Examkin

Neurocognitive Disorders

65 questions

All types65Multiple choice34Matching14Ordering17
Question 1Question →

Evaluate the following clinical scenarios detailing distinct neurocognitive or acute neuropsychiatric presentations. Pair each patient vignette with the single most appropriate next step in management or definitive therapeutic intervention.

Click a left item, then click its matching right item

Items

A hospitalized patient experiences severe rigidity, autonomic instability, and worsening confusion shortly after receiving haloperidol for well-formed visual hallucinations. The family reports a pre-existing history of acting out dreams.
An ambulatory patient presents with a newly developed 'glued-to-the-floor' ambulation pattern, concurrent with uninhibited detrusor contractions and mild executive dysfunction. Brain imaging demonstrates enlarged ventricles without proportional cortical atrophy.
A previously tactful executive begins making highly inappropriate comments to colleagues, exhibits profound emotional blunting, and develops a compulsive eating pattern focused exclusively on carbohydrates. Memory testing remains surprisingly intact.
A patient rapidly deteriorates into akinetic mutism and exhibits exaggerated myoclonic jerks upon exposure to loud noises. This catastrophic decline occurred over a period of mere weeks. EEG demonstrates characteristic periodic biphasic sharp waves.
An individual with known major neurocognitive disorder due to Alzheimer disease abruptly exhibits a fluctuating level of consciousness, disorganized thinking, and inattention on the second day following an orthopedic surgery.

Matches

Show answer & explanation

Answer

Match the DLB vignette with antipsychotic discontinuation; NPH with CSF removal; bvFTD with SSRI therapy; CJD with palliative care; and delirium with evaluation for systemic triggers.
Each correct pairing links the pathognomonic clinical presentation of a neurocognitive or acute neuropsychiatric syndrome with its evidence-based standard of care or immediate next management step.

Step-by-Step Solution

1
Analyze the first vignette focusing on haloperidol sensitivity in the context of visual hallucinations and dream enactment.
Diagnosis is Dementia with Lewy Bodies presenting with severe neuroleptic sensitivity.
Patients with DLB lack dopamine and are exquisitely sensitive to dopamine antagonists, requiring immediate cessation of haloperidol.
2
Identify the etiology behind the 'glued-to-the-floor' gait, incontinence, and enlarged ventricles.
Diagnosis is Normal Pressure Hydrocephalus.
The standard diagnostic and initial therapeutic step for NPH is high-volume CSF drainage to document gait improvement before considering permanent shunting.
3
Evaluate the isolated behavioral changes, loss of tact, and hyperorality without initial memory deficits.
Diagnosis is behavioral variant Frontotemporal Dementia.
Management for bvFTD relies heavily on symptom control using SSRIs to blunt impulsivity and compulsive behaviors.
4
Assess the rapidly progressive presentation featuring akinetic mutism, myoclonus, and specific EEG findings.
Diagnosis is Creutzfeldt-Jakob disease.
CJD is uniformly fatal and non-treatable; the focus shifts entirely to palliative care and appropriate prion precautions.
5
Differentiate acute post-surgical cognitive fluctuation from chronic progressive dementia.
Diagnosis is post-operative delirium superimposed on Alzheimer disease.
Delirium is a medical emergency necessitating rapid investigation of underlying causes (e.g., sepsis, medication effects) rather than primary psychiatric interventions.

Key Concept

Targeted management and definitive interventions for major neurocognitive disorders based on underlying pathophysiology.
Question 2Question →

A 48-year-old man is brought to the clinic by his sister due to a 5-month history of progressive forgetfulness, social withdrawal, and difficulty concentrating. The sister reports that he takes an unusually long time to answer simple questions and that his walking has become slow and uncoordinated. His medical history is significant for HIV infection, diagnosed 12 years ago. He admits to poor adherence to his antiretroviral therapy over the past 18 months. His most recent CD4+ T-cell count was 145/mm³. Vital signs are within normal limits. Neurological examination reveals marked psychomotor slowing, saccadic pursuit eye movements, and brisk deep tendon reflexes in the bilateral lower extremities. His Montreal Cognitive Assessment score is 19/30. Magnetic resonance imaging of the brain demonstrates diffuse cortical atrophy and symmetric, bilateral periventricular white matter hyperintensities without contrast enhancement or mass effect. Which of the following is the most likely diagnosis?

Show answer & explanation

Answer: HIV-associated neurocognitive disorder

Answer

The correct diagnosis is HIV-associated neurocognitive disorder.
HIV-associated neurocognitive disorder (HAND) is a neurodegenerative condition resulting from HIV infection of the central nervous system, typically seen in patients with long-standing, poorly controlled disease and low CD4+ counts. It classically presents with a subcortical pattern of dementia characterized by a triad of cognitive impairment (memory loss, executive dysfunction), behavioral changes (apathy, social withdrawal), and motor abnormalities (psychomotor retardation, slow gait, hyperreflexia, saccadic eye movements). Magnetic resonance imaging characteristically demonstrates diffuse cortical atrophy and symmetric periventricular white matter hyperintensities. Importantly, there is no mass effect, edema, or contrast enhancement, which perfectly matches this patient's presentation.

Step-by-Step Solution

1
Identify the core clinical syndrome based on the history and physical exam.
The patient exhibits a triad of cognitive decline (forgetfulness, MoCA 19/30), behavioral changes (apathy, social withdrawal), and motor symptoms (psychomotor retardation, hyperreflexia).
Establishing the specific pattern of neurological deficits is essential for narrowing the differential diagnosis in an immunocompromised patient.
2
Analyze the neuroimaging findings in the context of the patient's immune status.
MRI shows diffuse cortical atrophy and symmetric periventricular white matter hyperintensities, with no mass effect, edema, or contrast enhancement.
Imaging differentiates neurodegenerative processes from focal opportunistic infections or malignancies.
3
Synthesize the clinical and imaging data to determine the most likely etiology.
The insidious onset, symmetric subcortical imaging findings, and lack of focal deficits in a poorly controlled HIV patient point directly to a primary viral neurodegenerative process rather than an opportunistic infection.
This confirms HIV-associated neurocognitive disorder and rules out conditions like PML or toxoplasmosis.

Key Concept

HIV-associated neurocognitive disorder (HAND) typically presents with subcortical cognitive decline, behavioral apathy, and motor symptoms (hyperreflexia, psychomotor slowing). MRI classically shows diffuse atrophy and symmetric white matter changes without enhancement or mass effect.
Estimated Time:1m 15s
Question 3Question →

A 74-year-old retired teacher is brought to her primary care physician by her daughter due to progressive forgetfulness and difficulty managing her finances over the past two years. Her medical history includes well-controlled hypertension and hyperlipidemia. The physician suspects a major neurocognitive disorder. Arrange the following diagnostic steps in the most appropriate sequential clinical workflow, from the initial encounter to advanced diagnostic testing.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequential workflow is: 1) Clinical interview and medication review, 2) Objective bedside cognitive screening, 3) Laboratory testing for reversible causes, 4) Structural neuroimaging, and 5) Formal neuropsychological testing.
The evaluation of suspected major neurocognitive disorder follows a logical progression from least invasive and most fundamental to most specialized. It begins with a comprehensive history and medication review, as collateral information is vital and polypharmacy is a frequent culprit. This is immediately followed by a bedside cognitive screen (e.g., MoCA) to objectively quantify the deficit. Once impairment is confirmed, standard laboratory tests are drawn to rule out reversible metabolic or nutritional causes. Structural imaging follows to exclude macroscopic brain pathology such as tumors, bleeds, or hydrocephalus. Finally, if the diagnosis remains uncertain, formal neuropsychological testing is requested to clarify the specific neurocognitive domains affected.

Step-by-Step Solution

1
Initiate the evaluation with a comprehensive history and medication review.
Establishes the timeline of symptoms, incorporates caregiver collateral information, and rules out polypharmacy.
History is the most critical component of psychiatric and neurologic diagnoses.
2
Administer an objective screening tool like the MoCA or MMSE.
Provides quantifiable evidence of cognitive impairment.
Subjective memory complaints must be objectively verified before proceeding with an extensive medical workup.
3
Check routine blood tests (e.g., Vitamin B12, TSH).
Identifies or excludes common systemic, endocrine, or nutritional causes of pseudodementia or reversible cognitive decline.
Ruling out reversible medical conditions is a mandatory next step in the dementia algorithm.
4
Order structural neuroimaging (MRI or CT).
Visualizes the brain parenchyma to check for infarcts, masses, hydrocephalus, or distinct regional atrophy.
Imaging helps differentiate between neurodegenerative causes (like Alzheimer's) and structural/vascular causes.
5
Consider formal neuropsychological testing.
Yields a detailed profile of cognitive strengths and weaknesses across multiple domains.
This is a specialized, final diagnostic step used when standard evaluation fails to confidently differentiate between dementia subtypes or distinguish dementia from major depressive disorder.

Key Concept

Standard diagnostic evaluation pathway for major neurocognitive disorders.
Question 4Question →

A 75-year-old man is brought to the clinic by his daughter for a cognitive evaluation. Over the past 5 months, he has stopped managing his finances, spends most of the day sitting in a recliner, and frequently complains that his memory is 'completely gone.' When the physician asks him to perform serial sevens and recall three objects, he sighs loudly, states 'I just cannot do this anymore,' and refuses to try. Five months ago, he was forced to surrender his driver's license due to worsening macular degeneration. His daughter notes that he has lost 4.5 kg (10 lb) during this period. Neurologic examination is nonfocal. Which of the following is the most likely diagnosis?

Show answer & explanation

Answer: Major depressive disorder

Answer

Major depressive disorder
This patient is presenting with cognitive impairment secondary to major depressive disorder, a clinical picture often referred to as 'pseudodementia.' In the elderly, depression frequently manifests with prominent memory complaints. Key features that differentiate pseudodementia from genuine major neurocognitive disorder (like Alzheimer disease) include a more rapid onset (often following a stressor, such as losing driving privileges), intense distress or complaints about memory loss, and a characteristic lack of effort on cognitive testing. Instead of attempting to answer and making mistakes, depressed patients typically sigh, give up easily, or answer 'I do not know.' Furthermore, the patient's pervasive inactivity and significant weight loss are classic neurovegetative symptoms that confirm a major depressive episode.

Step-by-Step Solution

1
Identify the psychosocial stressor and timeline.
The patient lost his driver's license 5 months ago, correlating with the subacute onset of his symptoms.
A clear precipitating event with a subacute onset of cognitive complaints strongly suggests a psychiatric etiology rather than an insidious neurodegenerative disease.
2
Evaluate the patient's attitude toward his cognitive deficits.
He complains that his memory is 'completely gone' and refuses to try during the cognitive assessment.
Patients with depression-related cognitive impairment (pseudodementia) typically emphasize their deficits and show poor effort, unlike patients with genuine dementia who often lack insight and attempt to cover up their mistakes.
3
Look for neurovegetative symptoms of depression.
The patient exhibits severe anhedonia (sitting in a recliner all day) and a 10-lb weight loss.
These somatic symptoms confirm the presence of a major depressive episode.

Key Concept

Major depressive disorder in the elderly can present with prominent cognitive complaints (pseudodementia). It is differentiated from genuine major neurocognitive disorder by a subacute onset, exaggerated complaints about memory loss, poor effort on cognitive testing, and concurrent vegetative symptoms of depression.
Question 5Question →

Match each clinical presentation of cognitive decline to its most likely underlying pathophysiologic mechanism.

Click a left item, then click its matching right item

Items

A 67-year-old man presents with a 3-month history of rapidly progressive memory loss, akinetic mutism, and sudden, brief muscle jerks elicited by loud noises.
A 59-year-old woman exhibits a 2-year history of socially inappropriate comments, compulsive consumption of sweets, and profound apathy, with preserved visuospatial skills.
A 74-year-old man develops progressive cognitive impairment, pronounced fluctuations in daytime alertness, vivid hallucinations of animals, and a new-onset resting tremor.
A 71-year-old woman with a long-standing history of medication-noncompliant hypertension experiences abrupt declines in executive function separated by periods of stability, along with a right-sided Babinski sign.
A 76-year-old man presents with an insidious onset of a broad-based, magnetic gait, urinary urgency culminating in incontinence, and generalized cognitive slowing over 8 months.

Matches

Show answer & explanation

Answer

The correct pairings match Creutzfeldt-Jakob disease to prion misfolding, frontotemporal dementia to tau/TDP-43 accumulation, Lewy body dementia to alpha-synuclein inclusions, vascular dementia to ischemic white matter injury, and normal pressure hydrocephalus to impaired cerebrospinal fluid reabsorption.
Each clinical vignette provides classic hallmark features of a specific neurocognitive disorder, which directly corresponds to a unique pathophysiologic mechanism. Creutzfeldt-Jakob disease is caused by prion misfolding. Frontotemporal dementia is caused by tau or TDP-43 inclusions. Lewy body dementia is caused by alpha-synuclein aggregation. Vascular dementia is caused by ischemic white matter injury from small vessel disease. Normal pressure hydrocephalus is caused by impaired cerebrospinal fluid reabsorption leading to ventricular expansion.

Step-by-Step Solution

1
Analyze the first clinical presentation (rapid cognitive decline, startle myoclonus).
Identify Creutzfeldt-Jakob disease.
Recognize the classic triad of rapidly progressive dementia, myoclonus, and akinetic mutism.
2
Analyze the second presentation (social disinhibition, hyperorality).
Identify behavioral variant frontotemporal dementia.
Note the early personality changes and compulsive behaviors with relatively spared memory.
3
Analyze the third presentation (fluctuations, visual hallucinations, parkinsonism).
Identify Lewy body dementia.
Recognize the core criteria for this specific alpha-synucleinopathy.
4
Analyze the fourth presentation (stepwise decline, asymmetric reflexes).
Identify vascular dementia.
Note the temporal relationship with vascular risk factors (hypertension) and focal neurologic findings.
5
Analyze the fifth presentation (magnetic gait, incontinence, cognitive slowing).
Identify normal pressure hydrocephalus.
Recognize the classic triad of wacky, wobbly, and wet.
6
Match each identified syndrome to its underlying pathophysiology.
Map each clinical entity to its defining cellular or macroscopic mechanism.
To complete the matching set correctly by connecting clinical diagnoses with their established etiologies.

Key Concept

Distinct clinical presentations of neurocognitive disorders directly correlate with specific pathophysiologic mechanisms, such as abnormal protein aggregations or structural brain changes.
Question 6Question →

Evaluate the clinical scenarios describing older adult patients presenting with progressive cognitive or behavioral changes. Match each distinct clinical presentation with its definitive diagnostic finding or most likely underlying pathophysiological mechanism.

Click a left item, then click its matching right item

Items

A 67-year-old man is hospitalized for a 2-month history of rapidly progressing profound dementia, gait ataxia, and sudden jerky movements of his upper extremities when startled.
A 76-year-old nursing home resident develops severe lead-pipe rigidity and confusion shortly after receiving haloperidol for agitation. History includes fluctuating cognition and well-formed visual hallucinations.
A 59-year-old woman exhibits a 1-year history of worsening apathy, socially inappropriate comments, and a new compulsion to consume exclusively sweet foods, with relatively preserved memory.
A 71-year-old man exhibits a step-wise worsening of executive function over two years. Examination reveals asymmetric hyperreflexia, extensor plantar responses, and prominent emotional lability.
A 78-year-old woman presents with insidious, progressive short-term memory impairment over 3 years. She recently got lost driving in her own neighborhood but maintains appropriate social graces.

Matches

Show answer & explanation

Answer

Properly linking each clinical presentation to its pathophysiological mechanism requires recognizing the distinguishing features of the major neurocognitive disorders: rapid decline and myoclonus (CJD), neuroleptic sensitivity and hallucinations (DLB), personality changes (FTD), step-wise decline (Vascular), and insidious memory loss (Alzheimer).
Accurate matching requires recognizing the triad of rapid decline, ataxia, and myoclonus for CJD (14-3-3 protein, periodic sharp waves); early visual hallucinations, fluctuating cognition, and severe neuroleptic sensitivity for DLB (alpha-synuclein inclusions); early profound personality and dietary changes for FTD (Tau/TDP-43 aggregates); step-wise progression with focal signs for Vascular dementia (lacunar infarcts); and classic insidious short-term memory loss for Alzheimer disease (amyloid plaques and neurofibrillary tangles).

Step-by-Step Solution

1
Analyze each clinical vignette to identify the primary distinguishing symptoms and symptom onset pattern.
Identified rapid onset with myoclonus (CJD), antipsychotic sensitivity with hallucinations (DLB), behavioral/personality changes (FTD), step-wise decline with focal signs (Vascular), and slow progressive memory loss (Alzheimer).
Differentiation of neurocognitive disorders relies heavily on the temporal profile of decline and core clinical features present early in the disease course.
2
Correlate each established clinical diagnosis with its definitive molecular or imaging hallmark.
Matched CJD to CSF 14-3-3/EEG, DLB to alpha-synuclein, FTD to Tau/TDP-43, Vascular to lacunar infarcts, and Alzheimer to amyloid/tau plaques.
USMLE Step 2 CK frequently tests the ability to connect clinical presentations directly to underlying pathology and diagnostic workup results.

Key Concept

Differential diagnosis and pathophysiological mechanisms of major neurocognitive disorders.
Question 7Question →

A 58-year-old man is brought to the clinic by his husband due to a 14-month history of progressive behavioral changes. Previously known as a meticulous and empathetic high school teacher, the patient has become increasingly apathetic and frequently makes sexually explicit remarks to neighbors. He recently ate a stranger's sandwich off their plate at a local restaurant and showed no remorse when confronted by the staff. He denies feeling sad or anxious, stating, "Everything is perfectly fine." The patient has a remote history of a single depressive episode in his 20s. He takes over-the-counter diphenhydramine occasionally for sleep but takes no prescription medications. Vital signs are within normal limits. Laboratory studies, including a thyroid-stimulating hormone (TSH) level of 1.2 mU/L and a free T4 of 1.2 ng/dL (normal: 0.8-1.8 ng/dL), are normal. On mental status examination, he has a blunted affect and poor insight, but no delusions or hallucinations are elicited. Montreal Cognitive Assessment (MoCA) score is 23/30; he loses points primarily on clock drawing and verbal fluency tasks, but successfully recalls 3 out of 3 objects after a 5-minute delay. Neurological examination reveals no focal weakness, rigidity, or resting tremor. Which of the following is the most likely diagnosis?

Show answer & explanation

Answer: Frontotemporal neurocognitive disorder

Answer

Frontotemporal neurocognitive disorder
The correct answer is frontotemporal neurocognitive disorder. The behavioral variant of frontotemporal dementia (bvFTD) typically presents between the ages of 50 and 60. It is characterized by an insidious onset and gradual progression of profound personality changes, social disinhibition (e.g., making sexually explicit remarks to neighbors, stealing food), apathy, and hyperorality (changes in eating behaviors, such as eating off a stranger's plate). On formal cognitive testing, patients demonstrate marked executive dysfunction, often struggling with verbal fluency and clock drawing. Notably, visuospatial skills and memory are relatively preserved in the early stages, distinguishing it from Alzheimer disease. This patient's clinical picture perfectly aligns with bvFTD.

Step-by-Step Solution

1
Analyze the patient's demographic profile and the timeline of the symptoms.
The patient is a 58-year-old man with a 14-month insidious, progressive history of symptoms, which strongly suggests an early-onset primary neurocognitive disorder rather than an acute process like delirium or a typical psychiatric onset.
Establishing the tempo and age of onset narrows the differential diagnosis between acute, psychiatric, and neurodegenerative etiologies.
2
Evaluate the specific clinical features and mental status examination findings.
The patient exhibits prominent personality changes, disinhibition (inappropriate sexual remarks, stealing food), hyperorality (eating off others' plates), and executive dysfunction (poor clock drawing and verbal fluency), with relatively preserved memory (3/3 recall).
Different neurocognitive disorders have distinct early clinical hallmarks; characterizing the prominent deficits leads to the specific subtype.
3
Synthesize findings to identify the most likely diagnosis.
The combination of early personality changes, disinhibition, hyperorality, and prominent executive dysfunction with spared memory in a patient under 60 is the classic presentation of behavioral variant frontotemporal neurocognitive disorder.
Matching the symptom cluster to diagnostic criteria confirms the underlying etiology.

Key Concept

Recognizing the clinical presentation of behavioral variant frontotemporal dementia (bvFTD), which is characterized by early personality changes, disinhibition, apathy, and executive dysfunction with relatively preserved memory.
Estimated Time:1m 15s
Question 8Question →

A 72-year-old woman is evaluated in the outpatient geriatric clinic due to progressive memory impairment and behavioral changes. According to her son, who accompanies her, she has experienced significant day-to-day fluctuations in her alertness and attention over the last 10 months. Furthermore, she frequently describes seeing detailed, silent figures of people standing in her bedroom. Her sleep is often restless, and she frequently shouts and thrashes her arms as if she is acting out her dreams. On physical examination, the patient has a mask-like facial expression, a resting tremor in her left hand, and cogwheel rigidity in both upper extremities. The physician explains the likely diagnosis to the son and discusses management options. The physician strongly cautions against the use of a specific class of medications to treat her perceptual disturbances, noting that it could trigger a severe, potentially fatal reaction characterized by irreversible parkinsonism and autonomic dysfunction. Which of the following medications is most likely to cause the severe reaction described by the physician?

Show answer & explanation

Answer: Haloperidol

Answer

Haloperidol
This patient's clinical presentation is classic for Dementia with Lewy bodies (DLB), which is characterized by fluctuating cognition, recurrent well-formed visual hallucinations, REM sleep behavior disorder (acting out dreams), and spontaneous parkinsonism. A hallmark feature of DLB is severe neuroleptic sensitivity. Administration of first-generation (typical) antipsychotics, such as haloperidol, or some second-generation antipsychotics with strong dopamine D2 antagonism (e.g., risperidone), can precipitate a life-threatening reaction. This reaction is characterized by a dramatic worsening of parkinsonism, severe muscle rigidity, autonomic instability, and impaired consciousness. Because of this high risk, typical antipsychotics like haloperidol are strictly contraindicated in patients with DLB.

Step-by-Step Solution

1
Identify the underlying diagnosis based on the clinical presentation.
The patient has fluctuating cognition, well-formed visual hallucinations, REM sleep behavior disorder, and spontaneous parkinsonism, which are core clinical features of Dementia with Lewy bodies (DLB).
Accurate diagnosis is required to understand disease-specific pharmacological contraindications.
2
Recognize the specific pharmacological vulnerability associated with this condition.
Patients with DLB have extreme sensitivity to dopamine D2 receptor antagonists, particularly first-generation (typical) antipsychotics.
Administration of these agents can precipitate a life-threatening reaction known as severe neuroleptic sensitivity.
3
Select the medication from the options that represents this contraindicated class.
Haloperidol is a high-potency typical antipsychotic, making it highly likely to cause severe neuroleptic sensitivity in a patient with DLB.
The other medications listed are either indicated for DLB symptoms or do not cause this specific life-threatening reaction.

Key Concept

Severe neuroleptic sensitivity in Dementia with Lewy bodies (DLB)
Estimated Time:1m 0s
Question 9Question →

During morning rounds on a surgical ward, an internal medicine consultant is asked to evaluate a patient recovering from a right femoral neck fracture repair performed 48 hours ago. The nursing staff reports that the patient was awake, alert, and conversational yesterday, but overnight she became highly agitated, attempted to remove her urinary catheter, and claimed that insects were crawling on her bed sheets. The patient's daughter confirms her mother lived independently and had no history of memory issues or psychiatric illness prior to the fall. Physical examination reveals an inattentive patient who drifts off to sleep during questioning. Vital signs are stable, and a basic metabolic panel is unremarkable. Which of the following is the most likely diagnosis for this patient's acute presentation?

Show answer & explanation

Answer: Delirium

Answer

Delirium
The correct answer is delirium. This patient presents with an acute change in mental status, marked inattention (drifting off during questioning), a fluctuating level of consciousness, and visual hallucinations (seeing insects) following a major surgery. These features, combined with a lack of prior cognitive impairment, are the classic clinical hallmarks of delirium. Delirium is a neurocognitive disorder that is typically secondary to an underlying medical condition, medication effect, infection, or the physiological stress of surgery.

Step-by-Step Solution

1
Identify the timeline and onset of the patient's symptoms.
The patient developed acute behavioral changes and hallucinations over a matter of hours (overnight) on postoperative day 2.
Establishing the timeline helps distinguish acute conditions from chronic neurodegenerative diseases.
2
Analyze the specific clinical features present on examination.
The patient exhibits marked inattention, a fluctuating level of consciousness (drifting off to sleep), and visual hallucinations (seeing insects).
These specific signs are hallmark diagnostic features of a specific acute cognitive disorder.
3
Synthesize the findings to determine the most likely diagnosis.
An acute, fluctuating change in mental status with inattention in a hospitalized patient points directly to a secondary physiological effect rather than a primary psychiatric disorder.
Ruling out primary psychiatric illnesses and chronic cognitive decline confirms the diagnosis of delirium.

Key Concept

Clinical presentation and diagnostic criteria for delirium
Estimated Time:1m 0s
Question 10Question →

A 73-year-old retired architect is evaluated in the hospital for severe agitation. He was admitted 24 hours ago for cellulitis of the right lower extremity, for which wound cultures grew methicillin-resistant *Staphylococcus aureus* (MRSA). His medical history is significant for bipolar I disorder (not currently taking mood stabilizers), severe osteoarthritis (managed with scheduled tramadol), and a 3-year history of progressive cognitive decline, prominent visual hallucinations of small animals, and a resting tremor. He has a documented diagnosis of major neurocognitive disorder with Lewy bodies.

Currently, he is severely agitated, attempting to pull out his intravenous line, and striking at the nursing staff. He is unable to cooperate with a medical examination or verbal de-escalation. His husband, who is his legally appointed healthcare proxy, requests that the medical team administer medication to calm him down. However, the patient's daughter, who just arrived, demands that no mind-altering medications be given and suggests using physical restraints instead.

Which of the following is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: Administer low-dose quetiapine with the husband's consent

Answer

The most appropriate next step is to administer low-dose quetiapine with the consent of the patient's husband.
The correct action is to administer low-dose quetiapine. This patient has major neurocognitive disorder with Lewy bodies (DLB) and is presenting with acute delirium secondary to an infection, resulting in dangerous agitation. In DLB, patients have a severe sensitivity to neuroleptics (antipsychotics with strong dopamine D2 receptor antagonism, such as haloperidol or risperidone), which can cause irreversible parkinsonism, impaired consciousness, and autonomic dysfunction. When non-pharmacological interventions fail and the patient poses an immediate danger to themselves or staff, the safest pharmacological options are low-dose quetiapine or clozapine, as they have the lowest D2 receptor affinity. Furthermore, the patient's husband is the legally appointed healthcare proxy; his consent for pharmacological treatment legally overrides the daughter's objections.

Step-by-Step Solution

1
Identify the primary diagnosis and current acute complication.
The patient has Dementia with Lewy Bodies (DLB) and is experiencing acute hyperactive delirium secondary to an MRSA infection.
Understanding the underlying neurocognitive disorder is essential, as DLB dictates specific pharmacological contraindications.
2
Evaluate the ethical conflict regarding consent for treatment.
The husband's consent for pharmacological treatment is legally binding.
The husband is the legally appointed healthcare proxy, meaning his medical decisions override the conflicting requests of the daughter.
3
Select the most appropriate and safe intervention for severe agitation in DLB.
Low-dose quetiapine is the treatment of choice.
Patients with DLB have severe neuroleptic sensitivity. Typical antipsychotics and most atypicals (like risperidone) can cause life-threatening parkinsonism. Quetiapine has low D2 receptor affinity and is safer.
4
Rule out contraindicated medications based on the patient's history and current medication list.
Avoid linezolid (risk of serotonin syndrome with tramadol) and SSRI monotherapy (risk of manic switch in bipolar I).
Comprehensive management requires checking for dangerous drug-drug interactions and psychiatric contraindications.

Key Concept

Management of severe agitation in Dementia with Lewy Bodies (DLB)
Estimated Time:2m 0s
Question 11Question →

A 72-year-old woman is brought to the clinic by her son due to a 6-month history of progressive memory impairment, apathy, and severe psychomotor slowing. She frequently forgets conversations and has stopped participating in her usual social activities. She also reports worsening fatigue, constipation, and feeling cold constantly. Her medical history is significant for bipolar I disorder, which has been well-controlled on lithium monotherapy for 15 years, and hypertension. Current medications are lithium and lisinopril. Vital signs show a blood pressure of 130/80 mm Hg and a heart rate of 52/min. Physical examination reveals delayed relaxation of the deep tendon reflexes, dry skin, and a slightly puffy face. Cognitive assessment yields a Montreal Cognitive Assessment (MoCA) score of 19/30.

Laboratory results are as follows:

TestResultReference Range
Serum lithium0.8 mEq/L0.6-1.2 mEq/L
Thyroid-stimulating hormone (TSH)0.2 mIU/L0.4-4.0 mIU/L
Free thyroxine (T4)0.5 ng/dL0.9-1.7 ng/dL

Which of the following is the most appropriate next step in management?

Show answer & explanation

Answer: Magnetic resonance imaging of the brain

Answer

Magnetic resonance imaging of the brain
This patient presents with a major neurocognitive decline accompanied by classical signs of hypothyroidism (bradycardia, delayed deep tendon reflexes, constipation, cold intolerance). In the workup of a neurocognitive disorder, evaluating for reversible causes is mandatory. Her laboratory findings reveal a low free T4 level, confirming hypothyroidism. However, her thyroid-stimulating hormone (TSH) level is inappropriately low. In primary hypothyroidism, the lack of negative feedback from T4 leads to a dramatically elevated TSH. A low or inappropriately normal TSH in the setting of low free T4 indicates secondary (central) hypothyroidism, pointing to a failure of the pituitary gland or hypothalamus. The most common causes of central hypothyroidism are structural lesions, such as a pituitary macroadenoma, craniopharyngioma, or other compressive intracranial masses. Therefore, the most appropriate next step in management is a magnetic resonance imaging (MRI) scan of the brain to visualize the hypothalamic-pituitary axis.

Step-by-Step Solution

1
Identify the primary clinical syndrome.
The patient presents with reversible neurocognitive impairment (pseudodementia) accompanied by classic hypothyroid signs (bradycardia, delayed reflexes, cold intolerance, constipation).
Establishing the clinical phenotype is essential before interpreting laboratory values in the context of cognitive decline.
2
Interpret the thyroid function tests.
The free T4 is low (confirming hypothyroidism), but the TSH is inappropriately low (0.2 mIU/L), establishing a diagnosis of secondary (central) hypothyroidism.
Differentiating primary (high TSH) from secondary (low/normal TSH) hypothyroidism determines the anatomic location of the defect.
3
Differentiate the etiology from medication adverse effects.
Lithium induces primary hypothyroidism by inhibiting thyroid hormone release, which would elevate TSH. The patient's low TSH pattern rules out lithium-induced thyroid dysfunction.
Ruling out medication-induced effects prevents inappropriate cessation of a stable, long-term psychiatric regimen.
4
Determine the appropriate diagnostic intervention for central hypothyroidism.
Magnetic resonance imaging (MRI) of the brain is required.
Central hypothyroidism is most frequently caused by structural compressive lesions in the hypothalamic-pituitary axis (e.g., macroadenoma), which must be visualized radiographically.

Key Concept

Reversible neurocognitive impairment can be caused by central hypothyroidism (characterized by low free T4 and an inappropriately low TSH), which requires an MRI of the brain to evaluate for a pituitary or hypothalamic mass, independent of chronic lithium therapy which typically causes primary hypothyroidism (high TSH).
Question 12Question →

A 64-year-old man is brought to the neurologist by his wife due to a 3-month history of rapidly progressive cognitive decline and unusual involuntary movements. The wife notes that he initially had trouble concentrating at work and seemed unusually anxious. Over the past month, he has become profoundly disoriented, struggles to walk independently due to poor coordination, and frequently exhibits sudden, brief, shock-like muscle jerks, particularly when startled by a loud noise. He has no significant past medical history and takes no medications. Vital signs are normal. Neurological examination reveals marked gait ataxia, widespread myoclonus, and severe expressive aphasia. Magnetic resonance imaging (MRI) of the brain demonstrates hyperintensity in the basal ganglia and cerebral cortex on diffusion-weighted imaging. Which of the following best describes the underlying pathophysiology of this patient's condition?

Show answer & explanation

Answer: Conformational change of a normal cellular protein into a β\beta-pleated sheet isoform

Answer

Conformational change of a normal cellular protein into a β\beta-pleated sheet isoform
The patient's rapidly progressive dementia, prominent startle myoclonus, cerebellar ataxia, and characteristic MRI findings (hyperintensity in the basal ganglia and cerebral cortex on diffusion-weighted imaging) strongly suggest a diagnosis of Creutzfeldt-Jakob disease (CJD). CJD is a fatal spongiform encephalopathy caused by prions. The underlying pathophysiology involves the conformational change of the normal cellular prion protein (PrPCPrP^C), which is rich in α\alpha-helices, into an abnormal, disease-causing isoform (PrPScPrP^{Sc}) that is predominantly composed of β\beta-pleated sheets. These abnormal proteins are resistant to protease degradation and accumulate in the brain, leading to widespread neurodegeneration, vacuolization, and rapidly progressive clinical decline.

Step-by-Step Solution

1
Identify the key clinical features and timeline in the vignette.
The patient has a rapidly progressive dementia (over 3 months), startle myoclonus, cerebellar ataxia, and aphasia.
Establishing the pace of cognitive decline is crucial for narrowing the differential diagnosis of neurocognitive disorders.
2
Correlate the clinical presentation with the neuroimaging results.
MRI shows diffusion restriction (hyperintensity) in the basal ganglia and cerebral cortex, known as cortical ribboning.
These specific MRI findings, combined with the rapid clinical triad of dementia, myoclonus, and ataxia, are pathognomonic for Creutzfeldt-Jakob disease (CJD).
3
Determine the underlying pathophysiology of the diagnosed condition.
CJD is caused by the transformation of a normal α\alpha-helical cellular prion protein (PrPCPrP^C) into an abnormal β\beta-pleated sheet isoform (PrPScPrP^{Sc}).
The question explicitly asks for the pathophysiological mechanism of the patient's condition.

Key Concept

Creutzfeldt-Jakob disease (CJD) is a rapidly progressive neurocognitive disorder characterized by dementia, startle myoclonus, and ataxia, caused by the conformational change of normal prion proteins into abnormal β\beta-pleated sheets.
Question 13Question →

A 74-year-old woman is brought to the emergency department from her home by her daughter due to severe confusion and agitation that began yesterday. The daughter reports that the patient was previously able to manage her daily activities but has been 'talking to people who aren't there' and pacing the house incessantly over the past 24 hours. The patient has a history of major depressive disorder and mild cognitive impairment. Two days ago, she developed a runny nose and began taking an over-the-counter cold and allergy medication. Her prescribed medications include daily citalopram. Routine laboratory results from a clinic visit one week ago showed a decreased free thyroxine (T4) level with a normal thyroid-stimulating hormone (TSH) level. On physical examination, her temperature is 37.8°C (100.0°F), pulse is 112/min, and blood pressure is 142/86 mm Hg. She is disoriented to place and time. Her skin is warm, flushed, and dry. Her pupils are 7 mm bilaterally and sluggishly reactive to light. Bladder ultrasound reveals 600 mL of retained urine. Which of the following is the most likely cause of this patient's acute presentation?

Show answer & explanation

Answer: Anticholinergic medication toxicity

Answer

Anticholinergic medication toxicity
The correct answer is anticholinergic medication toxicity. This patient is presenting with acute-onset delirium characterized by confusion, agitation, and visual hallucinations. When combined with her physical examination findings—tachycardia, hyperthermia, dry and flushed skin, mydriasis (dilated pupils), and urinary retention—the clinical picture perfectly matches the anticholinergic toxidrome ('mad as a hatter, blind as a bat, red as a beet, hot as a hare, dry as a bone, full as a flask'). Elderly patients, particularly those with underlying mild cognitive impairment or dementia, are extremely sensitive to the central effects of anticholinergic drugs. Over-the-counter cold and allergy medications frequently contain first-generation antihistamines (such as diphenhydramine or chlorpheniramine) which have potent antimuscarinic properties.

Step-by-Step Solution

1
Identify the primary clinical syndrome from the patient's history.
The patient presents with acute-onset confusion, agitation, and visual hallucinations.
Recognizing the acute, fluctuating nature of the cognitive decline establishes the diagnosis of delirium.
2
Analyze the physical examination findings to identify an underlying etiology.
The patient exhibits tachycardia, low-grade fever, dry and flushed skin, dilated and sluggish pupils, and urinary retention.
These findings represent a specific toxidrome that must be matched to a pharmacological or physiological cause.
3
Correlate the toxidrome with the patient's recent medication history.
The combination of delirium and these autonomic signs is the classic presentation of anticholinergic toxicity, likely triggered by the recent use of an over-the-counter cold and allergy medication (which typically contain first-generation antihistamines).
Elderly patients with baseline cognitive impairment are highly susceptible to the central nervous system effects of anticholinergic medications.

Key Concept

Anticholinergic toxicity presents with delirium, hyperthermia, tachycardia, dry flushed skin, mydriasis, and urinary retention, and is a common cause of acute neurocognitive decline in the elderly.
Estimated Time:1m 30s
Question 14Question →

A 75-year-old man is brought to the neurology clinic by his son. Over the past 8 months, the patient has developed a progressively unsteady gait. The son describes his father's walking as feeling "glued to the ground" with very short steps. For the past 4 months, the patient has had difficulty managing his finances, exhibits new-onset apathy, and struggles with short-term memory. Over the last month, he has had multiple episodes of urinary incontinence, toward which he appears indifferent. His medical history includes hypertension and type 2 diabetes mellitus. Neurological examination reveals a broad-based, magnetic gait, but muscle strength and deep tendon reflexes are normal. A magnetic resonance imaging (MRI) scan of the brain is obtained and is shown below, demonstrating enlarged lateral and third ventricles with relatively normal, uncrowded cortical sulci. What is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: High-volume lumbar puncture

Answer

High-volume lumbar puncture
The correct answer is a high-volume lumbar puncture. The patient presents with the classic triad of Normal Pressure Hydrocephalus (NPH): abnormal gait (magnetic, broad-based, 'glued to the floor'), cognitive impairment, and urinary incontinence. Neuroimaging confirms communicating hydrocephalus, showing ventriculomegaly without significant cortical atrophy. The most appropriate next step in management is a high-volume lumbar puncture (also known as the tap test or Miller Fisher test) to remove 30-50 mL of cerebrospinal fluid. Improvement in gait and cognitive function following this procedure confirms the diagnosis and indicates that the patient is likely to benefit from definitive surgical treatment with a ventriculoperitoneal shunt.

Step-by-Step Solution

1
Identify the clinical syndrome based on the patient's presentation.
The patient exhibits the classic triad of gait apraxia ('magnetic' gait), cognitive impairment, and urinary incontinence.
Recognizing this specific symptom triad is essential for suspecting Normal Pressure Hydrocephalus (NPH).
2
Analyze the neuroimaging findings provided in the vignette.
The MRI shows ventriculomegaly out of proportion to cortical atrophy.
This confirms communicating hydrocephalus and supports the diagnosis of NPH over ex vacuo ventriculomegaly, which is typically seen in neurodegenerative diseases like Alzheimer's.
3
Determine the next best step in the diagnostic and management pathway.
A high-volume lumbar puncture (Miller Fisher tap test) is indicated.
Removing 30-50 mL of cerebrospinal fluid assesses whether the patient's gait and cognitive symptoms temporarily improve, which strongly predicts the success of definitive surgical treatment.

Key Concept

Diagnosis and management of Normal Pressure Hydrocephalus (NPH)
Estimated Time:1m 0s
Question 15Question →

A 58-year-old man is brought to the clinic by his wife due to an 88-month history of progressive behavioral changes. His wife reports that he has become increasingly apathetic and socially withdrawn, frequently neglecting his personal hygiene. He recently began compulsively hoarding empty glass bottles and has made sexually explicit remarks to neighbors, which is entirely out of character. The patient has a history of bipolar I disorder following a single manic episode at age 22, but he has been euthymic and off psychiatric medications for over 3030 years. Mental status examination reveals an alert and oriented patient with a blunted affect. He displays poor insight and disinhibition during the interview. Memory recall is 3/3 after 55 minutes, but he exhibits significant impairment on the Trail Making Test Part B. Laboratory studies show a thyroid-stimulating hormone (TSH) level of 0.2μU/mL0.2 \mu U/mL (Normal: 0.4−4.0μU/mL0.4-4.0 \mu U/mL) and a free thyroxine (T4) level of 0.6ng/dL0.6 ng/dL (Normal: 0.9−1.7ng/dL0.9-1.7 ng/dL). The patient has a legally executed advance directive designating his eldest daughter as his sole healthcare proxy. However, the daughter is not present, and the wife vehemently demands the physician immediately start an antidepressant, believing his symptoms represent a severe depressive relapse. Which of the following is the most appropriate next step in management?

Show answer & explanation

Answer: Obtain structural magnetic resonance imaging of the brain

Answer

Obtain structural magnetic resonance imaging of the brain
The correct action is to obtain a structural MRI of the brain. The patient presents with classic clinical features of behavioral variant frontotemporal dementia (bvFTD), characterized by early changes in personality, apathy, disinhibition, compulsive behaviors, and significant executive dysfunction with relative sparing of memory and visuospatial skills. Additionally, his laboratory results reveal central hypothyroidism (low TSH and low Free T4). The combination of a frontal lobe syndrome and a central pituitary/hypothalamic endocrinopathy should immediately raise suspicion for a structural brain lesion, such as a large frontal meningioma or tumor compressing the pituitary stalk, alongside primary neurodegenerative etiologies. An MRI is the most definitive next step to rule out space-occupying, vascular, or structural causes of his decline.

Step-by-Step Solution

1
Analyze the neurocognitive presentation and timeline.
The patient demonstrates new-onset apathy, disinhibition, hoarding, and executive dysfunction with preserved memory, highly suspicious for behavioral variant frontotemporal dementia (bvFTD).
Identifying the primary neurocognitive syndrome is essential for guiding the diagnostic workup.
2
Evaluate the laboratory findings.
TSH and Free T4 are both below normal limits, indicating central hypothyroidism.
These findings suggest a central hypothalamic-pituitary axis disruption rather than primary thyroid failure.
3
Synthesize clinical and laboratory data to determine the next step.
The combination of frontal lobe signs (bvFTD phenotype) and central endocrinopathy (central hypothyroidism) highly suggests a structural brain lesion (e.g., a frontal mass compressing the pituitary stalk) or a significant neurodegenerative process.
New-onset major neurocognitive disorders with atypical features or concurrent central endocrinopathies mandate neuroimaging to rule out reversible or structural causes.
4
Review the ethical constraints regarding surrogate decision-making.
The patient lacks capacity, and the daughter is the designated healthcare proxy. The wife's demands cannot override the legal proxy.
Medical interventions should only proceed with the consent of the legally appointed surrogate when an advance directive exists.

Key Concept

Patients presenting with new-onset major neurocognitive disorder featuring atypical symptoms (e.g., prominent frontal lobe behavioral changes) and concurrent objective medical abnormalities (e.g., central hypothyroidism) require prompt structural brain imaging to evaluate for potentially reversible or space-occupying lesions.
Estimated Time:1m 30s
Question 16Question →

A 7272-year-old woman is brought to the geriatrics clinic by her husband due to progressive memory loss and confusion over the past 33 months. Her husband states she spends most of her day in bed, has stopped cooking, and has lost 55 kg (1111 lb). Over the last 33 weeks, she has been repeatedly stating that "the government is coming to arrest me for tax fraud," which is completely unfounded.

Past medical history is significant for Parkinson disease, treated with selegiline, and bipolar I disorder. She previously took lithium but discontinued it a year ago of her own volition.

On mental status examination, she exhibits marked psychomotor retardation and poor eye contact. When asked to perform serial sevens or spell "WORLD" backwards, she gives minimal effort, frequently stating, "I don't know, my mind is completely gone."

Her daughter, who is her legally appointed healthcare proxy, lives in another state. Her husband is frustrated with the patient's decline and demands that the physician immediately authorize her placement in a local nursing home.

Which of the following is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: Recommend inpatient psychiatric admission for electroconvulsive therapy

Answer

Recommend inpatient psychiatric admission for electroconvulsive therapy
The correct response is to recommend inpatient psychiatric admission for electroconvulsive therapy. This patient is experiencing a severe bipolar depressive episode with psychotic features, which is presenting as pseudodementia. Key indicators of pseudodementia include a relatively rapid onset, highlighting of cognitive deficits, and poor effort on testing (giving 'I don't know' answers), unlike true neurocognitive disorders where patients often attempt to conceal their deficits. Given her severe depression, psychotic features, poor oral intake (weight loss), and complex medication history (recent MAOI use), electroconvulsive therapy (ECT) is the safest and most rapidly effective treatment. Additionally, ECT is known to transiently improve the motor symptoms of Parkinson disease.

Step-by-Step Solution

1
Analyze the patient's cognitive and behavioral presentation.
The relatively rapid onset of symptoms, poor effort on cognitive testing ('I don't know' answers), and severe depressive features indicate pseudodementia rather than a true major neurocognitive disorder.
Differentiating between dementia and depression-induced cognitive impairment is critical for appropriate management.
2
Evaluate the patient's psychiatric symptoms and history.
The presence of delusions (tax fraud) and a history of bipolar I disorder indicate a severe bipolar depressive episode with psychotic features.
Psychotic depression requires aggressive and specific interventions, often involving combination pharmacotherapy or somatic therapies.
3
Assess the medication history for pharmacological contraindications.
The patient takes selegiline, an MAOI, which strictly contraindicates SSRI use due to serotonin syndrome risk. Additionally, her bipolar history contraindicates antidepressant monotherapy.
Recognizing dangerous drug-drug interactions prevents iatrogenic harm.
4
Determine the optimal treatment step while navigating ethical constraints.
Electroconvulsive therapy (ECT) is the safest and most rapidly effective treatment. The husband's demand for nursing home placement must be deferred to the daughter, who is the legally appointed proxy.
ECT is the gold standard for severe psychotic depression in the elderly, particularly when complicated by poor oral intake and Parkinson disease. Legally, the proxy's authority cannot be bypassed.

Key Concept

Discriminating pseudodementia from true neurocognitive disorders and identifying appropriate management (ECT) while avoiding pharmacological contraindications and adhering to surrogate decision-making laws.
Question 17Question →

A 78-year-old man residing in an assisted living facility is evaluated for a decline in his cognitive abilities over the past 3 months. The nursing staff report that he has stopped participating in social activities, frequently stays in his room with the blinds drawn, and has lost 4.5 kg (10 lb) during this period. When asked about his memory, the patient becomes distressed and repeatedly states, "My mind is completely gone; I cannot remember anything anymore." On cognitive testing, he makes poor eye contact and frequently responds to questions with "I don't know," exhibiting minimal effort. However, when strongly encouraged by the examiner, he successfully performs complex attention tasks. His neurological examination shows no focal deficits. A non-contrast head CT performed 2 months ago after a mechanical fall was unremarkable. Laboratory studies, including thyroid-stimulating hormone and vitamin B12, are within normal limits. Which of the following is the most appropriate initial management for this patient?

Show answer & explanation

Answer: Initiate sertraline therapy

Answer

The most appropriate initial management is to initiate sertraline therapy.
The patient is exhibiting signs of major depressive disorder (MDD) presenting with prominent cognitive impairment, a condition historically referred to as pseudodementia. In elderly patients, MDD frequently manifests with cognitive deficits, psychomotor retardation, and neurovegetative symptoms such as weight loss and social withdrawal. Key features that differentiate MDD from a progressive major neurocognitive disorder (e.g., Alzheimer disease) include a relatively rapid, identifiable onset, the patient's acute awareness of and distress regarding their memory loss, and a tendency to give 'I don't know' answers on cognitive testing. Furthermore, when encouraged, these patients can often complete complex tasks, demonstrating intact underlying cognition. The most appropriate initial step in management is to treat the underlying depression with a selective serotonin reuptake inhibitor (SSRI) such as sertraline, which typically leads to improvement in both mood and cognitive symptoms.

Step-by-Step Solution

1
Analyze the time course and character of the cognitive decline.
The patient has a 3-month history of cognitive decline accompanied by social withdrawal and weight loss.
Establishing the timeline helps differentiate between the insidious onset of neurodegenerative dementias and the subacute onset typical of mood disorders or delirium.
2
Evaluate the patient's performance and attitude during cognitive testing.
The patient shows significant distress about memory loss, frequently answers with 'I don't know', but performs well when actively encouraged.
These testing behaviors are hallmark signs of depression-related cognitive impairment. In contrast, patients with Alzheimer disease often lack insight into their deficits and attempt to cover them up (confabulation).
3
Determine the most appropriate initial therapy based on the primary diagnosis.
The clinical picture is consistent with major depressive disorder, indicating the need for an antidepressant such as an SSRI (sertraline).
Treating the underlying unipolar depression will likely lead to improvement in both the patient's mood and cognitive deficits.

Key Concept

Depression-related cognitive impairment (historically called pseudodementia) presents with a subacute onset of memory issues, prominent distress regarding cognitive deficits, and frequent 'I don't know' responses on testing. Treatment involves addressing the underlying depression with antidepressants such as SSRIs.
Question 18Question →

A 78-year-old woman with a 6-year history of Alzheimer disease is brought to the clinic for a routine follow-up. Her family asks the physician about the natural progression of the disease to help them prepare for future care needs. The physician explains the typical chronological decline expected in this condition. Arrange the following clinical features in the correct chronological sequence that they typically appear during the natural course of Alzheimer disease, from earliest to latest.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct chronological progression is: mild short-term memory impairment, followed by the loss of instrumental activities of daily living (such as managing finances), then the loss of basic activities of daily living (such as bathing), and finally severe motor rigidity and mutism.
Alzheimer disease has a characteristic progressive pattern of cognitive and functional decline. It begins with prominent short-term memory impairment due to early hippocampal involvement. As the disease spreads to the frontal and parietal association cortices, higher-level executive functions are impaired, leading to a loss of ability to perform complex tasks (Instrumental ADLs). With further progression, basic self-care abilities (Basic ADLs) are lost. Finally, in the end-stages, global cortical damage results in severe neurologic deficits, including mutism, motor rigidity, and a bedbound state.

Step-by-Step Solution

1
Identify the initial presentation of Alzheimer disease.
Short-term memory impairment.
The disease typically begins in the medial temporal lobe (hippocampus), which is responsible for forming new memories.
2
Determine the next level of functional decline as cortical involvement spreads.
Impairment in instrumental activities of daily living (IADLs).
Complex tasks like managing finances and cooking require executive function and working memory, which are affected before basic self-care skills.
3
Identify the consequence of more diffuse cortical atrophy in moderate-to-severe disease.
Impairment in basic activities of daily living (ADLs).
Basic tasks such as bathing, dressing, and toileting become compromised as parietal and frontal lobe involvement worsens.
4
Identify the features of late/end-stage Alzheimer disease.
Motor rigidity, mutism, and total dependence.
Global severe brain atrophy eventually destroys nearly all cognitive and motor functions, leading to a bedbound, mute state.

Key Concept

The classic chronological progression of Alzheimer disease: memory loss -> IADL impairment -> ADL impairment -> severe motor/language loss.
Question 19Question →

A 72-year-old woman is brought to the outpatient geriatric psychiatry clinic by her son due to a 6-month history of significant cognitive decline. He reports that she has become increasingly withdrawn, spends most of the day in bed, and has stopped managing her household finances. During the interview, she makes poor eye contact, exhibits psychomotor retardation, and frequently answers "I don't know" rather than attempting to answer orientation or memory questions. Her Montreal Cognitive Assessment (MoCA) score is 19/30. Medical history is significant for bipolar I disorder that was well-controlled on lithium for two decades; however, she discontinued all medications 14 months ago following the death of her husband. Her son notes she has not had any periods of elevated mood, decreased need for sleep, or rapid speech since stopping her medication. Vital signs and physical examination are normal. Laboratory studies, including complete blood count, comprehensive metabolic panel, thyroid-stimulating hormone, and vitamin B12 levels, are within normal limits. The physician determines that her cognitive deficits are secondary to a severe mood episode rather than a primary neurodegenerative process. Which of the following is the most appropriate initial pharmacological intervention for this patient?

Show answer & explanation

Answer: Lurasidone

Answer

Lurasidone
The patient's presentation of cognitive decline, psychomotor retardation, apathy, and prominent "I don't know" answers in the setting of a recent stressor is classic for pseudodementia (cognitive impairment secondary to major depression). Because she has a history of bipolar I disorder, her current state is an acute episode of bipolar depression. Lurasidone is a second-generation (atypical) antipsychotic that is FDA-approved for the treatment of bipolar depression. It effectively targets both the mood and secondary cognitive symptoms without the high risk of inducing a manic switch.

Step-by-Step Solution

1
Analyze the patient's cognitive presentation.
The patient demonstrates psychomotor retardation and gives "I don't know" responses, which are classic signs of cognitive impairment secondary to depression (pseudodementia) rather than true dementia.
Differentiating pseudodementia from major neurocognitive disorder is the critical first step before initiating treatment.
2
Determine the specific type of affective episode.
The patient has a known history of bipolar I disorder and discontinued her mood stabilizer 14 months ago. Her current symptoms represent a bipolar depressive episode.
Major depressive episodes in bipolar disorder must be treated differently than unipolar major depressive disorder.
3
Select the appropriate pharmacotherapy.
Lurasidone is chosen as the initial intervention.
Lurasidone is an atypical antipsychotic approved for bipolar depression and does not carry the risk of precipitating mania, unlike SSRI monotherapy.

Key Concept

Patients with a history of bipolar I disorder who present with severe depression and secondary cognitive impairment (pseudodementia) should be treated with mood stabilizers or atypical antipsychotics approved for bipolar depression (e.g., lurasidone, cariprazine) to avoid SSRI-induced manic switching.
Estimated Time:1m 30s
Question 20Question →

A 70-year-old man is brought to the clinic by his son due to memory issues that began 2 months ago, shortly after the sudden death of his wife. The patient frequently complains about his memory, stating, "My brain is just broken; I can't remember anything." During cognitive testing, he puts forth poor effort and frequently answers "I don't know" to questions, though he can often provide the correct answers when gently prompted. He also reports early morning awakenings, decreased appetite, and a 4-kg (8.8-lb) weight loss over this period. His physical and neurological examinations are unremarkable. Which of the following is the most likely diagnosis?

Show answer & explanation

Answer: Major depressive disorder

Answer

Major depressive disorder
The correct answer is major depressive disorder. In elderly patients, severe depression can present with significant cognitive impairment, a condition historically termed 'pseudodementia'. Key distinguishing features from true neurocognitive disorders (like Alzheimer disease) include a rapid onset (often following a stressor), prominent complaints about memory loss (insight is intact), poor effort on testing (giving 'I don't know' answers rather than confabulating), and the presence of vegetative depressive symptoms like insomnia and weight loss.

Step-by-Step Solution

1
Analyze the time course of the cognitive symptoms.
The symptoms began acutely 2 months ago after a major life stressor (death of his wife).
Dementia typically has an insidious, chronic onset, whereas depression-related cognitive impairment (pseudodementia) often has a rapid onset linked to a stressor.
2
Evaluate the patient's attitude toward his cognitive deficits and his performance on cognitive testing.
He complains about his memory loss and frequently answers 'I don't know', but answers correctly when prompted.
Patients with genuine dementia typically lack insight, try to cover up their deficits, and guess or confabulate answers. Patients with depression highlight their deficits and put forth poor effort ('I don't know').
3
Identify any associated systemic or mood symptoms.
He has early morning awakenings, decreased appetite, and significant weight loss.
These are classic vegetative symptoms of major depressive disorder (SIGECAPS).

Key Concept

Major depressive disorder in the elderly can present with prominent cognitive deficits (pseudodementia), distinguished from true dementia by acute onset, prominent complaints of memory loss, 'I don't know' answers, and associated vegetative symptoms.
Page 1 / 4Next
Neurocognitive Disorders Practice Questions — USMLE Step 2 CK | Examkin