Understanding Inattention: Diagnosis and Misdiagnosis
Understanding Inattention: Diagnosis and Misdiagnosis
The main question at this point is whether phenotypic characteristics such as inattention, anxiety, depression, and overall executive dysfunction represent epiphenomena arising from common disrupted brain regions or pathways, or whether each DSM diagnostic entity should be understood individually as possessing discrete biological signatures. Current knowledge points to the former.
To better conceptualize attentional/executive/cognitive dysfunction, a step back from categorization and symptom description must be made, and a better understanding of the neuroanatomical and neurochemical commonalities of many of these symptoms should be sought. From a clinical-translational perspective, pharmacologic-challenge studies should continue to be done with and without the use of fMRI technology in randomized controlled trial designs with persons diagnosed with putative ADHD, anxiety, and depression, and ADHD comorbid with other DSM diagnoses.
An example of this approach would be the use of medications whose putative mechanism of action would render them theoretically useful in comorbid states. For instance, atomoxetine (Strattera®) has been studied in persons with comorbid ADHD and anxiety with promising results, although more and better-powered studies are needed. Another compound, modafinil (Provigil®), a cognitive enhancer that has also been studied as a possible alternative ADHD treatment, has been tested in healthy persons in whom threatening stimuli (those that would affect anxious individuals), as well as cognitive tasks, were used in fMRI protocols. Results showed decreases in prefrontal, anterior cingulate, and amygdala activity associated with decreases in reactivity to the threatening stimuli, as well as improvement in cognitive efficiency.
These two examples only attest to the complexities of brain function and its resultant behavioral output. Although ADHD is highly comorbid, its main features of inattention/impulsivity/executive dysfunction can be observed in mood and anxiety disorders, making proper diagnosis very difficult.
It is possible that inattention (as in ADD/ADHD), anxiety (as in generalized anxiety disorder), and depression (as in MDD) represent not a single diagnostic or symptomatic entity but separate entities sharing a single attentional/impulsive/executive dysfunction core, most likely the result of developmental inefficiencies in prefrontal cortical (thinking brain) function. But that, depending on genetic background and environmental influence, may therefore shift the original core toward a presentation more similar to either anxiety or mood disorders. It is likely that recruitment of brain regions other than the prefrontal cortex might be involved, as seen in imaging studies, as the core-attentional/impulsive/dysexecutive triad, plus or minus other anxiety or mood-like symptoms, moves from one end of the spectrum to the other.
It goes without saying that for the clinician, the diagnostic uncertainty is at best highly challenging, and, with the current state of the art in diagnosis, will require a higher degree of observation and data-gathering, incompatible with the current amount of time allotted for new psychiatric evaluations and follow-ups. To that extent, the over-/underdiagnosis of such attentional illnesses as ADHD—and of greater importance, the over-/underutilization of stimulant medication (the first line of treatment)—without a proper understanding and conceptualization of the patient and his/her illness could potentially exacerbate the illness, and in the worst-case scenario it could lead to further morbidity and suicide.
Treatment Options
The main question at this point is whether phenotypic characteristics such as inattention, anxiety, depression, and overall executive dysfunction represent epiphenomena arising from common disrupted brain regions or pathways, or whether each DSM diagnostic entity should be understood individually as possessing discrete biological signatures. Current knowledge points to the former.
To better conceptualize attentional/executive/cognitive dysfunction, a step back from categorization and symptom description must be made, and a better understanding of the neuroanatomical and neurochemical commonalities of many of these symptoms should be sought. From a clinical-translational perspective, pharmacologic-challenge studies should continue to be done with and without the use of fMRI technology in randomized controlled trial designs with persons diagnosed with putative ADHD, anxiety, and depression, and ADHD comorbid with other DSM diagnoses.
An example of this approach would be the use of medications whose putative mechanism of action would render them theoretically useful in comorbid states. For instance, atomoxetine (Strattera®) has been studied in persons with comorbid ADHD and anxiety with promising results, although more and better-powered studies are needed. Another compound, modafinil (Provigil®), a cognitive enhancer that has also been studied as a possible alternative ADHD treatment, has been tested in healthy persons in whom threatening stimuli (those that would affect anxious individuals), as well as cognitive tasks, were used in fMRI protocols. Results showed decreases in prefrontal, anterior cingulate, and amygdala activity associated with decreases in reactivity to the threatening stimuli, as well as improvement in cognitive efficiency.
These two examples only attest to the complexities of brain function and its resultant behavioral output. Although ADHD is highly comorbid, its main features of inattention/impulsivity/executive dysfunction can be observed in mood and anxiety disorders, making proper diagnosis very difficult.
Conclusion
It is possible that inattention (as in ADD/ADHD), anxiety (as in generalized anxiety disorder), and depression (as in MDD) represent not a single diagnostic or symptomatic entity but separate entities sharing a single attentional/impulsive/executive dysfunction core, most likely the result of developmental inefficiencies in prefrontal cortical (thinking brain) function. But that, depending on genetic background and environmental influence, may therefore shift the original core toward a presentation more similar to either anxiety or mood disorders. It is likely that recruitment of brain regions other than the prefrontal cortex might be involved, as seen in imaging studies, as the core-attentional/impulsive/dysexecutive triad, plus or minus other anxiety or mood-like symptoms, moves from one end of the spectrum to the other.
It goes without saying that for the clinician, the diagnostic uncertainty is at best highly challenging, and, with the current state of the art in diagnosis, will require a higher degree of observation and data-gathering, incompatible with the current amount of time allotted for new psychiatric evaluations and follow-ups. To that extent, the over-/underdiagnosis of such attentional illnesses as ADHD—and of greater importance, the over-/underutilization of stimulant medication (the first line of treatment)—without a proper understanding and conceptualization of the patient and his/her illness could potentially exacerbate the illness, and in the worst-case scenario it could lead to further morbidity and suicide.
Source...