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Medical Neuroscience

Week 13

Comprehensive Final Exam, part 1 (2 cases, 13 questions)

Quiz: Comprehensive Final Exam, part 1 (2 cases, 13 questions)

13 questions
Quiz: Comprehensive Final Exam, part 2 (2 cases, 7 questions)
7 questions
Quiz: Comprehensive Final Exam, part 3 (2 cases, 11 questions)
11 questions

Quiz: Comprehensive Final Exam, part 4 (2 cases, 12 questions)

12 questions

Comprehensive Final Exam, part 1 (2 cases, 13 questions)

Quiz30 minutes • 30 min
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Due October 18, 8:59 AM CESTOct 18, 8:59 AM CEST
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Comprehensive Final Exam, part 1 (2 cases, 13 questions)

Graded Quiz • 30 min

DueOct 18, 8:59 AM CEST
Comprehensive Final Exam, part 1 (2 cases, 13 questions)
Total points 13
1.
Question 1

Use the following case to answer question 1-7

Case 1

A 45-year-old woman was brought to the emergency room because of right face and arm
weakness and inability to speak. The patient had a past history of alcohol use,
cigarette smoking, and uncontrolled hypertension. On the morning of admission, she
staggered into her kitchen where her husband was eating breakfast; she was grunting
incoherently and grimacing in pain. Her foot caught on the leg of a chair; she
tripped and fell to the floor. Her husband called for emergency medical services
(ambulance) and she was transported to the emergency department of the closest
hospital. Upon examination, the following was noted:

Mental Status: She was alert, but only grunted producing no words. She
followed no commands except to close her eyes or and open her mouth, but she could
mimic gestures to raise her arms or legs.

Cranial nerves: Her pupils were 3 mm, constricting to 2 mm bilaterally when

the pupillary light reflex was tested. She had preserved blink to threat
bilaterally, meaning that when startled by rapid, close-range visual approach, she
blinked bilaterally in a normal fashion. Her extraocular movements were intact.
She did display a decreased, right nasolabial fold at rest (weakness in right lower
face), and she showed decreased movements of her right lower face; however, her
upper face was spared.

Motor: She showed no spontaneous or voluntary right arm movement, except for
flexion-withdrawal from a painful stimulus. She was able to raise her right leg
off the bed, but not with normal force against resistance. She did show good,
purposeful movements of her left arm and leg against resistance.

Somatic sensory: She grimaced in response to pinch in all extremities, but she
showed reduced mechanosensation (light touch and proprioception) over her right
face and right arm with sparing of the lower right leg. Similarly, she could not
accurately localize the sharp point of contact on her right face and right arm when
tested with the point of a pin, but localizations were normal elsewhere.

Over the next few days of in-patient care, the patient’s communication problems
evolved into a more focused problem making speech. By 6 days after admission, she
was only able to utter a few barely articulate words. She could not repeat words
spoken to her, but she could follow many simple commands and answer yes/no
questions appropriately.

What is the most likely pathological process that explains the development of this
patient’s symptoms?
1 point

multiple sclerosis

encephalitis

CNS neoplasm (tumor)

meningitis

Parkinson’s disease

Huntington’s chorea

hemorrhagic stroke
2.
Question 2

On the basis of the symptoms and signs described above, at what level of the
nervous system is this injury?
1 point

thalamus

cerebellum

spinal cord

medulla oblongata

basal ganglia

pons
midbrain

cerebral cortex
3.
Question 3

Which of the following statements below provides the BEST rationale for where you
think the stroke is localized?
1 point

The injury is likely to be in the midbrain because the pupils constricted rather
than dilated when the pupillary light reflex was tested.

The injury is most likely diffuse, being consistent with a widespread encephalitis
or meningitis, since widespread body parts are affected.

The injury is most likely in the left posterior limb of the internal capsule
because that’s where the corticobulbar, corticospinal, and somatic sensory
radiation come together in a small space.

The injury is likely to be in the left thalamus because that is the one location
where sensory and motor systems that govern the face, arm and leg are in close
proximity to one another.

The injury is likely to be in the pons because damage to the facial motor nucleus
and nerve are associated with lower facial weakness with sparing of the upper face.

The injury is likely to be in the medulla oblongata because the difficulty speaking
is most likely explained by damage to the lower motor neurons in the medulla that
govern the larynx and pharynx.

The injury is likely to be in the left cerebral cortex because the patient
has language production problems with somatic sensory and motor signs in the lower
right face and right arm.
4.
Question 4

What is the BEST characterization of this patient’s persistent communication

difficulties?
1 point

dysarthria (poorly articulated speech, resulting from interference in the control

of speech muscles)

upper motor neuron syndrome

dementia

lower motor neuron syndrome

Broca’s aphasia

left-sided deafness

Wernicke’s aphasia

global aphasia
5.
Question 5
What blood vessel was most likely involved in this case?
1 point

left anterior inferior cerebellar artery

left anterior choroidal artery

right anterior cerebral artery

left posterior cerebral artery

anterior spinal artery

basilar artery

right middle cerebral artery

right anterior choroidal artery

right posterior cerebral artery

left middle cerebral artery

left anterior cerebral artery

right posterior inferior cerebellar artery

6.
Question 6

With a focal stroke affecting gray matter, the core region of affected brain tissue
typically becomes necrotic. Such an area of necrotic tissue would be expected to
repair by which process?
1 point

By removal of the necrotic tissue by microglia and replacement of the volume of

gray matter with a dense plexus of axons and synaptic connections.

This area will remain acutely necrotic since it cannot be repaired.

By removal of the necrotic tissue by microglia and replacement of the volume of

gray matter with fibroblasts and collagen.

By removal of the necrotic tissue by microglia and partial replacement with

fibrillary astroglial scarring, and the rest of the volume becoming a cavity filled
with cerebrospinal fluid.

By removal of the necrotic tissue by microglia and repopulation of the volume of

gray matter with new neurons.
7.
Question 7

With focal stroke, the tissue surrounding the core region of infarction is referred
to as the “ischemic penumbra”, because it is a ‘shadowy’ region (penumbra means the
margins of shadow) that is deprived of adequate blood supply and subject to ongoing
excitotoxic injury. What is the best explanation of excitotoxicity in the adult
brain?
1 point
Excessive release of GABA that binds to GABA-A receptors, causing neurons to
atrophy and die by non-use.

Excessive release of neurotrophins that binds to p75 receptors, disrupting cellular

processes that are necessary for neuronal survival.

Activation of glia cells which release soluble factors that block neurotrophin
receptors.

Excessive release of neurotrophins that binds to Trk (tyrosine kinase) receptors,

disrupting cellular processes that are necessary for neuronal survival.

Excessive production of melatonin by the pineal gland, which produces chronic

insomnia.

Excessive release of glutamate that binds to AMPA and NMDA receptors,

exciting post synaptic neurons to death.

Excessive release of GABA that binds to GABA-A receptors, exciting post synaptic
neurons to death.
8.
Question 8

Use the following case to answer questions 8-13

Case 2

A 71-year-old woman was referred to your clinic because of difficulty walking. In

the course of interviewing this woman, you discover a 10-month history of
progressive gait difficulty, right leg numbness, and urinary problems. The patient
was in good health, walking 3 to 4 miles per day until about 10 months
ago, when she first noticed mild gait unsteadiness and bilateral leg stiffness.
She felt her feet were not fully under her control. Her left leg gradually
became weaker than her right, with occasional left leg buckling when she walked.

Meanwhile, her right leg developed progressive numbness to sharp pricks and
tingling sensations, and she had intermittent left-sided thoracic back pain.
More recently, she had increasing urinary frequency, with occasional incontinence,
and difficulty completing a bowel movement despite laxatives.
Upon physical examination, you note the following:

Rectal: normal tone; however, patient could not voluntarily contract anal
sphincter.

Cranial nerves: all sensory and motor functions were normal.

Motor: upper extremities—normal bulk and tone, with normal strength

throughout; lower extremities—normal bulk, with tone increased in left leg and
moderate impairments of strength throughout.

Coordination: normal throughout, except for some ataxia of left lower

extremity with heel-to-shin testing (left heel running up and down against right
shin).

Gait: stiff-legged and unsteady.

Somatic sensory: pinprick sensation was decreased on the right side below the
umbilicus; light touch, vibration and joint position sense were decreased in
the left foot and leg.
All sensory and motor functions appear to be intact in the arms and in the face.

What is the most likely pathological process that explains this patient’s symptoms?
1 point

Huntington’s chorea

encephalitis

multiple sclerosis

Parkinson’s disease

Alzheimer’s disease

meningitis

CNS neoplasm (tumor)

9.
Question 9

The stiffness of her left leg while walking, the increase in the tone of its
muscles, and the decrease in its strength are all signs and symptoms of injury to
which tract?
1 point

right spinocerebellar tract

(bilateral) lateral vestibulospinal tracts

left gracile tract

left lumbosacral spinal nerves

right gracile tract

right lateral corticospinal tract

right lumbosacral spinal nerves

spinothalamic tract axons in the left anterolateral white matter of the spinal cord

left spinocerebellar tract

left lateral corticospinal tract

spinothalamic tract axons in the right anterolateral white matter of the spinal
cord
10.
Question 10

Given the findings of the physical examination, which of the following tracts is
spared?
1 point

spinothalamic tract axons in the right anterolateral white matter of the spinal
cord

left lateral corticospinal tract

right cuneate tract

right gracile tract

left gracile tract

left cuneate tract

descending axons that control output from sacral somatic motor neurons to striated
sphincter muscles in the pelvic floor

right lateral corticospinal tract

spinothalamic tract axons in the left anterolateral white matter of the spinal cord
11.
Question 11

At what level do you think the lesion is in this patient?

1 point

NO sacral spinal cord

thalamus

NO medulla oblongata

midbrain

lumbar spinal cord

NO basal ganglia

cerebellum

pons

thoracic spinal cord

cervical spinal cord

12.
Question 12

What is the BEST statement that explains why the lesion in this patient is highly
unlikely to be at the level of the cerebral cortex involving the precentral and
postcentral gyri?
1 point

This patient displayed no language impairments, which indicates that the entire
precentral gyrus must be spared.

This patient displays localized impairments of sensation and motor function, which
is not consistent with focal damage to the cerebral cortex.

This patient displayed normal cranial nerve function, which indicates that the
entire precentral gyrus must be spared.

This patient displayed decreased pin-prick (sharp pain) perception, which is not
seen with damage to the postcentral gyrus.
This patient displayed an increase in muscle tone, which is not seen with damage to
the precentral gyrus.

This patient displayed “dissociated sensory loss” (loss of pain sensation on

one side and loss of mechanosensation on the other side), which is not seen with
damage to the postcentral gyrus.
13.
Question 13

How would you account for this patient’s problems with urinary incontinence and
bladder function?
1 point

There has been damage to axons that descend from reticular formation centers
to somatic motor neurons and visceral motor preganglionic neurons that govern
micturition.

There has been damage to the parasympathetic preganglionic neurons in the sacral
cord that motivate contraction of the detrusor muscle.

There has been breakdown of SNARE complexes in the presynaptic endings of

ganglionic parasympathetic axons that supply the detrusor (bladder wall) muscle.

There has been an autoimmune attack against the nicotinic acetylcholine receptors
in the external sphincter muscle that governs bladder voiding.

There has been damage to the somatic motor neurons in the sacral cord that motivate
contraction of the external sphincter muscle.
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