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The history and findings in this case are suggestive of Alzheimer's disease (AD), which probably was preceded by chronic traumatic encephalopathy (CTE).
AD is the most prevalent cause of cognitive impairment and dementia worldwide. Presently, approximately 50 million individuals are affected by AD; by 2050, the number of affected individuals globally is expected to reach 152 million. AD has a prolonged and progressive disease course that begins with neuropathologic changes in the brain years before onset of clinical manifestations. These changes include the accumulation of beta-amyloid plaques, neurofibrillary tangles, and neuroinflammation. Neuroimaging studies have shown that beta-amyloid plaques begin to deposit in the brain ≥ 10 years before the start of cognitive decline. Patients with AD normally present with slowly progressive memory loss; as the disease progresses, other areas of cognition are affected. Patients may experience language disorders (eg, anomic aphasia or anomia) and impairment in visuospatial skills and executive functions. Slowly progressive behavioral changes may also occur.
CTE is a neurodegenerative disorder that is believed to be the long-term consequence of repetitive head trauma. Its incidence is highest among athletes of high-impact sports, such as boxing or American football, and victims of domestic violence. Clinically, CTE can be indistinguishable from AD. Although neuropathologic differences exist, they can be confirmed only on postmortem examination. Patients with CTE may present with behavioral symptoms, such as aggression, depression, emotional lability, apathy, and suicidal feelings, as well as motor symptoms, including tremor, ataxia, incoordination, and dysarthria. Cognitive symptoms, including attention and concentration deficits and memory impairment, also occur. CTE is also associated with the development of dementia and may predispose patients to early-onset AD.
Curative therapies do not exist for AD; thus, management centers on symptomatic treatment for neuropsychiatric or cognitive symptoms. Cholinesterase inhibitors and a partial N-methyl-D-aspartate antagonist are the standard medical therapies used in patients with AD. For patients with mild cognitive impairment or mild dementia, several newly approved antiamyloid therapies are also available. 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. Presently, both aducanumab and lecanemab are recommended only for the treatment of patients with mild cognitive impairment or mild dementia, the population in which their safety and efficacy were demonstrated in clinical trials.
Psychotropic agents may be used to treat symptoms, such as depression, agitation, aggression, hallucinations, delusions, and sleep disorders, which can be problematic. Behavioral interventions may also be used, normally in combination with pharmacologic interventions (eg, anxiolytics for anxiety and agitation, neuroleptics for delusions or hallucinations, and antidepressants or mood stabilizers for mood disorders and specific manifestations). Regular physical activity and exercise may help to delay disease progression and are recommended as an adjunct to the medical management of AD.
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 Alzheimer's disease (AD), which probably was preceded by chronic traumatic encephalopathy (CTE).
AD is the most prevalent cause of cognitive impairment and dementia worldwide. Presently, approximately 50 million individuals are affected by AD; by 2050, the number of affected individuals globally is expected to reach 152 million. AD has a prolonged and progressive disease course that begins with neuropathologic changes in the brain years before onset of clinical manifestations. These changes include the accumulation of beta-amyloid plaques, neurofibrillary tangles, and neuroinflammation. Neuroimaging studies have shown that beta-amyloid plaques begin to deposit in the brain ≥ 10 years before the start of cognitive decline. Patients with AD normally present with slowly progressive memory loss; as the disease progresses, other areas of cognition are affected. Patients may experience language disorders (eg, anomic aphasia or anomia) and impairment in visuospatial skills and executive functions. Slowly progressive behavioral changes may also occur.
CTE is a neurodegenerative disorder that is believed to be the long-term consequence of repetitive head trauma. Its incidence is highest among athletes of high-impact sports, such as boxing or American football, and victims of domestic violence. Clinically, CTE can be indistinguishable from AD. Although neuropathologic differences exist, they can be confirmed only on postmortem examination. Patients with CTE may present with behavioral symptoms, such as aggression, depression, emotional lability, apathy, and suicidal feelings, as well as motor symptoms, including tremor, ataxia, incoordination, and dysarthria. Cognitive symptoms, including attention and concentration deficits and memory impairment, also occur. CTE is also associated with the development of dementia and may predispose patients to early-onset AD.
Curative therapies do not exist for AD; thus, management centers on symptomatic treatment for neuropsychiatric or cognitive symptoms. Cholinesterase inhibitors and a partial N-methyl-D-aspartate antagonist are the standard medical therapies used in patients with AD. For patients with mild cognitive impairment or mild dementia, several newly approved antiamyloid therapies are also available. 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. Presently, both aducanumab and lecanemab are recommended only for the treatment of patients with mild cognitive impairment or mild dementia, the population in which their safety and efficacy were demonstrated in clinical trials.
Psychotropic agents may be used to treat symptoms, such as depression, agitation, aggression, hallucinations, delusions, and sleep disorders, which can be problematic. Behavioral interventions may also be used, normally in combination with pharmacologic interventions (eg, anxiolytics for anxiety and agitation, neuroleptics for delusions or hallucinations, and antidepressants or mood stabilizers for mood disorders and specific manifestations). Regular physical activity and exercise may help to delay disease progression and are recommended as an adjunct to the medical management of AD.
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 Alzheimer's disease (AD), which probably was preceded by chronic traumatic encephalopathy (CTE).
AD is the most prevalent cause of cognitive impairment and dementia worldwide. Presently, approximately 50 million individuals are affected by AD; by 2050, the number of affected individuals globally is expected to reach 152 million. AD has a prolonged and progressive disease course that begins with neuropathologic changes in the brain years before onset of clinical manifestations. These changes include the accumulation of beta-amyloid plaques, neurofibrillary tangles, and neuroinflammation. Neuroimaging studies have shown that beta-amyloid plaques begin to deposit in the brain ≥ 10 years before the start of cognitive decline. Patients with AD normally present with slowly progressive memory loss; as the disease progresses, other areas of cognition are affected. Patients may experience language disorders (eg, anomic aphasia or anomia) and impairment in visuospatial skills and executive functions. Slowly progressive behavioral changes may also occur.
CTE is a neurodegenerative disorder that is believed to be the long-term consequence of repetitive head trauma. Its incidence is highest among athletes of high-impact sports, such as boxing or American football, and victims of domestic violence. Clinically, CTE can be indistinguishable from AD. Although neuropathologic differences exist, they can be confirmed only on postmortem examination. Patients with CTE may present with behavioral symptoms, such as aggression, depression, emotional lability, apathy, and suicidal feelings, as well as motor symptoms, including tremor, ataxia, incoordination, and dysarthria. Cognitive symptoms, including attention and concentration deficits and memory impairment, also occur. CTE is also associated with the development of dementia and may predispose patients to early-onset AD.
Curative therapies do not exist for AD; thus, management centers on symptomatic treatment for neuropsychiatric or cognitive symptoms. Cholinesterase inhibitors and a partial N-methyl-D-aspartate antagonist are the standard medical therapies used in patients with AD. For patients with mild cognitive impairment or mild dementia, several newly approved antiamyloid therapies are also available. 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. Presently, both aducanumab and lecanemab are recommended only for the treatment of patients with mild cognitive impairment or mild dementia, the population in which their safety and efficacy were demonstrated in clinical trials.
Psychotropic agents may be used to treat symptoms, such as depression, agitation, aggression, hallucinations, delusions, and sleep disorders, which can be problematic. Behavioral interventions may also be used, normally in combination with pharmacologic interventions (eg, anxiolytics for anxiety and agitation, neuroleptics for delusions or hallucinations, and antidepressants or mood stabilizers for mood disorders and specific manifestations). Regular physical activity and exercise may help to delay disease progression and are recommended as an adjunct to the medical management of AD.
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 51-year-old man presents with complaints of progressively worsening cognitive impairments, particularly in executive functioning and episodic memory, as well as depression, apathy, and emotional lability. The patient is accompanied by his wife, who states that he often becomes irritable and "flies off the handle" without provocation. The patient's depressive symptoms began approximately 18 months ago, shortly after his mother's death from heart failure. Both he and his wife initially attributed his symptoms to the grieving process; however, in the past 6 months, his depression and mood swings have become increasingly frequent and intense. In addition, he was recently mandated to go on administrative leave from his job as an IT manager because of poor performance and angry outbursts in the workplace. The patient believes that his forgetfulness and difficulty regulating his emotions are the result of the depression he is experiencing. His goal today is to "get on some medication" to help him better manage his emotions and return to work. Although his wife is supportive of her husband, she is concerned about her husband's rapidly progressing deficits in short-term memory and is uncertain that they are related to his emotional symptoms.
The patient's medical history is notable for nine concussions sustained during his time as a high school and college football player; only one resulted in loss of consciousness. He does not currently take any medications. There is no history of tobacco use, illicit drug use, or excessive alcohol consumption. There is no family history of dementia. His current height and weight are 6 ft 3 in and 223 lb, and his BMI is 27.9.
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 24 on the Mini-Mental State Examination, which is a set of 11 questions that doctors and other healthcare professionals commonly use to check for cognitive impairment. His clinician orders a brain MRI, which reveals a tau-positive neurofibrillary tangle in the neocortex.
