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Distinguishing comorbidities from differential diagnoses in bipolar disorder

Making a diagnosis of bipolar disorder (BD) can be challenging — comorbid psychiatric disorders are common and many symptoms overlap with those of the differential diagnoses, such as borderline personality disorder (BPD), major depressive disorder (MDD), attention deficit hyperactivity disorder (ADHD), and schizophrenia, explained Joseph Goldberg of Icahn School the Medicine, Mount Sinai New York, at Psych Congress 2019. It is important to distinguish the comorbidities from the differential diagnoses.

Before you treat a patient with bipolar-I disorder (BD-I), you need to know what you are treating, including all patient and history factors — a phenomenological description precedes treatment, said Professor Goldberg.

 

Distinguish comorbidities from differential diagnoses

Most patients with bipolar disorder have at least one comorbid psychiatric disorder

A careful clinical interview, longitudinal history and collateral historians are essential to make an accurate diagnosis of BD-I and enable the correct treatment, he explained. The challenges include:

  • the overlap of symptoms with those of the differential diagnoses — an online survey of 154 psychiatrists revealed that 36%, 31%, 20%, and 13% found it most difficult to differentiate BPD, MDD, ADHD, and schizophrenia from BD-I, respectively1
  • the presence of comorbid psychiatric disorders — a study of 288 patients with BD-I, revealed that 65%, 42%, and 24% had one, two, or three comorbid psychiatric disorders, respectively — most commonly anxiety and substance use disorders, and to a lesser extent, eating disorders2

Comorbidity is associated with an earlier age of BD-I onset and a worsening course of BD-I.2

 

Is the diagnosis BD-I or BD-I with comorbid BPD and/or PTSD?

Approximately 20% of people with BD-I have comorbid BPD3 and from 4% to 40% have comorbid PTSD,4 resulting in a complex diagnostic territory, said Professor Goldberg.

Bipolar disorder with comorbid PTSD is often associated with substance use disorder

Strategies to help determine whether or not the disorders are comorbid include:

  • a focus on overlapping and non-overlapping symptoms, for instance changes in sleep and energy can help clarifying a diagnosis of BD-I — excessive energy is a fundamental defining feature of BD-I and drives impulsive decision-making
  • distinguishing identifiable episodes from persistent trait characteristics by analyzing the baseline from which they deviate — there should be apparent on-off highs that may last weeks in BD-I
  • identifying interpersonal or environmental triggers, such as sleep deprivation and crossing time zones
  • recognizing that a history of trauma can complicate the course across all diagnoses

BD-I with comorbid PTSD is more common in women than in men and in BD-I than in BD-II, noted Professor Goldberg. Key features include shorter durations of euthymia, an increased risk for mood episode relapse, a higher depressive symptom burden, a poorer quality of life and a higher prevalence of comorbid substance use disorder.3

Different patterns of affective instability occur in BD-II and BPD, with more depression and euphoria in BD-II and more anger in BPD.

 

Is the diagnosis BD-II depression or MDD with comorbid BPD?

A variety of clinical features help in differentiating BD-II depression from MDD with comorbid BPD.

MDD comorbid with BPD is more often associated with PTSD than BD-II depression

A study of 206 patients with MDD with comorbid BPD and 62 patients with BD-II depression without BPD revealed that patients with MDD with comorbid BPD were significantly more often diagnosed with:

  • PTSD (p<0.001)
  • a substance use disorder (p<0.01)
  • somatoform disorder (p<0.05)
  • other nonborderline personality disorder (p<0.05).

Clinical ratings of anger, anxiety, paranoid ideation and somatization were significantly higher in the MDD with comorbid BPD group compared with the BD-II group and the MDD with comorbid BPD group made significantly more suicide attempts (all p<0.01).

Our correspondent’s highlights from the symposium are meant as a fair representation of the scientific content presented. The views and opinions expressed on this page do not necessarily reflect those of Lundbeck.

References
  1. McIntyre RS, et al. J Clin Psychiatry. 2019;80(3); doi: 10.4088/JCP.ot18043ah2.
  2. McElroy SL, et al. Am J Psychiatry. 2001;158:420–6.
  3. Cerimele JM, et al. J Clin Psychiatry 2017;78:e506–e514.
  4. Fomaro M, et al. J Affect Disord. 2016;195:105–18.
  5. Henry C, et al. J Psychiatr Res. 2001;35(6):307–12.
  6. Zimmerman M, et al. J Clin Psychiatry. 2013 Sep;74(9):880-6.
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