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:
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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.
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:
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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.
RESPONSES
What is the most likely pathological process that explains the development of this
patient’s symptoms?
CNS neoplasm (tumor)
hemorrhagic stroke
Parkinson’s disease
multiple sclerosis
encephalitis
Question 2
Case 1
On the basis of the symptoms and signs described above, at what level of the
nervous system is this injury?
pons
cerebellum
thalamus
medulla oblongata
cerebral cortex
Question 3
Case 1
Which of the following statements below provides the BEST rationale for where you
think the stroke is localized?
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.
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 most likely diffuse, being consistent with a widespread encephalitis or
meningitis, since widespread body parts are affected.
Question 4
Case 1
What is the BEST characterization of this patient’s persistent communication
difficulties?
Broca’s aphasia
dysarthria (poorly articulated speech, resulting from interference in the control of
speech muscles)
left-sided deafness
upper motor neuron syndrome
Wernicke’s aphasia
Question 5
Case 1
What blood vessel was most likely involved in this case?
right anterior cerebral artery
left posterior cerebral artery
left anterior cerebral artery
left middle cerebral artery
right posterior inferior cerebellar artery
Question 6
Case 1
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?
By removal of the necrotic tissue by microglia and repopulation of the volume of
gray matter with new neurons.
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.
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.
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.
Question 7
Case 1
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?
Activation of glia cells which release soluble factors that block neurotrophin
receptors.
Excessive release of neurotrophins that binds to p75 receptors, disrupting cellular
processes that are necessary for neuronal survival.
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, causing neurons to
atrophy and die by non-use.
Excessive release of GABA that binds to GABA-A receptors, exciting post synaptic
neurons to death.
Question 8
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?
multiple sclerosis
prion disease
CNS neoplasm (tumor)
meningitis
Parkinson’s disease
Question 9
Case 2
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?
(bilateral) lateral vestibulospinal tracts
left gracile tract
spinothalamic tract axons in the right anterolateral white matter of the spinal cord
left lateral corticospinal tract
right lateral corticospinal tract
Question 10
Case 2
Given the findings of the physical examination, which of the following tracts is spared?
left gracile tract
right lateral corticospinal tract
left lateral corticospinal tract
spinothalamic tract axons in the left anterolateral white matter of the spinal cord
descending axons that control output from sacral somatic motor neurons to striated
sphincter muscles in the pelvic floor
Question 11
Case 2
At what level do you think the lesion is in this patient?
midbrain
thalamus
thoracic spinal cord
cervical spinal cord
pons
Question 12
Case 2
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 (precentral and postcentral gyrus)?
This patient displayed no language impairments, which indicates that the entire
precentral gyrus must be spared.
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.
This patient displayed decreased pin-prick (sharp pain) perception, which is not
seen with damage to the postcentral gyrus.
This patient displayed normal cranial nerve function, 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.
Question 13
Case 2
How would you account for this patient’s problems with urinary
incontinence and bladder function?
There has been an autoimmune attack against the nicotinic acetylcholine receptors
in the external sphincter muscle that governs bladder voiding.
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 damage to the somatic motor neurons in the sacral cord that
motivate contraction of the external sphincter muscle.
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.