What do you suspect is responsible for this patient’s progressively worsening cognitive symptoms?
A 77-year-old Hispanic man is referred by his primary care physician (PCP) for evaluation of progressively worsening cognitive symptoms that began 5 to 7 years earlier, according to his son, who has accompanied him to the appointment. The man, who was formerly very social, has become increasingly withdrawn. Whereas he used to sit for hours on a park bench and talk with friends, now he spends most of his time inside watching TV or sleeping. Within the past year, he has started to forget where he placed items around the house, and he has trouble remembering names, including those of his grandchildren.
About 6 months earlier, his PCP prescribed an antidepressant because of his social withdrawal and increased sleep, but his symptoms have not improved.
The man grew up in Mexico and immigrated to the US at the age of 25. He has a high school education and completed one year of college during night school. He worked in construction until the age of 40, after which he started a successful Mexican restaurant. He retired 7 years ago, when his son took over management of the restaurant. He has been married for 45 years and has three children and six grandchildren.
He has a history of diabetes, high blood pressure, and hyperlipidemia. Medications include metformin, enalapril, and atorvastatin.
Family history is pertinent for dementia of unknown type in his mother.
Blood pressure is elevated (145/90 mm Hg). Heart rate and temperature are normal. No tremor is appreciated.
The man speaks English fluently but at a slow pace and with a strong accent. He has a flat affect but denies symptoms of depression and suicidal ideation.
On mental status examination, the patient is oriented to location and year but not to month or day of the week. He can recall one of four unrelated words at two minutes, completes two of five calculations correctly, can name three of four common objects correctly, and makes several errors in repeating a complex sentence. He can draw the face of a clock but has trouble placing the numbers and hands correctly.
Thyroid-stimulating hormone, vitamin B12, and vitamin D levels are within normal limits.
An MRI scan reveals no evidence of brain tumor or past stroke and shows changes suggestive of cerebral and hippocampal atrophy. A CT scan shows diffuse cerebral atrophy, widened sulci, dilatation of the lateral ventricles, and decreased hippocampal volume.
While a definitive diagnosis of Alzheimer disease (AD) relies on autopsy findings, the history of gradual withdrawal and memory problems; mental status examination results that suggest problems with memory, concentration, mathematical calculations, and visuospatial abilities; and imaging findings suggest a diagnosis of AD. Because the workup is negative for other common causes of cognitive decline, such as Parkinson disease, stroke, or brain tumor, donepezil is prescribed for the patient.
In the US, the overall prevalence of AD and related dementias is highest among African Americans (14.7%) and Hispanics (12.9%). Among non-Hispanic whites, the prevalence is 11.3%. The burden of disease falls most heavily on African Americans and Hispanics aged 85 years and older (43% and 40%, respectively).1
Because of a burgeoning population, Hispanics are expected to have the largest increase in total number of individuals with AD by 2060. By that year, researchers estimate that 3.2 million Hispanics and 2.2 million African Americans will have the disease.1
While the risk of AD is estimated to be about 1.5 times higher in Hispanics than in whites, Hispanics often receive a later diagnosis. Various factors may explain the delay in diagnosis, including health care disparities that affect access to care and patient education about signs and symptoms of AD onset.2
However, racial/ethnic differences in early symptoms of AD may also play a role. A recent study of 34 individuals with autopsy-confirmed AD found that although Hispanics and non-Hispanics had largely similar AD pathology, Hispanics had less impairment of memory, attention, and executive functioning than non-Hispanics. Hispanics also exhibited more disease in small cerebral blood vessels and more amyloid angiopathy than non-Hispanics.3
The study suggests symptoms that are usually prominent in early AD for non-Hispanic individuals may be less informative for Hispanics. That, in turn, may make it more difficult to make a clinical diagnosis in early to moderate disease, when medications are more likely to be effective.
The findings also highlight the need for more culturally sensitive public health campaigns to improve education, diagnosis, and treatment of AD among Hispanics.
1. Matthews KA, Xu W, Gaglioti AH, et al. Racial and ethnic estimates of Alzheimer’s disease and related dementias in the United States (2015-2060) in adults aged ≥65 years. Alzheimers Dement. 2019;15:17-24. doi: 10.1016/j.jalz.2018.06.3063.
2. Vega IE, Cabrera LY, Wygant CM, et al. Alzheimer’s disease in the Latino community: intersection of genetics and social determinants of health. J Alzheimers Dis. 2017;58:979-992. doi: 10.3233/JAD-161261.
3. Weissberger GH, Gollan TH, Bondi MW, et al. Neuropsychological deficit profiles, vascular risk factors, and neuropathological findings in Hispanic older adults with autopsy-confirmed Alzheimer’s disease. J Alzheimers Dis. 2019;67:291-302. doi: 10.3233/JAD-180351.
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