Medical Conditions and Elevated Mood

Diagnosable medical conditions have at least two interfaces with elevated mood. The first is when the medical condition is causative for the onset of elevated mood, leading to what has been called secondary mania. The second relates to medical comorbidities coexisting with elevated mood, but not necessarily having a causative effect.

Primary versus secondary mania

The elevated mood/hypomania/mania referred to in most of this text has also been labeled primary mania. Although the underlying cause of primary mania is usually unknown, in other situations, there appears to be a clearly identified medical cause for the onset of bipolar elevated mood. In this situation, referred to as secondary mania, identification and treatment of the medical cause are essential for adequate management of any mood alteration. This section discusses the evaluation, identification, and treatment of secondary mania.

Secondary mania may appear at any age but has a higher late-onset incidence because of medical causes and comorbidities. In an ideal world, every patient with new-onset elevated mood symptoms should be thoroughly evaluated medically and neurologically for identifiable medical causes. This, however, is neither cost effective nor always possible. Younger patients with new-onset elevated mood do require a thorough medical evaluation when they
show any of the symptoms listed in Table 12.1. The known physical causes of mania are shown in Table 12.2.

TABLE 12.1 Possible indications of secondary mania in younger patients

•	Manic symptoms interspersed with neurologic signs (e.g., gait, vision, or sensory disturbances)
•	Patients with no family history of affective disorder
•	Persistent sensitivity to mood stabilizing or antidepressant medications; side effects such as difficulty with balance, speech, or vision
•	History of recent head injury

Induction of mania has also been associated with a wide variety of disparate medications. These are shown in Table 12.3.

Corticosteroid-induced mania

Brought into the public eye by Jane Pauley’s autobiographic account of corticosteroid-induced mania, this common side effect occurs frequently and bears special mention. A variety of studies over the past 25 years have documented the frequency of mood-related symptoms secondary to the use of corticosteroids (1,2,3,4). Depending on the study, mania and hypomania were either more or less prevalent than depression, but in all studies both elevated mood and depression were common side effects. In these studies, mania and hypomania were shown to occur in 28% to 35% of patients who had been treated with steroids for a variety of medical conditions. Mixed mood episodes were also common, ranging from 8% to 12% of those treated with
corticosteroids (1,2). Because steroids are commonly indicated for a variety of medical conditions, including Addison’s disease, asthma, inflammatory bowel disease, multiple sclerosis, organ transplant, rheumatoid arthritis and systemic lupus erythematosus, this medical cause of elevated mood is seen frequently in medical and consultation services.

TABLE 12.2 Medical causes of secondary mania

1. Head injury

2. Stroke (including silent cerebral infarction)

3. Dementia

4. Infection

5. Tumor

6. Other neurologic disorders such as multiple sclerosis

7. Medication-induced elevated mood (see Table 12-3)

TABLE 12.3 Medications associated with the induction of mania

• Amphetamines

• Anticholinergics

• Benztropine

• Corticosteroids

• Cyclosporine

• Baclofen

• Bromocriptine

• Captopril

• Cimetidine

• Disulfiram

• Hydralazine

• Isoniazid

• Levodopa

• Levothyroxine

• Metrizamide

• Opioids

• Procarbazine

• Procyclidine

• Trihexyphenidyl

• Yohimbine

Adapted from Medicines that can cause mood disorders. Cleveland clinic health system 2004 accessed at www.cchs.net/health/health-info/2200/2284.asp?index=9287. (5)

A review of steroid-induced mania by Michael Cerullo (4) has studied the characteristics of this disorder. Typically, psychiatric symptoms emerge from 3 to 11 days after steroid therapy is begun and, when present, mania may persist for 3 weeks after steroids are discontinued. The incidence of psychiatric side effects is higher as the daily dose of steroid is increased with

1.3% incidence on <40 mg a day,
4.6% on 40 to 80 mg a day,
18.4% in those individuals taking >80 mg a day (6).

TABLE 12.4 Mood stabilizers with evidence of benefit in treating corticosteroid-induced mania

•	Preventing psychiatric effects in patients requiring long-term corticosteroids
	○ Lithium at 0.8 to 1.2 mEq/L
•	Preventing recurrence of manic symptoms in patients requiring additional steroid pulses
	○ Carbamazepine at 8-12 µg/mL
	○ Gabapentin 300 mg t.i.d.
•	Treating steroid-induced manic symptoms
	○ Olanzapine 2.5-30 mg/day
	○ Lithium 0.7 mEq/L
	○ Quetiapine 25-50 mg/day
	○ Carbamazepine at 8-12 µg/mL
	○ Haloperidol 2-20 mg/day
Adapted from Cerullo MA. Corticosteroid-induced mania: Prepare for the unpredictable. Current Psychiatry. 2006;5(6):43-58.

Psychiatric symptoms do not consistently appear with each exposure to steroids. Therefore, a history of previous exposure without psychiatric sequelae does not confer protection against such an occurrence during a subsequent exposure (1).

Although no double-blind, placebo-controlled studies have specifically examined the prevention or treatment of steroid-induced mania, patient reports and uncontrolled trials suggest that a variety of psychotropic agents may be beneficial in treating steroid-induced psychiatric symptoms (shown in Table 12.4).

Brain injury and elevated mood

There have been isolated case reports of hypomania, mania, or bipolar disorder with onset after traumatic brain injury (TBI). Most of these reports are on studies with one or two patients. One large-scale review, however, was performed by Jorge et al. (7). This comprehensive study reviewed a consecutive series of 66 patients with closed head injury who were followed at 3-, 6-, and 12-month intervals following the injury. Semistructured psychiatric interviews were conducted and activities of daily living, intellectual and social functioning were evaluated. Six patients (9%) met the criteria for mania at some point during follow-up. This secondary mania was not found to be associated with the severity of brain injury, degree of physical or cognitive impairment, level of social function, or previous family or personal history of psychiatric disorder. The duration of mania lasted for approximately 6 months; although methods of treatment that could affect this statistic were
not specified in the report. This frequency of mania is suggested by the authors to be significantly greater than that seen in other brain-injured populations (e.g., patients with stroke).

A smaller series (8) of eight patients looked at brain loci through neuroimaging for possible correlation between mania onset and the location of the TBI. None of the series showed a consistent pattern of TBI location with the onset of secondary mania, and to-date, it is unclear whether location is a crucial factor in the development of secondary mania from TBI. When treatment was indicated for the secondary mania in this group, the most successful outcome involved the use of anticonvulsants, most notably sodium valproate.

Late-onset secondary mania

Although elevated mood with a medical cause can occur at any age, it is particularly common in later life. The so-called late-onset hypomania/mania, that is, mania that occurs after the age of 50, is a form of mania that requires special consideration both in diagnosis and treatment. Late-onset elevated mood may have a clinical presentation among those identified in Table 12.5.

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