What to do when your depressed patient develops mania

It is not uncommon for a manic patient to report “depression” as the chief complaint or to omit elements related to psychomo­tor acceleration (such as racing thoughts or psychomotor agitation) in the description of symptoms. An accurate diagnosis often requires clinical probing and clarification of symptoms (eg, differentiating simple insom­nia with consequent next-day fatigue from loss of the need for sleep with intact or even enhanced next-day energy) or discriminating racing thoughts from anxious ruminations that might be more intrusive than rapid.

Presentations of frank mania also can come to light as a consequence of symp­toms, rather than as symptoms per se (eg, conflict in relationships, problems at work, financial reversals).

Particularly in patients who do not have a history of mania, avoid the temptation to begin or modify existing pharmacother­apy until you have performed a basic ini­tial evaluation. Immediate considerations for initial assessment and management include the following:

Provide containment. Ensure a safe setting, level of care, and frequency of monitoring. Evaluate suicide risk (particularly when mixed features are present), and risk of with­drawal from any psychoactive substances.

Engage significant others. Close family members can provide essential history, particularly when a patient’s insight about her illness and need for treatment are impaired. Family members and significant others also often play important roles in helping to restrict access to finances, fos­tering medication adherence, preventing access to weapons in the home, and shar­ing information with providers about sub­stance use or high-risk behavior.

Systematically assess for DSM-5 symp­toms of mania and depression. DSM-5 modified criteria for mania/hypomania to necessitate increased energy, in addition to change in mood, to make a syndromal diag­nosis. Useful during a clinical interview is the popular mnemonic DIGFAST to aid recognition of core mania symptoms^a:
• Distractibility
• Indiscretion/impulsivity
• Grandiosity
• Flight of ideas
• Activity increase
• Sleep deficit
• Talkativeness.

^aAlso see: “Mnemonics in a mnutshell: 32 aids to psychiatric diagnosis,” in the October 2008 issue Current Psychiatry and in the archive at CurrentPsychiatry.com.

These symptoms should represent a departure from normal baseline character­istics; it often is helpful to ask a significant other or collateral historian how the pres­ent symptoms differ from the patient’s usual state.

Assess for unstable medical conditions or toxicity states. When evaluating an acute change in mental status, toxicology screening is relatively standard and the absence of illicit substances should sel­dom, if ever, be taken for granted—espe­cially because occult substance use can lead to identification of false-positive BD “cases.”¹

Stop any antidepressant. During a manic episode, continuing antidepressant medi­cation serves no purpose other than to contribute to or exacerbate mania symp­toms. Nonetheless, observational studies demonstrate that approximately 15% of syndromally manic patients continue to receive an antidepressant, often when a clinician perceives more severe depression during mania, multiple prior depressive episodes, current anxiety, or rapid cycling.²

Importantly, antidepressants have been shown to harm, rather than alleviate, pre­sentations that involve a mixed state,³ and have no demonstrated value in preventing post-manic depression. Mere elimination of an antidepressant might ease symptoms during a manic or mixed episode.⁴

In some cases, it might be advisable to taper, not abruptly stop, a short half-life serotonergic antidepressant, even in the setting of mania, to minimize the potential for aggravating autonomic dysregulation that can result from antidepressant discon­tinuation effects.

Begin anti-manic pharmacotherapy. Initiation of an anti-manic mood stabilizer, such as lithium and divalproex, has been standard in the treatment of acute mania.

In the 1990s, protocols for oral loading of divalproex (20 to 30 mg/kg/d) gained popularity for achieving more rapid symp­tom improvement than might occur with lithium. In the current era, atypical anti­psychotics have all but replaced mood sta­bilizers as an initial intervention to contain mania symptoms quickly (and with less risk than first-generation antipsychotics for acute adverse motor effects from so-called rapid neuroleptization).

Because atypical antipsychotics often rapidly subdue mania, psychosis, and agitation, regardless of the underlying process, many practitioners might feel more comfortable initiating them than a mood stabilizer when the diagnosis is ambiguous or provisional, although their longer-term efficacy and safety, relative to traditional mood stabilizers, remains contested. Considerations for choosing from among feasible anti-manic pharma­cotherapies are summarized in Table 1.⁵

Normalize the sleep-wake cycle. Chronobiological and circadian vari­ables, such as irregular sleep patterns, are thought to contribute to the pathophysiol­ogy of affective switch in BD. Behavioral and pharmacotherapeutic efforts to impose a normal sleep−wake schedule are considered fundamental to stabilizing acute mania.

Facilitate next steps after acute stabili­zation. For inpatients, this might involve step-down to a partial hospitalization or intensive outpatient program, alongside taking steps to ensure continued treatment adherence and minimize relapse.