Editor’s note: Mild traumatic brain injury (mTBI) accounts for about 90% of all TBI cases in children and adolescents, or about 180 out of every 100,000 cases in the US. With 2 million cases between 2005 and 2009, we are seeing many patients who have TBI as part of their history. How does it affect them? What do we do about it? Dr. Jeffrey Max spoke on this topic when he was recently recognized for his significant contributions to the study of head injury in children and adolescents. He presented at the James Harris Symposium on Neurodevelopmental Disorders on the topic of mild traumatic brain injury (mTBI) in children and adolescents at the recent annual AACAP conference in Seattle, WA.

Traumatic brain injury vs concussion
Mild traumatic brain injury (mTBI) is used interchangeably with the term concussion. Specifically, in our studies, children with mTBI were included if they had an observed loss of consciousness, a Glasgow Coma Scale (GCS) score of 13 or 14, or a GCS score of 15 with at least two symptoms of concussion documented by the emergency department medical staff (eg, vomiting, nausea, headache, diplopia, dizziness, transient neurological deficits). As a reminder, the GCS ranges from 3 to 15. A GCS of 13–15 with no other findings is considered “uncomplicated mild”; GCS 13–15 with abnormal neuroimaging findings is called “complicated mild”; GCS 9–12 is considered “moderate”, and GCS 3–8 is classified as “severe” ­(­https://www.­glasgowcomascale.org).

Psychiatric disorders associated with TBI
In a multisite prospective psychiatric study, the rate of new-onset psychiatric disorders in children hospitalized for mTBI ranged from 28% to 36% during the first 2 years post-injury. Many disorders seemed to be enduring. This rate was substantially lower for mTBI in children treated in the emergency department and discharged.

A systematic review of controlled studies of mTBI (Emery CA et al, Can J Psychiatry 2016;61(5):259–269) found higher rates of psychiatric complications as compared with healthy non-injured children. ADHD is the most frequently cited new-onset disorder associated with mTBI. In one retrospective study, the rate of attention problems 2 years after mild TBI resulting in hospitalization was 6 times the rate in non-injured children. In another retrospective study, about a third (36%) of children hospitalized with mild TBI developed a new-onset ADHD, which has been termed “secondary ADHD” (SADHD).

SADHD has not yet been studied comprehensively in a cohort limited to mTBI. However, when this syndrome is identified in children with a history of mild to severe TBI that resulted in hospitalization, it is apparent that SADHD has differences compared with developmental ADHD. Results from prospective studies showed lower rates of SADHD than in retrospective studies (ie, in the region of 15%). SADHD is associated with lower pre-injury socioeconomic status, lower pre-injury adaptive function, higher pre-injury psychosocial adversity, more impaired pre-injury family function, greater severity of TBI, comorbid problematic post-injury emotional lability and disruptive behavior, and lower post-injury adaptive and intellectual function. Neuropsychological correlates of SADHD 6–12 months post-injury show deficient working memory, attention, and psychomotor speed compared to children with developmental ADHD. Limited treatment studies suggest a positive response to stimulants, but findings are mixed.

Rates of mood swings occur 8 times more often for children and teens with mTBI than for non-injured children and teens, and oppositional defiant disorder (ODD) occurs 5 times more often. Children injured before age 3 have been found to be more withdrawn between ages 4 and 6. In teens who suffered mTBI before age 5 and were hospitalized for it, the rate of later substance use disorders is 3 times the rate in uninjured teens.

Personality changes are not uncommon after mild TBI, including emotional lability, aggression, disinhibition, and trouble learning from mistakes.

Prior psychiatric history impacts the risk of having a TBI as well as a secondary psychiatric condition after head injury. Children who were already aggressive by age 5 are more likely to have TBI between ages 5 and 10. Up to half of those with psychiatric difficulties after mild TBI have a history of psychiatric conditions diagnosed prior to the injury. Pre-injury Child Behavioral Check List (CBCL) scores are higher for those who have had a mild TBI versus uninjured children and teens.

Assessing for new-onset psychiatric disorder
How do we define a new-onset psychiatric disorder? There needs to be a fairly distinct difference between pre-injury and post-injury symptomatology. For instance, the initial appearance of an anxiety disorder in a child with ­pre-existing ADHD would qualify as a new-onset disorder. However, if conduct disorder develops in the context of a pre-existing ODD, or if bipolar disorder develops when there is a diagnosis of ­pre-injury depression, these disorders would not be classified as new-onset disorders. The latter two disorders may be the natural progression of pre-injury disorders.

In an HMO study conducted in Seattle among children age 14 years or younger, hospitalization after mild TBI was associated with a three-fold greater prevalence of a new-onset psychiatric disorder vs non-injured matched controls: a general rate of 30% with a psychiatric diagnosis vs 20% (Massagli TL, Arch Phys Med Rehabil 2004;85(9):1428–1434). [Editor’s note: That 20% is consistent with the commonly cited rate of psychiatric diagnosis in children and teens.] There was a two-fold risk of psychiatric diagnosis when there was no such diagnosis prior to mild TBI; and the relative risk of hyperactivity was 8.

Treating mild TBI
How should we manage our patients with histories of mild TBI who manifest psychiatric symptoms? The CDC published new guidelines in fall 2018 emphasizing that patients tend to recover well, but that they need to rest and very gradually return to school (eg, 1 week post-injury), and only later return to sports (eg, 2 weeks post-injury). Patients must also have planned follow-up to track symptoms.

The research on specific treatment for psychiatric symptoms following mild TBI is scant. Cognitive behavioral therapy (CBT) has been suggested to help manage behavioral activation and reframe symptoms (eg, “recovering,” not “brain-injured” or “dumb”). The technique of using trauma narratives has been suggested as well as aerobic activity and psycho-education. There are multidisciplinary models of care such as the Seattle Sports Concussion Research Collaborative Concussion that may be helpful. Their approach involves weekly multidisciplinary meetings that include a case manager, CBT therapist, pediatrician, and psychiatrist. The case manager helps the family coordinate care with school and other health professionals. The psychiatrist manages psychopharmacotherapy as needed. The CBT therapist uses modular techniques that may involve behavior activation and a paced return to activities, teaching coping and problem-solving skills, relaxation techniques, cognitive reframing, and sleep hygiene (McCarty CA et al, Pediatrics 2016;138(4):e20160459).

Medication treatment after mTBI includes our usual pharmacopeia. Stimulants are effective for ADHD after mTBI, but exercise caution if the patient has had seizures, as there may be a higher seizure risk in this setting. Amitriptyline has been used for pain, and SSRIs have been used for mood and anxiety.

CCPR Verdict: You will see a lot of patients in your practice who have a history of mild TBI. Manage expectations, advocate for gradual return to school and sports activities, build collaborative resources, and treat symptomatically.

Editor’s note: Dr. Max is working on a long-term follow-up study of patients 24 years after their initial injuries, comparing psychiatric diagnoses of those who had severe TBI with those who had mild to moderate TBI and looking at the differences for those with and without psychiatric diagnoses prior to their original injury. The results may shed light on long-term outcomes for mild TBI and the possibility of a mediating effect of prior psychiatric disorders.