Cases That Test Your Skills

After 62 years, her husband is a ‘stranger’

Current Psychiatry. 2004 June;3(6):88-95

Ms. A, age 83, is increasingly confused and agitated. She attacks caregivers and distrusts her friends at church. The challenge: diagnose her dementia, quell her aggressive behavior, and slow her cognitive decline.

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References

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Presenting symptoms: Marital memories

Ms. A, age 83, has been experiencing increasing confusion, agitation, and memory loss across 4 to 5 years. Family members say her memory loss has become prominent within the last year. She can no longer cook, manage her finances, shop, or perform other basic activities. At times she does not recognize her husband of 62 years and needs help with bathing and grooming.

Ms. A’s Folstein Mini-Mental State Examination (MMSE) score is 18, indicating moderate dementia. She exhibits disorientation, diminished short-term memory, impaired attention including apraxia, and executive dysfunction. Her Geriatric Depression Scale (15-item short form) score indicates normal mood.

A neurologic exam reveals mild parkinsonism, including mild bilateral upper-extremity cogwheeltype rigidity and questionable frontal release signs including a possible mild bilateral grasp reflex. No snout reflex was seen.

This presentation suggests Ms. A has:

Alzheimer’s disease
Lewy body dementia
or vascular dementia

The authors’ observations:

Differentiating among Alzheimer’s, Lewy body, and vascular dementias is important (Table 1), as their treatments and clinical courses differ.

The initial workup’s goal is to diagnose a reversible medical condition that may be hastening cognitive decline. Brain imaging (CT or MRI) can uncover cerebrovascular disease, subdural hematomas, normal-pressure hydrocephalus, tumors, or other cerebral diseases. Laboratory tests can reveal systemic conditions such as hypothyroidism, vitamin B12 deficiency, hypercalcemia, neurosyphilis, or HIV infection.¹

Table 1

Differences in Alzheimer’s, Lewy body, and vascular dementias

Alzheimer’s dementia	Lewy body dementia	Vascular dementia
Gradual onset and chronic cognitive decline Memory difficulty combined with apraxia, aphasia, agnosia, or executive dysfunction	Cognitive, memory changes with one or more of the following: visual hallucinations fluctuating consciousness (“sundowning”) parkinsonian features	Early findings often include depression or personality changes, plus incontinence and gait disorder
Psychosis common in middle to late stages	Visual hallucinations, other psychoses in early stages Periods of marked delirium, “sundowning”	Temporal relationship between stroke and dementia onset, but variability in course
Day-to-day cognitive performance stable	Cognitive performance fluctuates during early stages.	Day-to-day cognitive performance stable
Parkinsonism not apparent in early stages, may present in middle to late stages	Parkinsonism in early stages Tremor not common	Gait disorder and parkinsonism common, especially with basal ganglia infarcts
Neurologic signs present in late stages	Exquisite sensitivity to neuroleptic therapy	Increased sensitivity to neuroleptics
Cannot be explained as vascular or mixed-type dementia	Cannot be explained as vascular or mixed-type dementia	Imaging necessary to document cerebrovascular disease

With a thorough history and laboratory testing, a diagnosis of “probable” AD can be as much as 85% accurate. Probable AD is characterized by progressive gradual decline of cognitive functions affecting memory and at least one other domain including executive dysfunction, apraxia, aphasia, and/or agnosia. These deficits must cause significant functional impairment.

Neurologic test results may support AD diagnosis after ruling out reversible causes of dementia. Neuropsychological testing can provide valuable early information when subtle findings cannot be ascertained on clinical screening. (For a listing of neuropsychological tests, see this article at currentpsychiatry.com.)

Diagnosis: An unpredictable patient

Ms. A received a CBC; comprehensive metabolic panel; urinalysis; screens for rapid plasma reagin, B12, folate, and homocysteine levels; and a brain MRI. Hemoglobin and serum albumin were mildly depressed, reflecting early malnutrition. MRI showed generalized cerebral atrophy. Significant vascular disease was not identified.

Ms. A was diagnosed as having probable Alzheimer’s-type dementia based on the test results and the fact that her cognition was steadily declining. Other explanatory mechanisms were absent. She did not exhibit hallucinatory psychosis or fluctuating consciousness, which would signal Lewy body dementia.

Table 2

Medications for treating agitation in Alzheimer’s dementia

Drug	Supporting evidence	Recommended dosage (mg/d)*	Rationale	Drawbacks
Anticonvulsants
Carbamazepine	Tariot et al²	200 to 1,200 mg/d in divided doses	Commonly used for impulse control disorders	Agranulocytosis, hyponatremia, liver toxicity (all rare)
Divalproex	Loy and Tariot³	250 to 2,000 mg/d	Increasing evidence points to neuroprotective qualities	Possible white blood cell suppression, liver toxicity, pancreatitis (all rare)
Gabapentin	Roane et al⁴	100 to 1,200 mg/d	Safe in patients with hepatic dysfunction	Scant data on use in Alzheimer’s disease
Lamotrigine	Tekin et al⁵	Start at 25 mg/d; titrate slowly to 50 to 200 mg/d	Possibly neuroprotective via N-methyl-D-aspartate mechanism	Rapid titration may cause Stevens-Johnson syndrome
Atypical antipsychotics
Olanzapine	Street et al⁶	2.5 to 10 mg/d	Sedating effects may aid sleep	Anticholinergic effects may increase confusion, compound cognitive deficit
Quetiapine	Tariot et al⁷	25 to 300 mg/d	Tolerable Sedating effects may aid sleep	Watch for orthostasis, especially at higher dosages
Risperidone	DeVane et al⁸	0.25 to 3 mg/d	Strong data support use	High orthostatic potential, possible extrapyramidal symptoms with higher dosages
Ziprasidone	None	Oral:20to80mgbid IM: 10 to 20 mg, maximum 40 mg over 24 hours	Effective in managing agitation	No controlled trials, case reports in AD-associated agitation
SSRIs
Citalopram	Pollock et al⁹	10 to 40 mg/d	Minimal CYP-2D6 inhibition	Effect may take 2 to 4 weeks
Sertraline	Lyketsos et al¹⁰	25 to 200 mg/d	Minimal CYP-2D6 inhibition	Effect may take 2 to 4 weeks
* No specific, widely accepted dosing guidelines exist for patients age > 65, but this group often does not tolerate higher dosages.
SSRI: Selective serotonin reuptake inhibitor
IM: Intramuscula