Confused and nearly naked after going on spending sprees

Mr. A’s age and severe cognitive impair­ment raise the possibility of dementia. Rapid onset, history of similar episodes, and apparent inter-episode recovery make dementia unlikely. The history of alcohol abuse and mildly elevated hepatic func­tion tests suggest a substance use disorder such as Wernicke-Korsakoff syndrome or a withdrawal syndrome. However, there is no evidence of excessive alcohol use over the past several months, toxicology studies were negative, and vital signs were stable. General medical causes for Mr. A’s presen­tation, such as hypoglycemia, head trauma, intracranial infection, and metabolic dis­turbance were considered, but physical examination and laboratory studies did not suggest any condition that would explain his condition.

Mr. A’s previous psychiatric hospitaliza­tion is critical in clarifying the more likely diagnosis. A similar presentation yielded the diagnosis of bipolar disorder, manic phase. Our working diagnosis, therefore, was bipolar disorder with features of delir­ious mania.

Delirious mania
Delirious mania was first described by Luther Bell in 1849 and is characterized by an acute and simultaneous onset of mania— severe insomnia, poor judgment, grandios­ity, excitement, emotional lability, bizarre hallucinations, and delusions—and delir­ium—altered consciousness, disorientation, and confusion.^2,3 Although there are no diag­nostic criteria, some authors suggest that delirious mania is characterized by inappro­priate toileting, denudation, profound lack of sleep, and episodic memory impairment that can last hours or days.⁴ Catatonia fre­quently is seen with delirious mania.⁵ Initial case descriptions described a high mortality rate, approaching 75% of patients.⁶ There is little published literature and no classifica­tion of delirious mania in DSM-5.1 Estimates are that delirium is concomitant in 20% to 33% of patients with mania.^7,8

Several theories try to clarify the underly­ing etiology of delirious mania. Jacobowski et al⁹ summarized the etiology and pro­posed that it is:
• 1 of 3 types of mania, including: acute and delusional manias, as initially pro­posed by Kraeplin
• a severe form of catatonia
• a condition akin to, but distinct from, delirium with similar underlying medi­cal causes
• a primary psychiatric disorder under­lying the cause of delirium.

EVALUATION Brain changes
For several days, Mr. A continues to engage in strange behavior. He tries to take patients’ belongings, is denudative, crawls on floors, licks walls, is unable to feed himself, and exhib­its odd motor movements with purposeless motor activity.

We consult our internal medicine team to iden­tify treatable, medical causes. Results of serum B12, thyroid-stimulating hormone, and rapid plasma reagin studies are within normal limits. Urinalysis is negative. A brain MRI reveals numerous white-matter T2-weighted and FLAIR hyperintensities, indicating small-vessel ischemic changes that are consistent with the findings of an MRI 3 years ago. A sleep-deprived EEG with temporal leads obtained on Day 4 of hospitalization demonstrates a diffusely slow and marginally to poorly organized background, believed to indicate global cerebral dysfunction that is most consistent with nonfocal global encephalopathy. There is no seizure activity. We do not perform a lumbar puncture because of Mr. A’s absence of focal neurologic deficits, lack of fever, and normal white blood cell count.

What is the most appropriate treatment?
a) electroconvulsive therapy (ECT)
b) high-dose benzodiazepine
c) mood stabilizer
d) antipsychotic

The authors’ observations
We strongly suspect that Mr. A has delirious mania. Symptoms and signs of mania include labile mood, excessive spending, grandios­ity, insomnia, and psychosis together with delirium (marked disorientation, confusion). We ascribed Mr. A’s odd motor behaviors to catatonia, a hallmark of delirious mania. The literature has little description of EEG find­ings in suspected cases of delirious mania; however, abnormal EEG tracings have been reported.¹⁰ We also speculated that Mr. A’s EEG reflected effects produced by his pre­scribed antipsychotic regimen.

Treatment
There is no clear consensus on treating deliri­ous mania. Because catatonia is a key feature of delirious mania—whether etiologically or as a prominent sign of the condition—ECT and benzodiazepines are proposed as pri­mary treatments. In a study of 16 patients with delirious mania, Karmacharya et al4 found ECT to be effective, with patients showing improvement after 1 to 4 treat­ments. Lee et al¹⁰ reported similar findings. Although a high-dose benzodiazepine is not as effective as ECT, a 1-time oral dose of 3 to 4 mg of lorazepam has been used to treat delirious mania.

The efficacy of antipsychotic and mood-stabilizing pharmacotherapy is not clear. Bond³ described 3 cases in which patients were treated effectively with a typical anti­psychotic (haloperidol or chlorpromazine) and lithium. Jung and Lee_¹¹demonstrated the efficacy of atypical antipsychotics, with a marked improvement in symptoms within 1 week. However, other studies do not sup­port these findings. Karmacharya et al⁴ found that typical antipsychotics 1) make the clinical picture worse by increasing extrapy­ramidal symptoms and 2) produce incon­sistent effects. Mood stabilizers sometimes proved beneficial.

Karmacharya et al⁴ further argued that the delay in improvement seen with any antipsychotics and mood stabilizers suggest they should not be considered a first-line treatment. These discordant findings are the result of a small number of studies and a lack of understanding of the exact nature of delirious mania.

TREATMENT Quick Response
Mr. A’s symptoms rapidly resolve with a com­bination of quetiapine, 800 mg/d, haloperidol, 10 mg/d, and lithium, 1,200 mg/d. His mood returns to euthymia and his psychotic symptoms abate. He is able to attend to all activities of daily living. Mental status clears and he is fully oriented and able to hold a logical conversation. He scores 28 out of 30 on a subsequent Montreal Cognitive Assessment, administered 11 days after the ini­tial assessment (Figure 2), indicating normal neurocognitive function. He returns to his baseline level of functioning and is discharged in psychiatrically stable condition. Mr. A has no recollection of the bizarre behaviors he dis­played earlier in his hospitalization.