Practical Guidelines for Diagnosing and Treating Mania and Bipolar Disorder in the Elderly

William M. McDonald, MD, Charles B. Nemeroff, MD, PhD


Medscape Psychiatry & Mental Health eJournal. 1998;3(2) 

In This Article

Diagnosis: Bipolar Disorder, Manic Phase

The clinical presentation of this patient with psychomotor agitation, marked impairment of functioning, a decreased need for sleep, hyperverbal speech, and complex paranoid delusions meets the DSM-IV criteria for bipolar disorder, manic phase.[11] In addition, elderly manic patients frequently present with confusion, disorientation, and distractibility.[12] Elderly patients with mania, particularly those patients with onset after age 60 years, have also been found to have an increased incidence of neurologic impairment, including gait ataxia and frontal release signs.[13,14,15,16] Frequently, even without evidence of comorbid dementia, there are neuropathologic changes observed with magnetic resonance imaging (MRI), including atrophy.[17] Elderly manic patients are sometimes misdiagnosed as having dementia, only to have complete resolution of affective and cognitive symptoms when treated with lithium.[18,19,20]

Younger patients with mania have presentations that include euphoric moods and grandiosity. In contrast, elderly patients are more likely to show a mixture of depressed affect and manic symptoms (pressured speech and a decreased need for sleep).[12] In addition, the family histories of older patients with new-onset mania have fewer first-degree relatives with affective illness compared with younger patients with mania.[21,22,23,24] However, a reliable family history of affective illness may be difficult to obtain, since many older relatives of the patient may have been diagnosed and treated before the advent of modern psychiatric diagnosis.

Incorrect diagnosis of the manic patient as having dementia causes significant problems. This often leads to ineffective treatment of the mood disorder, early nursing-home placement, continued disability, and possibly suicide. Patients misdiagnosed with agitated depression may be at risk for worsening of irritability and increased frequency of mood cycles when placed on an antidepressant medication.[25,26]

Mania should be included in the differential diagnosis of elderly patients with relatively acute onset of confusion and agitation. The diagnostic evaluation should first include a complete physical and neurologic examination, followed by appropriate laboratory assessment comprising, at least, a blood chemistry (Chem 7), complete blood cell count, electrocardiogram (ECG), thyroid panel, urinalysis, FTA-ABS, vitamin B12, folate, drug screen, and a head computerized tomography (CT) or MRI scan. After this initial screening, consideration should also be given to a more detailed blood chemistry to examine liver function, abnormalities in calcium and phosphorus related to the parathyroid gland, and metabolic and nutritional abnormalities.

Formal neuropsychological testing should be delayed until the patient is stabilized. Patients with even a remote history of alcoholism should be started on folate and thiamine. The patient's neurologic status and vital signs should be closely monitored for evidence of alcohol, narcotic, or benzodiazepine withdrawal, particularly during the first few days of hospitalization. All medications used by the patient should be reviewed carefully as playing a possible role in the patient's presentation. Drugs often associated with agitation and psychosis include anticholinergic medications, digoxin, antiparkinsonian medications, and steroids.

Manic patients may be difficult to distinguish from patients who have become delirious on medication, unless the clinician takes a careful history to determine whether the onset of symptoms coincided with the start of a new medication. Patients started on new medications that are coincident with psychotic symptoms, disinhibition, and/or delirium should be tapered off the medications to determine if they have a drug-induced psychiatric disorder or a primary psychiatric disturbance such as mania.

The patient should be treated conservatively until potential medical causes of agitation have been eliminated. Once the patient is stable and medical causes of an acute delirium have been eliminated, treatment of the psychiatric disorder may be initiated.

Acute pharmacologic management of the patient includes the use of antipsychotics and benzodiazepines. One approach is to treat the patient acutely with a combination of haloperidol and lorazepam in alternating doses until the patient is calm and coherent (Table I). Both medications have the advantage of either intramuscular or oral administration. The main disadvantage of haloperidol is the potential for extrapyramidal symptoms (EPS), including an agitated physical response (akathisia). However, alternating doses of lorazepam with haloperidol is likely to decrease the potential for the development of EPS. Thiothixene, molindone, risperidone, or olanzapine may be substituted for haloperidol.

Once the patient is stabilized with pharmacologic treatments she/he should be further evaluated to determine the cause of clinical presentation: dementia, mania, substance abuse, depression, or schizophrenia. Additional history and the clinical course of the patient's symptoms are important in determining the diagnosis. The demented patient demonstrates a slow decline in function and other symptoms associated with a progressive dementia such as Alzheimer's disease. A careful history reveals changes in cognition that have occurred over years, not months. The spouse typically describes difficulties with managing finances, getting lost while traveling, and language problems that predate the acute episode by years and, at first, appeared to be isolated episodes of confusion. The agitation in demented patients is associated with their cognitive problems, and their symptoms increase at night (ie, "sundowning"). More complete bedside neuropsychological testing for word fluency (eg, naming fewer than 18 animals in 1 minute) and visuospatial functioning (eg, drawing complex figures such as a 3-dimensional box) uncovers deficits consistent with Alzheimer's disease. The staff may describe difficulties dressing (apraxia), difficulty with speech and finding the right word (aphasia), and short-term memory loss (eg, finding their room, remembering their doctor's name).

The patient with subcortical dementia has evidence of CVA or other abnormalities on structural brain imaging scans (hyperintensities in greater than one third of their white matter) and classic neurologic/neuroimaging findings for Parkinson's disease, Huntington's chorea, or normal-pressure hydrocephalus.

The patient with alcoholic and other frontal lobe dementias appears inappropriate and disinhibited, with a flattened affect. As the patient's behavior comes under control, the symptoms of dementia become more apparent.

Patients with depression appear increasingly melancholic. They refuse to eat and withdraw to their rooms. The manic patient remains hyperverbal and intrusive. Compared with the delusions of a manic patient, which are often grandiose, paranoid, and complex, or the depressive delusions of a somatically preoccupied melancholic patient, the delusions of the demented patient are vague, mood incongruent, and often bizarre. Demented patients may feel that their possessions are being stolen, that imposters have replaced loved ones (Capgras's syndrome), or that their image in the mirror is someone else. Late-onset schizophrenia is relatively rare. Further history may reveal prodromal symptoms that mimic depression, such as poor personal hygiene, withdrawal, and lack of spontaneity. The delusions are bizarre and mood incongruent, and the patient's cognition is characterized by concrete thinking with sparse content.

Once stabilized, evaluation of the elderly patient with mania should continue. In clinical practice, elderly patients rarely fit within a single diagnostic category. The patient in our case study responded to a regimen of haloperidol 1mg bid and lorazepam 0.5mg bid. The initial laboratory testing was normal, except for evidence of mild dehydration and a urinary tract infection (UTI). Incidentally noted was extensive white matter disease on the head CT scan. The patient, although manageable on the ward, remained hyperverbal, intrusive, and delusional. He continued to show signs of cerebellar dysfunction and was placed on fall precautions. His alcohol history was reviewed with family members. The patient had been drinking daily for most of his adult life, which included up to one fifth of gin every night for the past 5 years. Further cognitive testing showed a pattern of intact cortical functions but clear evidence of subcortical and frontal lobe dementia, consistent with the diagnosis of alcoholic dementia.

The patient was given nutritional supplements, including folate and thiamine. His UTI was treated with the appropriate antibiotics and a fluid-intake increase. He was diagnosed with alcohol dependence and dementia as well as bipolar disorder, manic phase.


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