Wgu D574 Hlth 4360 Neuropsychology Bs Psychology Study
Guide Original Practice Questions And Answer With
Rationales| Instant Download
This exam assesses advanced understanding of nervous-system organization and the mapping of structure to
function, including cortical and subcortical systems, dissociation logic, vascular/connectional anatomy, and the
inferential limits of lesion-based localization. Items require synthesis across anatomy, physiology, and clinical
reasoning rather than surface recall. It contains 97 multiple-choice questions, each with four distractors and a
fully worked rationale that explains why the keyed answer is correct. Content is organized into 12 focused
sections: Neuroanatomy and Functional Localization, Neurons, Neurotransmission, and Neurophysiology,
Neuropsychological Assessment and Test Interpretation, Brain-Behavior Relationships and Cognitive Domains,
Neuroimaging and Diagnostic Methods, Neurodevelopmental and Pediatric Neuropsychology, Neurological
Disorders and Neuropsychiatric Conditions, Traumatic Brain Injury and Rehabilitation, Dementia, Aging, and
Neurodegenerative Disease, Psychopharmacology and Neuropsychological Interventions, Research Methods and
Evidence-Based Practice in Neuropsychology, Ethics, Cultural Competence, and Professional Issues. Targeted
learning outcomes include: Differentiate cortical and subcortical functional systems using dissociation and
double-dissociation logic; Apply vascular and connectional anatomy to predict structure-function consequences of
lesions; Critically evaluate lesion-based and neuroimaging evidence for functional localization claims. Every item
has been reviewed for clinical accuracy, current guidelines, and clarity so that students can study with confidence
Section 1: Neuroanatomy and Functional Localization (Questions 1-8)
1 A lesion produces impaired reading with preserved writing. Which inference
is strongest?
A) Reading and writing share one localized store, so the lesion is nonspecific.
B) The finding supports a double dissociation only if the reverse pattern is
also observed.
C) Reading is localized to the right hemisphere; writing to the left.
D) The lesion proves reading and writing are functionally independent
modules.
Answer: B
Rationale: A single dissociation (impaired reading, spared writing) is
compatible with shared or partially overlapping substrates and cannot establish
modular independence. Double dissociation-reverse pattern in another case-is
required to argue separate systems. Options A, C, and D overstate what one
case can show or assert unsupported lateralization.
2 Which vascular event best explains a fluent aphasia with preserved
repetition?
A) Superior division of left MCA, sparing arcuate fasciculus and Wernicke's
area.
,B) Left PCA infarct involving medial occipital cortex.
C) Inferior division of left MCA sparing Wernicke's area and arcuate
fasciculus.
D) Anterior communicating artery aneurysm rupture.
Answer: C
Rationale: Transcortical sensory aphasia (fluent, poor comprehension,
preserved repetition) reflects damage sparing Wernicke's area and the arcuate
fasciculus, often inferior-division MCA. Option A yields Broca-type nonfluent
output; B produces a visual-field defect; D typically causes frontal/executive or
memory findings, not this aphasia profile.
3 Which structure's damage most selectively impairs consolidation of new
declarative memories?
A) Mammillary bodies
B) Bilateral hippocampal formation
C) Basolateral amygdala
D) Dorsomedial thalamus
Answer: B
Rationale: Bilateral hippocampal damage produces profound anterograde
declarative amnesia with relatively preserved remote memory and procedural
learning. Mammillary body and dorsomedial thalamic lesions contribute to
diencephalic amnesia (often with additional deficits), and amygdala lesions
impair emotional modulation rather than consolidation itself.
4 Which pattern best localizes a lesion causing left hemispatial neglect with
right-hemisphere findings?
A) Right inferior parietal lobule and temporoparietal junction
B) Left dorsolateral prefrontal cortex
C) Bilateral medial temporal lobes
D) Right occipital pole
Answer: A
Rationale: Left neglect most commonly follows right inferior
parietal/temporoparietal lesions, reflecting right-hemisphere dominance for
spatial attention. Prefrontal lesions produce executive deficits, medial temporal
lesions produce amnesia, and occipital pole lesions produce field defects
without the attentional asymmetry of neglect.
,5 Which thalamic nucleus relays cerebellar and basal ganglia output to motor
cortex?
A) Pulvinar
B) Anterior nucleus
C) Ventral lateral (VL) nucleus
D) Lateral geniculate nucleus
Answer: C
Rationale: The VL nucleus receives dentatothalamic and pallidal projections
and relays to primary motor cortex, so its damage produces motor dysfunction.
Pulvinar and anterior nucleus serve attentional and limbic circuits, and the
LGN relays vision, not motor output.
6 Which finding best distinguishes frontal from posterior cortical dysfunction
on testing?
A) Impaired confrontation naming with circumlocution
B) Preserved repetition with impaired comprehension
C) Intact recall with poor strategy use and perseveration
D) Left homonymous hemianopia
Answer: C
Rationale: Frontal-executive dysfunction characteristically shows disorganized
encoding, poor strategy, and perseveration despite adequate storage, whereas
posterior lesions impair naming (temporal), repetition/comprehension
(perisylvian), or produce field cuts (occipital). Option C captures the executive
signature that separates frontal from posterior patterns.
7 A split-brain patient cannot name an object in the left visual field. Why?
A) Left visual field projects to right hemisphere, which lacks expressive
language.
B) Left visual field projects to left hemisphere, which is disconnected.
C) Callosal sparing permits interhemispheric transfer.
D) Right hemisphere dominates naming in most individuals.
Answer: A
Rationale: The left visual field is represented in the right hemisphere; with
callosal section, that information cannot reach left-hemisphere language areas
for naming. Option B reverses the projection, C contradicts the disconnection,
and D is false for most people.
, 8 Which best explains why lesion studies can overestimate localization
specificity?
A) Lesions always spare white matter tracts.
B) Lesions disrupt fibers of passage and connected regions, producing remote
effects.
C) Functional imaging cannot detect lesions.
D) Compensatory plasticity is never observed after focal injury.
Answer: B
Rationale: Focal lesions interrupt passing axons and deafferent connected
nodes, so deficits reflect network disruption, not only the lesioned site-an
argument for hodotopic or network-based localization. Options A, C, and D are
factually false and misstate imaging and plasticity evidence.
Section 2: Neurons, Neurotransmission, and Neurophysiology (Questions 9-17)
9 A drug blocks voltage-gated Na+ channels at nodes of Ranvier. What is the
most direct effect on axonal conduction?
A) Increased conduction velocity due to enhanced saltatory conduction
B) Failure of action potential regeneration and conduction block
C) Prolonged depolarization without affecting threshold
D) Selective loss of myelin integrity
Answer: B
Rationale: Voltage-gated Na+ channels at nodes of Ranvier are essential for
regenerating the action potential during saltatory conduction; blockade
prevents depolarization and halts propagation. Enhanced conduction (A) is
opposite; prolonged depolarization (C) would occur with persistent channel
opening, not block; myelin integrity (D) is unaffected by Na+ channel
blockade.
10 In a neuron with high intracellular Cl and low extracellular Cl, opening
GABA-A channels typically causes what?
A) Depolarization due to Cl efflux
B) Hyperpolarization due to Cl influx
C) No change because Cl is at equilibrium
D) Excitatory postsynaptic potential from K+ efflux
Answer: B
Guide Original Practice Questions And Answer With
Rationales| Instant Download
This exam assesses advanced understanding of nervous-system organization and the mapping of structure to
function, including cortical and subcortical systems, dissociation logic, vascular/connectional anatomy, and the
inferential limits of lesion-based localization. Items require synthesis across anatomy, physiology, and clinical
reasoning rather than surface recall. It contains 97 multiple-choice questions, each with four distractors and a
fully worked rationale that explains why the keyed answer is correct. Content is organized into 12 focused
sections: Neuroanatomy and Functional Localization, Neurons, Neurotransmission, and Neurophysiology,
Neuropsychological Assessment and Test Interpretation, Brain-Behavior Relationships and Cognitive Domains,
Neuroimaging and Diagnostic Methods, Neurodevelopmental and Pediatric Neuropsychology, Neurological
Disorders and Neuropsychiatric Conditions, Traumatic Brain Injury and Rehabilitation, Dementia, Aging, and
Neurodegenerative Disease, Psychopharmacology and Neuropsychological Interventions, Research Methods and
Evidence-Based Practice in Neuropsychology, Ethics, Cultural Competence, and Professional Issues. Targeted
learning outcomes include: Differentiate cortical and subcortical functional systems using dissociation and
double-dissociation logic; Apply vascular and connectional anatomy to predict structure-function consequences of
lesions; Critically evaluate lesion-based and neuroimaging evidence for functional localization claims. Every item
has been reviewed for clinical accuracy, current guidelines, and clarity so that students can study with confidence
Section 1: Neuroanatomy and Functional Localization (Questions 1-8)
1 A lesion produces impaired reading with preserved writing. Which inference
is strongest?
A) Reading and writing share one localized store, so the lesion is nonspecific.
B) The finding supports a double dissociation only if the reverse pattern is
also observed.
C) Reading is localized to the right hemisphere; writing to the left.
D) The lesion proves reading and writing are functionally independent
modules.
Answer: B
Rationale: A single dissociation (impaired reading, spared writing) is
compatible with shared or partially overlapping substrates and cannot establish
modular independence. Double dissociation-reverse pattern in another case-is
required to argue separate systems. Options A, C, and D overstate what one
case can show or assert unsupported lateralization.
2 Which vascular event best explains a fluent aphasia with preserved
repetition?
A) Superior division of left MCA, sparing arcuate fasciculus and Wernicke's
area.
,B) Left PCA infarct involving medial occipital cortex.
C) Inferior division of left MCA sparing Wernicke's area and arcuate
fasciculus.
D) Anterior communicating artery aneurysm rupture.
Answer: C
Rationale: Transcortical sensory aphasia (fluent, poor comprehension,
preserved repetition) reflects damage sparing Wernicke's area and the arcuate
fasciculus, often inferior-division MCA. Option A yields Broca-type nonfluent
output; B produces a visual-field defect; D typically causes frontal/executive or
memory findings, not this aphasia profile.
3 Which structure's damage most selectively impairs consolidation of new
declarative memories?
A) Mammillary bodies
B) Bilateral hippocampal formation
C) Basolateral amygdala
D) Dorsomedial thalamus
Answer: B
Rationale: Bilateral hippocampal damage produces profound anterograde
declarative amnesia with relatively preserved remote memory and procedural
learning. Mammillary body and dorsomedial thalamic lesions contribute to
diencephalic amnesia (often with additional deficits), and amygdala lesions
impair emotional modulation rather than consolidation itself.
4 Which pattern best localizes a lesion causing left hemispatial neglect with
right-hemisphere findings?
A) Right inferior parietal lobule and temporoparietal junction
B) Left dorsolateral prefrontal cortex
C) Bilateral medial temporal lobes
D) Right occipital pole
Answer: A
Rationale: Left neglect most commonly follows right inferior
parietal/temporoparietal lesions, reflecting right-hemisphere dominance for
spatial attention. Prefrontal lesions produce executive deficits, medial temporal
lesions produce amnesia, and occipital pole lesions produce field defects
without the attentional asymmetry of neglect.
,5 Which thalamic nucleus relays cerebellar and basal ganglia output to motor
cortex?
A) Pulvinar
B) Anterior nucleus
C) Ventral lateral (VL) nucleus
D) Lateral geniculate nucleus
Answer: C
Rationale: The VL nucleus receives dentatothalamic and pallidal projections
and relays to primary motor cortex, so its damage produces motor dysfunction.
Pulvinar and anterior nucleus serve attentional and limbic circuits, and the
LGN relays vision, not motor output.
6 Which finding best distinguishes frontal from posterior cortical dysfunction
on testing?
A) Impaired confrontation naming with circumlocution
B) Preserved repetition with impaired comprehension
C) Intact recall with poor strategy use and perseveration
D) Left homonymous hemianopia
Answer: C
Rationale: Frontal-executive dysfunction characteristically shows disorganized
encoding, poor strategy, and perseveration despite adequate storage, whereas
posterior lesions impair naming (temporal), repetition/comprehension
(perisylvian), or produce field cuts (occipital). Option C captures the executive
signature that separates frontal from posterior patterns.
7 A split-brain patient cannot name an object in the left visual field. Why?
A) Left visual field projects to right hemisphere, which lacks expressive
language.
B) Left visual field projects to left hemisphere, which is disconnected.
C) Callosal sparing permits interhemispheric transfer.
D) Right hemisphere dominates naming in most individuals.
Answer: A
Rationale: The left visual field is represented in the right hemisphere; with
callosal section, that information cannot reach left-hemisphere language areas
for naming. Option B reverses the projection, C contradicts the disconnection,
and D is false for most people.
, 8 Which best explains why lesion studies can overestimate localization
specificity?
A) Lesions always spare white matter tracts.
B) Lesions disrupt fibers of passage and connected regions, producing remote
effects.
C) Functional imaging cannot detect lesions.
D) Compensatory plasticity is never observed after focal injury.
Answer: B
Rationale: Focal lesions interrupt passing axons and deafferent connected
nodes, so deficits reflect network disruption, not only the lesioned site-an
argument for hodotopic or network-based localization. Options A, C, and D are
factually false and misstate imaging and plasticity evidence.
Section 2: Neurons, Neurotransmission, and Neurophysiology (Questions 9-17)
9 A drug blocks voltage-gated Na+ channels at nodes of Ranvier. What is the
most direct effect on axonal conduction?
A) Increased conduction velocity due to enhanced saltatory conduction
B) Failure of action potential regeneration and conduction block
C) Prolonged depolarization without affecting threshold
D) Selective loss of myelin integrity
Answer: B
Rationale: Voltage-gated Na+ channels at nodes of Ranvier are essential for
regenerating the action potential during saltatory conduction; blockade
prevents depolarization and halts propagation. Enhanced conduction (A) is
opposite; prolonged depolarization (C) would occur with persistent channel
opening, not block; myelin integrity (D) is unaffected by Na+ channel
blockade.
10 In a neuron with high intracellular Cl and low extracellular Cl, opening
GABA-A channels typically causes what?
A) Depolarization due to Cl efflux
B) Hyperpolarization due to Cl influx
C) No change because Cl is at equilibrium
D) Excitatory postsynaptic potential from K+ efflux
Answer: B
