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•1 •
A 63-year-old man who visits his doctor for a regular checkup admits that he is having trouble hea ring his
.2
wife when she speak s to him. However, he seems able to hear his favorite cowboys on the television
•3 Western, and this certainly angers his w ife. The physician conducts an aud itory test and reassures the
·4 patient that his pathology is part of the normal process of aging and not a newfound aversion to his wife.
•5
What physiologic changes would one expect to find in this patient on a cellular level?
:
A. Compression of cranial nerve VIII as it exits the internal auditory meatus
B. Degeneration of the distal hair cells at the apex of the organ of Corti
C. Degeneration of the proxima l hair cells of the organ of Corti
D. Degeneration of the utricle and the saccule
E. Trauma to the coch lear nuclei

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1 •
.2
The correct a n s wer is C. 64°/o chose this.
•3
Age-related degeneration of the organ of Corti (depicted in the Inner hair cel ls
·4 drawing) lies in the proximal portion of the basilar membrane
Tectorial membrane
•5 (farthest from the helicotrema or apex and closest to the ossicles
and oval w indow). Because this is the th innest and least compliant Outer hair cells
part of the basilar membrane, it is responsible for sensing high-
pitched sounds. The loss of hair cells in this region is called
presbycusis, and this is the classic pattern of sensorineural hearing
loss in older patients. It also explains why the patient is having
progressively more trouble hearing his wife's voice while hearing
most of the characters (cowboys with low-pitched voices) on
television just fine.
Helicotrema Presbycusis Basilar membrane Organ of Corti Sensorineural hearing loss Hair cell Basilar fi r
Ossicles Oval window Hearing loss Anatomical terms of location
Spiral gan ion
Coch lear nerve
Image courtesy of Wikimedia Commons

A is not correct. 2°/o chose this.

Compression or trauma to crania l nerve VIII wou ld not only disrupt al l frequencies of sound from one ear, but it
would also affect the vestibu lar system . Therefore, this man would present with hearing loss as well as vertigo,
nystagmus, nausea, and/or vomiting .
Vestibular system Nystagmus Vertigo Vestibulocochlear nerve Cranial nerves Nausea Vomiting Hearing loss Skull Vestibular exam Major trauma

B is not correct. 31°/o chose this.

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e - e - e e- • I - - e • - - :l - :f. U e I e e e :l e I a - -- e I - - e e I e e - e - - - - a I
1
would also affect the vestibular system. Therefore, this man would present with hearing loss as we ll as vertigo,
.2
nystagmus, nausea, and/or vomiting.
•3 Vestibular system Nystagmus Vertigo Vestibulocochlear nerve Cranial nerves Nausea Vomiting Hearing loss Skull Vestibular exam Major trauma

.4
B is not correct. 31% chose this.
•5
The ha ir cel ls located more distal ly near the apex of the organ of Corti rest on a broader and floppier portion of
the basilar membrane . Therefore, they process sounds that have a lower pitch, and they are usual ly spa red in
age-related hearing loss.
Basilar membrane Organ of Corti Hair cell Presbycusis Hearing loss

D is not correct. 2°/o chose this.

The utricle and the saccule are portions of the vestibular apparatus, and they are responsible fo r sensing
changes in head position with respect to linear acce leration . They are not involved in hearing.
Saccule Utricle (ear) Vestibular system linear particle accelerator

E is not correct. 1°/o chose this.

Trauma to a coch lear nucleus would result in the loss of hea ring of al l f requencies in the ipsilateral ea r.
Therefore, this man would not be able to hea r the te levision or his wife in one ear.
Cochlear nucleus Anatomical terms of location Ipsilateral Cell nucleus Major trauma

Bottom Line:
Hai r cel ls on the proximal region of the organ of Corti, where the basi lar membrane is thinnest, are responsible
for high-pitched sound perception and are frequently lost in presbycusis.
Basilar membrane Organ of Corti Presbycusis Hair cell

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1
- - - - -
- - - -- --- ------ - - - -- - - -
changes in head position with respect to linear acce leration . They are not involved in hearing.
.2 Saccule Utricle (ear) Vestibular system linear particle accelerator
•3
E is not correct. 1°/o chose this.
.4
Trauma to a coch lear nucleus would result in the loss of hea ring of al l frequencies in the ipsilateral ear.
•5 Therefore, this man would not be able to hear the te levision or his wife in one ear.
Cochlear nucleus Anatomical terms of location Ipsilateral Cell nucleus Major trauma

Bottom Line:
Hair cel ls on the proximal region of the organ of Corti, where the basi lar membrane is thinnest, are responsib le
for high-pitched sound perception and are frequently lost in presbycusis.
Basilar membrane Organ of Corti Presbycusis Hair cell

1iU;fii!1J•J for year:[ 2017

FI RST AID FA CTS
"

FA11 p 503.2
Diagnosing hearing loss
RINNE TEST WEBER TEST
Conduct ive Abnormal (bone> air) Localizes to affected ear
Sensorineural ormal (air> bone) Localizes to unaffected ear

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1 •
A 64-year-old woman is hospita lized in the intensive care unit after suffering an intracrania l hemorrhage.
.2
After 12 hours, she becomes unresponsive to both verbal and physical stimu lation. Physical examination
•3 revea ls a heart rate of 50/mi n, blood pressure of 170/ 100 mm Hg, and papilledema, with a left pupil that is
·4 d ilated and un reactive.
•5
What is the next best step in treatment of this patient?
:
A. Intubate and hyperventilate
B. Intubate and hypoventilate
C. Lower the head of the bed 30 degrees
D. Lu mbar puncture
E. Restrict fluids

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2 The correct answer is A. 53°/o chose this.

•3 This patient is presenting with al l the classic signs of increased intracrania l pressure (I CP), includ ing being
.4 comatose, bradycardic, and hypertensive, and having papilledema. I n add it ion, the di lated and unreactive pupil
•5 suggests a possib le herniation syndrome. This patient should be intubated as soon as possible to protect her
airway in case of increased pressure on the brain stem, which can lead to respiratory depression or arrest . In
addition, C0 2 is a powerfu l vasodi lator of cerebral vesse ls. The use of mechanical hyperventilation to lower
partial arteria l carbon dioxide pressure to 26-30 mm Hg has been shown to rapidly reduce ICP through
vasoconstriction and a decrease in the volume of intracran ial blood . A 1-mm Hg change in partia l arteria l carbon
dioxide pressure is associated with a 3% change in cerebral blood f low. The effect of hyperventilation on ICP is
short-lived, however, and thus is used to buy t ime to identify and treat the underlying cause of elevated I CP.
Other therapies for acute increases in ICP are the use of osmotic diuretics such as mann itol. However, these are
only temporizing measures and in a patient with such a poor clinica l presentation emergent surgical
decompression would be the definitive treatment.
Papilledema Hypoventilation Intracranial pressure Vasodilation Vasoconstriction Mannitol Bradycardia Hyperventilation Carbon dioxide Brainstem Diuretic

Respiratory tract Cerebral blood flow Osmosis Tracheal intubation Intubation Hypertension Decompressive craniectomy Human brain Major depressive disorder

Hernia Brain Depression (mood) Blood flow

B is not correct. 16% chose this.

Although intubation in this case wou ld be a correct measure, hypoventilation would lead to increased partia l
carbon dioxide pressure, causing cerebral vasodi lation and increased intracran ial pressure.
Carbon dioxide Vasodilation Intracranial pressure Hypoventilation Intubation Carbon

C is not correct. 7°/o chose this.

Patients with elevated intracranial pressure (ICP) shou ld be positioned to maximize venous outflow from the
head . The recommendation is to elevate the head of the bed 30 dearees. and mainta in the head in a straiaht •
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1 B is not correct. 16% chose this.

2 Although intubation in this case wou ld be a cor rect measure, hypoventilation would lead to increased partia l
•3 carbon dioxide pressure, causing cerebral vasodi lation and increased intracran ial pressure.
Carbon dioxide Vasodilation Intracranial pressure Hypoventilation Intubation Carbon
.4
•5 C is not correct. 7°/o chose this.
Patients with elevated intracranial pressure (I CP) shou ld be positioned to maximize venous outflow from the
head. The recommendation is to elevate the head of the bed 30 deg rees, and mainta in the head in a straight
position to avoid obstruction of jugula r venous return, thus lowering ICP. Lowering the head of the bed
(Trendelenburg position) cou ld decrease venous drainage from the head, and is not recommended for patients
with increased ICP.
Trendelenburg position Intracranial pressure Friedrich Trendelenburg Jugular vein Vein

D is not correct. 14% chose this.

Lumbar puncture shou ld not be performed in patients suspected of having elevated intracran ial pressure (ICP) .
I f lumbar puncture is performed, the ICP drops, wh ich can resu lt in depression of the entire ventricu lar system,
causing the brain to hern iate further. This is why CT is always perfor med before lumbar punctu re to rule out any
causes of increased I CP.
lumbar puncture Intracranial pressure Ventricular system lumbar vertebrae lumbar Brain herniation Major depressive disorder Human brain Depression (mood)

Brain

E is not correct. 10% chose this.

I n general, patients with elevated intracrania l pressure (ICP) do not need to be severely fluid restricted .
Although it might seem that lower blood pressu re wou ld result in lower ICP, this is not the case. Hypotension,
especia lly in conjunction with hypoxemia, can induce reactive vasod ilation and elevations in ICP. Patients shou ld
be kept euvolemic and normo- to hyperosmolar. While lowering of I CP is attempted, cerebral perfusion pressure
trnn\ ---...1- •- L...- J, __ ._ -L...- ~ ·- t=.n - - u- •- - ~ ·-:....1 -- .... -L... ... -1 =--1...--:- t rnn _ - - - - _ _._ .... ; _1 _.,.. ___ , ..... _ trn\

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1 Lumbar puncture shou ld not be performed in patients suspected of having elevated intracran ial pressure (ICP).
2 If lumbar puncture is performed, the ICP drops, wh ich can resu lt in depression of the entire ventricu lar system,
•3 causing the brain to hern iate further. This is why CT is always perfor med before lumbar punctu re to rule out any
causes of increased ICP.
.4
lumbar puncture Intracranial pressure Ventricular system lumbar vertebrae lumbar Brain herniation Major depressive disorder Human brain Depression (mood)
•5
Brain

E is not correct. 10% chose this.

In general, patients with elevated intracrania l pressure (ICP) do not need to be severely fluid restricted.
Although it might seem that lower blood pressu re wou ld result in lower ICP, this is not the case. Hypotension,
especia lly in conjunction with hypoxemia, can induce reactive vasod ilation and elevations in ICP. Patients shou ld
be kept euvolemic and normo- to hyperosmolar. While lowering of ICP is attempted, cerebral perfusion pressure
(CPP) needs to be kept above 60 mm Hg to avoid cerebral ischemia (CPP = mean arter ial pressu re- ICP).
Cerebral perfusion pressure Intracranial pressure Brain ischemia Hypoxemia Vasodilation Mean arterial pressure Hypotension Ischemia Blood pressure Perfusion

Fluid balance

Bottom Line:
The classic signs of increased intracranial pressu re (ICP) include coma, bradycardia, hypertension,
hyperventilation, and papilledema. A sing le fixed and di lated pupi l can be a sign of ipsilateral uncal herniation.
The immediate treatment for suspected increased ICP is intubation with mechanica l ventilation, elevating the
head of the bed to 30 degrees, and using osmotic diuretics such as mannitol.
Papilledema Bradycardia Hyperventilation Intracranial pressure Mannitol Mechanical ventilation Hypertension Diuretic Coma Osmosis Intubation Temporal lobe
Anatomical terms of location Hernia

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1 •
FA17 p472.1
2
•3 Cerebral perfusion Brain perfusion relies on tight autoregulation. Therapeutic hypen ·entilation - l Pco2
Cerebral perfusion is primarily driven b) - vasoconstriction - l cerebral blood Aow
·4
Pco1 (Po 1 also modulates perfusion in se,·ere - l intracranial pressure (IC P). ~ l ay be used
•5
h) poxia}. zo
to treat acute cerebral edema (eg, to st rokc)
Cerebral perfusion relies on a pressure gradient unresponsi,·e to other interventions.
between mean arterial pressure (\ lAP) and C PP =~ l AP- IC P. lf C PP = 0, there is no
JCP. l blood pressure or f IC P - l cerebral cerebral perfusion - brain death.
perfusion pressure (C PP).

50 100 150 40 80 120

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1 Cerebral perfusion Brain perfusion relies on tigh t aulorcgulalion. Therapeutic hyperventilation - l Pco2 •

2 Cerebral perfusion is primaril y driven by - vasoconstriction - l cerebral blood Aow

•3
Pco 1 (Po1 also modulates perfusion in se,·ere - l intracranial pressure (IC P). fay be used

·4
hypoxia). to treat acute cerebral edema (eg, zo
to sl rokc)
C erebral perfusion relies on a pressure gradient unresponsi,·e to other interventions.
•5 between mean arterial pressure (J\ lAP) and C PP = lAP- ICP. If C PP = 0, there is no
ICP. l blood pressure or t IC P - l cerebral cerebral perfusion .... brain death.
perfusion pressure (C PP).

50 100 150 40 80 120

Arterial gas pressure (mm Hg) Arterial gas pressure (mm Hg)

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2
A 40-year-old man presents to the office because of progressively worsen ing pain and weakness in his legs. IAA] •

He says the weakness is now so severe that he had to qu it his job as a construction worker. His father had a
•3 similar condition and required a wheelcha ir at the age of 35 years. His blood pressure is 130/8 5 mm Hg and
.4 pulse is 95/min. Part of his physical examination is shown in the video clip.
•5 OPE N MEDIA

What spinal levels are tested in this examination?

:
A. Ll and L2
B. L2 and L3
C. L3 and L4
D. 51 and 52
E. 52-54
F. Tl O and Tll
G. T l l and T12

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2 The correct answer is C. 77°/o chose this.

•3 Heredit ary spastic paraplegia is a prog ressive familial disorder that gene rally man ifests anyt ime between
4 ch ildhood and midd le age. Many different patterns of inhe ritance have been proposed, includ ing aut osomal
•5 dominant, autosoma l recessive, and X-linked forms . Most patients present with a symmetrical, stepwise
spasticit y and weakness in the legs. In genera l, sensat ion is spared. The only therapy is symptomatic treat ment
of the spasticit y . The hyperreflexia of the pate llar reflex demonst rat ed in t he video tests the L3 and L4 spinal
levels.
Hyperreflexia Spasticity Dominance (genetics) Hereditary spastic paraplegia Paraplegia Autosomal recessive Reflex Sex linkage Spastic Recessive

A is not correct. 4°/o chose this.

Ll and L2 are involved in t he cremasteric reflex . The Ll dermat ome is located close t o the inguina l ligament.
Cremasteric reflex Dermatome (anatomy) Inguinal ligament Somite ligament Inguinal canal Inguinal lymph node Reflex Inguinal

B is not correct. 8°/o chose this.

L3 and L4 must be functiona l for the patel lar reflex; however, L2 is not involved. The L2 and L3 der matomes are
locat ed over the anterior thigh.
Patellar reflex Dermatome (anatomy)

D is not correct. 5°/o chose this.

Sl and 52 is tested by the Ach illes reflex. They are not involved in the knee reflex.
E is not correct. 3°/o chose this.
Functional S2- S4 nerve roots are essential for ach ieving an erection, but they are not t ested by the Ach illes
reflex. Additiona lly, st roking the skin around t he anal sph incter and causing contraction ("anal wink")
demonstrates functiona l S3 - S4 leve ls.
Ankle jerk reflex Sphincter Nerve root

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1 L3 and L4 must be functiona l for the patel lar reflex; however, L2 is not involved . The L2 and L3 dermatomes are
2 located over the anterior thigh .
Patellar reflex Dermatome (anatomy)
•3
4 D is not correct. 5°/o chose this.
•5 Sl and 52 is tested by the Ach illes reflex. They are not involved in the knee reflex .
E is not correct. 3°/o chose this.
Funct ional S2- S4 nerve roots are essential for ach ieving an erection, but they are not tested by the Ach illes
reflex. Additiona lly, stroking the skin around the anal sph incter and causing contraction ("anal wink")
demonstrates functional S3 - S4 levels.
Ankle jerk reflex Sphincter Nerve root

F is not correct. 1 °/o chose this.

TlO and Tll are not tested by any common reflexes. The TlO dermatome is located over the umbi licus.
Dermatome (anatomy) Navel Somite Umbilicus (mollusc)

G is not correct. 2 °/o chose this.

Tll and T12 are not tested by any common reflexes.
T12 (classification)

Bottom Line :
L3 and L4 are the two nerve roots requ ired for the patel lar reflex, and med iation mostly occurs via L4 .
Patellar reflex

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2
G is not correct. 2°/o chose this.
Tll and T12 are not t est ed by any common reflexes.
•3
T12 (classification)
4

•5
Bottom Line:
L3 and L4 are the two nerve root s requ ired for the pat ellar reflex, and med iation mostly occurs via L4 .
Patellar reflex

liU;fiiJI•J
FIRST AID FACTS
for year: 20 17 " ]
.

FA17 p480.1

Clinical reflexes ReAexes count up in order (ma in nerve root Additional reAexes:
boldcd): Cremasteric reflex = Ll, L2 ("testicles move")
Achilles reflex = Sl , S2 (" buckle my shoe") Anal wink reflex = S3, S4 ("winks galore")
Patellar reflex = L3, L4 ("kick the door")
Biceps and brachioradialis reflexes = C5,
C6 ("pick up sticks")
Triceps reflex = C7, C8 ("'ay them straight")
Sl.2

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2
An elderly patient w ith chronic hypertension presents w ith loss of sensation on the left side of his face. On IAA] •

examination, he has complete lack of touch, vibration, and temperature sensation on the left side of his face,
•3 but his arms and legs have been spared as have his motor functions. The physician hypothesizes that t he
4 patient had a stroke, and imaging reveals the pathology to be in a division of the posterior cerebral artery.
•5
Which part of the brain most likely was affected?
:
A. Left lateral geniculate nucleus of the thalamus
B. Left medial geniculate nucleus of the thalamus
C. Left primary sensory cortex
D. Left ventra l posterolateral nucleus of the thalamus
E. Left ventra l posteromedia l nucleus of the thalamus
F. Right lateral genicu late nucleus of the thalamus
G. Right media l genicu late nucleus of the tha lamus
H. Right primary sensory cortex
I. Right ventra l posterolateral nucleus of the thalamus
J. Right ventra l posteromedial nucleus of the t ha lamus

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2 The correct answer is J. 28°/o chose this.

•3 Facia l senso ry pathways corresponding to the contralateral t rigemina l distribution ( left) pass th rough this
4
str ucture. When damaged, the contralatera l face is anesthetic.
Anesthesia Anatomical terms of location Anesthetic Trigeminal nerve Contralateral
5
•6 A is not correct. 3°/o chose this .
.7 The lateral genicu late nucleus (LGN) of the thalamus receives visual infor mation f rom the optic tract. A lesion to
the LGN wou ld likely produce a contralateral homonymous hemianopsia .
Homonymous hemianopsia lateral geniculate nucleus Optic tract Thalamus Contralateral lesion Anatomical terms of location Hemianopsia

B is not correct. 6°/o chose this.

The med ial geniculate nucleus of the thalamus receives auditory info rmation from the inferior col licul i. A lesion
in this location wou ld not produce somatosenso ry symptoms.
Medial geniculate nucleus Thalamus Inferior colliculus Somatosensory system Superior colliculus lesion Sound Cell nucleus Hearing

C is not correct. 6°/o chose this.

The primary sensory cortex of the lateral brain does receive sensory information from the face, but it is supplied
by the middle cerebral artery. Lesions to this reg ion usua lly do not lead to anesthesia .
Postcentral gyrus Middle cerebral artery Anesthesia Sensory cortex Human brain Cortex (anatomy) Brain Cerebral cortex

D is not correct. 9°/o chose this.

Al l the sensory modalities of the body, including the dorsal column and the spinothalamic t ract, pass through
the ventral posterolateral nucleus of the thalamus on their way to the cortex.
Ventral posterolateral nucleus Spinothalamic tract Thalamus Posterior column Anatomical terms of location Sensory system Cortex (anatomy) Dorsum (biology)

E is not correct. 15% chose this.

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2 E is not correct. 15% chose this.

•3 Al l the sensory modalities of the face ( light touch, proprioception, vibration, pain, and tempe ratu re) pass
through the ventral posteromed ial nucleus of the tha lamus on their way to the cortex, except for olfactory
4
sensation (cranial nerve I) . The tha lamus is suppl ied by branches of the poster ior cerebral artery. Keep in mind
5 that tha lamic nuclei are small, so it is rare that a lesion cou ld produce high ly specific eff ects. However, the
•6 sidedness is incorrect. Facial sensory pathways originating in the trigemina l distribution decussate lower in the
.7 brainstem pr ior to relaying th rough the tha lamus.
Ventral posteromedial nucleus Posterior cerebral artery Proprioception Thalamus Cranial nerves Brainstem Sensory system Decussation list of thalamic nuclei

Nucleus (neuroanatomy) Anatomical terms of location Olfaction lesion Trigeminal nerve Cortex (anatomy) Ventral

F is not correct. 6°/o chose this.

The lateral genicu late nucleus (LGN) of the thalamus receives visual infor mation from the optic tract. A lesion to
the LGN wou ld likely produce a contralateral homonymous hemianopsia .
Homonymous hemianopsia lateral geniculate nucleus Optic tract Thalamus Contralateral lesion Anatomical terms of location Hemianopsia

G is not correct. 7°/o chose this.

The med ial geniculate nucleus of the thalamus receives auditory information from the inferior col licul i. A lesion
in this location wou ld not produce somatosensory symptoms.
Medial geniculate nucleus Thalamus Inferior colliculus Somatosensory system Superior colliculus lesion Sound Cell nucleus Hearing

H is not correct. 8°/o chose this.

The primary sensory cortex of the lateral brain does receive sensory information from the face, but it is supplied
by the middle cerebral artery. Lesions to this reg ion usua lly do not lead to anesthesia .
Postcentral gyrus Middle cerebral artery Anesthesia Sensory cortex Human brain Cortex (anatomy) Brain Cerebral cortex

I is not correct. 12% chose this.

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lab 'lifllues

the LGN wou ld likely produce a contralateral homonymous hemianopsia .

Notes Calculator
.
2
Homonymous hemianopsia lateral geniculate nucleus Optic tract Thalamus Contralateral lesion Anatomical terms of location Hemianopsia
•3
4
G is not correct. 7°/o chose this.
The med ial geniculate nucleus of the thalamus receives auditory info rmation from the inferior col licul i. A lesion
5
in this location wou ld not produce somatosenso ry symptoms .
•6 Medial geniculate nucleus Thalamus Inferior colliculus Somatosensory system Superior colliculus lesion Sound Cell nucleus Hearing
.7
H is not correct. 8°/o chose this.
The primary sensory cortex of the lateral brain does receive sensory information from the face, but it is supplied
by the midd le cerebral artery. Lesions to this reg ion usua lly do not lead to anesthesia .
Postcentral gyrus Middle cerebral artery Anesthesia Sensory cortex Human brain Cortex (anatomy) Brain Cerebral cortex

I is not correct. 12% chose this.

Al l the sensory modalities of the body, including the dorsal column and the spinothalamic t ract, pass through
the ventral posterolateral nucleus of the thalamus on their way to the cortex.
Ventral posterolateral nucleus Spinothalamic tract Thalamus Posterior column Anatomical terms of location Sensory system Cortex (anatomy) Dorsum (biology)

Bottom Line:
The thalamus is supp lied by branches of the posterior cerebral artery. All t he sensory modal ities of the face,
except for o lfactory sensation, pass t hroug h the ventral posteromedial nucleus of t he thalamus on their way to
the cortex.
Ventral posteromedial nucleus Posterior cerebral artery Thalamus Olfaction Anatomical terms of location Sensory system Cortex (anatomy)

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1 FIRST AID FACTS

. . - •

2
•3 FA17 p468.1
Thalamus Major relay for all ascending sensory information except olfaction.
4
NUClEUS INPUT SENSES DESTINATION MNEMONIC
5
Ventral pinothalamic and dorsal columns/ \ ibration, Pain, Io somatosensory
•6 Postero- P ressure,
medial lemniscus corte"
.7 Lateral Proprioception.
nucleus Light touch.
temperature
Ventral Trigeminal and gustatory pathway J;~1ce
sensation, 1° somatosensory lakeup goes on
postero- taste cortex the face
Medial
nucleus
Lateral CN II Vision Calcarine sulcus Lateral =L ight
geniculate
nucleus
Medial Superior olive and inferior col liculus of Hearing Auditory cortex of l\ledial = 1\ l usic
geniculate tectum temporal lobe
nucleus
Ventral lateral Basal ganglia, cerebellum Motor f-. lotor cortex
nucleus

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1 •
During a routine office visit, physica l examination reveals that a 50-year-old man is unable to rapidly
2
alternate tapping the palm of one hand w ith the finger of another. The patient has also noted worsening
•3 problems with voluntary movement and has developed a t remor toward the end of some hand movements.
4 No nystagmus is noted on ocular examination. Gait and station are normal.
5
•6 What is the most likely cause of his symptoms?
.7 :
A . Alcohol intoxication
B. Degeneration of the cerebrocerebellum
C. Degeneration of the spinocerebellum
D. Degeneration of the vestibulocerebellum
E. Wernicke's encephalopathy

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2 The correct answer is B. 51°/o chose this.

•3 The neocerebel lum or cerebrocerebellum rests in the lateral cerebel lar hemispheres, and it is responsible for fine
4
movements of the hands and face . Lesions here would cause dysd iadochokinesis (t he impa irment in rapidly
alternat ing hand movements described above) and intention tremor (also as described above).
5 Intention tremor Anatomy of the cerebellum Cerebellum Dysdiadochokinesia Cerebrocerebellum Tremor Fine motor skill Cerebral hemisphere
6
A is not correct. 5°/o chose this.
.7
Acute alcohol intoxicat ion may present wit h many of these same symptoms, but t hey would relapse and remit
according to the pat ient's da ily drinking habits, and they wou ld not be likely to show progressive decl ine.
Acute alcohol intoxication Alcohol intoxication Alcoholic beverage Alcohol Substance intoxication Relapse

C is not correct. 27 % chose this.

The pa leocerebellum or spinocerebellum is found in the ant erior ver mis of the cerebellum, and is the area that is
most damaged by ch ron ic alcohol abuse. The vermis is responsible for trun k ba lance, voca l control, and
saccades of the eye. Det erioration of the vermis as a result of alcohol toxicit y leads to t he symptoms described
above as well as to slow or scanning speech .
Anatomy of the cerebellum Cerebellum Cerebellar vermis Saccade Alcohol Alcohol abuse Spinocerebellum Anterior Anatomical terms of location

D is not correct. 12% chose this.

The arch icerebel lum or vestibulocerebel lum is located in the floccu lonodu lar lobe. This portion is connected to
the vestibu lar nuclei, and it is mostly responsible for eye movements. Cond it ions affecting th is area lead to
problems of pursu it and nystagmus. However, saccades (the qu ick portion of eye movement seen in
nystagmus) are usua lly not affect ed by lesions in the arch icerebel lum.
Anatomy of the cerebellum Flocculonodular lobe Cerebellum Nystagmus Vestibular nuclei Vestibulocerebellum Nucleus (neuroanatomy) Saccade Vestibular system

Eye movement Vestibular exam

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1
C is not correct. 27% chose this.
2
The paleocerebellum or spinocerebellum is found in the anterior vermis of the cerebellum, and is the area that is
•3 most damaged by chron ic alcohol abuse. The vermis is responsible for trunk balance, voca l control, and
4 saccades of the eye. Deterioration of the vermis as a resu lt of alcohol toxicity leads to the symptoms described
5
above as well as to slow or scanning speech .
Anatomy of the cerebellum Cerebellum Cerebellar vermis Saccade Alcohol Alcohol abuse Spinocerebellum Anterior Anatomical terms of location
6
.7 D is not correct. 12% chose this.
The archicerebel lum or vestibulocerebellum is located in the floccu lonodular lobe. Th is portion is connected to
the vestibu lar nuclei, and it is mostly responsible for eye movements. Conditions affecting this area lead to
prob lems of pursu it and nystagmus. However, saccades (the qu ick portion of eye movement seen in
nystagmus) are usua lly not affected by lesions in the archicerebellum.
Anatomy of the cerebellum Flocculonodular lobe Cerebellum Nystagmus Vestibular nuclei Vestibulocerebellum Nucleus (neuroanatomy) Saccade Vestibular system

Eye movement Vestibular exam

E is not correct. 5°/o chose this.

Thiamine deficiency is common in alcohol ics, and it presents as Wernicke's encepha lopathy . Th is condition
involves a triad of symptoms: ophthalmoplegia or nystagmus, ataxia, and encephalopathy.
Wernicke' s encephalopathy Nystagmus Thiamine Ophthalmoparesis Ataxia Encephalopathy Thiamine deficiency Alcoholism Receptive aphasia

Bottom Line:
Lesions of the neocerebe llum can lead to dysdiadochokinesis and intention tremor.
Intention tremor Cerebellum Dysdiadochokinesia Tremor

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1 •
FA17 p481 .1
2 Common brain lesions
•3 AREA OFLESION CONSEQUENCE EXAMPLES
4 Frontal lobe Disinhibition and deficits in concentration,
5 orientation, judgment; may ha,·e reemergence
6
of primiti\'e reflexes.
.7 Frontal eye fie lds Eres look toward lesion.
'
Paramedian pontine Eyes look away from side of lesion.
reticular formation
Medial longitudinal Internuclear ophthalmoplegia (impaired ~ lultiple sclerosis.
fasciculus adduction of ipsilateral eye; nystagmus of
contralateral eye with abduction).
Dominant parietal Agraphia, acalculia, finger agnosia, left-right Cerstmann srndrome.
cortex disorientation.
Nondomlnant parietal Agnosia of the contralatera I side of the "oriel. ll emi~patial neglect syndrome.
cortex
Hippocampus Anterograde amnesia-inability to make new
(bilateral) memories.
Basal ganglia 1\ lay result in tremor at rest, chorea, athetosis. Parkinson disease, Huntington disease.
Subthalamic nucleus Contra lateral hemiballismus.
Mammillary bodies Wernicke-Korsakoff syndrome- Confusion, Wernicke problems come in a CAN 0 ' beer.
(bilateral) \ taxia, :\'ystagmus, Ophthalmoplegia,

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1 •
Mammillary bodies Wernicke-Korsakoff syndrome- Confusion, Wern icke problems come in a CAN 0 ' beer.
2 (bilateral) \ taxia, Kystagmus, O phthalmoplegia,
•3 memory loss (anterograde and retrograde
4 amnesia), confabulation, persona lit) changes.
5 Amygdala (bilateral) Kluver-Bucy syndrome-disinhibitcd behavior IISV-1 encephalitis.
6 (cg, hyperphagia, hypersexuality, h) pcrorality).
.7 Superior colliculus Parinaud syndrome- paralysis of conjugate Stroke, hydrocephalus, pinealoma.
vertical gaze (rostral interstitial nucleus also
involved).
Reticular activating Reduced levels of arousal and wal..cfulncss
system (midbrain) (eg, coma).
Cerebellar hemisphere Intention tremor, limb ataxia, loss of balance; Cercbcll:ar hemispheres are laterally located-
damage to cerebel lum - ipsilatera l deficits; affect lateral limbs.
fall toward side of lesion.
Cerebellar vermis Truncal ataxia, dysarthria. crmis is centrally located-affects central body.
Degeneration associated with chronic alcohol
usc.

FA17 p 541.2

Alcoholism Physiologic tolerance and dependence on alcohol with symptoms of withdrawal when intake is
interrupted.
Complications: alcoholic cirrhosis, hepatitis, pancreatitis, peripheral neuropathy, testicular atrophy.

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1 involved). •

2 Reticular activating Reduced levels of arousal and wakefulness

•3 system (midbrain) (eg, coma).
4 Cerebellar hemisphere Intention tremor, limb ataxia, loss of balance; Cerebellar hemispheres are laterally located-
5 damage to cerebellum - ipsilateral deficits; affect lateral limbs.
fall toward side of lesion.
6
.7 Cerebellar vermis Truncal ataxia, drsarthria. Vermis is centrally located-affects central body.
Degeneration associated with chronic alcohol
usc.

FA17 p 541.2

Alcoholism Physiologic tolerance and dependence on alcohol with symptoms of withdrawal when inte~kc is
interrupted.
Compl ications: alcoholic cirrhosis, hepatitis, pancreatitis, peripheral neuropathy, testicular atrophy.
Treatment: disullimm (to condition the patient to abstain from alcohol use), acamprosate,
naltrexone, supportive care. Support groups such as Alcoholics Anonymous are helpfu l in
sustaining abstinence and supporting patient and fami ly.
We rnicke-Korsakoff Caused by vitamin B1 deficiency. Triad of confusion, ophthalmoplegia, ataxia (Wernicke
syndrome encephalopathy). May progress to irreversible memory loss, confabulation, personality change
(Korsakoff syndrome). Symptoms may be precipitated by giving dextrose before administering
\·itamin B1 to a patient with thiamine deficiency. Associated with peri\·entricular hemorrhage/
necrosis of mammillary bodies. Treatment: I vitamin B1•

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1 •
The image below is a photomicrograph demonstrating normal cerebellar architecture. The large cells in the
2
image integrate the cerebellar cortical activity and transmit that information to the deep cerebellar nuclei.
•3
4
5
6
.7

What is the neurotransmitter used by the large integrating neurons?

:
A. y-Aminobutyric acid

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What is the neurotransmitter used by the large integrating neurons?
:
A. y-Aminobutyric acid
B. Acet ylcho line
C. Dopam ine
D. Glutamate
E. Glycine
F. Norepineph rine

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1 •

3
The correct answer is A. 36°/o chose this.
4
Cerebellar Purkinje cel ls are the only inhibitory cells in the cerebel lum. They
release GABA onto the neurons of the deep cerebellar nuclei.
5 Cerebel um Pu inje eel Gamma-Aminobutyric acid Deep cerebe lar nucle Nucleus oeuroanatomy) Neuron
6 Cerebellar nuclei
0 7

B is not correct. 16°/o chose this.

Acetylcholine is an excitatory neurotransmitter found in the brain and in the motor and autonomic systems .
Postsynaptic receptors for acetylcholine include both muscarinic and nicotinic receptors.
Neurotransmitter Acetylcholine Muscarinic acetylcholine receptor Nicotinic acetylcholine receptor Autonomic nervous system Chemical synapse Excitatory synapse

Human brain Brain Receptor (biochemistry) Excitatory postsynaptic potential

Cis not correct. 11°/o chose this.

Dopamine is a modulatory neurotransmitter found in various brain reg ions including the basal ganglia and
prefrontal cortex. Dopamine can be either excitatory or inhibitory depend ing on the receptor subtype upon
which it is acting.
Basal gang 1a Prefronta cortex Neurotransmitter Dopamine Ganglion Human brain Cortex (anatomy) Brain Excitatory postsynaptic potential Basal (phylogenetlcs)

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Human brain Brain Receptor (biochemistry) Excitatory postsynaptic potential
1

2 C is not correct. 11% chose this.

3 Dopamine is a modu latory neurotransmitter found in various brain reg ions including the basal gang lia and
4 prefronta l cortex. Dopamine can be either excitatory or inhibitory depend ing on the receptor subtype upon
wh ich it is acting.
5
Basal ganglia Prefrontal cortex Neurotransmitter Dopamine Ganglion Human brain Cortex (anatomy) Brain Excitatory postsynaptic potential Basal (phylogenetics)
6
.7
D is not correct. 24% chose this.
Glutamate is an excitatory neurotransmitter found in the brain . Other pathways in the cerebellum and cerebr um
that are excitatory use glutamate.
Cerebrum Neurotransmitter Cerebellum Glutamic acid Excitatory postsynaptic potential Human brain Excitatory synapse Brain

E is not correct. 9°/o chose this.

Glycine is an inh ibitory neurotransmitter, but it is found primarily in the neurons of the spina l cord.
Glycine Neurotransmitter Spinal cord Neuron

F is not correct. 4°/o chose this.

Norepineph r ine is an excitatory neu rotransmitter found in the brain and in the autonomic systems .
Norepinephrine Neurotransmitter Autonomic nervous system Human brain Brain Excitatory postsynaptic potential Excitatory synapse

Bottom Line:
Purkinje ce lls send inhibitory GABA projections to the deep cerebe llar nuclei, which are the so le output of the
cerebel lum.
Purkinje cell Cerebellum Gamma-Aminobutyric acid Deep cerebellar nuclei Nucleus (neuroanatomy) Cerebellar nuclei Cell nucleus

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1 •

2
FA17 p 469.1
3
Cerebellum lodulatcs mo,·cmcnt; aids in coordination and Lateral lesions-affect voluntary mo,·cmcnt of
4 balance. extremities (L imbs); when injured, propcnsit)
5 Input: to fall toward injured (ipsilateral) side.
6 Contralateral cortex via middle cerebellar \lediallesions- invoh-ement of \fidline
0 7 peduncle. structures (\ermal cortex, fastigial nuclei)
Ipsilateral proprioceptive information' ia and/or Aocculonodular lobe - truncal ataxia
inferior cerebellar peduncle from spinal ("ide-based cerebellar gait), nrstagmus, head
cord. tilting. Generally result in bilateral motor
Output: deficits affecting axiaJ and proximal limb
• The only output of cerebellar cortex = musculature.
Purkin je cells (always in hibitory) - deep
nuclei of cerebellum - contralateral cortex
,-ia superior cerebellar peduncle.
Deep nuclei (lateral - medial)- Dentate,
Emboliform, G lobose, Fast igial ("Don't Eat
C reasy Foods").

FA17 p 4 81 .1
Common brain lesions
AREA OFLESION CONSEQUENCE EXAMPLES
Frontal lobe Disinhibition and deficits in concentration,
• •
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1 •

2
3 Common brain lesions
4 AREA OFLESION
5 Frontal lobe
6 orientation, judgment; may ha\'e reemergence
0 7
Frontal eye fields
Paramedian pontine
reticular formation
Medial longitudinal
fasciculus
Dominant parietal
cortex
Nondomlnant parietal
cortex
Hippocampus
(bilateral)
Basal ganglia
Subthalamic nucleus
Mammillarv bodies
FA17 p 481 .1
CONSEQUENCE EXAMPLES
Disinhibition and deficits in concentration,
of primiti\'e reAexes.
E,·es look toward lesion.
'
Eyes look away from side of lesion.
Internuclear ophthalmoplegia {impaired t\ luhiple sclerosis.
adduction of ipsilateral eye; nystagmus of
contra lateral eye with abduction).
Agraphia, acalculia, finger agnosie~, left-right Cerstmann srndrome.
disorientation.
Agnosia of the contralatera l side or the \\Oriel. II em ispatial neglect syndrome.
Anterograde amnesia-inability to make new
memories.
.l\1av result in tremor at rest, chorea, athetosis. Parkinson disease, Huntington disease.
Contralateral hemiballismus.
Wernicke-Korsakoff svndrome - Conf••~ion . \ Vernicke nrohlems come in :1 C.A N ()' hf'f'r.

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1 •
Hippocampus Anterograde amnesia-inability to make new
2 (bilateral) memories.
3 Basal ganglia .I\ lay result in tremor at rest, chorea, athetosis. Parkinson disease, Huntington disease.
4
Subthalamic nucleus Contra lateraI hemiballismus.
5
Mammillary bodies Wernicke-Korsakoff syndrome- Confu ion, Wernicke problems come in a C Al\ 0 ' beer.
6 (bilateral) Ataxia, '\ystagmus, Ophthalmoplegia,
0 7 memory loss (anterograde and retrograde
amnesia), confabulation, personalit) changes.
Amygdala (bilateral) Kluver-Bucy syndrome- disinhibitcd behavior IISV-1 encephalitis.
(cg, hyperphagia, hypersexuality, h) perorality).
Superior colliculus Parinaud syndrome- paralysis of conjugate Stroke, hydrocephalus, pinealoma.
vertical gaze (rostral interstitial nucleus also
involved).
Reticular activating Reduced levels of arousal ;md wakefulness
system (midbrain) (eg, coma).
Cerebellar hemisphere Intention tremor, limb ataxia, loss of balance; Ccrcbclhtr hemispheres are laterally l oc;~t cd ­
damage to cerebellum - ipsilateral defi cits; affect lateral limbs.
fall toward side of lesion.
Cerebellar vermis Truncal ataxia, dysarthria. crmis is centrally located-affects central body.
Degeneration associated with chronic alcohol
usc.

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1 •
A 44-year-old woman visits her primary care physician comp laining of a drooping eyelid on her left side and
2
pupils of different sizes, as shown in the image. To localize the lesion, the physician administers two
3 medications in series to t he left eye. The first drop is a cocaine-based drop, and the second is
4 hyd roxyamphetamine. Based on the resu lts, the physician correctly diagnoses the patient as having Horner
syndrome, w ith a lesion in the postganglionic sympathetic nerve to the ciliary ganglion.
5
6
0 7

I mage courtesy of Nicholas Mahoney, MD

What is observed after the drops are admin istered?

:
A . Constriction of the pupil with both drops
B. Constriction with the first drop and no change with the second drop
C. Dilation of the pupil w ith both drops
D . Dilation w ith the first drop and no change with t he second drop

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 Image courtesy of Nicholas Mahoney, MD

What is observed after the drops are adm inistered?

:
A . Constriction of the pupil w ith both drops
B. Constriction w ith the first drop and no change with the second drop
C. Dilation of the pupil w ith both drops
D . Di lation w ith the first drop and no change with the second drop
E. No change with either drop
F. No change with the first drop and constriction with the second drop
G. No change with t he first drop and dilation w ith the second drop

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1 The correct answer is E. 30°/o chose this.

2 The patient has Horner syndrome with damage to the postgang lionic neu ron (third-order neuron), which is
3
character ized by the absence of norepineph r ine (NE) and thus no stimu lation of the long ci liary nerve, which
means no stimulation of the iris di lator pupi llae muscle to di late the pupil. This, in turn, prevents any dilation of
4
the pupil. The cocaine-based drop, which inhibits the reuptake of NE, wou ld not cause any change in the pupi l
5 because there is no NE in the neuromuscu lar synapse to beg in with. The add it ion of hydroxyamphetamine to a
6 norma l postgang lionic sympathetic neuron causes the release of NE. The lack of a response in the pupi l
indicates a problem with the postgangl ionic neuron because a damaged postgang lionic neu ron has no NE to
7
release. If we had not been given the infor mation in the vignette about the location of the lesion and were
simply to ld the patient had Horner syndrome and asked where the lesion was located, pre- or postgan lionic,
pupillary di lation wou ld ind icate damage to the pregang lionic (first- or second-order) neu ron such as the
brainstem, brachial plexus, or tumor of the lung apex (Pancoast) for example.
Sympathetic nervous system long ciliary nerves Horner' s syndrome Brachial plexus Norepinephrine Postganglionic nerve fibers Synapse Brainstem

Pupillary response Iris dilator muscle Neuron Preganglionic nerve fibers Neuromuscular junction Iris (anatomy) Mydriasis Ciliary nerves Neoplasm lung Muscle

Vasodilation lesion Reuptake

A is not correct. 6°/o chose this.

Both cocaine and hydroxyamphetamine drops wi ll cause di lation (mydriasis) of the pupil under norma l
physiology. Pilocar pine and other chol inergic agon ists cause pupil constriction (miosis) .
Pilocarpine Mydriasis Miosis Cholinergic Cocaine Pupillary reflex Physiology Vasodilation

B is not correct. 9°/o chose this.

Cocaine-based drops will cause mydriasis, not miosis. Administration of a cholinerg ic agonist to cause pupi llary
constr iction followed by a chol inergic antagonist (such as atropine) cou ld lead to th is reaction under normal
physiology.
Mydriasis Atropine Miosis Cholinergic Receptor antagonist Agonist Antagonist Physiology

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"......... ..... ....... .... . .......... .... . . ......,.. ...... ...
~ ~

2 A is not correct. 6°/o chose this.

3
Both cocaine and hydroxyamphetamine drops wi ll cause di lation (mydriasis) of the pupil under norma l
physiology. Pilocar pine and other chol inergic agon ists cause pupil constriction (miosis) .
4 Pilocarpine Mydriasis Miosis Cholinergic Cocaine Pupillary reflex Physiology Vasodilation
5
B is not correct. 9°/o chose this.
6
Cocaine-based drops will cause mydriasis, not miosis. Administration of a cholinerg ic agonist to cause pupi llary
7
constr iction followed by a chol inergic antagonist (such as atropine) cou ld lead to th is reaction under normal
physiology.
Mydriasis Atropine Miosis Cholinergic Receptor antagonist Agonist Antagonist Physiology

C is not correct. 16% chose this.

This describes the reaction that occu rs in normal physiology . However, in Horner synd rome there is an absence
of norepinephrine (NE); therefore cocaine drops (wh ich inhibit NE reupta ke) with not induce a response .
Likewise, in Horner syndrome there is a postsynaptic defect that interferes with the norma l dilation of
hydroxyamphetamine.
Horner' s syndrome Norepinephrine Cocaine Chemical synapse Physiology Vasodilation

D is not correct. 16% chose this.

Although no change is expected with the second drop, the first shou ld also elicit no change.
F is not correct. 9°/o chose this.
No change is expected with the first drop as there is an absence of norepinehpr ine in Horner synd rome.
However, hydroxyamphetamine will not cause constriction . Under normal circumstances it wil l cause pupi llary
dilation .
Horner' s syndrome Pupillary response Mydriasis Vasodilation

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1 Likewise, in Horner syndrome there is a postsynaptic defect that interferes with the norma l dilation of
2
hydroxyamphetamine.
Horner's syndrome Norepinephrine Cocaine Chemical synapse Physiology Vasodilation
3
4
D is not correct. 16% chose this.
5
Although no change is expected with the second drop, the first shou ld also elicit no change.
6 F is not correct. 9°/o chose this.
7
No change is expected with the first drop as there is an absence of norepinehpr ine in Horner synd rome.
However, hydroxyamphetamine will not cause constriction . Under normal circumstances it wil l cause pupi llary
dilation .
Horner's syndrome Pupillary response Mydriasis Vasodilation

G is not correct. 14% chose this.

Dilation with the hydroxyamphetamine drop ind icates damgage to first or second order neurons. In the vignette
we are told that damage has occu red to the postgang lionic fibers wh ich are third-order neurons. These
medications work by causing release of stored endogenous norepinephrine, becasue they are damaged they
have no epinephrine to release.
Epinephrine Norepinephrine Neuron Vasodilation Postganglionic nerve fibers Endogeny (biology)

Bottom Line:
Horner synd rome invo lves a disruption of sympathetic output to the iris. It can occu r anywhere along the
sympathetic t ract. I f the damage is to the third-order neuron (postgang lionic fi bers) the pupil wi ll not di late. I f
the damage is to fi rst- or second-order neurons the pupil will di late .
Horner's syndrome Neuron Pupillary response Iris (anatomy) Postganglionic nerve fibers

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3 ljl;fil;1i•J for year: 20 17 •

FIRST AID FACTS
4
5
FA17 p 509.3
6
Horner syndrome Sympathetic denervation of face - : P \\I is horny (llorner).
7
Ptosis (slight drooping of C)elid: superior Pto~h. anhidro~il>. and mio~i~.
tarsal muscle)
\ nhidrosis (absence of S\\ eating) and
Rushing of affected side of fa ce Long coltaty ~e

Yliosis (pupil constriction) To sweat glands

Associated with lesion of spinal cord above ot foreheild

Tl (eg, Brown-Sequard syndrome, late-stage I"(1~';:::/.::::;::;:::p.~ To smooth muscle of eyetod

To pupollill)' dilator
syringomyelia) or of the stellate ganglion
- -- - - - <To sweat glands of face
alongside the spinal cord (eg, Pancoast tumor). External carotid artery
Any interruption results in I Iorncr syndrome.
First neuron
Superior cervical ganglion

Sy~~apse l.s
In lateral horn T1
""'---r-Second neuron
Sponal cord

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