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The history and findings in this case are suggestive of early-onset Alzheimer's disease (AD) with aphasia.
AD is a neurodegenerative disorder characterized by cognitive and behavioral impairment that significantly interferes with a patient's social and occupational functioning. There is currently no cure for AD, which has a long preclinical period and a progressive course. Individuals with AD develop amyloid plaques in the hippocampus, a structure deep in the brain that helps to encode memories, and in other areas of the cerebral cortex that are involved in thinking and making decisions.
Patients with AD typically present with insidiously progressive memory loss; over the course of several years, other areas of cognition are impaired. Subsequent to memory loss, patients may also experience language disorders (eg, anomic aphasia or anomia) and impairment in visuospatial skills and executive functions. In many patients, slowly progressive behavioral changes are also observed.
AD is most prevalent in individuals older than 65 years; however, early‐onset AD (in individuals aged 60 years or older) can also occur. Early-onset AD shares the same essential neuropathological characteristics (ie, amyloid plaques and neurofibrillary tangles) as late-onset (65 years or older) AD, but it differs in several ways. For example, memory loss is an extremely common presenting symptom in late-onset AD, whereas nonamnestic presentation (ie, language, visuospatial, or executive impairment) is very rare, occurring in only about 5% of cases. Conversely, nonamnestic presentations may occur in 30%-40% of patients with early-onset AD. Frequent nonamnestic cognitive manifestations in patients with early-onset AD are those seen in mild to moderate AD, including visual agnosia (55.1%), aphasia (57.9%), and behavioral changes (61.7%). In addition, several studies have suggested that early-onset AD may have a more aggressive course than late-onset AD does, including faster cognitive and functional decline.
Presently, only symptomatic therapies are available for AD. The standard medical treatment for AD includes cholinesterase inhibitors and a partial N-methyl-D-aspartate antagonist. Newly approved antiamyloid therapies are also available for patients with mild cognitive impairment or mild dementia. These include aducanumab, a first-in-class amyloid beta–directed antibody that was approved in 2021, and lecanemab, another amyloid beta–directed antibody that was approved in 2023. Both aducanumab and lecanemab are recommended for the treatment of patients with mild cognitive impairment or mild dementia stage of disease, the population in which the safety and efficacy of these newer agents were demonstrated in clinical trials.
Psychotropic agents may be used to treat the secondary symptoms of AD (eg, depression, agitation, aggression, hallucinations, delusions, sleep disorders), which can be problematic. Behavioral interventions ranging from patient-centered approaches to caregiver training may also be used to help manage cognitive and behavioral manifestations of AD, often in combination with pharmacologic interventions, such as anxiolytics for anxiety and agitation, neuroleptics for delusions or hallucinations, and antidepressants or mood stabilizers for mood disorders and specific manifestations (eg, episodes of anger or rage). Routine physical activity and exercise may affect AD progression and may possibly exert a protective effect on brain health.
Jasvinder Chawla, MD, Professor of Neurology, Loyola University Medical Center, Maywood; Director, Clinical Neurophysiology Lab, Department of Neurology, Hines VA Hospital, Hines, IL.
Jasvinder Chawla, MD, has disclosed no relevant financial relationships.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
The history and findings in this case are suggestive of early-onset Alzheimer's disease (AD) with aphasia.
AD is a neurodegenerative disorder characterized by cognitive and behavioral impairment that significantly interferes with a patient's social and occupational functioning. There is currently no cure for AD, which has a long preclinical period and a progressive course. Individuals with AD develop amyloid plaques in the hippocampus, a structure deep in the brain that helps to encode memories, and in other areas of the cerebral cortex that are involved in thinking and making decisions.
Patients with AD typically present with insidiously progressive memory loss; over the course of several years, other areas of cognition are impaired. Subsequent to memory loss, patients may also experience language disorders (eg, anomic aphasia or anomia) and impairment in visuospatial skills and executive functions. In many patients, slowly progressive behavioral changes are also observed.
AD is most prevalent in individuals older than 65 years; however, early‐onset AD (in individuals aged 60 years or older) can also occur. Early-onset AD shares the same essential neuropathological characteristics (ie, amyloid plaques and neurofibrillary tangles) as late-onset (65 years or older) AD, but it differs in several ways. For example, memory loss is an extremely common presenting symptom in late-onset AD, whereas nonamnestic presentation (ie, language, visuospatial, or executive impairment) is very rare, occurring in only about 5% of cases. Conversely, nonamnestic presentations may occur in 30%-40% of patients with early-onset AD. Frequent nonamnestic cognitive manifestations in patients with early-onset AD are those seen in mild to moderate AD, including visual agnosia (55.1%), aphasia (57.9%), and behavioral changes (61.7%). In addition, several studies have suggested that early-onset AD may have a more aggressive course than late-onset AD does, including faster cognitive and functional decline.
Presently, only symptomatic therapies are available for AD. The standard medical treatment for AD includes cholinesterase inhibitors and a partial N-methyl-D-aspartate antagonist. Newly approved antiamyloid therapies are also available for patients with mild cognitive impairment or mild dementia. These include aducanumab, a first-in-class amyloid beta–directed antibody that was approved in 2021, and lecanemab, another amyloid beta–directed antibody that was approved in 2023. Both aducanumab and lecanemab are recommended for the treatment of patients with mild cognitive impairment or mild dementia stage of disease, the population in which the safety and efficacy of these newer agents were demonstrated in clinical trials.
Psychotropic agents may be used to treat the secondary symptoms of AD (eg, depression, agitation, aggression, hallucinations, delusions, sleep disorders), which can be problematic. Behavioral interventions ranging from patient-centered approaches to caregiver training may also be used to help manage cognitive and behavioral manifestations of AD, often in combination with pharmacologic interventions, such as anxiolytics for anxiety and agitation, neuroleptics for delusions or hallucinations, and antidepressants or mood stabilizers for mood disorders and specific manifestations (eg, episodes of anger or rage). Routine physical activity and exercise may affect AD progression and may possibly exert a protective effect on brain health.
Jasvinder Chawla, MD, Professor of Neurology, Loyola University Medical Center, Maywood; Director, Clinical Neurophysiology Lab, Department of Neurology, Hines VA Hospital, Hines, IL.
Jasvinder Chawla, MD, has disclosed no relevant financial relationships.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
The history and findings in this case are suggestive of early-onset Alzheimer's disease (AD) with aphasia.
AD is a neurodegenerative disorder characterized by cognitive and behavioral impairment that significantly interferes with a patient's social and occupational functioning. There is currently no cure for AD, which has a long preclinical period and a progressive course. Individuals with AD develop amyloid plaques in the hippocampus, a structure deep in the brain that helps to encode memories, and in other areas of the cerebral cortex that are involved in thinking and making decisions.
Patients with AD typically present with insidiously progressive memory loss; over the course of several years, other areas of cognition are impaired. Subsequent to memory loss, patients may also experience language disorders (eg, anomic aphasia or anomia) and impairment in visuospatial skills and executive functions. In many patients, slowly progressive behavioral changes are also observed.
AD is most prevalent in individuals older than 65 years; however, early‐onset AD (in individuals aged 60 years or older) can also occur. Early-onset AD shares the same essential neuropathological characteristics (ie, amyloid plaques and neurofibrillary tangles) as late-onset (65 years or older) AD, but it differs in several ways. For example, memory loss is an extremely common presenting symptom in late-onset AD, whereas nonamnestic presentation (ie, language, visuospatial, or executive impairment) is very rare, occurring in only about 5% of cases. Conversely, nonamnestic presentations may occur in 30%-40% of patients with early-onset AD. Frequent nonamnestic cognitive manifestations in patients with early-onset AD are those seen in mild to moderate AD, including visual agnosia (55.1%), aphasia (57.9%), and behavioral changes (61.7%). In addition, several studies have suggested that early-onset AD may have a more aggressive course than late-onset AD does, including faster cognitive and functional decline.
Presently, only symptomatic therapies are available for AD. The standard medical treatment for AD includes cholinesterase inhibitors and a partial N-methyl-D-aspartate antagonist. Newly approved antiamyloid therapies are also available for patients with mild cognitive impairment or mild dementia. These include aducanumab, a first-in-class amyloid beta–directed antibody that was approved in 2021, and lecanemab, another amyloid beta–directed antibody that was approved in 2023. Both aducanumab and lecanemab are recommended for the treatment of patients with mild cognitive impairment or mild dementia stage of disease, the population in which the safety and efficacy of these newer agents were demonstrated in clinical trials.
Psychotropic agents may be used to treat the secondary symptoms of AD (eg, depression, agitation, aggression, hallucinations, delusions, sleep disorders), which can be problematic. Behavioral interventions ranging from patient-centered approaches to caregiver training may also be used to help manage cognitive and behavioral manifestations of AD, often in combination with pharmacologic interventions, such as anxiolytics for anxiety and agitation, neuroleptics for delusions or hallucinations, and antidepressants or mood stabilizers for mood disorders and specific manifestations (eg, episodes of anger or rage). Routine physical activity and exercise may affect AD progression and may possibly exert a protective effect on brain health.
Jasvinder Chawla, MD, Professor of Neurology, Loyola University Medical Center, Maywood; Director, Clinical Neurophysiology Lab, Department of Neurology, Hines VA Hospital, Hines, IL.
Jasvinder Chawla, MD, has disclosed no relevant financial relationships.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
A 53-year-old woman, who is a high school mathematics teacher, presents with reports of progressively increasing cognitive impairments. Specifically, she notes increasing difficulty with remembering words as well as challenges with her executive functioning. She was recently reprimanded by her principal for missing several mandatory staff meetings and deadlines for submitting student grades. The patient states her symptoms began approximately 2 years ago. She initially attributed them to hormonal changes because of menopause but is becoming concerned about the impact they are having on her ability to function. She recently began experiencing difficulties with spatial perception, which resulted in her falling down the stairs of her home and spraining an ankle. The patient lives alone and has no children. Her medical history is unremarkable except for a motor vehicle accident 5 years earlier that resulted in her sustaining a concussion and a fractured wrist. She does not currently take any medications. There is no history of tobacco use or excessive alcohol consumption. Her current height and weight are 5 ft 3 in and 147 lb, respectively.
No abnormalities are noted on physical exam; the patient's blood pressure, pulse oximetry, and heart rate are within normal ranges. Laboratory tests are all within normal ranges, including thyroid-stimulating hormone and vitamin B12 levels. The patient scores 16 on the Montreal Cognitive Assessment test. Her clinician orders an MRI, which reveals deep indentations around the front and sides of the brain.
