,CONTENT
Chapter 1: Introduction to Clinical Case Presentations
Chapter 2: Neuroanatomy Overview and Basic Definitions
Chapter 3: The Neurologic Exam as a Lesson in Neuroanatomy
Chapter 4: Introduction to Clinical Neuroradiology
Chapter 5: Brain and Environs: Cranium, Ventricles, and Meninges
Chapter 6: Corticospinal Tract and Other Motor Pathways
Chapter 7: Somatosensory Pathways
Chapter 8: Spinal Nerve Roots
Chapter 9: Major Plexuses and Peripheral Nerves
Chapter 10: Cerebral Hemispheres and Vascular Supply
Chapter 11: Visual System
Chapter 12: Brainstem I: Surface Anatomy and Cranial Nerves
Chapter 13: Brainstem II: Eye Movements and Pupillary Control
Chapter 14: Brainstem III: Internal Structures and Vascular Supply
Chapter 15: Cerebellum
Chapter 16: Basal Ganglia
Chapter 17: Pituitary and Hypothalamus
Chapter 18: Limbic System: Homeostasis, Olfaction, Memory and Emotion
Chapter 19: Higher-Order Cerebral Function
,Chapter 1: Introduction to Clinical Case
Presentations
Chapter 1: Introduction to Clinical Case Presentations (Blumenfeld).
Each question is aligned to the chapter theme . Every question has 4 choices (A–D), the answer
shown only as Answer: X, a deep rationale for the correct answer (including why the other
choices are incorrect), and a short list of Key words.
1. Which of the following best captures the primary pedagogical advantage of using real
patient cases to teach neuroanatomy?
A. They let students memorize anatomical names faster.
B. They emphasize rare, exotic disorders that students rarely see.
C. They integrate anatomical knowledge with clinical reasoning, exam findings and
imaging interpretation.
D. They replace the need to learn foundational anatomy.
Answer: C
Rationale: Real patient cases force learners to apply anatomical knowledge to problems
encountered in practice: mapping symptoms to structures, interpreting exam findings, and
choosing/reading imaging. This builds diagnostic reasoning and pattern recognition rather than
rote memorization. (A) is reductive — cases improve application, not just rote recall. (B) is false
— cases emphasize common patterns and diagnostic thinking, not just rare diseases. (D) is
incorrect: cases complement, not replace, foundational anatomy.
Key words: case-based learning, clinical reasoning, applied anatomy, imaging integration
2. According to the case format Blumenfeld emphasizes, what is the optimal sequence for
presenting information to maximize localization and diagnostic reasoning?
A. Physical exam → History → Diagnosis → Imaging
B. History → Physical exam → Imaging → Diagnosis
C. Imaging → History → Physical exam → Diagnosis
D. Diagnosis → History → Physical exam → Imaging
Answer: B
Rationale: The clinical workflow and reasoning proceed from history (timing, onset, associated
features) to targeted physical exam that tests hypotheses from the history, then to imaging
selected to answer unresolved questions, culminating in a diagnosis that integrates all
information. Presenting history first avoids anchoring to imaging and enables proper hypothesis
generation. Other orders (A, C, D) disrupt the hypothesis-driven approach and can encourage
premature closure.
Key words: history first, hypothesis-driven exam, imaging selection, diagnostic integration
, 3. A 62-year-old man is described as having “maximal neurologic deficit at onset” (sudden
hemiparesis). Which aspect of the history most strongly supports a vascular (ischemic or
hemorrhagic) cause rather than tumor or infection?
A. Gradual worsening over months
B. Episodic fluctuating deficits over weeks
C. Immediate maximal deficit at onset without prodrome
D. Low-grade fever and night sweats for weeks
Answer: C
Rationale: Sudden, maximal deficit at onset is classic for vascular events (ischemic stroke or
intracerebral hemorrhage). Tumors and chronic infections more commonly produce progressive
symptoms over weeks–months; inflammatory processes may fluctuate but often have different
patterns. Fever and constitutional symptoms point toward infection or systemic disease, not
primary vascular stroke. Recognizing time course in the history narrows the initial differential
and directs urgent imaging (non-contrast CT for hemorrhage).
Key words: sudden onset, vascular, stroke, time course
4. On neurologic exam you find spasticity, hyperreflexia, and an extensor plantar response
(Babinski). These findings best localize to which system?
A. Lower motor neurons (anterior horn cell/peripheral nerve)
B. Neuromuscular junction
C. Upper motor neurons / corticospinal tract
D. Primary muscle (myopathy)
Answer: C
Rationale: Spasticity, increased deep tendon reflexes and Babinski indicate an upper motor
neuron lesion affecting corticospinal pathways. Lower motor neuron lesions produce flaccidity,
decreased reflexes, atrophy and possibly fasciculations. Neuromuscular junction disorders and
myopathies produce weakness but not true hyperreflexia with Babinski. In case-based learning,
these exam features are critical to discriminate central vs peripheral processes and guide
localization to brain, brainstem or spinal cord motor pathways.
Key words: UMN signs, corticospinal, spasticity, Babinski
5. A patient arrives 90 minutes after sudden focal weakness. Which initial imaging choice
best balances speed and the key diagnostic question of hemorrhage vs ischemia?
A. Non-contrast head CT (fast, detects acute blood)
B. Routine MRI T2 (better soft tissue contrast)
C. PET scan (metabolic information)
D. Lumbar puncture (diagnostic for stroke)
Answer: A
, Rationale: In the hyperacute setting, non-contrast head CT is the fastest and most sensitive test
to detect acute intracranial hemorrhage — a crucial first question since hemorrhage alters acute
management. MRI (including DWI) is more sensitive for acute ischemia but may not be
available emergently and takes longer. PET is not used emergently. Lumbar puncture is not first-
line for acute focal deficits. This is a classic example of how case chronology directs imaging
choice.
Key words: acute stroke, non-contrast CT, hemorrhage detection, emergent imaging
6. A 28-year-old woman reports subacute diplopia and sensory changes evolving over
several days to weeks. Which diagnosis should be high on your differential based on this
history?
A. Acute embolic stroke
B. Demyelinating disease (e.g., multiple sclerosis)
C. Chronic neurodegenerative disorder (e.g., ALS)
D. Single large intracranial tumor with months of symptoms
Answer: B
Rationale: Young adult with subacute, multifocal neurologic symptoms evolving over days–
weeks is classic for inflammatory/demyelinating disorders such as MS. Vascular stroke is
typically abrupt and maximal at onset; degenerative disorders evolve over months–years. A
tumor would usually produce progressively worsening focal deficits over longer periods. The
history’s time course and multiplicity of symptoms help localize to a process that can involve
different CNS regions at separate times (dissemination in space and time).
Key words: subacute, demyelination, MS, young adult
7. Which clinical exam feature most reliably distinguishes a central (supranuclear) facial
palsy from a peripheral (facial nerve) palsy?
A. Presence of hyperacusis
B. Loss of forehead wrinkling on the affected side
C. Sparing of forehead movement (ability to raise eyebrows) with contralateral lower
face weakness
D. Taste loss from the anterior 2/3 of the tongue
Answer: C
Rationale: Central (supranuclear) facial weakness typically spares the forehead because upper
facial muscles receive bilateral cortical input; therefore forehead function is preserved while
contralateral lower face is weak. Peripheral facial nerve palsy involves the whole hemiface
including the forehead. Hyperacusis and taste disturbance are features of peripheral facial nerve
(CN VII) involvement but are not as reliable for separating central versus peripheral as forehead
sparing is. This exam distinction is a staple of localization taught via cases.
Key words: forehead sparing, central vs peripheral, facial palsy, CN VII
, 8. A patient has right homonymous hemianopia and right-sided hemiparesis from an
acute onset event. Which localization best explains both deficits?
A. Right occipital lobe lesion only
B. Left middle cerebral artery (MCA) territory lesion affecting optic radiations and motor
cortex
C. Optic chiasm lesion and contralateral motor cortex lesion
D. Right optic tract lesion and left thalamic stroke
Answer: B
Rationale: Right homonymous hemianopia means loss of the right visual fields of both eyes —
implying a lesion in the left visual pathway posterior to the chiasm (left optic
tract/radiation/occipital lobe). Right-sided hemiparesis means left motor pathway involvement. A
left MCA territory infarct can affect left motor cortex (producing right weakness) and adjacent
optic radiations (producing contralateral visual field loss). Option A (right occipital) would
produce left visual field loss and not explain right weakness. Understanding laterality and
pathways is essential in case analysis.
Key words: homonymous hemianopia, laterality, MCA territory, motor + visual
9. Which of the following is a classic false localizing sign that may mislead localization if
considered in isolation?
A. Ipsilateral pupillary dilation with severe oculomotor palsy from herniation
B. Papilledema indicating local optic nerve lesion
C. Isolated abducens (VI) palsy due to increased intracranial pressure producing lateral
rectus weakness
D. Focal weakness corresponding exactly to a cortical lesion on imaging
Answer: C
Rationale: The abducens nerve (VI) is particularly susceptible to stretch from raised
intracranial pressure and can show palsy even when the primary lesion is remote — a false
localizing sign. Papilledema indicates raised ICP rather than a primary optic nerve lesion.
Pupillary dilation from third nerve compression is more localizing for transtentorial
herniation/uncal compression. Focal weakness matching cortical lesion is a true localizing sign.
Recognizing false localizing signs prevents diagnostic error when integrating exam and imaging.
Key words: false localizing sign, abducens palsy, increased ICP, VI nerve
10. In a patient whose history documents subacute (days–weeks) worsening of focal
neurologic deficits accompanied by fever and elevated inflammatory markers, which
etiologies should be prioritized in the differential?
A. Acute embolic stroke only
B. Infectious or inflammatory central nervous system processes (e.g., encephalitis,
, abscess)
C. Idiopathic neurodegenerative disease (onset over years)
D. Purely functional (psychogenic) disorder
Answer: B
Rationale: Subacute progression with systemic or inflammatory signs suggests infectious or
inflammatory CNS disease (encephalitis, brain abscess, autoimmune encephalitis). Acute
embolic stroke typically has abrupt onset; degenerative diseases evolve slowly over months-to-
years. Functional disorders may present variably but are diagnoses of exclusion and do not
commonly present with objective fever/inflammation. History directs what diagnostic tests
(bloodwork, MRI with contrast, CSF) to prioritize.
Key words: subacute, fever, inflammation, encephalitis, abscess
11. On MRI, which feature most strongly suggests an extra-axial lesion such as a
meningioma rather than an intra-axial glial tumor?
A. Central necrosis with irregular margins
B. Lesion that crosses through the corpus callosum ("butterfly" glioma)
C. Broad dural base with a dural tail and displacement of brain parenchyma rather than
infiltration
D. Predominant involvement of white matter tracts with diffuse infiltration
Answer: C
Rationale: Extra-axial lesions (meningiomas) characteristically have a broad dural attachment
and may demonstrate a dural tail; they displace adjacent brain tissue rather than infiltrate it.
Gliomas, especially high-grade, often show central necrosis, irregular margins, and can cross
midline via corpus callosum. Recognizing radiologic patterns is essential in case-based teaching
to generate anatomy-based differential diagnoses before histology.
Key words: extra-axial, dural tail, meningioma, displacement vs infiltration
12. Which diagnostic strategy most effectively guards against premature closure (accepting
a diagnosis without sufficient evidence) when discussing clinical cases?
A. Anchoring to the first imaging report and not re-evaluating the exam
B. Generating a prioritized differential diagnosis from the history and clinical exam
before ordering confirmatory tests
C. Relying exclusively on the most probable diagnosis without alternatives
D. Avoiding systematic checklists to keep reasoning flexible
Answer: B
Rationale: Creating a prioritized differential based on history and exam before ordering tests
promotes hypothesis-driven testing and reduces premature closure. Anchoring to initial imaging
(A) increases bias; relying solely on a single most likely diagnosis (C) or avoiding systematic
approaches (D) can cause missed alternative diagnoses. The chapter emphasizes structured
, reasoning and disciplined sequencing (history → exam → imaging) to minimize cognitive errors.
Key words: premature closure, differential diagnosis, hypothesis-driven testing, cognitive bias
13. A patient presents with a thunderclap headache and neck stiffness. Non-contrast head CT
done 6 hours after onset is normal. What is the next best diagnostic step to evaluate
suspected subarachnoid hemorrhage (SAH)?
A. MRI brain with T2 FLAIR only
B. Lumbar puncture to look for xanthochromia / red blood cells in CSF
C. No further testing — normal CT excludes SAH
D. EEG for seizure activity
Answer: B
Rationale: Non-contrast CT is highly sensitive early for SAH, but sensitivity falls with time. If
CT is negative and clinical suspicion remains high (thunderclap headache, meningismus), a
lumbar puncture to detect xanthochromia or RBCs is indicated. MRI FLAIR can sometimes
detect SAH but is not the standard next step. EEG is irrelevant here. This question links clinical
chronology and test sensitivity — a chapter 1 theme.
Key words: thunderclap headache, SAH, lumbar puncture, xanthochromia
14. A case documents ascending symmetric weakness over several days after a
gastrointestinal infection, with areflexia on exam. Which element of the history-exam-
imaging triad most strongly points to Guillain-Barré syndrome (GBS)?
A. Presence of upper motor neuron signs (spasticity, Babinski)
B. Symmetric, progressive, ascending weakness with areflexia and recent infection
C. Unilateral cranial nerve palsy with localized cortical lesion on MRI
D. Chronic fluctuating weakness improving with steroids
Answer: B
Rationale: GBS is characterized by rapidly progressive, symmetric, ascending weakness with
decreased/absent reflexes often following infection. UMN signs would argue against GBS
(central process). A unilateral cranial nerve palsy with a focal MRI lesion suggests a structural
lesion. Chronic fluctuating steroid-responsive weakness might suggest inflammatory myopathy
or MS relapse, not classic GBS. Recognizing classic clinical patterns from history/exam
streamlines the diagnostic plan (electrodiagnostics, CSF testing).
Key words: ascending weakness, areflexia, GBS, postinfectious
15. Which exam feature most specifically localizes weakness to the neuromuscular
junction (e.g., myasthenia gravis) rather than to nerve or muscle fiber disease?
A. Elevated serum CK with proximal weakness
B. Fasciculations and muscle wasting
Chapter 1: Introduction to Clinical Case Presentations
Chapter 2: Neuroanatomy Overview and Basic Definitions
Chapter 3: The Neurologic Exam as a Lesson in Neuroanatomy
Chapter 4: Introduction to Clinical Neuroradiology
Chapter 5: Brain and Environs: Cranium, Ventricles, and Meninges
Chapter 6: Corticospinal Tract and Other Motor Pathways
Chapter 7: Somatosensory Pathways
Chapter 8: Spinal Nerve Roots
Chapter 9: Major Plexuses and Peripheral Nerves
Chapter 10: Cerebral Hemispheres and Vascular Supply
Chapter 11: Visual System
Chapter 12: Brainstem I: Surface Anatomy and Cranial Nerves
Chapter 13: Brainstem II: Eye Movements and Pupillary Control
Chapter 14: Brainstem III: Internal Structures and Vascular Supply
Chapter 15: Cerebellum
Chapter 16: Basal Ganglia
Chapter 17: Pituitary and Hypothalamus
Chapter 18: Limbic System: Homeostasis, Olfaction, Memory and Emotion
Chapter 19: Higher-Order Cerebral Function
,Chapter 1: Introduction to Clinical Case
Presentations
Chapter 1: Introduction to Clinical Case Presentations (Blumenfeld).
Each question is aligned to the chapter theme . Every question has 4 choices (A–D), the answer
shown only as Answer: X, a deep rationale for the correct answer (including why the other
choices are incorrect), and a short list of Key words.
1. Which of the following best captures the primary pedagogical advantage of using real
patient cases to teach neuroanatomy?
A. They let students memorize anatomical names faster.
B. They emphasize rare, exotic disorders that students rarely see.
C. They integrate anatomical knowledge with clinical reasoning, exam findings and
imaging interpretation.
D. They replace the need to learn foundational anatomy.
Answer: C
Rationale: Real patient cases force learners to apply anatomical knowledge to problems
encountered in practice: mapping symptoms to structures, interpreting exam findings, and
choosing/reading imaging. This builds diagnostic reasoning and pattern recognition rather than
rote memorization. (A) is reductive — cases improve application, not just rote recall. (B) is false
— cases emphasize common patterns and diagnostic thinking, not just rare diseases. (D) is
incorrect: cases complement, not replace, foundational anatomy.
Key words: case-based learning, clinical reasoning, applied anatomy, imaging integration
2. According to the case format Blumenfeld emphasizes, what is the optimal sequence for
presenting information to maximize localization and diagnostic reasoning?
A. Physical exam → History → Diagnosis → Imaging
B. History → Physical exam → Imaging → Diagnosis
C. Imaging → History → Physical exam → Diagnosis
D. Diagnosis → History → Physical exam → Imaging
Answer: B
Rationale: The clinical workflow and reasoning proceed from history (timing, onset, associated
features) to targeted physical exam that tests hypotheses from the history, then to imaging
selected to answer unresolved questions, culminating in a diagnosis that integrates all
information. Presenting history first avoids anchoring to imaging and enables proper hypothesis
generation. Other orders (A, C, D) disrupt the hypothesis-driven approach and can encourage
premature closure.
Key words: history first, hypothesis-driven exam, imaging selection, diagnostic integration
, 3. A 62-year-old man is described as having “maximal neurologic deficit at onset” (sudden
hemiparesis). Which aspect of the history most strongly supports a vascular (ischemic or
hemorrhagic) cause rather than tumor or infection?
A. Gradual worsening over months
B. Episodic fluctuating deficits over weeks
C. Immediate maximal deficit at onset without prodrome
D. Low-grade fever and night sweats for weeks
Answer: C
Rationale: Sudden, maximal deficit at onset is classic for vascular events (ischemic stroke or
intracerebral hemorrhage). Tumors and chronic infections more commonly produce progressive
symptoms over weeks–months; inflammatory processes may fluctuate but often have different
patterns. Fever and constitutional symptoms point toward infection or systemic disease, not
primary vascular stroke. Recognizing time course in the history narrows the initial differential
and directs urgent imaging (non-contrast CT for hemorrhage).
Key words: sudden onset, vascular, stroke, time course
4. On neurologic exam you find spasticity, hyperreflexia, and an extensor plantar response
(Babinski). These findings best localize to which system?
A. Lower motor neurons (anterior horn cell/peripheral nerve)
B. Neuromuscular junction
C. Upper motor neurons / corticospinal tract
D. Primary muscle (myopathy)
Answer: C
Rationale: Spasticity, increased deep tendon reflexes and Babinski indicate an upper motor
neuron lesion affecting corticospinal pathways. Lower motor neuron lesions produce flaccidity,
decreased reflexes, atrophy and possibly fasciculations. Neuromuscular junction disorders and
myopathies produce weakness but not true hyperreflexia with Babinski. In case-based learning,
these exam features are critical to discriminate central vs peripheral processes and guide
localization to brain, brainstem or spinal cord motor pathways.
Key words: UMN signs, corticospinal, spasticity, Babinski
5. A patient arrives 90 minutes after sudden focal weakness. Which initial imaging choice
best balances speed and the key diagnostic question of hemorrhage vs ischemia?
A. Non-contrast head CT (fast, detects acute blood)
B. Routine MRI T2 (better soft tissue contrast)
C. PET scan (metabolic information)
D. Lumbar puncture (diagnostic for stroke)
Answer: A
, Rationale: In the hyperacute setting, non-contrast head CT is the fastest and most sensitive test
to detect acute intracranial hemorrhage — a crucial first question since hemorrhage alters acute
management. MRI (including DWI) is more sensitive for acute ischemia but may not be
available emergently and takes longer. PET is not used emergently. Lumbar puncture is not first-
line for acute focal deficits. This is a classic example of how case chronology directs imaging
choice.
Key words: acute stroke, non-contrast CT, hemorrhage detection, emergent imaging
6. A 28-year-old woman reports subacute diplopia and sensory changes evolving over
several days to weeks. Which diagnosis should be high on your differential based on this
history?
A. Acute embolic stroke
B. Demyelinating disease (e.g., multiple sclerosis)
C. Chronic neurodegenerative disorder (e.g., ALS)
D. Single large intracranial tumor with months of symptoms
Answer: B
Rationale: Young adult with subacute, multifocal neurologic symptoms evolving over days–
weeks is classic for inflammatory/demyelinating disorders such as MS. Vascular stroke is
typically abrupt and maximal at onset; degenerative disorders evolve over months–years. A
tumor would usually produce progressively worsening focal deficits over longer periods. The
history’s time course and multiplicity of symptoms help localize to a process that can involve
different CNS regions at separate times (dissemination in space and time).
Key words: subacute, demyelination, MS, young adult
7. Which clinical exam feature most reliably distinguishes a central (supranuclear) facial
palsy from a peripheral (facial nerve) palsy?
A. Presence of hyperacusis
B. Loss of forehead wrinkling on the affected side
C. Sparing of forehead movement (ability to raise eyebrows) with contralateral lower
face weakness
D. Taste loss from the anterior 2/3 of the tongue
Answer: C
Rationale: Central (supranuclear) facial weakness typically spares the forehead because upper
facial muscles receive bilateral cortical input; therefore forehead function is preserved while
contralateral lower face is weak. Peripheral facial nerve palsy involves the whole hemiface
including the forehead. Hyperacusis and taste disturbance are features of peripheral facial nerve
(CN VII) involvement but are not as reliable for separating central versus peripheral as forehead
sparing is. This exam distinction is a staple of localization taught via cases.
Key words: forehead sparing, central vs peripheral, facial palsy, CN VII
, 8. A patient has right homonymous hemianopia and right-sided hemiparesis from an
acute onset event. Which localization best explains both deficits?
A. Right occipital lobe lesion only
B. Left middle cerebral artery (MCA) territory lesion affecting optic radiations and motor
cortex
C. Optic chiasm lesion and contralateral motor cortex lesion
D. Right optic tract lesion and left thalamic stroke
Answer: B
Rationale: Right homonymous hemianopia means loss of the right visual fields of both eyes —
implying a lesion in the left visual pathway posterior to the chiasm (left optic
tract/radiation/occipital lobe). Right-sided hemiparesis means left motor pathway involvement. A
left MCA territory infarct can affect left motor cortex (producing right weakness) and adjacent
optic radiations (producing contralateral visual field loss). Option A (right occipital) would
produce left visual field loss and not explain right weakness. Understanding laterality and
pathways is essential in case analysis.
Key words: homonymous hemianopia, laterality, MCA territory, motor + visual
9. Which of the following is a classic false localizing sign that may mislead localization if
considered in isolation?
A. Ipsilateral pupillary dilation with severe oculomotor palsy from herniation
B. Papilledema indicating local optic nerve lesion
C. Isolated abducens (VI) palsy due to increased intracranial pressure producing lateral
rectus weakness
D. Focal weakness corresponding exactly to a cortical lesion on imaging
Answer: C
Rationale: The abducens nerve (VI) is particularly susceptible to stretch from raised
intracranial pressure and can show palsy even when the primary lesion is remote — a false
localizing sign. Papilledema indicates raised ICP rather than a primary optic nerve lesion.
Pupillary dilation from third nerve compression is more localizing for transtentorial
herniation/uncal compression. Focal weakness matching cortical lesion is a true localizing sign.
Recognizing false localizing signs prevents diagnostic error when integrating exam and imaging.
Key words: false localizing sign, abducens palsy, increased ICP, VI nerve
10. In a patient whose history documents subacute (days–weeks) worsening of focal
neurologic deficits accompanied by fever and elevated inflammatory markers, which
etiologies should be prioritized in the differential?
A. Acute embolic stroke only
B. Infectious or inflammatory central nervous system processes (e.g., encephalitis,
, abscess)
C. Idiopathic neurodegenerative disease (onset over years)
D. Purely functional (psychogenic) disorder
Answer: B
Rationale: Subacute progression with systemic or inflammatory signs suggests infectious or
inflammatory CNS disease (encephalitis, brain abscess, autoimmune encephalitis). Acute
embolic stroke typically has abrupt onset; degenerative diseases evolve slowly over months-to-
years. Functional disorders may present variably but are diagnoses of exclusion and do not
commonly present with objective fever/inflammation. History directs what diagnostic tests
(bloodwork, MRI with contrast, CSF) to prioritize.
Key words: subacute, fever, inflammation, encephalitis, abscess
11. On MRI, which feature most strongly suggests an extra-axial lesion such as a
meningioma rather than an intra-axial glial tumor?
A. Central necrosis with irregular margins
B. Lesion that crosses through the corpus callosum ("butterfly" glioma)
C. Broad dural base with a dural tail and displacement of brain parenchyma rather than
infiltration
D. Predominant involvement of white matter tracts with diffuse infiltration
Answer: C
Rationale: Extra-axial lesions (meningiomas) characteristically have a broad dural attachment
and may demonstrate a dural tail; they displace adjacent brain tissue rather than infiltrate it.
Gliomas, especially high-grade, often show central necrosis, irregular margins, and can cross
midline via corpus callosum. Recognizing radiologic patterns is essential in case-based teaching
to generate anatomy-based differential diagnoses before histology.
Key words: extra-axial, dural tail, meningioma, displacement vs infiltration
12. Which diagnostic strategy most effectively guards against premature closure (accepting
a diagnosis without sufficient evidence) when discussing clinical cases?
A. Anchoring to the first imaging report and not re-evaluating the exam
B. Generating a prioritized differential diagnosis from the history and clinical exam
before ordering confirmatory tests
C. Relying exclusively on the most probable diagnosis without alternatives
D. Avoiding systematic checklists to keep reasoning flexible
Answer: B
Rationale: Creating a prioritized differential based on history and exam before ordering tests
promotes hypothesis-driven testing and reduces premature closure. Anchoring to initial imaging
(A) increases bias; relying solely on a single most likely diagnosis (C) or avoiding systematic
approaches (D) can cause missed alternative diagnoses. The chapter emphasizes structured
, reasoning and disciplined sequencing (history → exam → imaging) to minimize cognitive errors.
Key words: premature closure, differential diagnosis, hypothesis-driven testing, cognitive bias
13. A patient presents with a thunderclap headache and neck stiffness. Non-contrast head CT
done 6 hours after onset is normal. What is the next best diagnostic step to evaluate
suspected subarachnoid hemorrhage (SAH)?
A. MRI brain with T2 FLAIR only
B. Lumbar puncture to look for xanthochromia / red blood cells in CSF
C. No further testing — normal CT excludes SAH
D. EEG for seizure activity
Answer: B
Rationale: Non-contrast CT is highly sensitive early for SAH, but sensitivity falls with time. If
CT is negative and clinical suspicion remains high (thunderclap headache, meningismus), a
lumbar puncture to detect xanthochromia or RBCs is indicated. MRI FLAIR can sometimes
detect SAH but is not the standard next step. EEG is irrelevant here. This question links clinical
chronology and test sensitivity — a chapter 1 theme.
Key words: thunderclap headache, SAH, lumbar puncture, xanthochromia
14. A case documents ascending symmetric weakness over several days after a
gastrointestinal infection, with areflexia on exam. Which element of the history-exam-
imaging triad most strongly points to Guillain-Barré syndrome (GBS)?
A. Presence of upper motor neuron signs (spasticity, Babinski)
B. Symmetric, progressive, ascending weakness with areflexia and recent infection
C. Unilateral cranial nerve palsy with localized cortical lesion on MRI
D. Chronic fluctuating weakness improving with steroids
Answer: B
Rationale: GBS is characterized by rapidly progressive, symmetric, ascending weakness with
decreased/absent reflexes often following infection. UMN signs would argue against GBS
(central process). A unilateral cranial nerve palsy with a focal MRI lesion suggests a structural
lesion. Chronic fluctuating steroid-responsive weakness might suggest inflammatory myopathy
or MS relapse, not classic GBS. Recognizing classic clinical patterns from history/exam
streamlines the diagnostic plan (electrodiagnostics, CSF testing).
Key words: ascending weakness, areflexia, GBS, postinfectious
15. Which exam feature most specifically localizes weakness to the neuromuscular
junction (e.g., myasthenia gravis) rather than to nerve or muscle fiber disease?
A. Elevated serum CK with proximal weakness
B. Fasciculations and muscle wasting
