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16 May 2017

Karam RG et al. Acta Psychiatr Scand; Epub ahead of print

In an attempt to address the lack of available information on the trajectories of ADHD dimensions during adulthood, the current study aimed to: 1) verify ADHD symptom domain trajectories, and 2) analyse the clinical and sociodemographic predictors of change in inattention, hyperactivity and impulsivity domains in a well-characterised clinical sample of adults with ADHD.

At baseline (T1), Brazilian adults of European descent from the Porto Alegre cohort (n=344; mean age 34.1 years [range: 18–68 years]) were diagnosed with ADHD as per DSM-IV criteria between 2003 and 2007. A diagnosis of ADHD was made using a semi-structured interview devised from a modified version of the Epidemiological Version of the Schedule for Affective Disorders and Schizophrenia for School-Aged Children (K-SADS-E), with wording adapted for adults. A total of 227 adults met the diagnostic criteria for follow-up (T2), occurring a mean 7.3 years (SD, 1.5) later.

6 months prior to T2, ADHD symptoms were re-evaluated and grouped into their respective domains of inattention, hyperactivity and impulsivity. The K-SADS-E was then used to evaluate variations in the number of symptoms occurring within each domain between T1 and T2.

Confirmation of a rise in ADHD symptom number as a possible ADHD domain trajectory was attempted by applying a cut-off of ≥2 symptoms at T2 compared with T1.

  • At T1, predictor variables examined were: 1) baseline number of ADHD domain symptoms; 2) other ADHD measures; 3) sociodemographic profile and medical history; 4) psychiatric comorbidities present up to T1; 5) temperament profile; and 6) cognitive performance.
  • At T2, predictor variables examined were: 1) methylphenidate (MPH) treatment duration between T1 and T2 (months); 2) time span between T1 and T2; and 3) psychiatric comorbidities occurring between T1 and 6 months prior to T2.

Despite an overall reduction in symptom numbers from baseline of all 3 ADHD domains (inattention, 66.7% reduction from baseline; hyperactivity, 55.1%; impulsivity, 42.2%), rises were also observed. For inattention and impulsivity, rates of rise were 13.3% and 17.3%, respectively, with a greater rise of 25.3% for hyperactivity.

Analysis of eligible predictors of changes in ADHD symptom numbers indicated that:

  • A reduction in the number of inattention symptoms were negatively correlated with a history of school suspension (p=0.02) and methylphenidate use prior to T1 (p<0.001), and positively correlated with the number of inattention symptoms at T1 (p=0.01), up to T1.
  • A smaller reduction in the number of inattention symptoms were correlated with oppositional defiant disorder (ODD) (p=0.03) and social phobia (p=0.03) in the period between T1 and 6 months prior to T2.
  • A reduction in the number of hyperactivity symptoms were negatively correlated with the number of impulsivity symptoms (p=0.005); the number of inattention symptoms (p=0.009) and alcohol use disorder (AUD) (p=0.006), and positively correlated with the number of hyperactivity symptoms (p<0.001), up to T1.
  • A reduction in the number of hyperactivity symptoms were negatively correlated with ODD (p=0.05) and AUD in the period between T1 and 6 months prior to T2.
  • A reduction in the number of impulsivity symptoms were negatively correlated with the number of impulsivity symptoms (p<0.001).
  • A reduction in the number of hyperactivity/impulsivity symptoms were negatively correlated with the number of inattention symptoms (p=0.008) and AUD (p=0.02), and positively correlated with the number of hyperactivity symptoms (p<0.001), up to T1.
  • A reduction in the number of hyperactivity/impulsivity symptoms were negatively correlated with ODD (p=0.003) in the period between T1 and T2.

Predictors of a rise in the number of symptoms within the 3 ADHD domains include a lower number of symptoms in the respective domain at T1. Additionally, a rise in the number of hyperactivity symptoms were associated with AUD up to T1. Inclusion of psychiatric comorbidities between T1 and T2 in the analysis showed that a rise in ADHD symptom number were associated with a lower number of symptoms at T1.

This study had several limitations: 1) to be able to draw inference from adults with sub-threshold ADHD symptoms and without ADHD, a population-based study is required; 2) additional time points are required for more robust trajectories; 3) participation of an ‘active AUD non-ADHD control’ group is required to confirm the significance of AUD as a predictor; 4) there is a risk of recall bias resulting from retrospective assessment of covariate information prior to T1; 5) potential bias arising from inclusion of covariates occurring between T1 and T2 as a predictor of change during this time period exists; 6) assessment of changes in impulsivity using only 3 symptoms to define this domain means caution while interpreting results should be exercised; 7) non-independence exists within domains between the number of symptoms at T1 and change in the number of symptoms from T1 to T2.

The authors conclude that, over time, a rise in ADHD symptoms can occur in adults with the disorder, and that psychiatric comorbidities can negatively influence the trajectory of these symptoms.

Read more about trajectories of ADHD dimensions in adults here

 

DSM-IV, Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition

Karam RG, Rovaris DL, Breda V, et al. Trajectories of attention-deficit/hyperactivity disorder dimensions in adults. Acta Psychiatr Scand 2017; Epub ahead of print.

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