Image Quizzes

This patient’s presentation is indicative of moderate-stage Alzheimer’s disease (AD), which is confirmed by physical exam and testing; most notably, her MMSE score of 18 (a score of ≥ 25 is considered normal) and MRI results showing distinct cortical atrophy. At this stage of disease, signs and symptoms become more pronounced and widespread to include not only language deficiencies, prominent memory loss, and sensory processing, but also motor deficits and behavioral issues, all of which are clearly present in this patient.

A very important clinical consideration is a possible delay in diagnosis. It is atypical for an initial diagnosis of AD to be made when a patient is in the moderate stage of disease. This patient’s history over 5 years before her diagnosis included complaints of forgetfulness and low-level dyspraxia, which were not pursued. Reasons for this can vary. Broadly, patient interactions in a primary care setting tend to be brief, thus, many patients are not engaged in their care. Early symptoms — eg, memory impairment — can be missed during routine office visits.

There are also significant racial disparities in the diagnosis of dementia. According to National Institute of Aging-funded studies that were conducted in 39 AD Research Centers, White patients > 65 years old had a significantly higher prevalence of dementia diagnoses at baseline visits than Black patients in the same age group. Black patients, especially Black women, tend not to be diagnosed with AD until it has progressed. Conversely, Black patients had more risk factors for AD, greater cognitive impairment, and more severe neuropsychiatric symptoms (delusions and hallucinations) than those of other races and ethnicities.

Another barrier to timely diagnosis in Black patients is disparity in access to neuroimaging. In a study conducted by Wibecan and colleagues at Boston Medical Center, researchers found that among neuroimaging assessments conducted at the facility, Black patients who received MRI or CT scan for the diagnosis of cognitive impairment were older than White patients (72.5 years vs 67 years). Additionally, Black patients were significantly less likely to undergo MRI (the gold standard of care for dementia diagnosis) than CT scan.  

Hypothyroidism is an endocrine disorder that occurs because of a deficiency in thyroid hormone. Symptoms tend to be subtle and non-specific but vary greatly. Some of the hallmark symptoms are fatigue, weight gain, cold intolerance, dry skin, and hair loss. Additionally, emotional lability and depressed mood with mental impairment, slowed speech, and movement, as evident in this patient. However, hypothyroidism was ruled out when her laboratory results returned with all values within normal range.  

Vascular dementia is the second-most prevalent form of dementia after AD. It is characterized as cognitive impairment that occurs after one, or a series of, neurologic events and does not refer to a single disease but to a variety of vascular disorders. Patients with vascular dementia often exhibit mood and behavioral changes, deficits in executive function, and severe memory loss, all of which are present in this patient. However, as there were no (known) neurologic events in this patient — and no evidence thereof on imaging — and her hypertension is relatively well controlled, this is not a diagnostic consideration for this patient.  

Normal pressure hydrocephalus (NPH) is caused by the build-up of cerebrospinal fluid in the brain. It is characterized by abnormal gait, dementia, and urinary incontinence. Patients with NPH experience decreased attention, significant memory loss, bradyphrenia, bradykinesia, and broad-based gait, all of which feature in this patient. However, brain MRI was negative for structural abnormalities of this type, and there was no indication of NPH, which rules it out as a potential diagnosis.  

Shaheen E. Lakhan, MD, PhD, MS, MEd, Chief of Pain Management, Carilion Clinic and Virginia Tech Carilion School of Medicine, Roanoke, Virginia.

Disclosure: Shaheen E. Lakhan, MD, PhD, MS, MEd, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
 

This patient’s presentation is indicative of moderate-stage Alzheimer’s disease (AD), which is confirmed by physical exam and testing; most notably, her MMSE score of 18 (a score of ≥ 25 is considered normal) and MRI results showing distinct cortical atrophy. At this stage of disease, signs and symptoms become more pronounced and widespread to include not only language deficiencies, prominent memory loss, and sensory processing, but also motor deficits and behavioral issues, all of which are clearly present in this patient.

A very important clinical consideration is a possible delay in diagnosis. It is atypical for an initial diagnosis of AD to be made when a patient is in the moderate stage of disease. This patient’s history over 5 years before her diagnosis included complaints of forgetfulness and low-level dyspraxia, which were not pursued. Reasons for this can vary. Broadly, patient interactions in a primary care setting tend to be brief, thus, many patients are not engaged in their care. Early symptoms — eg, memory impairment — can be missed during routine office visits.

There are also significant racial disparities in the diagnosis of dementia. According to National Institute of Aging-funded studies that were conducted in 39 AD Research Centers, White patients > 65 years old had a significantly higher prevalence of dementia diagnoses at baseline visits than Black patients in the same age group. Black patients, especially Black women, tend not to be diagnosed with AD until it has progressed. Conversely, Black patients had more risk factors for AD, greater cognitive impairment, and more severe neuropsychiatric symptoms (delusions and hallucinations) than those of other races and ethnicities.

Another barrier to timely diagnosis in Black patients is disparity in access to neuroimaging. In a study conducted by Wibecan and colleagues at Boston Medical Center, researchers found that among neuroimaging assessments conducted at the facility, Black patients who received MRI or CT scan for the diagnosis of cognitive impairment were older than White patients (72.5 years vs 67 years). Additionally, Black patients were significantly less likely to undergo MRI (the gold standard of care for dementia diagnosis) than CT scan.  

Hypothyroidism is an endocrine disorder that occurs because of a deficiency in thyroid hormone. Symptoms tend to be subtle and non-specific but vary greatly. Some of the hallmark symptoms are fatigue, weight gain, cold intolerance, dry skin, and hair loss. Additionally, emotional lability and depressed mood with mental impairment, slowed speech, and movement, as evident in this patient. However, hypothyroidism was ruled out when her laboratory results returned with all values within normal range.  

Vascular dementia is the second-most prevalent form of dementia after AD. It is characterized as cognitive impairment that occurs after one, or a series of, neurologic events and does not refer to a single disease but to a variety of vascular disorders. Patients with vascular dementia often exhibit mood and behavioral changes, deficits in executive function, and severe memory loss, all of which are present in this patient. However, as there were no (known) neurologic events in this patient — and no evidence thereof on imaging — and her hypertension is relatively well controlled, this is not a diagnostic consideration for this patient.  

Normal pressure hydrocephalus (NPH) is caused by the build-up of cerebrospinal fluid in the brain. It is characterized by abnormal gait, dementia, and urinary incontinence. Patients with NPH experience decreased attention, significant memory loss, bradyphrenia, bradykinesia, and broad-based gait, all of which feature in this patient. However, brain MRI was negative for structural abnormalities of this type, and there was no indication of NPH, which rules it out as a potential diagnosis.  

Shaheen E. Lakhan, MD, PhD, MS, MEd, Chief of Pain Management, Carilion Clinic and Virginia Tech Carilion School of Medicine, Roanoke, Virginia.

Disclosure: Shaheen E. Lakhan, MD, PhD, MS, MEd, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
 

This patient’s presentation is indicative of moderate-stage Alzheimer’s disease (AD), which is confirmed by physical exam and testing; most notably, her MMSE score of 18 (a score of ≥ 25 is considered normal) and MRI results showing distinct cortical atrophy. At this stage of disease, signs and symptoms become more pronounced and widespread to include not only language deficiencies, prominent memory loss, and sensory processing, but also motor deficits and behavioral issues, all of which are clearly present in this patient.

A very important clinical consideration is a possible delay in diagnosis. It is atypical for an initial diagnosis of AD to be made when a patient is in the moderate stage of disease. This patient’s history over 5 years before her diagnosis included complaints of forgetfulness and low-level dyspraxia, which were not pursued. Reasons for this can vary. Broadly, patient interactions in a primary care setting tend to be brief, thus, many patients are not engaged in their care. Early symptoms — eg, memory impairment — can be missed during routine office visits.

There are also significant racial disparities in the diagnosis of dementia. According to National Institute of Aging-funded studies that were conducted in 39 AD Research Centers, White patients > 65 years old had a significantly higher prevalence of dementia diagnoses at baseline visits than Black patients in the same age group. Black patients, especially Black women, tend not to be diagnosed with AD until it has progressed. Conversely, Black patients had more risk factors for AD, greater cognitive impairment, and more severe neuropsychiatric symptoms (delusions and hallucinations) than those of other races and ethnicities.

Another barrier to timely diagnosis in Black patients is disparity in access to neuroimaging. In a study conducted by Wibecan and colleagues at Boston Medical Center, researchers found that among neuroimaging assessments conducted at the facility, Black patients who received MRI or CT scan for the diagnosis of cognitive impairment were older than White patients (72.5 years vs 67 years). Additionally, Black patients were significantly less likely to undergo MRI (the gold standard of care for dementia diagnosis) than CT scan.  

Hypothyroidism is an endocrine disorder that occurs because of a deficiency in thyroid hormone. Symptoms tend to be subtle and non-specific but vary greatly. Some of the hallmark symptoms are fatigue, weight gain, cold intolerance, dry skin, and hair loss. Additionally, emotional lability and depressed mood with mental impairment, slowed speech, and movement, as evident in this patient. However, hypothyroidism was ruled out when her laboratory results returned with all values within normal range.  

Vascular dementia is the second-most prevalent form of dementia after AD. It is characterized as cognitive impairment that occurs after one, or a series of, neurologic events and does not refer to a single disease but to a variety of vascular disorders. Patients with vascular dementia often exhibit mood and behavioral changes, deficits in executive function, and severe memory loss, all of which are present in this patient. However, as there were no (known) neurologic events in this patient — and no evidence thereof on imaging — and her hypertension is relatively well controlled, this is not a diagnostic consideration for this patient.  

Normal pressure hydrocephalus (NPH) is caused by the build-up of cerebrospinal fluid in the brain. It is characterized by abnormal gait, dementia, and urinary incontinence. Patients with NPH experience decreased attention, significant memory loss, bradyphrenia, bradykinesia, and broad-based gait, all of which feature in this patient. However, brain MRI was negative for structural abnormalities of this type, and there was no indication of NPH, which rules it out as a potential diagnosis.  

Shaheen E. Lakhan, MD, PhD, MS, MEd, Chief of Pain Management, Carilion Clinic and Virginia Tech Carilion School of Medicine, Roanoke, Virginia.

Disclosure: Shaheen E. Lakhan, MD, PhD, MS, MEd, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
 

Early-onset AD (EOAD) is the most likely diagnosis for this patient. Her symptoms — cognitive decline, executive function deficits, and visuospatial dysfunction — and brain imaging results are consistent with EOAD. But importantly, her father’s diagnosis of EOAD at age 58 suggests a hereditary component, which greatly increases the genetic risk for this patient. Moreover, neuroimaging shows cortical atrophy in the temporal lobes. A key radiologic feature of AD in this patient is the large increase in the subarachnoid spaces affecting the parietal region.

Between one third to just over one half of patients with EOAD have at least one first-degree relative with the disease. Given the patient’s neuroimaging results and family history of EOAD, she was sent for genetic testing, which revealed mutations in the PSEN1 gene; one the most common genetic causes of EOAD (along with mutations in the APP gene). For those who do have an autosomal dominant familial form of EOAD, clinical presentation is often atypical and includes headaches, myoclonus, seizures, hyperreflexia, and gait abnormalities. This patient did experience headaches but not the other symptoms.

Traumatic brain injury (TBI) is an insult to the brain from an outside mechanical force. It is both non-congenital and non-degenerative but can lead to permanent physical, cognitive, and/or psychosocial functioning. Patients often experience an altered or diminished state of consciousness in the aftermath of such an event. TBI is a diagnostic consideration for this patient, given that she was in a car accident and has experienced unusual cognitive and behavioral symptoms — eg, memory loss and visuospatial dysfunction. However, imaging does not reveal evidence of TBI, with no concussion or cerebral hemorrhage. Thus, TBI is not an accurate diagnosis for this patient.    

Parkinson’s disease (PD) is one of the most common neurologic disorders that is marked by three hallmark features: resting tremor, rigidity, and bradykinesia that generally affects people over the age of 60. Even though many patients with PD exhibit some measure of executive function impairment early in the course of the disease, substantial impairment and dementia usually manifest about 8 years after the onset of motor symptoms. Dementia occurs in approximately 20%-40% of patients with PD. Although patients with PD demonstrate executive function deficits, memory loss, and visuospatial dysfunction, they do not experience aphasia. This patient does not have any of the cardinal features of PD, which rules it out as a diagnosis.  

Frontotemporal dementia is a progressive dysfunction of the frontal lobes of the brain, primarily manifesting as language abnormalities, including reduced speech, perseveration, mutism, and echolalia, also known as primary progressive aphasia (PPA). Over time, patients develop other psychiatric symptoms: disinhibition, impulsivity, loss of social awareness, neglect of personal hygiene, mental rigidity, and utilization behavior. Given the patient’s language difficulties, frontotemporal dementia may be an initial diagnostic consideration. However, per the neurologic imaging results, brain abnormalities are located in the temporal regions. Additionally, the patient does not exhibit any of the psychiatric symptoms associated with frontotemporal dementia but does experience short-term memory loss and visuospatial dysfunction, which are not typical of this diagnosis. This patient does not have frontotemporal dementia.  

EOAD is characterized by deficits in language, visuospatial skills and executive function. Often, these patients do not exhibit amnestic disorder early in the disease. While their memory recognition and semantic memory is higher than for patients who present with late-onset (normal course) AD, their attention scores are typically lower. As a result of this atypical presentation, patients with EOAD tend to have a longer duration of disease before diagnosis (~1.6 years). They are also likely to have a history of TBI, which is a risk factor for dementia.

In comparison to late-onset AD (LOAD), EOAD has a larger genetic predisposition (92%-100% vs 70%-80%), a more aggressive course, a more frequent delay in initial diagnosis, higher prevalence of TBI, and less memory impairment. However, EOAD has greater decline in other cognitive domains, and because of the young age of onset, greater psychosocial impairment. Overall disease progression in these patients is much faster compared with patients who have LOAD. Neuroimaging in these patients generally features greater hippocampal sparing and posterior neocortical atrophy, with brain changes that affect the frontoparietal networks rather than the classic presentation found in LOAD. 

An important aspect of the workup of patients for whom EOAD is a diagnostic consideration is to thoroughly determine their family history and to perform genetic testing along with counseling.

The pharmacological treatment of patients with early-onset AD is identical to patients who have normal course or late-onset AD. Cholinesterase inhibitors (ChEIs) — eg, donepezil, galantamine, and rivastigmine, with the usual titration schedules — are indicated in these patients. Although these medications target memory, they also provide support to patients with other variants of EOAD — eg, logopenic variant PPA. However, it is imperative that providers monitor these patients carefully, as ChEIs may exacerbate some behaviors.

Management of patients with EOAD varies based on the patient's specific variant. It is vital for clinicians to coordinate patient-centered care individually. For example, patients with logopenic variant PPA should be referred for speech therapy assessment and treatment should focus on improving communication, while patients with posterior cortical atrophy benefit most from interventions for those who experience vision impairments. As this patient’s symptoms revolve primarily around cognition and visuospatial dysfunction, her treatment will focus on interventions to improve coordination, balance, and cognitive function.

Perhaps the most important part of managing a patient with EOAD is providing adequate and appropriate psychosocial support. These patients are most often in their most productive time of life, balancing careers and families. EOAD can bring about feelings of loss of independence, anticipatory grief, and anxiety about the future and the increased difficulty in managing the tasks of daily life. It is vital that these patients — and their families — receive adequate education and psychiatric support via therapists, support groups, and community resources that are age appropriate.  

Shaheen E. Lakhan, MD, PhD, MS, MEd, Chief of Pain Management, Carilion Clinic and Virginia Tech Carilion School of Medicine, Roanoke, Virginia.

Disclosure: Shaheen E. Lakhan, MD, PhD, MS, MEd, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Early-onset AD (EOAD) is the most likely diagnosis for this patient. Her symptoms — cognitive decline, executive function deficits, and visuospatial dysfunction — and brain imaging results are consistent with EOAD. But importantly, her father’s diagnosis of EOAD at age 58 suggests a hereditary component, which greatly increases the genetic risk for this patient. Moreover, neuroimaging shows cortical atrophy in the temporal lobes. A key radiologic feature of AD in this patient is the large increase in the subarachnoid spaces affecting the parietal region.

Between one third to just over one half of patients with EOAD have at least one first-degree relative with the disease. Given the patient’s neuroimaging results and family history of EOAD, she was sent for genetic testing, which revealed mutations in the PSEN1 gene; one the most common genetic causes of EOAD (along with mutations in the APP gene). For those who do have an autosomal dominant familial form of EOAD, clinical presentation is often atypical and includes headaches, myoclonus, seizures, hyperreflexia, and gait abnormalities. This patient did experience headaches but not the other symptoms.

Traumatic brain injury (TBI) is an insult to the brain from an outside mechanical force. It is both non-congenital and non-degenerative but can lead to permanent physical, cognitive, and/or psychosocial functioning. Patients often experience an altered or diminished state of consciousness in the aftermath of such an event. TBI is a diagnostic consideration for this patient, given that she was in a car accident and has experienced unusual cognitive and behavioral symptoms — eg, memory loss and visuospatial dysfunction. However, imaging does not reveal evidence of TBI, with no concussion or cerebral hemorrhage. Thus, TBI is not an accurate diagnosis for this patient.    

Parkinson’s disease (PD) is one of the most common neurologic disorders that is marked by three hallmark features: resting tremor, rigidity, and bradykinesia that generally affects people over the age of 60. Even though many patients with PD exhibit some measure of executive function impairment early in the course of the disease, substantial impairment and dementia usually manifest about 8 years after the onset of motor symptoms. Dementia occurs in approximately 20%-40% of patients with PD. Although patients with PD demonstrate executive function deficits, memory loss, and visuospatial dysfunction, they do not experience aphasia. This patient does not have any of the cardinal features of PD, which rules it out as a diagnosis.  

Frontotemporal dementia is a progressive dysfunction of the frontal lobes of the brain, primarily manifesting as language abnormalities, including reduced speech, perseveration, mutism, and echolalia, also known as primary progressive aphasia (PPA). Over time, patients develop other psychiatric symptoms: disinhibition, impulsivity, loss of social awareness, neglect of personal hygiene, mental rigidity, and utilization behavior. Given the patient’s language difficulties, frontotemporal dementia may be an initial diagnostic consideration. However, per the neurologic imaging results, brain abnormalities are located in the temporal regions. Additionally, the patient does not exhibit any of the psychiatric symptoms associated with frontotemporal dementia but does experience short-term memory loss and visuospatial dysfunction, which are not typical of this diagnosis. This patient does not have frontotemporal dementia.  

EOAD is characterized by deficits in language, visuospatial skills and executive function. Often, these patients do not exhibit amnestic disorder early in the disease. While their memory recognition and semantic memory is higher than for patients who present with late-onset (normal course) AD, their attention scores are typically lower. As a result of this atypical presentation, patients with EOAD tend to have a longer duration of disease before diagnosis (~1.6 years). They are also likely to have a history of TBI, which is a risk factor for dementia.

In comparison to late-onset AD (LOAD), EOAD has a larger genetic predisposition (92%-100% vs 70%-80%), a more aggressive course, a more frequent delay in initial diagnosis, higher prevalence of TBI, and less memory impairment. However, EOAD has greater decline in other cognitive domains, and because of the young age of onset, greater psychosocial impairment. Overall disease progression in these patients is much faster compared with patients who have LOAD. Neuroimaging in these patients generally features greater hippocampal sparing and posterior neocortical atrophy, with brain changes that affect the frontoparietal networks rather than the classic presentation found in LOAD. 

An important aspect of the workup of patients for whom EOAD is a diagnostic consideration is to thoroughly determine their family history and to perform genetic testing along with counseling.

The pharmacological treatment of patients with early-onset AD is identical to patients who have normal course or late-onset AD. Cholinesterase inhibitors (ChEIs) — eg, donepezil, galantamine, and rivastigmine, with the usual titration schedules — are indicated in these patients. Although these medications target memory, they also provide support to patients with other variants of EOAD — eg, logopenic variant PPA. However, it is imperative that providers monitor these patients carefully, as ChEIs may exacerbate some behaviors.

Management of patients with EOAD varies based on the patient's specific variant. It is vital for clinicians to coordinate patient-centered care individually. For example, patients with logopenic variant PPA should be referred for speech therapy assessment and treatment should focus on improving communication, while patients with posterior cortical atrophy benefit most from interventions for those who experience vision impairments. As this patient’s symptoms revolve primarily around cognition and visuospatial dysfunction, her treatment will focus on interventions to improve coordination, balance, and cognitive function.

Perhaps the most important part of managing a patient with EOAD is providing adequate and appropriate psychosocial support. These patients are most often in their most productive time of life, balancing careers and families. EOAD can bring about feelings of loss of independence, anticipatory grief, and anxiety about the future and the increased difficulty in managing the tasks of daily life. It is vital that these patients — and their families — receive adequate education and psychiatric support via therapists, support groups, and community resources that are age appropriate.  

Shaheen E. Lakhan, MD, PhD, MS, MEd, Chief of Pain Management, Carilion Clinic and Virginia Tech Carilion School of Medicine, Roanoke, Virginia.

Disclosure: Shaheen E. Lakhan, MD, PhD, MS, MEd, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Early-onset AD (EOAD) is the most likely diagnosis for this patient. Her symptoms — cognitive decline, executive function deficits, and visuospatial dysfunction — and brain imaging results are consistent with EOAD. But importantly, her father’s diagnosis of EOAD at age 58 suggests a hereditary component, which greatly increases the genetic risk for this patient. Moreover, neuroimaging shows cortical atrophy in the temporal lobes. A key radiologic feature of AD in this patient is the large increase in the subarachnoid spaces affecting the parietal region.

Between one third to just over one half of patients with EOAD have at least one first-degree relative with the disease. Given the patient’s neuroimaging results and family history of EOAD, she was sent for genetic testing, which revealed mutations in the PSEN1 gene; one the most common genetic causes of EOAD (along with mutations in the APP gene). For those who do have an autosomal dominant familial form of EOAD, clinical presentation is often atypical and includes headaches, myoclonus, seizures, hyperreflexia, and gait abnormalities. This patient did experience headaches but not the other symptoms.

Traumatic brain injury (TBI) is an insult to the brain from an outside mechanical force. It is both non-congenital and non-degenerative but can lead to permanent physical, cognitive, and/or psychosocial functioning. Patients often experience an altered or diminished state of consciousness in the aftermath of such an event. TBI is a diagnostic consideration for this patient, given that she was in a car accident and has experienced unusual cognitive and behavioral symptoms — eg, memory loss and visuospatial dysfunction. However, imaging does not reveal evidence of TBI, with no concussion or cerebral hemorrhage. Thus, TBI is not an accurate diagnosis for this patient.    

Parkinson’s disease (PD) is one of the most common neurologic disorders that is marked by three hallmark features: resting tremor, rigidity, and bradykinesia that generally affects people over the age of 60. Even though many patients with PD exhibit some measure of executive function impairment early in the course of the disease, substantial impairment and dementia usually manifest about 8 years after the onset of motor symptoms. Dementia occurs in approximately 20%-40% of patients with PD. Although patients with PD demonstrate executive function deficits, memory loss, and visuospatial dysfunction, they do not experience aphasia. This patient does not have any of the cardinal features of PD, which rules it out as a diagnosis.  

Frontotemporal dementia is a progressive dysfunction of the frontal lobes of the brain, primarily manifesting as language abnormalities, including reduced speech, perseveration, mutism, and echolalia, also known as primary progressive aphasia (PPA). Over time, patients develop other psychiatric symptoms: disinhibition, impulsivity, loss of social awareness, neglect of personal hygiene, mental rigidity, and utilization behavior. Given the patient’s language difficulties, frontotemporal dementia may be an initial diagnostic consideration. However, per the neurologic imaging results, brain abnormalities are located in the temporal regions. Additionally, the patient does not exhibit any of the psychiatric symptoms associated with frontotemporal dementia but does experience short-term memory loss and visuospatial dysfunction, which are not typical of this diagnosis. This patient does not have frontotemporal dementia.  

EOAD is characterized by deficits in language, visuospatial skills and executive function. Often, these patients do not exhibit amnestic disorder early in the disease. While their memory recognition and semantic memory is higher than for patients who present with late-onset (normal course) AD, their attention scores are typically lower. As a result of this atypical presentation, patients with EOAD tend to have a longer duration of disease before diagnosis (~1.6 years). They are also likely to have a history of TBI, which is a risk factor for dementia.

In comparison to late-onset AD (LOAD), EOAD has a larger genetic predisposition (92%-100% vs 70%-80%), a more aggressive course, a more frequent delay in initial diagnosis, higher prevalence of TBI, and less memory impairment. However, EOAD has greater decline in other cognitive domains, and because of the young age of onset, greater psychosocial impairment. Overall disease progression in these patients is much faster compared with patients who have LOAD. Neuroimaging in these patients generally features greater hippocampal sparing and posterior neocortical atrophy, with brain changes that affect the frontoparietal networks rather than the classic presentation found in LOAD. 

An important aspect of the workup of patients for whom EOAD is a diagnostic consideration is to thoroughly determine their family history and to perform genetic testing along with counseling.

The pharmacological treatment of patients with early-onset AD is identical to patients who have normal course or late-onset AD. Cholinesterase inhibitors (ChEIs) — eg, donepezil, galantamine, and rivastigmine, with the usual titration schedules — are indicated in these patients. Although these medications target memory, they also provide support to patients with other variants of EOAD — eg, logopenic variant PPA. However, it is imperative that providers monitor these patients carefully, as ChEIs may exacerbate some behaviors.

Management of patients with EOAD varies based on the patient's specific variant. It is vital for clinicians to coordinate patient-centered care individually. For example, patients with logopenic variant PPA should be referred for speech therapy assessment and treatment should focus on improving communication, while patients with posterior cortical atrophy benefit most from interventions for those who experience vision impairments. As this patient’s symptoms revolve primarily around cognition and visuospatial dysfunction, her treatment will focus on interventions to improve coordination, balance, and cognitive function.

Perhaps the most important part of managing a patient with EOAD is providing adequate and appropriate psychosocial support. These patients are most often in their most productive time of life, balancing careers and families. EOAD can bring about feelings of loss of independence, anticipatory grief, and anxiety about the future and the increased difficulty in managing the tasks of daily life. It is vital that these patients — and their families — receive adequate education and psychiatric support via therapists, support groups, and community resources that are age appropriate.  

Shaheen E. Lakhan, MD, PhD, MS, MEd, Chief of Pain Management, Carilion Clinic and Virginia Tech Carilion School of Medicine, Roanoke, Virginia.

Disclosure: Shaheen E. Lakhan, MD, PhD, MS, MEd, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Individuals with DS are at significantly increased risk of developing Alzheimer’s disease (AD) because of the overexpression of the amyloid precursor protein (APP) gene on chromosome 21.

The patient exhibits hallmark symptoms of AD, including progressive memory loss, disorientation, difficulty performing daily tasks, and behavioral changes such as irritability and social withdrawal. The MRI findings of ventricular enlargement and cortical atrophy are consistent with brain changes commonly seen in AD, particularly in individuals with DS who often develop these changes earlier in life (typically in their thirties or forties).

Frontotemporal dementia primarily causes behavioral and language changes with relative memory sparing early on, making it inconsistent with this patient's prominent memory loss, disorientation, and generalized cortical atrophy — features more typical of AD.

Vascular dementia often presents with stepwise decline and focal neurologic deficits; it is unlikely in this patient, given the absence of cerebrovascular events or risk factors like hypertension or diabetes.

While normal pressure hydrocephalus can cause ventricular enlargement, its classic triad of gait disturbance, urinary incontinence, and dementia is incomplete here, making this answer unlikely.

DS is the most common genetic cause of intellectual disability, occurring in approximately 1 in 700 live births worldwide. Nearly all adults with DS develop neuropathologic changes associated with AD by age 40, and the lifetime risk of developing dementia exceeds 90%; by the age of 55-60, at least 70% of individuals with DS exhibit clinical signs of dementia.

The link between DS and neurodegeneration is largely attributed to the triplication of chromosome 21, which includes the APP gene. Overexpression of APP leads to excessive production and accumulation of amyloid-β (Aβ), which forms the hallmark plaques seen in AD. In DS, amyloid plaques begin to form as early as the teenage years, and by the fourth decade, neurofibrillary tangles (tau protein aggregates) and widespread neurodegeneration are nearly universal. 

Initial symptoms of AD often include memory impairment, particularly short-term memory deficits, and executive dysfunction, difficulty with planning and problem-solving, and visuospatial deficits. Behavioral and personality changes, such as irritability, withdrawal, or apathy, are also commonly reported. Compared with sporadic AD, individuals with DS often show earlier behavioral symptoms, including impulsivity and changes in social interactions, which may precede noticeable memory deficits. Additionally, late-onset myoclonic epilepsy is common in individuals with DS and dementia, further complicating diagnosis and care.

The diagnosis of dementia in DS is challenging because of baseline intellectual disability, which makes it difficult to assess cognitive decline using standard neuropsychological tests. However, a combination of clinical history, caregiver reports, neuroimaging, and biomarker analysis can aid in early detection. Structural MRI of the brain often reveals ventricular enlargement and cortical atrophy, while PET imaging can detect early amyloid and tau accumulation. 

Because AD is now the leading cause of death in individuals with DS, the lack of effective disease-modifying treatments highlights an important need for clinical trials focused on this population. Current research aims to explore the role of anti-amyloid monoclonal antibodies, neuroprotective agents, and lifestyle interventions to delay or prevent neurodegeneration.

Shaheen E. Lakhan, MD, PhD, MS, MEd, Chief of Pain Management, Carilion Clinic and Virginia Tech Carilion School of Medicine, Roanoke, Virginia.

Disclosure: Shaheen E. Lakhan, MD, PhD, MS, MEd, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Individuals with DS are at significantly increased risk of developing Alzheimer’s disease (AD) because of the overexpression of the amyloid precursor protein (APP) gene on chromosome 21.

The patient exhibits hallmark symptoms of AD, including progressive memory loss, disorientation, difficulty performing daily tasks, and behavioral changes such as irritability and social withdrawal. The MRI findings of ventricular enlargement and cortical atrophy are consistent with brain changes commonly seen in AD, particularly in individuals with DS who often develop these changes earlier in life (typically in their thirties or forties).

Frontotemporal dementia primarily causes behavioral and language changes with relative memory sparing early on, making it inconsistent with this patient's prominent memory loss, disorientation, and generalized cortical atrophy — features more typical of AD.

Vascular dementia often presents with stepwise decline and focal neurologic deficits; it is unlikely in this patient, given the absence of cerebrovascular events or risk factors like hypertension or diabetes.

While normal pressure hydrocephalus can cause ventricular enlargement, its classic triad of gait disturbance, urinary incontinence, and dementia is incomplete here, making this answer unlikely.

DS is the most common genetic cause of intellectual disability, occurring in approximately 1 in 700 live births worldwide. Nearly all adults with DS develop neuropathologic changes associated with AD by age 40, and the lifetime risk of developing dementia exceeds 90%; by the age of 55-60, at least 70% of individuals with DS exhibit clinical signs of dementia.

The link between DS and neurodegeneration is largely attributed to the triplication of chromosome 21, which includes the APP gene. Overexpression of APP leads to excessive production and accumulation of amyloid-β (Aβ), which forms the hallmark plaques seen in AD. In DS, amyloid plaques begin to form as early as the teenage years, and by the fourth decade, neurofibrillary tangles (tau protein aggregates) and widespread neurodegeneration are nearly universal. 

Initial symptoms of AD often include memory impairment, particularly short-term memory deficits, and executive dysfunction, difficulty with planning and problem-solving, and visuospatial deficits. Behavioral and personality changes, such as irritability, withdrawal, or apathy, are also commonly reported. Compared with sporadic AD, individuals with DS often show earlier behavioral symptoms, including impulsivity and changes in social interactions, which may precede noticeable memory deficits. Additionally, late-onset myoclonic epilepsy is common in individuals with DS and dementia, further complicating diagnosis and care.

The diagnosis of dementia in DS is challenging because of baseline intellectual disability, which makes it difficult to assess cognitive decline using standard neuropsychological tests. However, a combination of clinical history, caregiver reports, neuroimaging, and biomarker analysis can aid in early detection. Structural MRI of the brain often reveals ventricular enlargement and cortical atrophy, while PET imaging can detect early amyloid and tau accumulation. 

Because AD is now the leading cause of death in individuals with DS, the lack of effective disease-modifying treatments highlights an important need for clinical trials focused on this population. Current research aims to explore the role of anti-amyloid monoclonal antibodies, neuroprotective agents, and lifestyle interventions to delay or prevent neurodegeneration.

Shaheen E. Lakhan, MD, PhD, MS, MEd, Chief of Pain Management, Carilion Clinic and Virginia Tech Carilion School of Medicine, Roanoke, Virginia.

Disclosure: Shaheen E. Lakhan, MD, PhD, MS, MEd, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Individuals with DS are at significantly increased risk of developing Alzheimer’s disease (AD) because of the overexpression of the amyloid precursor protein (APP) gene on chromosome 21.

The patient exhibits hallmark symptoms of AD, including progressive memory loss, disorientation, difficulty performing daily tasks, and behavioral changes such as irritability and social withdrawal. The MRI findings of ventricular enlargement and cortical atrophy are consistent with brain changes commonly seen in AD, particularly in individuals with DS who often develop these changes earlier in life (typically in their thirties or forties).

Frontotemporal dementia primarily causes behavioral and language changes with relative memory sparing early on, making it inconsistent with this patient's prominent memory loss, disorientation, and generalized cortical atrophy — features more typical of AD.

Vascular dementia often presents with stepwise decline and focal neurologic deficits; it is unlikely in this patient, given the absence of cerebrovascular events or risk factors like hypertension or diabetes.

While normal pressure hydrocephalus can cause ventricular enlargement, its classic triad of gait disturbance, urinary incontinence, and dementia is incomplete here, making this answer unlikely.

DS is the most common genetic cause of intellectual disability, occurring in approximately 1 in 700 live births worldwide. Nearly all adults with DS develop neuropathologic changes associated with AD by age 40, and the lifetime risk of developing dementia exceeds 90%; by the age of 55-60, at least 70% of individuals with DS exhibit clinical signs of dementia.

The link between DS and neurodegeneration is largely attributed to the triplication of chromosome 21, which includes the APP gene. Overexpression of APP leads to excessive production and accumulation of amyloid-β (Aβ), which forms the hallmark plaques seen in AD. In DS, amyloid plaques begin to form as early as the teenage years, and by the fourth decade, neurofibrillary tangles (tau protein aggregates) and widespread neurodegeneration are nearly universal. 

Initial symptoms of AD often include memory impairment, particularly short-term memory deficits, and executive dysfunction, difficulty with planning and problem-solving, and visuospatial deficits. Behavioral and personality changes, such as irritability, withdrawal, or apathy, are also commonly reported. Compared with sporadic AD, individuals with DS often show earlier behavioral symptoms, including impulsivity and changes in social interactions, which may precede noticeable memory deficits. Additionally, late-onset myoclonic epilepsy is common in individuals with DS and dementia, further complicating diagnosis and care.

The diagnosis of dementia in DS is challenging because of baseline intellectual disability, which makes it difficult to assess cognitive decline using standard neuropsychological tests. However, a combination of clinical history, caregiver reports, neuroimaging, and biomarker analysis can aid in early detection. Structural MRI of the brain often reveals ventricular enlargement and cortical atrophy, while PET imaging can detect early amyloid and tau accumulation. 

Because AD is now the leading cause of death in individuals with DS, the lack of effective disease-modifying treatments highlights an important need for clinical trials focused on this population. Current research aims to explore the role of anti-amyloid monoclonal antibodies, neuroprotective agents, and lifestyle interventions to delay or prevent neurodegeneration.

Shaheen E. Lakhan, MD, PhD, MS, MEd, Chief of Pain Management, Carilion Clinic and Virginia Tech Carilion School of Medicine, Roanoke, Virginia.

Disclosure: Shaheen E. Lakhan, MD, PhD, MS, MEd, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Posttraumatic stress disorder (PTSD) is the most likely diagnosis considering this patient’s symptoms of anxiety, hypervigilance, recurring nightmares, agitation, flashbacks, and violent outbursts. His experience of being robbed at gunpoint outside his gym seems to have been the triggering event for his PTSD, which may have also been influenced by his history of multiple concussions incurred in a fight setting in which he is forced to defend himself. His avoidance of continued training and appearing at scheduled fights further support this diagnosis. His CT scan, although not diagnostic for PTSD directly, does show evidence of minor brain injury, with the remaining hematomas.

Anxiety disorder may account for the patient’s severe anxiety, agitation, and headaches, but his symptoms are new and started after the robbery, which indicates PTSD and not a long-standing anxiety disorder.

Schizophrenia is an unlikely diagnosis for this patient. Although he is within the typical age range of symptom onset, has had violent outbursts, and is prone to vast changes in mood that come on quickly, he is not psychotic and does not experience any of the hallmark symptoms of schizophrenia: delusions, hallucinations, and disorganized speech/behavior, at least two of which would need to be present to support a diagnosis of schizophrenia.

Given this patient’s circumstances, post-traumatic epilepsy initially may be a potential diagnostic consideration. However, he is not experiencing seizures, but rather mood and behavioral disturbances, the onset of which occurred after a specific event. Additionally, posttraumatic epilepsy results from traumatic brain injury.

According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision, an update to the 2017 clinical treatment guidelines published by the American Psychiatric Association (APA), the diagnostic criteria for PTSD in an individual older than 6 years are:

1.    Exposure to actual or threatened death, serious injury or sexual assault
2.    The traumatic event is persistently re-experienced via flashbacks, nightmares, and intrusive thoughts that cause strong emotional reactions and psychological distress
3.    Avoidance behaviors either in thoughts or conversations about the event or of people and places associated with the event
4.    At least two examples of negative alterations in cognition and mood
5.    At least two examples of hyperarousal
6.    Duration of symptoms > 1 month
7.    Significant distress or impairment in function because of these symptoms

Trauma-focused therapy is the gold standard of treatment for patients with PTSD. A recent review of current treatment strategies for PTSD found that cognitive processing therapy, cognitive-behavioral therapy, prolonged exposure therapy, and eye movement desensitization and reprocessing, all with a strong trauma focus, are the most effective treatments for PTSD.

The use of pharmacology to treat PTSD is controversial and varies by guideline. The APA and US Department of Veterans Affairs both recommend the use of antidepressants, particularly selective serotonin reuptake inhibitors, as a first-line treatment of PTSD. This is particularly important for patients who have psychiatric comorbid conditions, such as depression, who may not be able to effectively engage in cognitive- behavioral therapy. However, use of benzodiazepines or hypnotics should be strictly avoided in these patients because these drugs increase intrusive and avoidance symptoms over time. Medication should be continued for 6 to 12 months to help prevent relapse. 

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.
 

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Posttraumatic stress disorder (PTSD) is the most likely diagnosis considering this patient’s symptoms of anxiety, hypervigilance, recurring nightmares, agitation, flashbacks, and violent outbursts. His experience of being robbed at gunpoint outside his gym seems to have been the triggering event for his PTSD, which may have also been influenced by his history of multiple concussions incurred in a fight setting in which he is forced to defend himself. His avoidance of continued training and appearing at scheduled fights further support this diagnosis. His CT scan, although not diagnostic for PTSD directly, does show evidence of minor brain injury, with the remaining hematomas.

Anxiety disorder may account for the patient’s severe anxiety, agitation, and headaches, but his symptoms are new and started after the robbery, which indicates PTSD and not a long-standing anxiety disorder.

Schizophrenia is an unlikely diagnosis for this patient. Although he is within the typical age range of symptom onset, has had violent outbursts, and is prone to vast changes in mood that come on quickly, he is not psychotic and does not experience any of the hallmark symptoms of schizophrenia: delusions, hallucinations, and disorganized speech/behavior, at least two of which would need to be present to support a diagnosis of schizophrenia.

Given this patient’s circumstances, post-traumatic epilepsy initially may be a potential diagnostic consideration. However, he is not experiencing seizures, but rather mood and behavioral disturbances, the onset of which occurred after a specific event. Additionally, posttraumatic epilepsy results from traumatic brain injury.

According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision, an update to the 2017 clinical treatment guidelines published by the American Psychiatric Association (APA), the diagnostic criteria for PTSD in an individual older than 6 years are:

1.    Exposure to actual or threatened death, serious injury or sexual assault
2.    The traumatic event is persistently re-experienced via flashbacks, nightmares, and intrusive thoughts that cause strong emotional reactions and psychological distress
3.    Avoidance behaviors either in thoughts or conversations about the event or of people and places associated with the event
4.    At least two examples of negative alterations in cognition and mood
5.    At least two examples of hyperarousal
6.    Duration of symptoms > 1 month
7.    Significant distress or impairment in function because of these symptoms

Trauma-focused therapy is the gold standard of treatment for patients with PTSD. A recent review of current treatment strategies for PTSD found that cognitive processing therapy, cognitive-behavioral therapy, prolonged exposure therapy, and eye movement desensitization and reprocessing, all with a strong trauma focus, are the most effective treatments for PTSD.

The use of pharmacology to treat PTSD is controversial and varies by guideline. The APA and US Department of Veterans Affairs both recommend the use of antidepressants, particularly selective serotonin reuptake inhibitors, as a first-line treatment of PTSD. This is particularly important for patients who have psychiatric comorbid conditions, such as depression, who may not be able to effectively engage in cognitive- behavioral therapy. However, use of benzodiazepines or hypnotics should be strictly avoided in these patients because these drugs increase intrusive and avoidance symptoms over time. Medication should be continued for 6 to 12 months to help prevent relapse. 

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.
 

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Posttraumatic stress disorder (PTSD) is the most likely diagnosis considering this patient’s symptoms of anxiety, hypervigilance, recurring nightmares, agitation, flashbacks, and violent outbursts. His experience of being robbed at gunpoint outside his gym seems to have been the triggering event for his PTSD, which may have also been influenced by his history of multiple concussions incurred in a fight setting in which he is forced to defend himself. His avoidance of continued training and appearing at scheduled fights further support this diagnosis. His CT scan, although not diagnostic for PTSD directly, does show evidence of minor brain injury, with the remaining hematomas.

Anxiety disorder may account for the patient’s severe anxiety, agitation, and headaches, but his symptoms are new and started after the robbery, which indicates PTSD and not a long-standing anxiety disorder.

Schizophrenia is an unlikely diagnosis for this patient. Although he is within the typical age range of symptom onset, has had violent outbursts, and is prone to vast changes in mood that come on quickly, he is not psychotic and does not experience any of the hallmark symptoms of schizophrenia: delusions, hallucinations, and disorganized speech/behavior, at least two of which would need to be present to support a diagnosis of schizophrenia.

Given this patient’s circumstances, post-traumatic epilepsy initially may be a potential diagnostic consideration. However, he is not experiencing seizures, but rather mood and behavioral disturbances, the onset of which occurred after a specific event. Additionally, posttraumatic epilepsy results from traumatic brain injury.

According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision, an update to the 2017 clinical treatment guidelines published by the American Psychiatric Association (APA), the diagnostic criteria for PTSD in an individual older than 6 years are:

1.    Exposure to actual or threatened death, serious injury or sexual assault
2.    The traumatic event is persistently re-experienced via flashbacks, nightmares, and intrusive thoughts that cause strong emotional reactions and psychological distress
3.    Avoidance behaviors either in thoughts or conversations about the event or of people and places associated with the event
4.    At least two examples of negative alterations in cognition and mood
5.    At least two examples of hyperarousal
6.    Duration of symptoms > 1 month
7.    Significant distress or impairment in function because of these symptoms

Trauma-focused therapy is the gold standard of treatment for patients with PTSD. A recent review of current treatment strategies for PTSD found that cognitive processing therapy, cognitive-behavioral therapy, prolonged exposure therapy, and eye movement desensitization and reprocessing, all with a strong trauma focus, are the most effective treatments for PTSD.

The use of pharmacology to treat PTSD is controversial and varies by guideline. The APA and US Department of Veterans Affairs both recommend the use of antidepressants, particularly selective serotonin reuptake inhibitors, as a first-line treatment of PTSD. This is particularly important for patients who have psychiatric comorbid conditions, such as depression, who may not be able to effectively engage in cognitive- behavioral therapy. However, use of benzodiazepines or hypnotics should be strictly avoided in these patients because these drugs increase intrusive and avoidance symptoms over time. Medication should be continued for 6 to 12 months to help prevent relapse. 

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.
 

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Posttraumatic stress disorder (PTSD) is the most likely diagnosis given the patient's symptoms — recurrent nightmares, flashbacks, and anxiety triggered by trauma-related noises, all of which are classic indicators of the disorder. His history of witnessing traumatic events at work, including a fatal accident, further reinforces this diagnosis and strongly suggests PTSD as the most fitting explanation. Although the brain scan does not diagnose PTSD directly, it plays an important role in ruling out other potential causes, such as structural brain damage, that could be contributing to his symptoms. Thus, the patient's symptoms are more likely a result of PTSD rather than an underlying organic brain injury.

Although major depressive disorder could explain some of the patient's symptoms, such as impaired daily functioning and withdrawal, the presence of recurrent nightmares, flashbacks, and trauma-specific triggers are more indicative of PTSD.

Generalized anxiety disorder might account for the patient's heightened anxiety, but it typically involves chronic, pervasive worry rather than the trauma-specific symptoms seen here.

Chronic traumatic encephalopathy (CTE) is a possible concern given the patient's occupation and the findings on the CT scan. However, CTE generally presents with cognitive and behavioral changes over time, such as memory loss and aggression, rather than the distinctive trauma-related symptoms characteristic of PTSD.

Individuals with PTSD often display heightened emotional, cognitive, and behavioral responses when exposed to trauma-related cues; these responses include severe anxiety, dissociative episodes, flashbacks, and heightened reactivity. To manage their increased arousal, individuals with PTSD frequently engage in avoidance behaviors, which can result in emotional numbing, diminished interest in daily activities, and, in more severe cases, social withdrawal.

According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR), the diagnostic criteria for PTSD in individuals older than 6 years include (A) exposure to actual or threatened death, serious injury, or sexual violence; (B) the presence of one or more intrusion symptoms related to the trauma; (C) persistent avoidance of trauma-related stimuli; (D) negative changes in cognition and mood associated with the trauma; and (E) marked alterations in arousal and reactivity, with at least two specific symptoms.

Trauma-focused psychotherapy is generally recommended as the first-line treatment for most adults with PTSD, with exposure-based therapies often preferred over other therapeutic approaches or pharmacologic treatments, such as selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors. However, in patients with comorbid conditions such as depression or psychosis that hinder their ability to engage in trauma-focused therapy, initial pharmacologic management is recommended until symptoms stabilize, allowing for the later introduction of psychotherapy. Clinical trials and meta-analyses have demonstrated the effectiveness of various trauma-focused therapies, including trauma-focused cognitive-behavioral therapy, prolonged exposure therapy, and eye movement desensitization and reprocessing. Treatment selection should be made collaboratively, considering the patient's presentation and preferences and the therapist's expertise.

For effective management of PTSD, medication regimens should be maintained for at least 6 months to 1 year to prevent relapse or recurrence. Multiple clinical trials have shown that patients who continue SSRIs after acute treatment are less likely to experience a relapse than those who switch to placebo.

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Posttraumatic stress disorder (PTSD) is the most likely diagnosis given the patient's symptoms — recurrent nightmares, flashbacks, and anxiety triggered by trauma-related noises, all of which are classic indicators of the disorder. His history of witnessing traumatic events at work, including a fatal accident, further reinforces this diagnosis and strongly suggests PTSD as the most fitting explanation. Although the brain scan does not diagnose PTSD directly, it plays an important role in ruling out other potential causes, such as structural brain damage, that could be contributing to his symptoms. Thus, the patient's symptoms are more likely a result of PTSD rather than an underlying organic brain injury.

Although major depressive disorder could explain some of the patient's symptoms, such as impaired daily functioning and withdrawal, the presence of recurrent nightmares, flashbacks, and trauma-specific triggers are more indicative of PTSD.

Generalized anxiety disorder might account for the patient's heightened anxiety, but it typically involves chronic, pervasive worry rather than the trauma-specific symptoms seen here.

Chronic traumatic encephalopathy (CTE) is a possible concern given the patient's occupation and the findings on the CT scan. However, CTE generally presents with cognitive and behavioral changes over time, such as memory loss and aggression, rather than the distinctive trauma-related symptoms characteristic of PTSD.

Individuals with PTSD often display heightened emotional, cognitive, and behavioral responses when exposed to trauma-related cues; these responses include severe anxiety, dissociative episodes, flashbacks, and heightened reactivity. To manage their increased arousal, individuals with PTSD frequently engage in avoidance behaviors, which can result in emotional numbing, diminished interest in daily activities, and, in more severe cases, social withdrawal.

According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR), the diagnostic criteria for PTSD in individuals older than 6 years include (A) exposure to actual or threatened death, serious injury, or sexual violence; (B) the presence of one or more intrusion symptoms related to the trauma; (C) persistent avoidance of trauma-related stimuli; (D) negative changes in cognition and mood associated with the trauma; and (E) marked alterations in arousal and reactivity, with at least two specific symptoms.

Trauma-focused psychotherapy is generally recommended as the first-line treatment for most adults with PTSD, with exposure-based therapies often preferred over other therapeutic approaches or pharmacologic treatments, such as selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors. However, in patients with comorbid conditions such as depression or psychosis that hinder their ability to engage in trauma-focused therapy, initial pharmacologic management is recommended until symptoms stabilize, allowing for the later introduction of psychotherapy. Clinical trials and meta-analyses have demonstrated the effectiveness of various trauma-focused therapies, including trauma-focused cognitive-behavioral therapy, prolonged exposure therapy, and eye movement desensitization and reprocessing. Treatment selection should be made collaboratively, considering the patient's presentation and preferences and the therapist's expertise.

For effective management of PTSD, medication regimens should be maintained for at least 6 months to 1 year to prevent relapse or recurrence. Multiple clinical trials have shown that patients who continue SSRIs after acute treatment are less likely to experience a relapse than those who switch to placebo.

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Posttraumatic stress disorder (PTSD) is the most likely diagnosis given the patient's symptoms — recurrent nightmares, flashbacks, and anxiety triggered by trauma-related noises, all of which are classic indicators of the disorder. His history of witnessing traumatic events at work, including a fatal accident, further reinforces this diagnosis and strongly suggests PTSD as the most fitting explanation. Although the brain scan does not diagnose PTSD directly, it plays an important role in ruling out other potential causes, such as structural brain damage, that could be contributing to his symptoms. Thus, the patient's symptoms are more likely a result of PTSD rather than an underlying organic brain injury.

Although major depressive disorder could explain some of the patient's symptoms, such as impaired daily functioning and withdrawal, the presence of recurrent nightmares, flashbacks, and trauma-specific triggers are more indicative of PTSD.

Generalized anxiety disorder might account for the patient's heightened anxiety, but it typically involves chronic, pervasive worry rather than the trauma-specific symptoms seen here.

Chronic traumatic encephalopathy (CTE) is a possible concern given the patient's occupation and the findings on the CT scan. However, CTE generally presents with cognitive and behavioral changes over time, such as memory loss and aggression, rather than the distinctive trauma-related symptoms characteristic of PTSD.

Individuals with PTSD often display heightened emotional, cognitive, and behavioral responses when exposed to trauma-related cues; these responses include severe anxiety, dissociative episodes, flashbacks, and heightened reactivity. To manage their increased arousal, individuals with PTSD frequently engage in avoidance behaviors, which can result in emotional numbing, diminished interest in daily activities, and, in more severe cases, social withdrawal.

According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR), the diagnostic criteria for PTSD in individuals older than 6 years include (A) exposure to actual or threatened death, serious injury, or sexual violence; (B) the presence of one or more intrusion symptoms related to the trauma; (C) persistent avoidance of trauma-related stimuli; (D) negative changes in cognition and mood associated with the trauma; and (E) marked alterations in arousal and reactivity, with at least two specific symptoms.

Trauma-focused psychotherapy is generally recommended as the first-line treatment for most adults with PTSD, with exposure-based therapies often preferred over other therapeutic approaches or pharmacologic treatments, such as selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors. However, in patients with comorbid conditions such as depression or psychosis that hinder their ability to engage in trauma-focused therapy, initial pharmacologic management is recommended until symptoms stabilize, allowing for the later introduction of psychotherapy. Clinical trials and meta-analyses have demonstrated the effectiveness of various trauma-focused therapies, including trauma-focused cognitive-behavioral therapy, prolonged exposure therapy, and eye movement desensitization and reprocessing. Treatment selection should be made collaboratively, considering the patient's presentation and preferences and the therapist's expertise.

For effective management of PTSD, medication regimens should be maintained for at least 6 months to 1 year to prevent relapse or recurrence. Multiple clinical trials have shown that patients who continue SSRIs after acute treatment are less likely to experience a relapse than those who switch to placebo.

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.