quadrant I (low severity of brain injury and substance misuse) includes acute medical and primary care settings and interventions that provide screening and brief interventions. Quadrant II (low severity of substance misuse and high severity of brain injury) includes brain injury rehabilitation settings and interventions that provide education, screening, brief interventions, and linkages to community supports and referral for ongoing substance use treatment. Quadrant III (high severity of substance misuse and low severity of brain injury) includes substance use treatment settings and interventions that provide screening, accommodations (for cognitive-linguistic deficits), and service linkage. Quadrant IV (high severity of substance misuse and brain injury) includes specialized brain injury and substance use services, including integrated programming.

Alcoholics Anonymous (AA) and Narcotics Anonymous (NA) have also been suggested as helpful resources in providing education and social support and promoting personal responsibility/accountability.

Finally, pharmacological treatments of substance misuse in the ABI population have been recommended as an adjunct to traditional therapies, or when therapy alone has been unsuccessful.

 Naltrexone, acamprosate, and disulfiram (Antabuse) are US Food and Drug Administration (FDA)-approved medications for the treatment of alcohol use disorder. Naltrexone and acamprosate act to reduce alcohol cravings, whereas disulfiram operates via aversive counterconditioning. It is recommended that these medications be initiated after a period of abstinence, and they may require liver function tests. Naltrexone, methadone, and buprenorphine are FDA-approved to treat opioid dependence. These medications also reduce cravings by binding with opioid receptors.

is the regional director of clinical services at the Centre for Neuro Skills, which operates post-acute brain injury rehabilitation programs in California and Texas. He is licensed in Texas as a chemical dependency counselor and psychological associate with independent practice. He also holds a clinical appointment at the University of Texas Medical Branch (UTMB) in Galveston in the Department of Rehabilitation Sciences.

Substance abuse as a mediating factor in outcome from traumatic brain injury

Non-lethal opioid overdose and acquired brain injury: a position statement of the Brain Injury Association of America

. Brain Injury Association of America; 2018.

Cocaine use and risk of stroke: a systematic review

Stroke and methamphetamine use in young adults: a review

6. Ponsford J, Whelan-Goodinson R, Bahar-Fuchs A. 

Alcohol and drug use following traumatic brain injury: a prospective study

7. Zgaljardic DJ, Seale GS, Schaefer LA, et al. 

Psychiatric disease and post-acute traumatic brain injury

Motivational Interviewing: Helping People Change

Addiction and Change: How Addictions Develop and Addicted People Recover

Detecting alcoholism. the CAGE questionnaire

AUDIT: The Alcohol Use Disorders Identification Test: Guidelines for Use in Primary Health Care. 2nd Edition

The Alcohol, Smoking and Substance Involvement Screening Test (ASSIST)

. World Health Organization. January 1, 2010.

The Substance Abuse Subtle Screening Inventory (SASSI) Manual, Second Edition

14. Bogner J, Corrigan JD, Peng J, et al. 

Comparative effectiveness of a brief intervention for alcohol misuse following traumatic brain injury: a randomized controlled trial

Substance abuse treatment for persons with brain injuries: identifying models and modalities

Motivational interviewing to prevent alcohol abuse after traumatic brain injury: a case series

Interventions to promote retention in substance abuse treatment

18. Vungkhanching M, Heinemann AW, Langley MJ, et al. 

Feasibility of a skills-based substance abuse prevention program following traumatic brain injury

Family role in substance abuse and traumatic brain injury rehabilitation

. In: High WM, Sander AM, Struchen MA, Hart KA, eds. 

Rehabilitation for Traumatic Brain Injury

21. Corrigan JD. The treatment of substance abuse. In: Zasler ND, Katz DL, Zafonte RD, et al, eds. 

Brain Injury Medicine: Principles and Practice

22. Corrigan JD, Mysiw WJ. Substance abuse among persons with TBI. In: Zasler ND, Katz DL, Zafonte RD, et al, eds. 

Understanding the intersection between substance misuse and acquired brain injury can assist clinicians in accurately diagnosing and treating these cooccurring conditions.

Substance Misuse and Acquired Brain Injury

 has featured cover stories providing expert perspectives on multiple important psychiatric issues such as the state of mental health care in the United States, the link between COVID-19 and psychosis, and the future of psychiatry. Halfway through 2022, here are some highlights from this year’s cover stories so far.

Psychosis in the Patient With COVID-19: An Emerging Psychopathology?

The link between viral infections and effects on the central nervous system has been studied with viruses such as influenza, H1N1, and previous coronaviruses, including SARS and MERS. It has been documented that like COVID-19, these viruses have been able to produce symptoms of psychosis in patients with no prior psychiatric conditions.

Recently published studies have shown that COVID-19 can cause severe neuropsychological stress-inducing psychosis in affected patients.

 The literature covering correlations between COVID-19 and psychosis has demonstrated that there has been an increase in the rate of psychotic symptoms such as paranoia, delusions of persecution, and auditory and visual hallucinations in populations with high incidence rates of COVID-19 infection.

Thought, CircRNAs, and a Neurodigital Hypothesis

If you ask a cardiologist, “Physiologically speaking, what is a heartbeat?” they can bore you to tears with details on anatomy, electrophysiology, hemodynamics, innervation, and pulmonary and peripheral circulation. But if you ask a psychiatrist the entirely pertinent question, “Physiologically speaking, what is a thought?” the truth is, we have been without a clue—until now.

Of all psychiatry’s mysteries, this is the most crucial void in our scientific knowledge: how the brain executes the higher functions that are the actual focus of psychiatric practice—the generation of thought and behavior. This knowledge gap has been responsible for psychiatry’s own split personality—historically swinging back and forth between a biological focus on the brain and a psychological focus on the mind. Just as physics sought a unified “theory of everything” to incorporate the mystery of gravity, this missing piece of science has eluded psychiatry since its inception. 

Psychiatric Care in the US: Are We Facing a Crisis?

By the end of 2021, many American adults found themselves in the worst mental state in years. According to the US Census Bureau’s Household Pulse Survey, 47% of adults reported symptoms of anxiety,

 and 1 in 5 adults disclosed suffering from a mental illness.

 Despite this, it is estimated that less than half of Americans with a mental disorder get adequate treatment.

“It has been just over a year now since the COVID-19 pandemic struck the United States full force. A year of hunkering down and Zooming in, teleworking and telepsychiatry, economic and social upheaval, and steady scientific progress. Looking back to last March, we knew this would be difficult. But we didn’t know how difficult. And we certainly didn’t know that the challenge of COVID-19 would last this long,” said Joshua A. Gordon, MD, PhD, director of the National Institute of Mental Health, in a 2021 director’s message.

Psychedelics and the Future of Psychiatry

Over the past several years, we have witnessed a psychedelic renaissance, and a growing body of evidence suggests that several psychedelic compounds hold strong therapeutic potential for a wide array of mental health conditions.

Once dismissed as dangerous and having little therapeutic potential, psychedelic drugs are gaining mainstream acceptance. Research data continue to demonstrate that, on the whole, these medicines are not only safe, but mostly well tolerated. Although more research is needed to better understand safety, especially in the context of at-risk conditions, these favorable safety profiles are enabling deeper exploration of these medicines. 

See more 2022 cover stories and download complete issues of 

. And be sure to stay up-to-date by subscribing to the 

Do you have a comment on any of these or other articles? Have a good idea for an article and want to write? Interested in sharing your perspectives? Write to us at 

Over the past 6 months, Psychiatric Times has featured expert opinions on important psychiatric issues from psychosis to psychedelics.

From the Pages of Psychiatric Times: 6 Months of Cover Stories

 was onsite for the 2022 American Psychiatric Association (APA) Annual Meeting in New Orleans, Louisiana, covering expert opinions and the latest research on a wide variety of important psychiatric issues. Here are some highlights from our coverage.

“Why is it that people with ADHD can do some specific things that they happen to be really interested in, or where they feel like, if they don’t take care of this 

 want to see happen is going to happen fast?”

Thomas E. Brown, PhD, of the Brown Clinic for ADHD and Related Disorders and the University of California-Riverside School of Medicine shared with 2022 American Psychiatric Association (APA) Annual Meeting attendees that attention-deficit/hyperactivity disorder (ADHD) may appear to be a problem of motivation, or “willpower,” but it is not. 

More Than a Knockout: Structural Brain Effects in MMA Sparring

In a first-of-its-kind study, researchers looked at the effect of practice sparring on possible brain changes in mixed martial arts (MMA) fighters. The results were presented at the 2022 American Psychiatric Association Annual Meeting by study author Aaron I. Esagoff, a medical student at Johns Hopkins University School of Medicine.

Although previous studies have looked at other sports that involve repetitive brain injury, the real risk for MMA fighters occur during practice sessions, explained Esagoff. Fights/matches only happen a few times per year, but individuals can spend hundreds of hours sparring and practicing. MMA is a hybrid combat sport that includes moves from boxing, wrestling, karate, judo, and jujitsu. 

“I think until we really understand the underlying neurobiology of PTSD, we’re stuck with a situation where the patient gets better, but they don’t get well.”

Charles B. Nemeroff, MD, PhD, Matthew P. Nemeroff Endowed Chair and professor in the University of Texas at Austin (UT Austin) Dell Medical School Department of Psychiatry & Behavioral Sciences, discussed the neurobiology of posttraumatic stress disorder (PTSD) at the 2022 American Psychiatric Association Annual Meeting. In the session—moderated by Edmond Hsin T. Pi, MD—Nemeroff described the diagnosis, epidemiology, and pathophysiology of PTSD, along with notable risk factors and some current and emerging treatments for PTSD. 

Leading the Artificial Intelligence Revolution

“Artificial intelligence (AI) is here to stay, and it’s really very important for the psychiatric field to take a leading role in developing it.”

P. Murali Doraiswamy, MBBS, FRCP, of the Duke University School of Medicine discussed some of the latest developments in AI and its current and potential applications for psychiatry at the 2022 American Psychiatric Association (APA) Annual Meeting. He was joined in a panel discussion by Robert M. Califf, MD, MACC, commissioner of food and drugs for the US Food and Drug Administration (FDA), and moderator Samantha Boardman, MD, psychiatrist and author of 

Everyday Vitality: Turning Stress Into Strength

 coverage from the 2022 APA Annual Meeting 

Catch up on the latest research on ADHD, PTSD, and more with Psychiatric Times.

In Case You Missed It: Highlights From the 2022 APA Annual Meeting

Catatonia is a psychomotor syndrome that features too little (hypokinetic), too much (hyperkinetic), or abnormal (parakinetic) movements. It presents in association with either primary mental illness or other medical conditions.

 An individual with catatonia can develop life-threatening autonomic abnormalities, a condition called malignant catatonia. Severe or persistent catatonia can also lead to a variety of medical complications including thromboembolic disease, pressure ulcers, contractures, aspiration pneumonia, malnutrition, and dehydration.

 Prompt identification and management are imperative.

An estimated 5% to 10% of acute psychiatric inpatients have catatonia, with a growing body of literature describing catatonia in acute medical settings as well.

 Despite the prevalence of catatonia and its clinical impact, catatonia remains widely underdiagnosed. In fact, 2 separate studies found that roughly only 1 in 10 cases of catatonia was recognized by psychiatric inpatient treatment teams.

 Although several factors likely play a role, we believe that a widespread lack of understanding catatonia’s clinical diversity may be a large reason catatonia so often goes undiagnosed.

To explore this possibility, we collaborated with Andrew Francis, MD, PhD, senior author of the Bush-Francis Catatonia Rating Scale (BFCRS). Published in 1996, the BFCRS is the most widely used scale to assess catatonia in clinical and research settings.

 We began by creating a detailed BFCRS Training Manual and Coding Guide to describe each item on the scale and to provide a semi-structured interview to guide scoring.

Next, we created an online module to assess how well clinicians and trainees in psychiatry could identify the features of catatonia. The module consisted of standardized patient videos that participants were asked to score using the 23-item BFCRS and multiple-choice questions on individual BFCRS items. A total of 482 medical students, psychiatry trainees, and psychiatrists from more than 150 medical institutions globally participated in our study.

 Overall, participants answered correctly 69% of the BFCRS items when scoring standardized patient videos and 55% of multiple-choice items. After adjusting for demographics using multivariable regression, we found that, compared to medical students, psychiatrists correctly identified only 2 more items on the BFCRS when scoring standardized videos.

We were also curious whether a video-based online educational module could improve the accuracy of catatonia recognition. After taking the assessments above, participants were invited to take a 1-hour educational course on catatonia that reviewed each of the items on the BFCRS as illustrated through a series of narrated standardized patient exams and onscreen explanations. Participants’ knowledge was reassessed directly after completing the module and 3 months later. We found substantial improvements in catatonia recognition on follow-up assessments across all stages of training.

 Across the sample, post-module scoring of standardized patient videos improved from 69% to 87% correct, with limited attrition in performance to 81% correct at 3 months. After completing this module, medical students outperformed psychiatrists who had not yet taken the educational module, and, at 3 months, psychiatry resident participants still outperformed psychiatrists at study baseline.

Based on favorable responses to this project and participant feedback, we subsequently created a set of 23 point-of-care videos on how to score each BFCRS item. With these videos, we illustrate some of the diversity of how each BFCRS item can present. For example, grimacing can involve a variety of facial movements; mannerism pertains to patterns of speech or body movements; and negativism can manifest as physical resistance to examination or as relational opposition. These videos also offer guidance on scoring item severity. Finally, to enhance clinical utility, we have created a hyperlinked version of the BFCRS that links users to these point-of-care videos and to the corresponding pages on the BFCRS Training Manual and Coding Guide.

Now that this project is complete, we have made this suite of catatonia educational materials freely available online at 

 Our goal in creating these resources is to equip clinicians to identify catatonia both accurately and reliably. Catatonia involves a variety of motoric and behavioral findings, so education to improve its identification should prioritize audiovisual depictions of its features. We hope that these video-based resources will serve this role.

These videos also reinforce comments in the ICD-11, clarifying that several of catatonia’s diagnostic features require physical examination (ie, catalepsy, waxy flexibility, and rigidity).

 We invite psychiatric clerkships and residency programs to incorporate these materials into their curricula, researchers to use these resources to ensure standardized definitions across studies, and practicing psychiatrists to learn more about this compelling clinical condition.

 is an assistant professor of psychiatry at the University of Rochester Medical Center. 

 is chief resident in psychiatry at the University of Rochester Medical Center. The authors are indebted to Andrew Francis, MD, PhD, for his collaboration on this project and to Hochang B. Lee, MD, for supporting this work.

The project described in this piece was supported by the Department of Psychiatry at the University of Rochester Medical Center, including internal funds and statistical analysis by the Quantitative Methods Core.The authors declare no relevant conflicts of interest. Dr Oldham is supported by a K23 award through the National Institute on Aging (AG072383).

Diagnostic and Statistical Manual of Mental Disorders (DSM5-TR)

. American Psychiatric Association Publishing; 2022.

2. Walther S, Stegmayer K, Wilson JE, Heckers S. 

Structure and neural mechanisms of catatonia

Prevalence of catatonia and its moderators in clinical samples: results from a meta-analysis and meta-regression analysis

4. van der Heijden FM, Tuinier S, Arts NJ, et al. 

Catatonia: disappeared or under-diagnosed? 

5. Ghaziuddin N, Dhossche D, Marcotte K. 

Retrospective chart review of catatonia in child and adolescent psychiatric patients

Catatonia. I. rating scale and standardized examination

7. Wortzel JR, Maeng DD, Francis A, Oldham MA. 

Prevalent gaps in understanding the features of catatonia among psychiatrists, psychiatry trainees, and medical students

8. Wortzel JR, Maeng DD, Francis A, Oldham MA. 

Evaluating the effectiveness of an educational module for the Bush-Francis Catatonia Rating Scale

9. Wortzel JR, Oldham MA. Bush-Francis Catania Rating Scale assessment resources. University of Rochester Medical Center. 2022. Accessed May 17, 2022. 

https://www.urmc.rochester.edu/psychiatry/divisions/collaborative-care-and-wellness/bush-francis-catatonia-rating-scale.aspx

10. ICD-11 for mortality and morbidity statistics. World Health Organization. 2022. Accessed May 31, 2022. 

https://icd.who.int/browse11/l-m/en#/http://id.who.int/icd/entity/486722075

Despite its prevalence and clinical impact, catatonia remains widely underdiagnosed. What are clinicians missing?

So That’s What Catatonia Looks Like?

“The amount of devastation that has occurred from this infection is unparalleled by any pandemic that we have faced on this continent or any war that we have faced.”

Avindra Nath, MD, a neurologist in Bethesda, Maryland, discussed the neurological and neuropsychiatric complications of COVID-19 at the 2022 American Psychiatric Association (APA) Annual Meeting, beginning with the recent statistics related to COVID-19. To date, there have been 100 million infections and 1 million deaths in the United States alone, with 500 million infections and 50 million deaths globally. 

The effects of long COVID—particularly on the brain—are also of concern. “The brain gets overlooked. But what is primary and most important at the end of any pandemic is what happens to the brain because those are the things that cause the long-term consequences,” said Nath, who is also senior investigator and clinical director in the Section of Infections of the Nervous System, Division of Neuroimmunology & Neurovirology, at the National Institute of Neurological Disorders and Stroke.

Nath explained that individuals who develop COVID-19 can be divided into 2 groups: (1) those who have very severe symptoms at the time of COVID-19 onset, but then gradually improve, and (2) those who have mild symptoms at onset or even improve for a while, but then develop new symptoms weeks or months later.

“If you look at patients acutely and they have lots of symptoms, over 3 to 5 months, many will get better, but some will not. And if they don’t get better by then, chances are they won’t,” Nath said.

Some of these symptoms that may occur in cases of long COVID—or the chronic stage of COVID-19—include exercise intolerance; mood, cognition, and sleep disorders; pain syndromes (eg, myalgia, neuropathic pain, paresthesia, headache, tinnitus); and dysautonomia (eg, palpitations, postural orthostatic tachycardia syndrome, hypotension, hypothermia, fever).

“First onset of major depressive illness, anxiety, or psychosis [with none] in the past history is directly related to this infection,” Nath added, also noting that some symptoms of long COVID overlap with symptoms of other diseases such as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), Gulf War illness, and post Lyme disease syndrome. “It’s quite possible that all of these are related to one another,” Nath said. “It’s just that the event that precipitated them may be somewhat different.”

In order to learn more about what happens to the brain during and following COVID-19 infection, Nath shared that he and colleagues analyzed the brains of individuals who had died of COVID-19 in MRIs. They found, in part, that perivascular fibrinogen leakage indicated vascular injury, and that platelets were activated and formed clots in small blood vessels. 

Based on this and additional neurological and neuropsychiatric research, Nath suggested that future directions should include more clinical trials involving immunomodulatory agents and more research involving biomarkers for neuronal injury (NfL, pNfH, GFAP, SNAP-25), vascular injury (sICAM, VEGF, P-selectin, E-selectin, MMP-3, antibodies to ACE2), and immune activation.

In terms of treatment, “there is symptomatic treatment—but can you affect the course of the disease?” Nath said. “…I think you need to tailor the treatment to the patient you’re seeing and depending on what you think is the major underlying pathophysiological mechanism. And now we have the tools to be able to refer to that.”

An expert discusses the effects of long COVID on the brain at the 2022 APA Annual Meeting.

Neurological and Neuropsychiatric Complications of COVID-19

The prevalence of attention-deficit/hyperactivity disorder (

) in the worldwide pediatric population has been stable over the past 30 years except in the United States, where cases have increased.

 According to a 2016 parent survey, approximately 6.1 million US children (9.4%) had received a diagnosis of ADHD.

 Worldwide, ADHD is the third most common mental health disorder, following depression and anxiety.

 Overall, girls (5.6%) are less likely to be diagnosed with ADHD than boys (12.9%).

A 2021 global systematic review and meta-analysis suggested that the prevalence of persistent adult ADHD was 2.58% and the prevalence of symptomatic adult ADHD was 6.76%, with 139.84 million and 366.33 million affected adults worldwide in 2020, respectively.

 ADHD appears to impact men more than women. In adults, ADHD appears to decrease as an individual ages.

Etiology is still not clearly understood; however, combinations of genetic, neurological, and environmental factors likely contribute to its pathogenesis and symptom expression.

 Genetic factors are implicated, but the mechanism of action is not completely clear. Family, twin, and adoption studies have strongly suggested that ADHD is highly inheritable. Moreover, genetic studies have documented the gene sets interfering with neurotransmitter pathways in the brain that implicate rare copy number variants or the collection of higher deletions, as well as the duplications impacting gene transcriptions that are more likely to be found in individuals with ADHD.

Pre-, peri-, and postnatal environmental factors play a significant role in the development of ADHD. Some evidence suggests prenatal factors include the mother’s lifestyle during pregnancy.

 For example, prenatal alcohol exposure can lead to hyperactive, disruptive, and impulsive behaviors and increase the risk of psychiatric disorders.

 Maternal smoking during the prenatal developmental period has been linked to increased risk of ADHD

 Perinatal factors, such as very low birthweight, can result in a 2-fold increase in the likelihood of ADHD.

ADHD is conceptualized as a disorder of childhood that gradually diminishes over the lifespan.

 However, several prospective longitudinal studies have challenged the prevailing assumption that childhood ADHD and adult ADHD affect the same individuals, and that they share the same neurodevelopmental vulnerabilities.

 The results of these studies suggest that more than two-thirds of individuals with adult ADHD never had childhood ADHD. Adult ADHD had been generally neglected in epidemiological studies, until recently, as researchers attempt to estimate the true prevalence of ADHD in adults. Furthermore, researchers are exploring whether ADHD is solely a neurodevelopmental disorder that presents in childhood, or whether ADHD can be acquired during other developmental periods. The prevalence of persistent adult ADHD from childhood and that of symptomatic adult ADHD were 2.58% and 6.76% in 2020, respectively.

The diagnostic assessment of ADHD can be complicated, as inattention, impulsivity, and difficulties with concentration can be driven by myriad factors. It is well documented that children and adolescents diagnosed with ADHD often have 1 or more cooccurring disorders

According to a study by Elia and colleagues, oppositional defiance disorder was the most common comorbid disorder at 41%, followed by depression/dysthymia at 22% and general anxiety disorder at 15%.

Approximately 60% to 100% of children with ADHD have 1 or more comorbid disorders that persist into adulthood. Autism spectrum disorder, with a comorbid rate of 42%, and learning disorders (math, reading, and spelling), account for 10% and 92% of comorbidities. Tourette syndrome accounts for 55% comorbidity. Children with ADHD experience major depression at a rate higher than children without ADHD (12% to 50%). Regarding anxiety symptoms, children with ADHD have a prevalence rate between 15% and 35%.

In adults with ADHD, the most common cooccurring psychiatric disorders are bipolar disorder, depression, anxiety disorders, substance use disorders (SUDs), and personality disorders.

 ADHD has a high cooccurring prevalence with bipolar disorder: Estimates range between 9.5% and 21.2%, with bipolar I disorder being more likely.

 ADHD and depression commonly cooccur at even higher rates, ranging from 18.6% to 53.3%.

 Individuals with ADHD are also at higher risk for developing anxiety disorders than the general population, with rates approaching 50%.

 SUDs are likely the most common cooccurring condition with ADHD—specifically, alcohol and/or nicotine, cannabis, and cocaine use.

Research support for the intersection of ADHD and personality disorders is scant compared with the support of other psychiatric cooccurring conditions. However, reports indicate that personality pathology is present in approximately 50% of adults with ADHD—most commonly cluster B and C personality structures—and up to 25% of adults with ADHD have 2 or more personality conditions.

Diagnosing ADHD can be a complicated process. It is imperative to obtain historical information such as academic performance records and previous psychological testing reports, if ever tested.

There are several significant barriers to diagnosis and treatment in ADHD, including overlapping symptomology between ADHD and mood and anxiety disorders, SUDs, learning disabilities, information processing disorders, auditory processing disorders, and psychosocial factors. It is important to note that some individuals overcome ADHD-related deficits by developing and mastering compensating skills. This also can impact the accuracy of ADHD diagnosis.

Evidenced-based assessment includes multi-informant/multimethod procedures and validated measures. This approach should be guided by current research and include test data to support clinical observations and, ultimately, an accurate ADHD diagnosis. 

 highlights several measures used in ADHD assessments.

Treatment considerations should be informed by functional outcomes including symptom reduction, increased quality of life, and improved daily, academic, and occupational functioning.

 Efficiency at working or studying, maintaining stable relationships, containing or curbing impulsivity, and being satisfied with life overall are indicators of improved functioning. Moreover, adherence to treatment is key to successful management of ADHD.

First-line treatments for ADHD are pharmacologic: stimulants and nonstimulants. Stimulant medications include methylphenidate, mixed amphetamine salts, and lisdexamfetamine dimesylate. Nonstimulants used in ADHD treatment include atomoxetine and alpha-2-adrenergic agonists. 

 highlights several ADHD medication options, although the effectiveness of psychopharmacological treatments is beyond the scope of this paper.

For children and adolescents, a well-established body of evidence supports the effectiveness of psychosocial treatments, including behavioral management interventions (eg, parent training, classroom interventions, peer-based interventions), training interventions (eg, cognitive training, neurofeedback, organization), cognitive behavioral therapy (CBT), and physiological treatments (eg, play and other physical activities).

CBT, the preferred nonpharmacological treatment for adult ADHD, consistently reduces its core behavioral symptoms.

Usually first diagnosed in childhood and sometimes persisting into adulthood, ADHD has extensive implications for academic achievement, relationships, finances, and employment. In addition, untreated ADHD carries greater risk of accidental injuries and substance abuse. Thus, careful assessment is of utmost importance to properly diagnose and then treat the disorder.

is an assistant professor and licensed clinical psychologist at Harris Health System in the Menninger Department of Psychiatry and Behavioral Sciences at Baylor College of Medicine in Houston, Texas. 

 is a psychology fellow at Baylor College of Medicine.

1. Polanczyk GV, Willcutt EG, Salum GA, et al. 

ADHD prevalence estimates across three decades: an updated systematic review and meta-regression analysis

2. Danielson ML, Bitsko RH, Ghandour RM, et al. 

Prevalence of parent-reported ADHD diagnosis and associated treatment among U.S. children and adolescents, 2016

3. Bélanger SA, Andrews D, Gray C, Korczak D. 

ADHD in children and youth: part 1 - etiology, diagnosis, and comorbidity

The prevalence of adult attention-deficit hyperactivity disorder: a global systematic review and meta-analysis

Molecular genetics of attention deficit hyperactivity disorder

6. Stergiakouli E, Hamshere M, Holmans P, et al; deCODE Genetics; Psychiatric GWAS Consortium. 

Investigating the contribution of common genetic variants to the risk and pathogenesis of ADHD

7. Williams NM, Franke B, Mick E, et al. 

Genome-wide analysis of copy number variants in attention deficit hyperactivity disorder: the role of rare variants and duplications at 15q13.3

9. D’Onofrio BM, Van Hulle CA, Waldman ID, et al. 

Causal inferences regarding prenatal alcohol exposure and childhood externalizing problems

Is it ADHD—or something else? The importance of careful assessment for the proper diagnosis and effective treatment of the third most common mental health disorder worldwide.

Neuropsychiatry

Substance Misuse and Acquired Brain Injury

From the Pages of Psychiatric Times: 6 Months of Cover Stories

In Case You Missed It: Highlights From the 2022 APA Annual Meeting

So That’s What Catatonia Looks Like?

Neurological and Neuropsychiatric Complications of COVID-19

ADHD Update: Diagnosis, Assessment, and Treatment Issues

Assessing Gaps and Opportunities in ECT, rTMS, and DBS Guidelines

Stroke Awareness: Issues for Psychiatrists to Consider

Clearing the ‘Brain Fog’ in Long COVID

More Than a Knockout: Structural Brain Effects in MMA Sparring