Multidisciplinary Self Assessment Examination Flashcards
Clinical features of the Brown-Sequard syndrome include
all of the following EXCEPT?
A. Contralateral loss of pain and temperature sensation
beginning one to two spinal segments below the lesion
B. Ipsilateral loss of proprioception and vibratory sense
below the level of the lesion
C. Ipsilateral Horner’s syndrome if the lesion is cervical
D. Ipsilateral loss of crude touch below the level of the lesion
E. Ipsilateral loss of sweating below the level of the lesion
D. Ipsilateral loss of crude touch below the level of the lesion
What is depicted in the photomicrograph below (Figure 8.2Q)?
A. Palisading cells around a necrotic region in a patient
with glioblastoma
B. Spongiform change in a patient with prion disease
C. Homer-Wright rosette in a 3-year-old male with
medulloblastoma
D. Acute infarct in a patient with myoclonic epilepsy with
ragged red fibers (MERRF)
E. Fibrinoid necrosis in a patient with acute hemorrhagic
leulwencephalopathy
**A. Palisading cells around a necrotic region in a patient
with glioblastoma **
Note the “picket fence” arrangement (pseudopalisading) of the nuclei surrounding a region of necrosis in this
photomicrograph, which depicts a glioblastoma (Ellison,
pp.628- 631).
What is the most sensitive laboratory test for the detection of neurocysticercosis (NCC)?
A. Peripheral eosinophil count
B. Complete serum white blood cell count
C. Stool for ova and parasites
D. Enzyme-linked immunosorbent assay (ELISA)
E. Electroimmunotransfer blot (EITB)
E. Electroimmunotransfer blot (EITB)
Complete white blood cell count, peripheral eosinophil
level, and serum anticysticercal antibody levels should be
obtained in all patients suspected of having NCC. Patients
requiring ventriculostomy placement should have cerebrospinal fluid (CSF) analyzed for eosinophil and anticysticercal antibody levels. Stool testing for ova and parasites is
helpful in patients with simultaneous intestinal tapeworm
infection but is insensitive and nonspecific for T. SOhll:1ll
species and is found in less than 33% of cases. Severallaboratory methods have been developed to detect host antibodies
against circulating cysticercal antigens. From the many
tests performed , current data indicate that enzyme-linked
immunosorbent assay (ELISA) and electroimmunotransfer
blot (EITB) tests are the most effective. Studies comparing
these diagnostic modalities have shown that the EITB assay
is more sensitive overall than ELISA, especially when serum
is being tested. Both techniques are more sensitive in cases
with multiple cysts than in cases with solitary or confined
lesions. Additionally, no globa l difference among cases
was found with parasites located in different compartments
(ventricles, subarachnoid space, parenchyma) of the central nervous system (Greenberg, pp. 236- 238; Proano-Narvaez
et aI., p. 2118)
Match each of the following spinal cord lesions
with the appropriate clinical syndrome (Figure 8.4-8.9Q),
using each answer once, more than once, or not at all.
Early subacute combined degeneration
E
Match each of the following spinal cord lesions
with the appropriate clinical syndrome (Figure 8.4-8.9Q),
using each answer once, more than once, or not at all.
Syringomyelia
F
Match each of the following spinal cord lesions
with the appropriate clinical syndrome (Figure 8.4-8.9Q),
using each answer once, more than once, or not at all.
Tabes dorsalis
D
Match each of the following spinal cord lesions
with the appropriate clinical syndrome (Figure 8.4-8.9Q),
using each answer once, more than once, or not at all.
PoliomyelitiS
A
Match each of the following spinal cord lesions
with the appropriate clinical syndrome (Figure 8.4-8.9Q),
using each answer once, more than once, or not at all.
Amyotrophic lateral sclerosis
C
Match each of the following spinal cord lesions
with the appropriate clinical syndrome (Figure 8.4-8.9Q),
using each answer once, more than once, or not at all.
Familial spastic paraplegia
B
\Vhich of the following tumors may share certain
histopathologic features with the lesion depicted below
(Figure S.10Q) ?
1. Clear cell ependymoma
2. Central neurocytoma
3. Dysembryoplastic neuroepithelial tumor
4. Fibrous meningioma
A. 1,2, and3
B. 1 and3
C. 2 and 4
D. Only 4 is correct
E. All of the above
**A. 1,2, and3 **
The differential diagnosis of oligodendroglia I tllI110rS
includes clear cell ependymoma, central neurocytoma, and
dysembryoplastic neuroepithelial tumor. All of these entities
exhibit the presence of neoplastic cells with a uniform round
nucleus and clear cytoplasm. A rare differential diagnosis
of oligodendroglioma is clear cell meningioma (not fibrous
meningioma), which can be differentiated from oligodendroglioma by abundant diastase-sensitive PAS positivity
and immunoreactivity for EMA. Note the prominent calcification , “chicken wire” capillaries (prominent branching),
“fried egg” cells with round monomorphic nuclei, and perinuclear halos arranged in a back-to-back fashion in this
photomicrograph depicting an oligodendroglioma (Ellison,
pp. 641- 644; WHO, p. 59).
Which of the following abdominal wall layers will best
hold suture (highest tensile strength) during placement of a
ventriculoperitoneal shunt?
A. Colles fascia
B. Cruveilhier’s fascia
C. Buck’s fascia
**D. Scarpa’s fascia **
E. Camper’s fascia
**D. Scarpa’s fascia **
The anterior abdominal wall consists of the epidermis, superficial layer of superficial fascia (of Camper), the
deep layer of superficial fascia (of Scarpa), the deep fascia
(investing fascia of musculature), the external and internal
oblique muscles, the transverse abclominis muscle , transversalis fascia, loose extraperitoneal connective tissue , and
peritoneum. Camper’s fascia is predominately an adipose layer that contains most of the fat of the subdermis. It continues over the pubis as the superficial layer (of Cruveilhier) of
the superficial perineal faSCia, crosses the inguinal ligament
to merge with the superficial fascia of the thigh, and continues over the chest as the superficial layer of superficial
thoracic fascia. Scarpa’s fascia is a fibrous layer that will best
hold sutures (highest tensile strength). It continues over the
pubis as the deep layer of superficial perineal fascia (of
Colles) and passes into the upper thigh, where it attaches to
the fascia lata. The deep fascia is the investing fascia of the
musculature, aponeuroses, and large neurovascular structures and is not easily separated from the underlying epimysium of muscle. It extends into the penis as Buck’s faSCia,
continues over the spermatic cord as the externa l spermatic
faSCia, and passes over the pubis and perineal musculature as
the deep perineal fascia of Gallaudet (April, p. 173)
What is the diagnosis ?
A. Fatty filum with tethered cord
B. Myxopapillaryependymoma
C. Dermal sinus tract
D. Epidural hematoma
E. Dermoid tumor
**A. Fatty filum with tethered cord **
Note the cord tethering and fatty filum on this sagittal
MRl (Ramsey, pp. 104- 106).
Which of the following is correct about the lesion
depicted on the angiogram below (Figure 8.13Q)?
A. Annual risk of bleeding is approximately 3% per year
B. Associated with cranial bruit and congestive heart
failure during the neonatal period
C. The loss of a tumor suppressor gene on chromosome 22
**D. Tills lesion is usually found within normal brain
parenchyma **
E. Represents an extreme anatomic variant of cortical
arterial blood supply
**D. Tills lesion is usually found within normal brain
parenchyma **
This angiogram depicts the classic “caput medusae”
pattern of a venous angioma , which is an extreme anatomic
variant of medullary (white matter) venous drainage. The
precise etiology of this lesion remains unclear, although
some authors have proposed that it results from arrested
development of parts of the venous vasculature at a time
when normal arterial development is nearly complete. This
results in the retention of primitive venous channels that
typically empty into a single large draining vein (Osborn,
pp.294- 295).
Which of the following structures are connected by the stria medullaris thalami ?
A. Nucleus basalis (of Meynert) and septal nuclei
B. Septal nuclei and habenular nuclei
C. Habenular nuclei and occipital cortex
D. Septal nuclei and anterior thalamic nuclei
E. Pineal gland and anterior commissure
**B. Septal nuclei and habenular nuclei **
The stria medullaris thalami contains projections
that originate in the septal nuclei, anterior thalamic nuclei,
and hypothalamus (preoptic region) and terminate in the
habenular nuclei. The habenular nuclei then project to the
raphe nuclei of the midbrain via the fasciculus retroflexus.
In this manner, the stria medullaris thalami act as a relay
point for limbic system information that is transmitted to the
midbrain (Carpenter, p. 252; Martin, p. 473).
Which retinal cell provides a mechanism for mediating
opposite responses in adjacen t groups of photoreceptor cells
that is used to enhance contrast between objects?
A. Plexiform cells
B. Amacrine
C. Horizontal cells
D. Ganglion
E. Bipolar cells
C. Horizontal cells
Visual information flows vertically from photoreceptor cells (outer nuclear layer) to bipolar cells (inner nuclear
layer) to ganglion cells (ganglion cell layer) as well as laterally via horizontal cells (outer plexiform layer) and amacrine
cells (inner plexiform layer). Light produces opposite effects
on the rate of bipolar cell firing depending on whether it stimulates the center or surrounding part of the cell’s receptive
field. Additionally, a lateral network of horizontal cells that
directly interconnect neighboring groups of photoreceptor
cells helps mediate this antagonist property. Hence, horizontal cells provide a mechanism for mediating opposite
responses in adjacent photoreceptor cells, which is used to
enhance luminance contrast. The precise role of amacrine
cells remains unclear, although some amacrine cells function like horizontal cells. They mediate antagonistic inputs
between bipolar cells and ganglion cells in the inner plexiform layer. Other amacrine cells have been implicated in
shaping the complex receptive field properties of various
types of ganglion cells, such as M-type cells that process
orientation information (Pritchard, pp. 292- 302; Kandel,
p.515).
What deficit may result from damage to Exner’s area?
A. Alexia
B. Aphasia
C. Agraphia
D. Anosmia
E. Apathy
C. Agraphia
Match the following structures with the appropriate letterhead on the following axial CT scans (Figures 8.17-
8.24Q a, b, c) of the right petrous temporal bone, using each
answer only once
Vestibule
F
Match the following structures with the appropriate letterhead on the following axial CT scans (Figures 8.17-
8.24Q a, b, c) of the right petrous temporal bone, using each
answer only once
Cochlea
H
Match the following structures with the appropriate letterhead on the following axial CT scans (Figures 8.17-
8.24Q a, b, c) of the right petrous temporal bone, using each
answer only once
Posterior semicircular canal
E
Match the following structures with the appropriate letterhead on the following axial CT scans (Figures 8.17-
8.24Q a, b, c) of the right petrous temporal bone, using each
answer only once
Lateral semicircular cana
A
Match the following structures with the appropriate letterhead on the following axial CT scans (Figures 8.17-
8.24Q a, b, c) of the right petrous temporal bone, using each
answer only once
Vestibular aqueduct
D
Match the following structures with the appropriate letterhead on the following axial CT scans (Figures 8.17-
8.24Q a, b, c) of the right petrous temporal bone, using each
answer only once
Facial nerve
B
Match the following structures with the appropriate letterhead on the following axial CT scans (Figures 8.17-
8.24Q a, b, c) of the right petrous temporal bone, using each
answer only once
Superior semicircular canal
B
Match the following structures with the appropriate letterhead on the following axial CT scans (Figures 8.17-
8.24Q a, b, c) of the right petrous temporal bone, using each
answer only once
Endolymphatic duct
I
Which of the following is a flow-regulated valve?
A. Orbis-Sigma valve
B. PS Medical Delta valve
C. Cordis horizontal-vertical valve
D. Codman Hakim programmable valve
E. Holter-Hausner valve
**A. Orbis-Sigma valve **
What is the diagnosis ?
A. Porencephaly
B. Cortical dysplasia
C. Open-lip schizencephaly
D. Arachnoid cyst
E. Closed-lip schizencephaly
**C. Open-lip schizencephaly **
This abnormality is believed to result from failure of
what embryologic stage of development?
A. Primary neurulation
B. Secondary neurulation
C. Disjunction
**D. Cellular migration **
E. Myelination
**D. Cellular migration **
All of the following are derived from a common precursor
EXCEPT?
A. ACTH
B. ~I’lelanocyte-stimulating hormone
C. Beta lipotropin
D. Beta endorphin
E. Leucine-enkephalin
E. Leucine-enkephalin
A 62-year-old female undergoes uncomplicated transsphenoidal resection of a pituitary macroadenoma and is recovering in the intensive care unit. Postoperatively, she
develops increased thirst, nausea, elevated urine output (> 300
mL for 3 consecutive hours), hyperna tremia (149 mEq/L),
and a serum osmolarity of 323 mEq/L. At this point, optimal
trea tment for this patient should include what?
A. Fludrocortisone acetate
B. Urea
C. Oral desmopressin acetate (DDAVP)
D. r.rgilline vasopressin (aqueous Pitressin) intravenously
E. Pitressin in tannic oil suspension intramuscularly
D. r.rgilline vasopressin (aqueous Pitressin) intravenously
What is depicted on the EEG below (Figure S.30Q)?
A. Absence seizure
B. Left temporal lobe spike-and-wave discharges
C. Alpha rhythm
D. Theta rhythm
E. K complexes
**C. Alpha rhythm **
A 54-year-old female awakens from surgery for an
elective right ophthalmic artery aneurysm clipping with
complete right eye blindness and no other neurologic deficit.
A cerebral angiogram reveals incorporation of the ophthalmic
artery origin into the clip construct. What other finding(s)
may be present on the angiogram?
A. Occlusion of the right internal carotid artery with
inadequate posterior or anterior communicating
artery collaterals
B. Vasospasm of the right internal carotid artery
C. Poor collateral filling of the right globe from the
maxillary and facial arteries
D. Inadequate ascending pharyngeal artery collateral flow
to the right globe
E. All of the above
**C. Poor collateral filling of the right globe from the
maxillary and facial arteries **
A 28-year-old obese male presents with a 2-montl1 history of headaches and diplopia. He is found to harbor the
lesion depicted in the photomicrograph below (Figure 8.32-
8.33Q). What should be the next course of treatment after
surgical resection of this lesion?
A. Whole-brain radiation therapy
B. Radiosurgery
C. Chemotherapy
D. Observation and serial MRI
E. Proton-beam radiotherapy
D. Observation and serial MRI
What does the arrow in this photomicrograph depict?
A. Capillary telangiectasia
B. Gemistocytes
C. Rosenthal fibers
D. Normal blood vessels
E. Melanin granules
**C. Rosenthal fibers **
An infant is able to transfer objects from hand to hand,
bear some of his weight, lift his head off the table prior to
being pulled up, and turn his head to voice. ‘'’hat is the
approximate age of this child?
A. 2 months
B. 4 months
C. 6 months
D. 8 months
E. 10 months
C. 6 months
All of the following reflexes generally disappear by 4 to
6 months of age EXCEPT?
A. Suck
B. Palmar grasp
C. Tonic neck
D. Ventral suspension (Landau)
E. Placing/stepping
**D. Ventral suspension (Landau) **
What is the earliest visual field cut experienced by
patients with ophthalmic artery aneurysms?
A. Monocular inferior temporal quadrantanopsia
B. Monocular superior temporal quadrantanopsia
C. lvlonocular superior nasal quadrantanopsia
D. Binocular inferior nasal quadrantanopsia
E. Binocular temporal hemianopsia
**D. Binocular inferior nasal quadrantanopsia **
Which of the following structures are usually either
drilled or sectioned during surgical exposure of large
ophthalmic artery aneurysms?
1. Falciform ligament
2. Distal dural ring
3. Anterior clinoid process
4. Optic strut
A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above
**E. All of the above **
A 42-year-old right-handed male presents to an emergency department with seizures. I-lis CT and MRI studies
show a fairly well circumscribed, heterogenously enhancing
right frontal lesion with patchy calcification and surrounding
edema suggestive of an oligodendroglioma. All of the following are true about this tumor EXCEPT?
A. The polypeptide glial fibrillary acidic protein (GFAP) is
not expressed by oligodendrocytes
B. They account for approximately 5% of all primary
intracranial neoplasms
C. Identifying the oligodendroglial component on frozen
section is usually facilitated by the classic “fried egg”
appearance of the perinuclear halo
D. The greater the degree of anaplasia, the shorter the
survival
E. There is a strong association between response to
PCV (procarbazine, CCNU, and vincristine) chemotherapy and allelic loss on 1p/19q in anaplastic
oligodendrogliomas
**C. Identifying the oligodendroglial component on frozen
section is usually facilitated by the classic “fried egg”
appearance of the perinuclear halo **
Which of the following structures contains second-order
neurons of the spinocerebellar tracts ?
A. Clarke’s nucleus
B. Nucleus gracilis/cuneatus
C. Accessory cuneate nucleus
D. Inferior olives
E. Both A and C
**E. Both A and C **
Where is the cortical representation of macular vision?
A. Occipital poles
B. Lower bank of the calcarine sulcus
C. Temporoparieto-occipital junction
D. Precuneus
E. Superior bank of calcarine sulcus
**A. Occipital poles **
What is the first site of binaural convergence within the
auditory pathway?
A. Dorsal cochlear nuclei
B. Laterallemniscus
C. Superior olive
D. ivredial geniculate bodies
E. Inferior colliculi
A. Dorsal cochlear nuclei
The superior olivary nuclei receive the ventral acoustic striae and contain third-order auditory neurons that subsequently project to the contralateral lateral lemniscus. The
superior olives are the initial sites of binaural convergence
within the auditory pathway (Kandel, pp. 606- 608)
A 42-year-old male underwent a therapeutic interventional neuroradiologic procedure. What is depicted on his
angiogram below (Figure 8.42Q)?
A. Intraprocedural aneurysmal rupture
B. Poor distal middle cerebral artery perfusion
C. An enlarged tentorial artery supplying a lateral pontine
arterial-venous malformation
D. A dural arterial-venous fistula
E. Type II carotid-cavernous fistula
**A. Intraprocedural aneurysmal rupture **
The angiogram depicts a right posterior carotid wall
aneurysm as well as extravasation of contrast dye from
the aneurysm in a patient about to be treated with GDC
embolization (microcatheter evident in internal carotid
artery). Intraprocedural aneurysmal rupture is reported to
occur in 2 to 8% of patients treated with GDC embolization.
It seems to be more prevalent during treatment of smaller
aneurysms, especially in the acute phase following SAl-I. It
may occur during several phases of the embolization procedure. When the microcatheter is responsible for the rupture,
it is important to avoid withdrawing the device prematurely,
as the offending device often plugs the ruptured site and
prevents additional extravasation of blood. Similarly, if the
aneurysm ruptures during the coiling phase, it is important
that the clinician deploy the coil in an attempt to seal
the leak. In general, once rupture occurs, the remaining
aneurysmal sac should be packed as quickly as possible. In
refractory cases, temporary or permanent balloon occlusion
of the parent vessel or immediate surgical clipping may be
warranted (Youmans, pp. 2071-2072).
What is depicted on the ECG below (Figure 8.43Q)
A. Myocardial infarction
B. Hyperkalemia
C. Torsades de pointes
D. Digoxin toxicity
E. Atrial flutter
**A. Myocardial infarction **
Note the prominent ST-segment elevation in leads VI
through V” on this ECG, depicting an anterior wallmyocardial infarction. In general, ST-segment and T-wave changes
appear over the first minutes to hours of an infarction, and Q
waves appear over hours to days. An evolving myocardial
infarction may first manifest with peaked ‘1’ waves followed
by ST segment elevation and T-wave inversion. Eventually Q
waves may appear. In a large anterior wall infarction, these
changes are most apparent in leads VI through V(“ while in
an inferior infarction, these changes often occur in leads II,
III, and aVF. Of note, if a patient’s T waves are chronically
inverted> the peaking may make them appear normal-a
process referred to as pseudonormalization. T waves are
the least reliable of ST- and T-wave segment abnormalities
because many noncardiac events may influence them (i.e.,
elevated IC+) . Dying myocardial cells release their enzymes
into the bloodstream, and the increased concentration
should be confirmed in the peripheral blood (Fishman,
pp . 9 - 24; Marino, pp. 301-313).
A 16-year-old male with the MRl depicted
below (Figure 8.44-8.45Q) is referred to your office for
surgical evaluation. His laboratory studies reveal that he has
hypothyroidism, cortisol deficiency, and a prolactin level of
69. I-lis family states that they have noted behavior changes
and a recent increase in his weight. I-Ie has no vision with the
left eye and a dense temporal field cut of the right eye.
What is the most likely diagnosis?
A. Pituitary macroadenoma
B. Metastatic tumor invading the posterior pituitary gland
C. Craniopharyngioma
D. Sphenoid sinusitis
E. Invasive mucocele of the sphenoid sinus
**C. Craniopharyngioma **
The clinical history and MRl are most consistent
with a cystic craniopharyngioma. The modestly elevated
prolactin level is likely the result of the “stalk effect,”
whereby injury of the hypothalamus or pituitary stalk (i.e.,
from large tumors) results in modest elevations of prolactin
from reduced prolactin inhibitory factor levels (dopamine).
As a general rule, prolactin levels> 150 ng/mL are rarely
secondary to a stalk effect, whereas levels < 90 usually suggest a stalk injury. Large components of this tumor
extend inferiorly into the sphenoid sinus and superiorly into
the suprasellar space. Moreover, the optic chiasm appears
draped over the rostral margin of the tumor. Although these
are worrisome findings that warrant special concern, they
are not uncommon with craniopharyngioma. This sagittal
MRl shows that the posterior component of this tumor has
eroded through a significant portion of the tuberculum sella
and clivus, a relatively rare but significant finding. This latter
detail is especially concerning, since failure to recognize this
degree of bony erosion on preoperative MRl may result
in inadvertent injury to major posterior fossa structures
(basilar artery, perforating vessels) during transsphenoidal
tumor resection. Thyroxin (‘1’4) is generally preferred over
thyroid extract (‘1’.1) because blood levels are often more predictable. This is especially true for patients with concomitant
liver injury, as ‘1’.1 is converted to T4 in the liver. Patients with
ci’rrhosis may remain hypothyroid even while taking T..
Although it is preferable to correct hypothyroidism preoperatively, it is important to correct any cortisol deficiency as
well, as premature thyroid replacement can precipitate an
adrenal crisis in this group of patients. Thyroxine has been
shown to decrease phenytoin levels (Committee on Education
in Neurological Surgery, p. 102; Greenberg, pp. 419- 436).
A 16-year-old male with the MRl depicted
below (Figure 8.44-8.45Q) is referred to your office for surgical evaluation. His laboratory studies reveal that he has hypothyroidism, cortisol deficiency, and a prolactin level of 69. I-lis family states that they have noted behavior changes and a recent increase in his weight. I-Ie has no vision with the left eye and a dense temporal field cut of the right eye.
The prolactin level is elevated most likely secondary to what process?
A. Hook effect
B. Stalk effect
C. Avengaard effect
D. Tumor secretion
E. Prolactin-secreting lung nodule
B. Stalk effect
The clinical history and MRl are most consistent
with a cystic craniopharyngioma. The modestly elevated
prolactin level is likely the result of the “stalk effect,”
whereby injury of the hypothalamus or pituitary stalk (i.e.,
from large tumors) results in modest elevations of prolactin
from reduced prolactin inhibitory factor levels (dopamine).
As a general rule, prolactin levels> 150 ng/mL are rarely
secondary to a stalk effect, whereas levels < 90 usually suggest a stalk injury. Large components of this tumor
extend inferiorly into the sphenoid sinus and superiorly into
the suprasellar space. Moreover, the optic chiasm appears
draped over the rostral margin of the tumor. Although these
are worrisome findings that warrant special concern, they
are not uncommon with craniopharyngioma. This sagittal
MRl shows that the posterior component of this tumor has
eroded through a significant portion of the tuberculum sella
and clivus, a relatively rare but significant finding. This latter
detail is especially concerning, since failure to recognize this
degree of bony erosion on preoperative MRl may result
in inadvertent injury to major posterior fossa structures
(basilar artery, perforating vessels) during transsphenoidal
tumor resection. Thyroxin (‘1’4) is generally preferred over
thyroid extract (‘1’.1) because blood levels are often more predictable. This is especially true for patients with concomitant
liver injury, as ‘1’.1 is converted to T4 in the liver. Patients with
ci’rrhosis may remain hypothyroid even while taking T..
Although it is preferable to correct hypothyroidism preoperatively, it is important to correct any cortisol deficiency as
well, as premature thyroid replacement can precipitate an
adrenal crisis in this group of patients. Thyroxine has been
shown to decrease phenytoin levels (Committee on Education
in Neurological Surgery, p. 102; Greenberg, pp. 419- 436).
All of the following are typically associated with Behget’s
syndrome EXCEPT?
A. Uveitis
B. Genital ulcers
C. Aphthous stomatitis
D. Arthritis
E. Elevation of serum angiotensin-converting enzyme
E. Elevation of serum angiotensin-converting enzyme
Sarcoidosis, not Behget’s syndrome, is associated
with elevated levels of angiotensin-converting enzyme
(Merritt, pp. 121- 122).
Match the following questions with the associated EMG finding, using each answer only ONCE
Postexercise facilitation
A. Myasthenia gravis
B. Lambert-Eaton syndrome
C. Polymyositis
D. Carpal tunnel syndrome
E. Myotonia
F. None of the above
B. Lambert-Eaton syndrome
Match the following questions with the associated EMG finding, using each answer only ONCE
Decrementalmotor response
**A. Myasthenia gravis **
B. Lambert-Eaton syndrome
C. Polymyositis
D. Carpal tunnel syndrome
E. Myotonia
F. None of the above
**A. Myasthenia gravis **
Match the following questions with the associated EMG finding, using each answer only ONCE
“Dive bomber” frequency
A. Myasthenia gravis
B. Lambert-Eaton syndrome
C. Polymyositis
D. Carpal tunnel syndrome
E. Myotonia
F. None of the above
**E. Myotonia **
Match the following questions with the associated EMG finding, using each answer only ONCE
Myopathic motor units, fibrillation, pseudo myotonia
A. Myasthenia gravis
B. Lambert-Eaton syndrome
C. Polymyositis
D. Carpal tunnel syndrome
E. Myotonia
F. None of the above
**C. Polymyositis **
Match the following questions with the associated EMG finding, using each answer only ONCE
Sensory> motor latencies
A. Myasthenia gravis
B. Lambert-Eaton syndrome
C. Polymyositis
D. Carpal tunnel syndrome
E. Myotonia
F. None of the above
**D. Carpal tunnel syndrome **
A 13-year-old boy with a lytic skull lesion presents
with diabetes insipidus and the coronal Mill depicted below.
What is the most likely diagnosis?
A. Granular cell tumor
B. Sarcoidosis
C. Pituitary adenoma
D. Langerhans’ cell histiocytosis
E. Germinoma
D. Langerhans’ cell histiocytosis
Note the abnormally thickened stalk
with high signal intensity on this coronal MRl depicting
Langerhans’ cell histiocytosis. The etiology of this condition
is unlmown, but it is believed to result from overproliferation
of an antigen-presenting dendritic cell of bone marrow
origin. Although it is usually treated as a neoplastic process,
some speculate that it is due to malfunction of the immune
system. Other manifestations of this disease may include
lytic skull lesions (approximately 80% of cases) as well
as hematopoietic, hepatic, and pulmonary abnormalities.
A pathognomic finding of this condition on electron
microscopy is the presence of Birbeck granules, a unique
organelle of the Langerhans’ cell (Ramsey, pp. 381- 385;
Merritt, p. 872).
A 13-year-old boy with a lytic skull lesion presents
with diabetes insipidus and the coronal Mill depicted below.
This disorder is marked by proliferation of what cell type?
A. Fibroblasts
B. T-ceillymphocytes
C. Antigen-presenting dendritic cells
D. Eosinophils
E. Cells derived from Rathke’s pouch
**C. Antigen-presenting dendritic cells **
Note the abnormally thickened stalk
with high signal intensity on this coronal MRl depicting
Langerhans’ cell histiocytosis. The etiology of this condition
is unlmown, but it is believed to result from overproliferation
of an antigen-presenting dendritic cell of bone marrow
origin. Although it is usually treated as a neoplastic process,
some speculate that it is due to malfunction of the immune
system. Other manifestations of this disease may include
lytic skull lesions (approximately 80% of cases) as well
as hematopoietic, hepatic, and pulmonary abnormalities.
A pathognomic finding of this condition on electron
microscopy is the presence of Birbeck granules, a unique
organelle of the Langerhans’ cell (Ramsey, pp. 381- 385;
Merritt, p. 872).
A 13-year-old boy with a lytic skull lesion presents
with diabetes insipidus and the coronal Mill depicted below.
A pathognomonic finding of this condition on microscopy includes the presence of
A. Birbeck granules
B. Junctional complexes
c. Cholesterol crystals
D. Keratohyaline granules
E. Stippled chromatin
**A. Birbeck granules **
Note the abnormally thickened stalk
with high signal intensity on this coronal MRl depicting
Langerhans’ cell histiocytosis. The etiology of this condition
is unlmown, but it is believed to result from overproliferation
of an antigen-presenting dendritic cell of bone marrow
origin. Although it is usually treated as a neoplastic process,
some speculate that it is due to malfunction of the immune
system. Other manifestations of this disease may include
lytic skull lesions (approximately 80% of cases) as well
as hematopoietic, hepatic, and pulmonary abnormalities.
A pathognomic finding of this condition on electron
microscopy is the presence of Birbeck granules, a unique
organelle of the Langerhans’ cell (Ramsey, pp. 381- 385;
Merritt, p. 872).
What is depicted in the photolnicrograph below?
A. N eurofi broma
B. Transitional meningioma
C. Acoustic neuroma
D. Pilocytic astrocytoma
E. Pleomorphic xanthoastrocytoma
C. Acoustic neuroma
Acoustic neuroma. Note the palisading of nuclei
(picket fence-like arrangement) separated by an anuclear
area (arrow) on this photomicrograph, which depicts a
Verocay body (Ellison, pp. 695- 699).
What does the arrow depict?
A. Verocay body
B. Whorls
C. Psammoma body
D. Pseudopalisading
E. Antoni B area
**A. Verocay body **
Acoustic neuroma. Note the palisading of nuclei
(picket fence-like arrangement) separated by an anuclear
area (arrow) on this photomicrograph, which depicts a
Verocay body (Ellison, pp. 695- 699).
When a patient cannot adduct the right eye in attempting to.look to the left but the eye adducts on convergence, the
lesion is most likely in what location?
A. Right medial longitudinal fasciculus
B. Left mecliallongituclinal fasciculus
C. Left abducens nucleus
D. Right abducens nucleus
E. Nucleus of cranial nerve III
**A. Right medial longitudinal fasciculus **
A lesion of the MLF does not allow for transfer of information from the abducens nucleus (CN VI) to the opoculomotor nucleus (CN III) and results in internuclear
ophthalmoplegia (INO). It is characterized by deficient
adduction during attempted conjugate gaze away from the
side of the lvILF lesion and monocular nystagmus of the
abducting eye. An i’vILF lesion is on the same side as
the eye with the adduction wealmess, and INO is named
for the side of the J’vILF lesion. 1\ lesion in the nucleus of CN
III would paralyze volitional movements and convergence
(Kline, pp. 63-64).
Match the following peripheral nerve injuries
with the appropriate hand abnormality (Figure 8.58-8.63Q),
using each answer once , more than once, or not at all.
Injury of the median nerve at the level of the elbow
B
Compressive lesions of the
ulnar nerve at the level of the elbow, forea rm, or wrist can
produce a “claw hand” (A) in severe cases. The ulnar half
of the flexor digitorum profundus, lumbricals 3 and 4, the
dorsal and palmar interossei, and the hypothenar muscles
are typically paralyzed. When the metacarpophalangeal
joints are extended, the distal and proximal interphalangeal
joints cannot be extended because the interossei and half the
IUl11bricais are not functional, which results in a “claw-like”
posture. Laceration of the ulnar nerve in the wrist leaves
the innervation of the ulnar side of the flexor digitorum
profundus intact but can also result in a claw hand. There is
also loss of abduction of the thumb, so that a piece of paper
cannot be held between the side of the thumb and the index
finger.
Match the following peripheral nerve injuries
with the appropriate hand abnormality (Figure 8.58-8.63Q),
using each answer once , more than once, or not at all.
Injury of the ulnar nerve at the elbow
A
Compressive lesions of the
ulnar nerve at the level of the elbow, forea rm, or wrist can
produce a “claw hand” (A) in severe cases. The ulnar half
of the flexor digitorum profundus, lumbricals 3 and 4, the
dorsal and palmar interossei, and the hypothenar muscles
are typically paralyzed. When the metacarpophalangeal
joints are extended, the distal and proximal interphalangeal
joints cannot be extended because the interossei and half the
IUl11bricais are not functional, which results in a “claw-like”
posture. Laceration of the ulnar nerve in the wrist leaves
the innervation of the ulnar side of the flexor digitorum
profundus intact but can also result in a claw hand. There is
also loss of abduction of the thumb, so that a piece of paper
cannot be held between the side of the thumb and the index
finger.
Match the following peripheral nerve injuries
with the appropriate hand abnormality (Figure 8.58-8.63Q),
using each answer once , more than once, or not at all.
Injury of the ulnar nerve at the wrist
A
Compressive lesions of the
ulnar nerve at the level of the elbow, forea rm, or wrist can
produce a “claw hand” (A) in severe cases. The ulnar half
of the flexor digitorum profundus, lumbricals 3 and 4, the
dorsal and palmar interossei, and the hypothenar muscles
are typically paralyzed. When the metacarpophalangeal
joints are extended, the distal and proximal interphalangeal
joints cannot be extended because the interossei and half the
IUl11bricais are not functional, which results in a “claw-like”
posture. Laceration of the ulnar nerve in the wrist leaves
the innervation of the ulnar side of the flexor digitorum
profundus intact but can also result in a claw hand. There is
also loss of abduction of the thumb, so that a piece of paper
cannot be held between the side of the thumb and the index
finger.
Match the following peripheral nerve injuries
with the appropriate hand abnormality (Figure 8.58-8.63Q),
using each answer once , more than once, or not at all.
Anterior interosseous nerve injury
C
Compressive lesions of the
ulnar nerve at the level of the elbow, forea rm, or wrist can
produce a “claw hand” (A) in severe cases. The ulnar half
of the flexor digitorum profundus, lumbricals 3 and 4, the
dorsal and palmar interossei, and the hypothenar muscles
are typically paralyzed. When the metacarpophalangeal
joints are extended, the distal and proximal interphalangeal
joints cannot be extended because the interossei and half the
IUl11bricais are not functional, which results in a “claw-like”
posture. Laceration of the ulnar nerve in the wrist leaves
the innervation of the ulnar side of the flexor digitorum
profundus intact but can also result in a claw hand. There is
also loss of abduction of the thumb, so that a piece of paper
cannot be held between the side of the thumb and the index
finger.
Match the following peripheral nerve injuries
with the appropriate hand abnormality (Figure 8.58-8.63Q),
using each answer once , more than once, or not at all.
Klumpke’s paralysis
D
Compressive lesions of the
ulnar nerve at the level of the elbow, forea rm, or wrist can
produce a “claw hand” (A) in severe cases. The ulnar half
of the flexor digitorum profundus, lumbricals 3 and 4, the
dorsal and palmar interossei, and the hypothenar muscles
are typically paralyzed. When the metacarpophalangeal
joints are extended, the distal and proximal interphalangeal
joints cannot be extended because the interossei and half the
IUl11bricais are not functional, which results in a “claw-like”
posture. Laceration of the ulnar nerve in the wrist leaves
the innervation of the ulnar side of the flexor digitorum
profundus intact but can also result in a claw hand. There is
also loss of abduction of the thumb, so that a piece of paper
cannot be held between the side of the thumb and the index
finger.
Match the following peripheral nerve injuries
with the appropriate hand abnormality (Figure 8.58-8.63Q),
using each answer once , more than once, or not at all.
C8 root lesion
C
Compressive lesions of the
ulnar nerve at the level of the elbow, forea rm, or wrist can
produce a “claw hand” (A) in severe cases. The ulnar half
of the flexor digitorum profundus, lumbricals 3 and 4, the
dorsal and palmar interossei, and the hypothenar muscles
are typically paralyzed. When the metacarpophalangeal
joints are extended, the distal and proximal interphalangeal
joints cannot be extended because the interossei and half the
IUl11bricais are not functional, which results in a “claw-like”
posture. Laceration of the ulnar nerve in the wrist leaves
the innervation of the ulnar side of the flexor digitorum
profundus intact but can also result in a claw hand. There is
also loss of abduction of the thumb, so that a piece of paper
cannot be held between the side of the thumb and the index
finger.
Match each of the following lesion sites with the
associated clinical deficit.
Posterior end of the inferior frontal gyrus
A. Dressing apncda
B. Writing apraxia
C. Speech apraxia
D. Gait apraxia
E. Prosopagnosia
F. Astereognosis
G. None of the above
**C. Speech apraxia **
Apraxia is defined as the
inability to execute a normal volitional act despite the fact
that the motor systems and mental status are relatively
intact. Speech apraxia often results from a lesion near the
posterior part of the inferior frontal gyrus (approximately
area 44), while writing apraxia or dysgraphia results from
damage in the left angular gyrus. Dressing apraxia results
from damage in the posterior right parietal lobe, while gait
apraxia is usually associated with diffuse cerebral disease
such as Alzheimer’s disease. Lesions that affect the inferomedial part of the temporo-occipital region tend to cause an
inability to recognize facial features (pl:osopagnosia), while
lesions of either parietal lobe rnay produce astereognosis, in
which patients fail to recognize the forms of objects when felt
but not when viewed (Brazis, pp. 481-508).
Match each of the following lesion sites with the
associated clinical deficit.
Left angular gyrus
A. Dressing apncda
B. Writing apraxia
C. Speech apraxia
D. Gait apraxia
E. Prosopagnosia
F. Astereognosis
G. None of the above
**B. Writing apraxia **
Apraxia is defined as the
inability to execute a normal volitional act despite the fact
that the motor systems and mental status are relatively
intact. Speech apraxia often results from a lesion near the
posterior part of the inferior frontal gyrus (approximately
area 44), while writing apraxia or dysgraphia results from
damage in the left angular gyrus. Dressing apraxia results
from damage in the posterior right parietal lobe, while gait
apraxia is usually associated with diffuse cerebral disease
such as Alzheimer’s disease. Lesions that affect the inferomedial part of the temporo-occipital region tend to cause an
inability to recognize facial features (pl:osopagnosia), while
lesions of either parietal lobe rnay produce astereognosis, in
which patients fail to recognize the forms of objects when felt
but not when viewed (Brazis, pp. 481-508).
Match each of the following lesion sites with the
associated clinical deficit.
Posterior part of right parietal lobe
A. Dressing apncda
B. Writing apraxia
C. Speech apraxia
D. Gait apraxia
E. Prosopagnosia
F. Astereognosis
G. None of the above
**A. Dressing apncda **
Apraxia is defined as the
inability to execute a normal volitional act despite the fact
that the motor systems and mental status are relatively
intact. Speech apraxia often results from a lesion near the
posterior part of the inferior frontal gyrus (approximately
area 44), while writing apraxia or dysgraphia results from
damage in the left angular gyrus. Dressing apraxia results
from damage in the posterior right parietal lobe, while gait
apraxia is usually associated with diffuse cerebral disease
such as Alzheimer’s disease. Lesions that affect the inferomedial part of the temporo-occipital region tend to cause an
inability to recognize facial features (pl:osopagnosia), while
lesions of either parietal lobe rnay produce astereognosis, in
which patients fail to recognize the forms of objects when felt
but not when viewed (Brazis, pp. 481-508).
Match each of the following lesion sites with the
associated clinical deficit.
Diffuse cerebral disease
A. Dressing apncda
B. Writing apraxia
C. Speech apraxia
D. Gait apraxia
E. Prosopagnosia
F. Astereognosis
G. None of the above
**D. Gait apraxia **
Apraxia is defined as the
inability to execute a normal volitional act despite the fact
that the motor systems and mental status are relatively
intact. Speech apraxia often results from a lesion near the
posterior part of the inferior frontal gyrus (approximately
area 44), while writing apraxia or dysgraphia results from
damage in the left angular gyrus. Dressing apraxia results
from damage in the posterior right parietal lobe, while gait
apraxia is usually associated with diffuse cerebral disease
such as Alzheimer’s disease. Lesions that affect the inferomedial part of the temporo-occipital region tend to cause an
inability to recognize facial features (pl:osopagnosia), while
lesions of either parietal lobe rnay produce astereognosis, in
which patients fail to recognize the forms of objects when felt
but not when viewed (Brazis, pp. 481-508).
Match each of the following lesion sites with the
associated clinical deficit.
Medial inferior temporo-occipital region
A. Dressing apncda
B. Writing apraxia
C. Speech apraxia
D. Gait apraxia
E. Prosopagnosia
F. Astereognosis
G. None of the above
**E. Prosopagnosia **
Apraxia is defined as the
inability to execute a normal volitional act despite the fact
that the motor systems and mental status are relatively
intact. Speech apraxia often results from a lesion near the
posterior part of the inferior frontal gyrus (approximately
area 44), while writing apraxia or dysgraphia results from
damage in the left angular gyrus. Dressing apraxia results
from damage in the posterior right parietal lobe, while gait
apraxia is usually associated with diffuse cerebral disease
such as Alzheimer’s disease. Lesions that affect the inferomedial part of the temporo-occipital region tend to cause an
inability to recognize facial features (pl:osopagnosia), while
lesions of either parietal lobe rnay produce astereognosis, in
which patients fail to recognize the forms of objects when felt
but not when viewed (Brazis, pp. 481-508).
Match each of the following lesion sites with the
associated clinical deficit.
Either parietal lobe
A. Dressing apncda
B. Writing apraxia
C. Speech apraxia
D. Gait apraxia
E. Prosopagnosia
F. Astereognosis
G. None of the above
**F. Astereognosis **
Apraxia is defined as the
inability to execute a normal volitional act despite the fact
that the motor systems and mental status are relatively
intact. Speech apraxia often results from a lesion near the
posterior part of the inferior frontal gyrus (approximately
area 44), while writing apraxia or dysgraphia results from
damage in the left angular gyrus. Dressing apraxia results
from damage in the posterior right parietal lobe, while gait
apraxia is usually associated with diffuse cerebral disease
such as Alzheimer’s disease. Lesions that affect the inferomedial part of the temporo-occipital region tend to cause an
inability to recognize facial features (pl:osopagnosia), while
lesions of either parietal lobe rnay produce astereognosis, in
which patients fail to recognize the forms of objects when felt
but not when viewed (Brazis, pp. 481-508).
Where do afferent axons serving the muscle stretch
reflex synapse?
A. Dorsal root ganglia
B. Dorsal horn neurons
C. Ventral motoneuron
D. Clarke’s nucleus
E. Rexedlamina III
**C. Ventral motoneuron **
The muscle stretch reflex is a monosynaptic circuit
that is dependent on two neurons. Afferent axons serving
the muscle stretch reflex synapse directly with ventralmotoneurons (Carpenter, p. 79).
A 35-year-old construction worker fell from a three-story
building while at work and suffered a complete spinal cord
injury at the C2 level. Which of the following functions may
be preserved after a complete spinal cord injury at this level?
1. J’dicturition
2. Ejaculation
3. Peristalsis
4. Breathing
A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above
A. 1,2, and 3 are correct
After a complete spinal cord injury, all voluntary
movements and sensation below the level of the lesion are
lost, but a number of visceral reflexes may be preserved
in some cases. A patient with a complete C2 spinal cord
injury is unlikely to be able to breathe, since the spinal cord
does not contain intrinsic circuitry for breathing. Retained
reflexes may include micturition, defecation, peristalsis, and
possibly even ejaculation, although there may be no sensation of the sexual act (Brazis, pp. 85- 88; DeMyer, pp. 142-
143).
A 15-year-old-girl sees her physician for a physical
examination prior to the start of soccer season. The physician notices that the palate fails to elevate on the left side
when the patient says “Ah.” What other associated deficits
may be seen in this patient?
1. Swallowing
2. Phonation
3. Taste
4. Salivation
A. 1,2, and 3
B. 1 and 3
C. 2 and4
D. Only 4 is correct
E. All of the above
**A. 1,2, and 3 **
The most important cranial nerve for palatal elevation
is generally CN X. Interruption of the left CN X can cause
paralysis of palatal elevation on the left side. Taste, swallowing, and phonation are also partially subserved by CN Xi
therefore an insult to this cranial nerve may result in problems with speech, swallowing, and taste. Salivation problems
may be evident with deficits in CN VII and IX (Carpenter,
pp.137-144,172-173).
Match each of the spinal cord tracts with the
appropriate clinical correlate (Figure 8.73- 8.80), using each
answer once, more than once, or not at all. Major ascending
tracts are depicted on the left, while descending tracts are
shown on the right.
Small peripheral myelinated fibers of tills pathway
synapse in the substantia gelatinosa of the dorsal horn
I
The major ascending tracts of the spinal cord (left) are the dorsal columns,
spinothalamic tract, dOl’sal spinocerebellar tract, and ventral
spinocerebellar tract. The dOl’sal columns convey tactile
discrimination (Meissner corpuscles), vibration (pacinian
corpuscle), joint position sense (muscle spindles and Golgi
tendon organs), and conscious proprioception. First-order
neurons give rise to axons that ascend in the fasciculus
cuneatus (A, upper extremity fibers) and gracilis (E, lower
extremity), which terminate in the gracile and cuneate
nuclei of the medulla. Second-order neurons, known as
arcuate fibers, cross to the contralateral side as the medial
lemniscus and ascend to the ventral posterolateral (VPL)
nucleus of the thalamus. Synaptic connections are then
made in the thalamus with third-order neurons, which travel
through the posterior limb of the internal capsule to reach
the postcentral gyrus of the cerebral cortex.
Match each of the spinal cord tracts with the
appropriate clinical correlate (Figure 8.73- 8.80), using each
answer once, more than once, or not at all. Major ascending
tracts are depicted on the left, while descending tracts are
shown on the right.
These fibers pass through the superior cerebellar peduncle
J
The major ascending tracts of the spinal cord (left) are the dorsal columns,
spinothalamic tract, dOl’sal spinocerebellar tract, and ventral
spinocerebellar tract. The dOl’sal columns convey tactile
discrimination (Meissner corpuscles), vibration (pacinian
corpuscle), joint position sense (muscle spindles and Golgi
tendon organs), and conscious proprioception. First-order
neurons give rise to axons that ascend in the fasciculus
cuneatus (A, upper extremity fibers) and gracilis (E, lower
extremity), which terminate in the gracile and cuneate
nuclei of the medulla. Second-order neurons, known as
arcuate fibers, cross to the contralateral side as the medial
lemniscus and ascend to the ventral posterolateral (VPL)
nucleus of the thalamus. Synaptic connections are then
made in the thalamus with third-order neurons, which travel
through the posterior limb of the internal capsule to reach
the postcentral gyrus of the cerebral cortex.
Match each of the spinal cord tracts with the
appropriate clinical correlate (Figure 8.73- 8.80), using each
answer once, more than once, or not at all. Major ascending
tracts are depicted on the left, while descending tracts are
shown on the right.
This tract arises from Dieter’s nucleus
F
The major ascending tracts of the spinal cord (left) are the dorsal columns,
spinothalamic tract, dOl’sal spinocerebellar tract, and ventral
spinocerebellar tract. The dOl’sal columns convey tactile
discrimination (Meissner corpuscles), vibration (pacinian
corpuscle), joint position sense (muscle spindles and Golgi
tendon organs), and conscious proprioception. First-order
neurons give rise to axons that ascend in the fasciculus
cuneatus (A, upper extremity fibers) and gracilis (E, lower
extremity), which terminate in the gracile and cuneate
nuclei of the medulla. Second-order neurons, known as
arcuate fibers, cross to the contralateral side as the medial
lemniscus and ascend to the ventral posterolateral (VPL)
nucleus of the thalamus. Synaptic connections are then
made in the thalamus with third-order neurons, which travel
through the posterior limb of the internal capsule to reach
the postcentral gyrus of the cerebral cortex.
Match each of the spinal cord tracts with the
appropriate clinical correlate (Figure 8.73- 8.80), using each
answer once, more than once, or not at all. Major ascending
tracts are depicted on the left, while descending tracts are
shown on the right.
Conscious proprioception from the legs is mainly transmitted in this tract
B
The major ascending tracts of the spinal cord (left) are the dorsal columns,
spinothalamic tract, dOl’sal spinocerebellar tract, and ventral
spinocerebellar tract. The dOl’sal columns convey tactile
discrimination (Meissner corpuscles), vibration (pacinian
corpuscle), joint position sense (muscle spindles and Golgi
tendon organs), and conscious proprioception. First-order
neurons give rise to axons that ascend in the fasciculus
cuneatus (A, upper extremity fibers) and gracilis (E, lower
extremity), which terminate in the gracile and cuneate
nuclei of the medulla. Second-order neurons, known as
arcuate fibers, cross to the contralateral side as the medial
lemniscus and ascend to the ventral posterolateral (VPL)
nucleus of the thalamus. Synaptic connections are then
made in the thalamus with third-order neurons, which travel
through the posterior limb of the internal capsule to reach
the postcentral gyrus of the cerebral cortex.
Match each of the spinal cord tracts with the
appropriate clinical correlate (Figure 8.73- 8.80), using each
answer once, more than once, or not at all. Major ascending
tracts are depicted on the left, while descending tracts are
shown on the right.
Carries fibers from medial and inferior vestibular nuclei,
tectospinal tract, and interstitial nucleus of Cajal
G
The major ascending tracts of the spinal cord (left) are the dorsal columns,
spinothalamic tract, dOl’sal spinocerebellar tract, and ventral
spinocerebellar tract. The dOl’sal columns convey tactile
discrimination (Meissner corpuscles), vibration (pacinian
corpuscle), joint position sense (muscle spindles and Golgi
tendon organs), and conscious proprioception. First-order
neurons give rise to axons that ascend in the fasciculus
cuneatus (A, upper extremity fibers) and gracilis (E, lower
extremity), which terminate in the gracile and cuneate
nuclei of the medulla. Second-order neurons, known as
arcuate fibers, cross to the contralateral side as the medial
lemniscus and ascend to the ventral posterolateral (VPL)
nucleus of the thalamus. Synaptic connections are then
made in the thalamus with third-order neurons, which travel
through the posterior limb of the internal capsule to reach
the postcentral gyrus of the cerebral cortex.
Match each of the spinal cord tracts with the
appropriate clinical correlate (Figure 8.73- 8.80), using each
answer once, more than once, or not at all. Major ascending
tracts are depicted on the left, while descending tracts are
shown on the right.
Fibers from this tract originate from layer V of the
cerebral cortex
C
The major ascending tracts of the spinal cord (left) are the dorsal columns,
spinothalamic tract, dOl’sal spinocerebellar tract, and ventral
spinocerebellar tract. The dOl’sal columns convey tactile
discrimination (Meissner corpuscles), vibration (pacinian
corpuscle), joint position sense (muscle spindles and Golgi
tendon organs), and conscious proprioception. First-order
neurons give rise to axons that ascend in the fasciculus
cuneatus (A, upper extremity fibers) and gracilis (E, lower
extremity), which terminate in the gracile and cuneate
nuclei of the medulla. Second-order neurons, known as
arcuate fibers, cross to the contralateral side as the medial
lemniscus and ascend to the ventral posterolateral (VPL)
nucleus of the thalamus. Synaptic connections are then
made in the thalamus with third-order neurons, which travel
through the posterior limb of the internal capsule to reach
the postcentral gyrus of the cerebral cortex.
Match each of the spinal cord tracts with the
appropriate clinical correlate (Figure 8.73- 8.80), using each
answer once, more than once, or not at all. Major ascending
tracts are depicted on the left, while descending tracts are
shown on the right.
Carries fibers that ascend to either the thalamus, periaqueductal gray, reticular formation , or superior colliculus
I
The major ascending tracts of the spinal cord (left) are the dorsal columns,
spinothalamic tract, dOl’sal spinocerebellar tract, and ventral
spinocerebellar tract. The dOl’sal columns convey tactile
discrimination (Meissner corpuscles), vibration (pacinian
corpuscle), joint position sense (muscle spindles and Golgi
tendon organs), and conscious proprioception. First-order
neurons give rise to axons that ascend in the fasciculus
cuneatus (A, upper extremity fibers) and gracilis (E, lower
extremity), which terminate in the gracile and cuneate
nuclei of the medulla. Second-order neurons, known as
arcuate fibers, cross to the contralateral side as the medial
lemniscus and ascend to the ventral posterolateral (VPL)
nucleus of the thalamus. Synaptic connections are then
made in the thalamus with third-order neurons, which travel
through the posterior limb of the internal capsule to reach
the postcentral gyrus of the cerebral cortex.
Match each of the spinal cord tracts with the
appropriate clinical correlate (Figure 8.73- 8.80), using each
answer once, more than once, or not at all. Major ascending
tracts are depicted on the left, while descending tracts are
shown on the right.
Uncrossed pyramidal fibers mainly supplying the axial
musculature
H
The major ascending tracts of the spinal cord (left) are the dorsal columns,
spinothalamic tract, dOl’sal spinocerebellar tract, and ventral
spinocerebellar tract. The dOl’sal columns convey tactile
discrimination (Meissner corpuscles), vibration (pacinian
corpuscle), joint position sense (muscle spindles and Golgi
tendon organs), and conscious proprioception. First-order
neurons give rise to axons that ascend in the fasciculus
cuneatus (A, upper extremity fibers) and gracilis (E, lower
extremity), which terminate in the gracile and cuneate
nuclei of the medulla. Second-order neurons, known as
arcuate fibers, cross to the contralateral side as the medial
lemniscus and ascend to the ventral posterolateral (VPL)
nucleus of the thalamus. Synaptic connections are then
made in the thalamus with third-order neurons, which travel
through the posterior limb of the internal capsule to reach
the postcentral gyrus of the cerebral cortex.
Facial nerve displacement by an acoustic neuroma is most commonly (in decreasing order of frequency) in what
direction?
A. Inferior, followed by anterior, superior, and posterior
B. Anterior, followed by superior, inferior, and posterior
C. Anterior, followed by inferior, superior, and posterior
D. Posterior, followed by anterior, inferior, and rarely
superior
E. Superior, followed by inferior, anterior, and posterior
**B. Anterior, followed by superior, inferior, and posterior **
Facial nerve displacement by an acoustic neuroma is
most commonly (in deCI’easing order of frequency) anterior,
followed by superior, inferior, and posterior. The facial nerve
is often stretched during microdissection and is most susceptible to injury at the proximal rim of the porus acusticus
(Connolly, p. 475)
Paralysis of pelvic floor muscles, symmetric saddle
anesthesia, impaired erection and ejaculation, constipation,
and an autonomous neurogenic bladder best describe what spinal cord lesion?
A. Lesion of the first and second sacral segments
B. Cauda equina syndrome
C. Conus medullaris syndrome
D. Tethered cord syndrome
E. Syringomyelia
**C. Conus medullaris syndrome **
Paralysis of pelvic floor muscles, early sphincter
and bladder dysfunction, symmetric saddle anestheSia, impaired erection and ejaculation, constipation, and minimal
pain best characterize the conus medullaris syndrome.
A tethered cord may present with a combination of neurologic, urologic , orthopediC, and dermatologic manifestations.
Commonly patients present with numb feet, muscle atrophy,
upper motor neuron Signs, bowel and bladder dysfunction,
foot deformities, scoliOSiS, and cutaneous stigmata of spinal
dysraphism. Compression of the lumbar and sacral roots
below L3 often results in cauda equina syndrome, which is
characterized by early pain, asymmetric saddle anesthesia,
and a variable patellar reflex response . Sphincter changes
are often similar to those of the conus medullaris syndrome
but tend to occur late in the clinical course. With Sllesions,
there is weakness of the triceps surae, flexor digitorum
longus (FDL), flexor hallucis longus (FHL), and small foot
muscles. The Achilles reflexes are absent, whereas the patellar reflexes are preserved. There is complete sensory loss
over the sole, heel, and outer part of the foot and ankle .
The gastrocnemius and soleus muscles are stronger with S2
segmental lesions, however, the FDL, FHL, and foot muscles
remain weak. The sensory loss tends to involve the upper
part of the dOl’sal calf, dorsolateral thigh, and the saddle area
(Brazis, pp. 99-100)
The finding depicted on the CT scan below (Figure 8.83Q) is most likely to occur after
A. Berry aneurysm rupture
B. Infection
C. Extradural carotid artery dissection
D. Trauma
E. Contrast administration
**D. Trauma **
This CT demonstrates a subarachnoid hemorrhage
(SAH), which is most commonly seen after trauma. Although
the blood pattern may vary, traumatic SAH often involves the
convexities of the cerebral hemispheres, while aneurysmal
subarachnoid hemorrhages generally have a preponderance
of blood in the basal cisterns (Greenberg, p. 754)
Vhat is the region of cerebral cortex most closely associated with the conscious perception of smell?
A. Temporal association cortex
B. Cingulate gyrus
C. Limbic system
D. Orbitofrontal cortex
E. Amygdala
D. Orbitofrontal cortex
Experimental studies indicate the orbitofrontal cortex is a key region involved with the conscious perception
of smell, as lesions in this region have been shown to result
in failure to discriminate between various odorants (Kandel,
p.633).
What is the most likely
diagnosis ?
A. Pilocytic astrocytoma
B. Medulloblastoma
C. Subacute infarct
D. Lhermitte-Duclos disease
E. Ependymoma
D. Lhermitte-Duclos disease
This T2-weighted image shows the hyperintense
and thickened folia in a characteristic laminated pattern
that is most consistent with Lhermitte-Duclos disease. It is
associated with hypertrophy of granular cell neurons and
axonal hypennyelination in the molecular layer (Osborn ON,
pp.69-70).
Which of the following best characterizes this abnormality?
A. These lesions typically have an abundance of Rosenthal
fibers
B. Most often secondary to vertebral artery occlusion
C. Hypertrophy of granular-cell neurons and axonal
hypermyelination in the molecular layer
D. Evidence of Homer-Wright rosettes on histopathologic
sectioning
E. Pseudorosettes on histopathologic sectioning
**C. Hypertrophy of granular-cell neurons and axonal
hypermyelination in the molecular layer **
This T2-weighted image shows the hyperintense
and thickened folia in a characteristic laminated pattern
that is most consistent with Lhermitte-Duclos disease. It is
associated with hypertrophy of granular cell neurons and
axonal hypennyelination in the molecular layer (Osborn ON,
pp.69-70).
A 42-year-old female presents to the emergency
department with staring spells and the T2-weighted MR
image depicted below (Figure 8.87Q). What is the most likely
diagnosis ?
A. Temporal lobe ganglioglioma
B. Dysembryoplastic neuroepithelial tumor
C. Epidermoid cyst
D. Aneurysm
E. Neurocysticercosis
**D. Aneurysm **
This T2-weighted MRI shows a right temporal lobe
mass with signal loss (flow void), which is most consistent
with a large middle cerebral artery anemysm (Osborn ON,
pp. 266- 268)
Match each of the following types of nystagmus
with the specific lesion areas, using each answer once, more
than once, or not at all.
Posterior diencephalon/pretectum (interstitial nucleus
of Cajal); suprasellar region
A. Downbeat nystagmus
B. Upbeat nystagmus
C. Seesaw nystagmus
D. Spasmus nutans
E. Ocular bobbing
F. Ocular flutter
G. Convergence-retraction nystagmus
H. Ocular myoclonus
I. Abducting nystagmus
J. Bruns nystagmus
**C. Seesaw nystagmus **
Match each of the following types of nystagmus
with the specific lesion areas, using each answer once, more
than once, or not at all.
Dorsal midbrain
A. Downbeat nystagmus
B. Upbeat nystagmus
C. Seesaw nystagmus
D. Spasmus nutans
E. Ocular bobbing
F. Ocular flutter
G. Convergence-retraction nystagmus
H. Ocular myoclonus
I. Abducting nystagmus
J. Bruns nystagmus
**G. Convergence-retraction nystagmus **
Match each of the following types of nystagmus
with the specific lesion areas, using each answer once, more
than once, or not at all.
Pons (medial longitudinal faSCiculus)
A. Downbeat nystagmus
B. Upbeat nystagmus
C. Seesaw nystagmus
D. Spasmus nutans
E. Ocular bobbing
F. Ocular flutter
G. Convergence-retraction nystagmus
H. Ocular myoclonus
I. Abducting nystagmus
J. Bruns nystagmus
**I. Abducting nystagmus **
Match each of the following types of nystagmus
with the specific lesion areas, using each answer once, more
than once, or not at all.
Central pons
A. Downbeat nystagmus
B. Upbeat nystagmus
C. Seesaw nystagmus
D. Spasmus nutans
E. Ocular bobbing
F. Ocular flutter
G. Convergence-retraction nystagmus
H. Ocular myoclonus
I. Abducting nystagmus
J. Bruns nystagmus
**E. Ocular bobbing **
Match each of the following types of nystagmus
with the specific lesion areas, using each answer once, more
than once, or not at all.
Ipsilateral inferior olive, red nucleus, contralateral
dentate nucleus (Mollaret triangle)
A. Downbeat nystagmus
B. Upbeat nystagmus
C. Seesaw nystagmus
D. Spasmus nutans
E. Ocular bobbing
F. Ocular flutter
G. Convergence-retraction nystagmus
H. Ocular myoclonus
I. Abducting nystagmus
J. Bruns nystagmus
H. Ocular myoclonus
Match each of the following types of nystagmus
with the specific lesion areas, using each answer once, more
than once, or not at all.
Medulla , ventral tegmentum of pons, cerebellar pathway
A. Downbeat nystagmus
B. Upbeat nystagmus
C. Seesaw nystagmus
D. Spasmus nutans
E. Ocular bobbing
F. Ocular flutter
G. Convergence-retraction nystagmus
H. Ocular myoclonus
I. Abducting nystagmus
J. Bruns nystagmus
**B. Upbeat nystagmus **
Match each of the following types of nystagmus
with the specific lesion areas, using each answer once, more
than once, or not at all.
Cervicomedullary junction
A. Downbeat nystagmus
B. Upbeat nystagmus
C. Seesaw nystagmus
D. Spasmus nutans
E. Ocular bobbing
F. Ocular flutter
G. Convergence-retraction nystagmus
H. Ocular myoclonus
I. Abducting nystagmus
J. Bruns nystagmus
**A. Downbeat nystagmus **
Match each of the following types of nystagmus
with the specific lesion areas, using each answer once, more
than once, or not at all.
Pontomedullary junction, vestibular pathways
A. Downbeat nystagmus
B. Upbeat nystagmus
C. Seesaw nystagmus
D. Spasmus nutans
E. Ocular bobbing
F. Ocular flutter
G. Convergence-retraction nystagmus
H. Ocular myoclonus
I. Abducting nystagmus
J. Bruns nystagmus
**J. Bruns nystagmus **
A patient suffers a closed head injury after a motor
vehicle collision and is noted to have ecchymosis over the
right eye, with diplopia when looking down and to the left.
The diplopia most likely represents wealmess of what muscle?
A. Right superior oblique
B. Left superior rectus
C. Right inferior rectus
D. Left inferior oblique
E. Right inferior oblique
**A. Right superior oblique **
Orbital injuries often impair the action of the superior
oblique muscle because of displacement of the trochlea,
which attaches to the anterior rim of the orbit and acts as a
sling for the recurrent course of the trochlear tendon.
Looking down and to the left typically involves the right
superior oblique (trochlear nerve , IV) and left inferior rectus
(oculomotor nerve , III) muscles. \Vhen the eyes look conjuga tely toward any object, the muscle that is the prime mover works in unison with the muscle of the opposite eye (Kline,
pp. 105- 114).
The lesion depicted on the photomicrograph below (Figure
8.97Q) may be associated with all of the following EXCEPT?
A. Autosomal dominant inheritance
B. Renal cell carcinoma
C. Pancreatic cysts
D. Overproduction of erythropoietin
E. Tumor suppressor gene that maps to chromosome 9p25
**E. Tumor suppressor gene that maps to chromosome 9p25 **
Note the numerous capillaries and cells with a vacuolated appearance in this photomicrograph depicting a
hemangioblastoma. This tumor is associated with VI-IL in
about 25% of cases, is carried in an autosomal dominant
fashion (chromosome 3p25), and is associated with retinal
angioma, renal cell carcinoma, renal and pancreatic cysts,
pheochromocytoma, or epididymal papillary cystadenoma .
This tumor may cause polycythemia in about 10% of cases
due to inappropriate production of erythropoietin (Ellison,
pp. 736- 738).
A 47-year-old female underwent clipping of a
ruptured middle cerebral artery bifurcation aneurysm and
required a blood transfusion while recovering in the ICU.
The patient developed hypotension, fever, confusion, and
back pain shortly after receiving the first unit of packed red
blood cells (PRECs).
What is the most likely etiology of these findings?
A. A prior sensitization in a patient who had a nondetectable level of antibody at the time of blood typing
B. ABO incompatibility
C. Antileukocyte antibodies in a patient with a prior
blood transfusion
D. Viral contamination of the PRECs
E. None of the above
**B. ABO incompatibility **
Acute hemolytic transfusion reactions are
uncommon and are rarely life-threatening. They are produced by antibodies in the recipient that bind to ABO surface
antigens or erythrocytes of mismatched donor blood. These
antibodies /L: complement and can produce rapid cell lysis
within minutes. Lysis then provokes a severe inflammatory
reaction, which can lead to hypotension, multiorgan dysfunction, and a host of other clinical findings. This type of
transfusion reaction is often the result of identification
errors, leading to ABO mismatched blood . The transfusion
should be stopped immediately; the volume status, urine
output, and blood pressure should be monitored and maintained; and the patient’s blood sent for free hemoglobin,
haptoglobin levels, and a Coombs’ test. Treatment includes
supportive care with maintenance of good urine out.
A 47-year-old female underwent clipping of a
ruptured middle cerebral artery bifurcation aneurysm and
required a blood transfusion while recovering in the ICU.
The patient developed hypotension, fever, confusion, and
back pain shortly after receiving the first unit of packed red
blood cells (PRECs).
What should be the next course of management in this
patient’s care?
A. The transfusion should be continued, but hemoglobin
and bilirubin levels should be checked
B. Administer diphenhydramine (25 mg) IV immediately
and continue the transfusion
C. Administer epinephrine (1:1000) 0.5 mg every 10 to
15 minutes until the adverse reaction subsides
D. The transfusion should be stopped and the patient’s
blood sent for free hemoglobin, haptoglobin levels, and
Coombs’ test
E. Stop the transfusion; administer acetaminophen and
diphenhydramine 30 minutes prior to any subsequent
blood transfusion
**D. The transfusion should be stopped and the patient’s blood sent for free hemoglobin, haptoglobin levels, and Coombs’ test **
Acute hemolytic transfusion reactions are
uncommon and are rarely life-threatening. They are produced by antibodies in the recipient that bind to ABO surface
antigens or erythrocytes of mismatched donor blood. These
antibodies /L: complement and can produce rapid cell lysis
within minutes. Lysis then provokes a severe inflammatory
reaction, which can lead to hypotension, multiorgan dysfunction, and a host of other clinical findings. This type of
transfusion reaction is often the result of identification
errors, leading to ABO mismatched blood . The transfusion
should be stopped immediately; the volume status, urine
output, and blood pressure should be monitored and maintained; and the patient’s blood sent for free hemoglobin,
haptoglobin levels, and a Coombs’ test. Treatment includes
supportive care with maintenance of good urine out.
What is the most common intradural spinal cord tumor
in patients with neurofibromatosis type II (NF-2)?
A. Schwannoma
B. Meningioma
C. Paraganglioma
D. Astrocytoma
E. Ependymoma
E. Ependymoma
The presence of l11ultiple intradural spinal cord
tumors is relatively common with NF-2 and may include
ependymomas (most common), schwannomas, and meningiomas (Greenberg, p. 478).
Destruction of the pyramidal cells of Ammon’s horn
would most likely produce severe ~”onal projection loss to
what structure?
A. Subiculum and entorhinal cortex
B. Premotor cortex
C. Amygdala
D. Ventrolateral thalamus
E. Superior colliculus
A. Subiculum and entorhinal cortex
The pyramidal neurons of the hippocampus
(Aml11on’s horn) send numerous fiber projections to the
subiculuIll and entorhinal cortex (area 28), which form
the anterior part of the parahippocampal gyrus (Carpenter,
pp. 369- 382).
What is depicted in the photomicrograph below (Figure 8.102Q)?
A. Hemangiopericytoma
B. IvIedulioblastoma
C. Melanoma
D. Rhabdoid tumor
E. Germinoma
**A. Hemangiopericytoma **
Note the “staghorn” vascular channel in this grade II
hemangiopericytoma. These tumors are vimentin-positive ,
ENlA-negative, have a dense arrangement of sheet-like cells,
and have a high nuclear-cytoplasmic ratio. Other characteristics include focallobularity, paucicellular areas, and dense
periceIJular reticulin (Ellison, pp. 736- 738).
A patient presents to a neurologist with a 2-week
history of wealmess in the muscles of the lower right face. If
this patient was also aphasic, what type of aphasia is IllOSt
likely to accompany the facial wealmess?
A. Agraphia
B. Alexia without agraphia
C. Expressive aphasia
D. Fluent aphasia
E. Auditory word agnosia
**C. Expressive aphasia **
Lesions that occupy the anterior part of the left
parasylvian fissure may cause a nontluent type of aphasia
(Broca’s). This region may abut the parts of the motor
cortex that supply the upper motor neuron fibers for
the contralateral facial nucleus. Therefore a patient with
right-sided upper motor neuron facial deficit may also have
an expressive-type of aphasia originating from Broca’s area
(Brazis, pp. 511- 516)
A coronal section through the plane of the genu of the internal capsule would bisect what structure?
A. Putamen
B. Globus pallidus
C. Caudate nucleus
D. Hypothalamus
E. Thalamus
**B. Globus pallidus **
A coronal section through the genu of the internal
capsule would almost exclusively bisect the globus pallid us,
which is triangle-shaped, with its apex fitting into the genu of
the intcrnal capsule (Carpenter, pp. 337- 344).
The lesion depicted below (Figure 8.10SQ) most likely
originates from what blood vessel?
A. Accessory middle cerebral artery
B. Frontopolar artery
C. Anterior temporal artery
D. Posterior temporal artery
E. Lenticulostriate
**C. Anterior temporal artery **
The middle cerebral artery (MCA) is divided
anatomically into four major segments: M1 (horizontal) segment, M2 (insular segment), M3 (opercular segment), and
M4 (cortical) segment. The anterior temporal artery typically arises from the 1-11 segment of the MCA before the
bifurcation. It passes directly anteriorly and inferiorly over
the temporal tip and usually does not course toward the
sylvian fissure. Although relatively uncommon, aneurysms
can form at the origin or further distally along this vessel (as depicted here). An accessory middle cerebral artery is an
MCA branch that arises from either the ACA (more common)
or the ICA and parallels the M1 segment toward the sylvian
fissure. The lenticulostriate arteries are divided into a
smaller medial group and a larger lateral group that originate
from the distal half of the M1 segment and project superiorly
to enter the anterior perforated substance to supply parts of
the lentiform nuclei, caudate nucleus, and internal capsule.
The posterior temporal artery usually originates from the
M4 segment of the MCA and supplies the posterior temporal
lobe. The frontopolar artery is a branch of the anterior cerebral artery (A2 portion), which originates below the rostrum
or genu of the corpus callosum and extends anteriorly to
supply the frontal pole (Osborn DCA, pp. 135- 137).
What percentage of patients with subarachnoid hemorrhage secondary to aneurysmal rupture develops angiographic
vasospasm at some time during their hospital course?
A. 20%
B.30%
C. 70%
0.80%
E. 90%
**C. 70% **
Most patients develop some degree of vessel narrowing after aneurysmal subarachnoid hemorrhage. About 70%
will develop angiographic vasospasm, and approximately
30% will go on to develop symptomatic vasospasm (Youmans,
p.1545).
A 43-year-old female presents to your clinic with
acromegaly and an i’“IIU revealing a 3-cm pituitary macroadenoma with extension into the right cavernous sinus. The
patient has normal vision and a serum growth hormone
level after induced hyperglycemia of 220 mg/dL. The most
appropriate next step in the management of this patient may
include
A. Transsphenoidal surgery
B. Radiosurgery
C. Octreotide
D. Conventional radiation therapy
E. Aand C
E. Aand C
Over the past few decades a variety of medical,
surgical, and radiation interventions have evolved that have
proven effective in reducing GH levels. No one treatment is
uniformly effective, and often a combination of interventions
is required. \Then a macroadenoma is surgically resected
transsphenoidally, endocrine remission rates vary between
65 and 90%. When a macroadenoma is resected, immediate
postoperative remission is reported to be even lower (30 and
79%). The rate of remission is adversely affected by a higher
preoperative GH level and larger invasive tumors. Therefore
biochemical cure with surgery for large GH-secreting macroadenomas is typically not expected. Conventional radiation
therapy can usually shrinl, pituitary tumors when up to
50 Gy is delivered in 1.8-Gy fractions over 6 weeks, but a
decrease or normalization of GIl levels usually takes many
years. When initial GI-I levels are> 100 pg/mL, only 60% of
patients will attain GH levels < 5 ~lg/mL after 18 years following radiation, and about 50% will develop hypopituitarism
within 10 years. Radiosurgery has the same disadvantages as
conventional radiation and would add increased risk in this
patient due to the proximity of the lesion to the optic nerves
and chiasm. Although perhaps controversial, some endocrinologists are advocating primary drug therapy in patients
with GI-I-secreting macroadenomas (especially with normal
vision). Bromocriptine, a dopamine agonist, has been documented to lower GH levels in up to 71% of patients, and
octreotide, a somatostatin analogue, has achieved similar
results. If there is no shrinkage of the tumor after 16 weeks of
therapy, further use of medication has been shown to have
little impact. Patients with rapidly deteriorating vision or
other neurologic problems related to the lesion (unlike our
patient) are often not good candidates for a trial of medical
therapy and often require more urgent surgical intervention.
Nevertheless, the most effective treatment strategy for acromegaly secondary to a GIl-secreting macroadenoma
usually requires a combination of surgical and medical
options (Berger, pp. 405- 406).
Figure 8.108-8.116Q depicts an endoscopic
approach to the third ventricle. Iatch the following ana tomic
structures to the corresponding letterhead , using each
answer either once, more than once, or not at all
Thalamostriate vein
A
Figure 8.108-8.116Q demonstrates the surgical anatomy of
the right lateral and anterior third ventricle during endoscopic third ventriculostomy for aqueductal stenosis. The
ventriculostomy site is depicted in the floor of the third
ventricle in this figure. The veins of the third ventricular system collect into deeper veins that course in a subependymal
location as they travel through the margins of the choroidal
fissure to empty into the internal cerebral, basal, and great
veins. In general, the veins draining the frontal horn and
body of the third ventricle drain into the internal cerebral
vein (not depicted here) as it courses through the velum
interpositum; those draining the temporal horn drain into a
segment of the basal vein of Rosenthal coursing through the
ambient cistern; and the veins from the atrium drain into
segments of the basal, internal cerebral, and great veins
coursing through the quadrigeminal cistern. Of note , the
thalamostriate vein passes forward in the sulcus between the
caudate nucleus and thalamus toward the foramen of Monro
(FOM), where it turns sharply posterior to enter the velum
interpositum to join the internal cerebral vein. The angle
formed by the junction of the internal cerebral vein and
thalamostriate vein, referred to as the venous angle, approximates the level of the FOM 011 the lateral view of a cerebral
angiogram (Will~ins, pp. 1427-1429; Youmans, pp. 1237-
1240).
Figure 8.108-8.116Q depicts an endoscopic
approach to the third ventricle. Iatch the following ana tomic
structures to the corresponding letterhead , using each
answer either once, more than once, or not at all
Septal vein
D
Figure 8.108-8.116Q demonstrates the surgical anatomy of
the right lateral and anterior third ventricle during endoscopic third ventriculostomy for aqueductal stenosis. The
ventriculostomy site is depicted in the floor of the third
ventricle in this figure. The veins of the third ventricular system collect into deeper veins that course in a subependymal
location as they travel through the margins of the choroidal
fissure to empty into the internal cerebral, basal, and great
veins. In general, the veins draining the frontal horn and
body of the third ventricle drain into the internal cerebral
vein (not depicted here) as it courses through the velum
interpositum; those draining the temporal horn drain into a
segment of the basal vein of Rosenthal coursing through the
ambient cistern; and the veins from the atrium drain into
segments of the basal, internal cerebral, and great veins
coursing through the quadrigeminal cistern. Of note , the
thalamostriate vein passes forward in the sulcus between the
caudate nucleus and thalamus toward the foramen of Monro
(FOM), where it turns sharply posterior to enter the velum
interpositum to join the internal cerebral vein. The angle
formed by the junction of the internal cerebral vein and
thalamostriate vein, referred to as the venous angle, approximates the level of the FOM 011 the lateral view of a cerebral
angiogram (Will~ins, pp. 1427-1429; Youmans, pp. 1237-
1240).
Figure 8.108-8.116Q depicts an endoscopic
approach to the third ventricle. Iatch the following ana tomic
structures to the corresponding letterhead , using each
answer either once, more than once, or not at all
Thalamus
G
Figure 8.108-8.116Q demonstrates the surgical anatomy of
the right lateral and anterior third ventricle during endoscopic third ventriculostomy for aqueductal stenosis. The
ventriculostomy site is depicted in the floor of the third
ventricle in this figure. The veins of the third ventricular system collect into deeper veins that course in a subependymal
location as they travel through the margins of the choroidal
fissure to empty into the internal cerebral, basal, and great
veins. In general, the veins draining the frontal horn and
body of the third ventricle drain into the internal cerebral
vein (not depicted here) as it courses through the velum
interpositum; those draining the temporal horn drain into a
segment of the basal vein of Rosenthal coursing through the
ambient cistern; and the veins from the atrium drain into
segments of the basal, internal cerebral, and great veins
coursing through the quadrigeminal cistern. Of note , the
thalamostriate vein passes forward in the sulcus between the
caudate nucleus and thalamus toward the foramen of Monro
(FOM), where it turns sharply posterior to enter the velum
interpositum to join the internal cerebral vein. The angle
formed by the junction of the internal cerebral vein and
thalamostriate vein, referred to as the venous angle, approximates the level of the FOM 011 the lateral view of a cerebral
angiogram (Will~ins, pp. 1427-1429; Youmans, pp. 1237-
1240).
Figure 8.108-8.116Q depicts an endoscopic
approach to the third ventricle. Iatch the following ana tomic
structures to the corresponding letterhead , using each
answer either once, more than once, or not at all
Choroid plexus
B
Figure 8.108-8.116Q demonstrates the surgical anatomy of
the right lateral and anterior third ventricle during endoscopic third ventriculostomy for aqueductal stenosis. The
ventriculostomy site is depicted in the floor of the third
ventricle in this figure. The veins of the third ventricular system collect into deeper veins that course in a subependymal
location as they travel through the margins of the choroidal
fissure to empty into the internal cerebral, basal, and great
veins. In general, the veins draining the frontal horn and
body of the third ventricle drain into the internal cerebral
vein (not depicted here) as it courses through the velum
interpositum; those draining the temporal horn drain into a
segment of the basal vein of Rosenthal coursing through the
ambient cistern; and the veins from the atrium drain into
segments of the basal, internal cerebral, and great veins
coursing through the quadrigeminal cistern. Of note , the
thalamostriate vein passes forward in the sulcus between the
caudate nucleus and thalamus toward the foramen of Monro
(FOM), where it turns sharply posterior to enter the velum
interpositum to join the internal cerebral vein. The angle
formed by the junction of the internal cerebral vein and
thalamostriate vein, referred to as the venous angle, approximates the level of the FOM 011 the lateral view of a cerebral
angiogram (Will~ins, pp. 1427-1429; Youmans, pp. 1237-
1240).
Figure 8.108-8.116Q depicts an endoscopic
approach to the third ventricle. Iatch the following ana tomic
structures to the corresponding letterhead , using each
answer either once, more than once, or not at all
Anterior caudate vein
F
Figure 8.108-8.116Q demonstrates the surgical anatomy of
the right lateral and anterior third ventricle during endoscopic third ventriculostomy for aqueductal stenosis. The
ventriculostomy site is depicted in the floor of the third
ventricle in this figure. The veins of the third ventricular system collect into deeper veins that course in a subependymal
location as they travel through the margins of the choroidal
fissure to empty into the internal cerebral, basal, and great
veins. In general, the veins draining the frontal horn and
body of the third ventricle drain into the internal cerebral
vein (not depicted here) as it courses through the velum
interpositum; those draining the temporal horn drain into a
segment of the basal vein of Rosenthal coursing through the
ambient cistern; and the veins from the atrium drain into
segments of the basal, internal cerebral, and great veins
coursing through the quadrigeminal cistern. Of note , the
thalamostriate vein passes forward in the sulcus between the
caudate nucleus and thalamus toward the foramen of Monro
(FOM), where it turns sharply posterior to enter the velum
interpositum to join the internal cerebral vein. The angle
formed by the junction of the internal cerebral vein and
thalamostriate vein, referred to as the venous angle, approximates the level of the FOM 011 the lateral view of a cerebral
angiogram (Will~ins, pp. 1427-1429; Youmans, pp. 1237-
1240).
Figure 8.108-8.116Q depicts an endoscopic
approach to the third ventricle. Iatch the following ana tomic
structures to the corresponding letterhead , using each
answer either once, more than once, or not at all
Superior choroidal vein
C
Figure 8.108-8.116Q demonstrates the surgical anatomy of
the right lateral and anterior third ventricle during endoscopic third ventriculostomy for aqueductal stenosis. The
ventriculostomy site is depicted in the floor of the third
ventricle in this figure. The veins of the third ventricular system collect into deeper veins that course in a subependymal
location as they travel through the margins of the choroidal
fissure to empty into the internal cerebral, basal, and great
veins. In general, the veins draining the frontal horn and
body of the third ventricle drain into the internal cerebral
vein (not depicted here) as it courses through the velum
interpositum; those draining the temporal horn drain into a
segment of the basal vein of Rosenthal coursing through the
ambient cistern; and the veins from the atrium drain into
segments of the basal, internal cerebral, and great veins
coursing through the quadrigeminal cistern. Of note , the
thalamostriate vein passes forward in the sulcus between the
caudate nucleus and thalamus toward the foramen of Monro
(FOM), where it turns sharply posterior to enter the velum
interpositum to join the internal cerebral vein. The angle
formed by the junction of the internal cerebral vein and
thalamostriate vein, referred to as the venous angle, approximates the level of the FOM 011 the lateral view of a cerebral
angiogram (Will~ins, pp. 1427-1429; Youmans, pp. 1237-
1240).
Figure 8.108-8.116Q depicts an endoscopic
approach to the third ventricle. Iatch the following ana tomic
structures to the corresponding letterhead , using each
answer either once, more than once, or not at all
Fornix
E
Figure 8.108-8.116Q demonstrates the surgical anatomy of
the right lateral and anterior third ventricle during endoscopic third ventriculostomy for aqueductal stenosis. The
ventriculostomy site is depicted in the floor of the third
ventricle in this figure. The veins of the third ventricular system collect into deeper veins that course in a subependymal
location as they travel through the margins of the choroidal
fissure to empty into the internal cerebral, basal, and great
veins. In general, the veins draining the frontal horn and
body of the third ventricle drain into the internal cerebral
vein (not depicted here) as it courses through the velum
interpositum; those draining the temporal horn drain into a
segment of the basal vein of Rosenthal coursing through the
ambient cistern; and the veins from the atrium drain into
segments of the basal, internal cerebral, and great veins
coursing through the quadrigeminal cistern. Of note , the
thalamostriate vein passes forward in the sulcus between the
caudate nucleus and thalamus toward the foramen of Monro
(FOM), where it turns sharply posterior to enter the velum
interpositum to join the internal cerebral vein. The angle
formed by the junction of the internal cerebral vein and
thalamostriate vein, referred to as the venous angle, approximates the level of the FOM 011 the lateral view of a cerebral
angiogram (Will~ins, pp. 1427-1429; Youmans, pp. 1237-
1240).
Figure 8.108-8.116Q depicts an endoscopic
approach to the third ventricle. Iatch the following ana tomic
structures to the corresponding letterhead , using each
answer either once, more than once, or not at all
Superior superficial thalamic veins
H
Figure 8.108-8.116Q demonstrates the surgical anatomy of
the right lateral and anterior third ventricle during endoscopic third ventriculostomy for aqueductal stenosis. The
ventriculostomy site is depicted in the floor of the third
ventricle in this figure. The veins of the third ventricular system collect into deeper veins that course in a subependymal
location as they travel through the margins of the choroidal
fissure to empty into the internal cerebral, basal, and great
veins. In general, the veins draining the frontal horn and
body of the third ventricle drain into the internal cerebral
vein (not depicted here) as it courses through the velum
interpositum; those draining the temporal horn drain into a
segment of the basal vein of Rosenthal coursing through the
ambient cistern; and the veins from the atrium drain into
segments of the basal, internal cerebral, and great veins
coursing through the quadrigeminal cistern. Of note , the
thalamostriate vein passes forward in the sulcus between the
caudate nucleus and thalamus toward the foramen of Monro
(FOM), where it turns sharply posterior to enter the velum
interpositum to join the internal cerebral vein. The angle
formed by the junction of the internal cerebral vein and
thalamostriate vein, referred to as the venous angle, approximates the level of the FOM 011 the lateral view of a cerebral
angiogram (Will~ins, pp. 1427-1429; Youmans, pp. 1237-
1240).
Figure 8.108-8.116Q depicts an endoscopic
approach to the third ventricle. Iatch the following ana tomic
structures to the corresponding letterhead , using each
answer either once, more than once, or not at all
Caudate nucleus
I
Figure 8.108-8.116Q demonstrates the surgical anatomy of
the right lateral and anterior third ventricle during endoscopic third ventriculostomy for aqueductal stenosis. The
ventriculostomy site is depicted in the floor of the third
ventricle in this figure. The veins of the third ventricular system collect into deeper veins that course in a subependymal
location as they travel through the margins of the choroidal
fissure to empty into the internal cerebral, basal, and great
veins. In general, the veins draining the frontal horn and
body of the third ventricle drain into the internal cerebral
vein (not depicted here) as it courses through the velum
interpositum; those draining the temporal horn drain into a
segment of the basal vein of Rosenthal coursing through the
ambient cistern; and the veins from the atrium drain into
segments of the basal, internal cerebral, and great veins
coursing through the quadrigeminal cistern. Of note , the
thalamostriate vein passes forward in the sulcus between the
caudate nucleus and thalamus toward the foramen of Monro
(FOM), where it turns sharply posterior to enter the velum
interpositum to join the internal cerebral vein. The angle
formed by the junction of the internal cerebral vein and
thalamostriate vein, referred to as the venous angle, approximates the level of the FOM 011 the lateral view of a cerebral
angiogram (Will~ins, pp. 1427-1429; Youmans, pp. 1237-
1240).
Injury to the thalamostriate vein during surgery may
produce which of the following complications?
1. Drowsiness
2. Hemorrhagic infarct in the basal ganglia
3. Hemiparesis
4. Mutism
A. 1,2,and3
B. 1 and 3
C. 2 and4
D. Only 4 is correct
E. All of the above
E. All of the above
Occlusion or injury of the thalamostriate vein may
cause drowsiness, hemiplegia, mutism, and hemorrhagic
infarction of the basal ganglia (Will~ins, pp. 1427-1429).
Characteristic microscopic fea tures of diffuse a.-xonal
injury (DAI) 12 to 24 hours after the insult may include
1. Astrogliosis
2. A;wnal retraction balls
3. Hemosiderin-laden macrophages
4. Perivascular hemorrhages
A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above
**C. 2 and 4 are correct **
Acute microscopic changes after DAI typically include
axonal retraction balls and perivascular hemorrhages, while
in later stages there can be astrogliosis, endothelial proliferation, and accumulation of hemosiderin-laden macrophages
(Marion, pp. 40-45; Ellison, pp. 249- 257; Ramsey, pp. 431-
434).
How far below the iliac crest does the sciatic notch lie?
A. 3 to 4 cm
B. 4 to 5 cm
C. 7 to B cm
D. 10 to 12 cm
E. 14 cm
**C. 7 to B cm **
In approaching the posterior ilium during autogenous iliac bone graft harvesting, a limited incision that stays
within 8 cm of the posterior superior iliac spine typically
avoids the superior cluneal nerves. Dissection is then carried
down to the gluteal fascia, which should be opened directly
above the iliac crest to facilitate fascial closure. During subcrestal exposure, the lateral subperiosteal dissection should
be carried to the gluteus medius and tensor fascia lata muscles. Subperiosteal dissection usually avoids damage to the
superior gluteal artery, which courses through the musculature. The sciatic notch usually lies approximately 7 to 8 cm
below the iliac crest and must not be violated, as it harbors
the main trunk of the sciatic artery, the sciatic nerve , and the ureter, which runs ventral to the superior gluteal artery.
j’dedially, the dissection should extend to the iliacus muscle ,
which prevents injury to the iliohypogastric and ilioinguinal
nerves (Connolly, pp. 819- 820)
The etiology of the abnormality depicted on the MRJ
scan below (Figure B.120-B.122Q) is most likely
A. Iatrogenic
B. Infectious
C. Traumatic
D. Developmental
E. Neoplastic
**D. Developmental **
Note the absence of the corpus
callosum and the high-riding third ventricle on this sagittal
MRI depicting agenesis of the corpus callosum. This condition is usually not associated with Chiari I malformation
but rather with the Chiari II malformation (Osborn DN,
pp.29- 33).
What is the diagnosis ?
A. Diffuse axonal injury
B. Obstruction of the aqueduct of Sylvius
C. Meningitis
D. Agenesis of the corpus callosum
E. Obstruction of the foramen of Monro
D. Agenesis of the corpus callosum
Note the absence of the corpus
callosum and the high-riding third ventricle on this sagittal
MRI depicting agenesis of the corpus callosum. This condition is usually not associated with Chiari I malformation
but rather with the Chiari II malformation (Osborn DN,
pp.29- 33).
Associated conditions may include all of the following
EXCEPT?
A. Schizencephaly
B. Chiari I malformation
C. Dandy-Walker malformation
D. Cephaloceles
E. Azygos anterior cerebral artery
**B. Chiari I malformation **
Note the absence of the corpus
callosum and the high-riding third ventricle on this sagittal
MRI depicting agenesis of the corpus callosum. This condition is usually not associated with Chiari I malformation
but rather with the Chiari II malformation (Osborn DN,
pp.29- 33).
A 45-year-old telemarketing agent has noticed
a gradual decline in his hearing over the course of a few
months and, only recently, some right ann wealmess. Physical
exam discloses full extraocular motion , symmetric facial
movements, a Weber test that lateralizes to the right, a Rinne
test revealing bone conduction better than air conduction on
the left Side, a uvula that deviates slightly to the right, and a
tongue that deviates to the left. His MRl is depicted below
(Figure 8.124-8.125Q).
\Vha t is the most likely diagnosis ?
A. Foramen magnum meningioma
B. Acoustic neuroma
C. Glomus jugulare tumor
D. Hemangiopericytoma
E. Chordoma
**C. Glomus jugulare tumor **
This patient harbors a glomus jugulare tumor,
which often presents with unilate ral hearing loss or pulsatile
tinnitus. Intracranial extension usually affects multiple
cranial nerves, which may result in a number of clinical
problems including dysphagia . Angiography is essential
because it helps with surgical planning. It helps delineate the
blood supply to the tumor as well as collateral blood flow
to the brain. Often preoperative embolization is a useful
adjunct for these highly vascular and locally invasive tumors.
Although observation with serial imaging studies to determine tumor progression may be an appropriate option for
medically frail patients, gross total resection is considered
the trea tment of choice for symptomatic lesions (Youmans,
pp.1295-1308).
A 45-year-old telemarketing agent has noticed
a gradual decline in his hearing over the course of a few
months and, only recently, some right ann wealmess. Physical
exam discloses full extraocular motion , symmetric facial
movements, a Weber test that lateralizes to the right, a Rinne
test revealing bone conduction better than air conduction on
the left Side, a uvula that deviates slightly to the right, and a
tongue that deviates to the left. His MRl is depicted below
(Figure 8.124-8.125Q).
The best treatment strategy for this patient wound entail
A. Radiosurgery
B. Proton-beam radiation
C. Observation with seriallvlRl scans
D. Attempted gross total resec tion
E. Conventional external-beam radiation
**D. Attempted gross total resec tion **
This patient harbors a glomus jugulare tumor,
which often presents with unilate ral hearing loss or pulsatile
tinnitus. Intracranial extension usually affects multiple
cranial nerves, which may result in a number of clinical
problems including dysphagia . Angiography is essential
because it helps with surgical planning. It helps delineate the
blood supply to the tumor as well as collateral blood flow
to the brain. Often preoperative embolization is a useful
adjunct for these highly vascular and locally invasive tumors.
Although observation with serial imaging studies to determine tumor progression may be an appropriate option for
medically frail patients, gross total resection is considered
the trea tment of choice for symptomatic lesions (Youmans,
pp.1295-1308).
What is the most likely mechanism accounting for the
fracture pattern depicted in Figure 8.126-8.127Q)?
A. Direct axial load on a neutral neck
B. Direct axial load on a flexed neck
C. Distraction
D. Direct axial load on a laterally bent necll
E. Hyperextension
**A. Direct axial load on a neutral neck **
The fracture-pattern (Jefferson fracture)
depicted on this axial CT scan most often results from an
axial load on a neutral neck. These patients are usually neurologically intact due to the large diameter of the spinal canal
at this level. If the sum of overhang of both lateral masses on
C2 is :2: 7 mm, the transverse ligament is probably disrupted,
which requires rigid immobilization (usually with a halo
vest) or surgical n.xation if additional fractures are present
(Greenberg, pp. 702-703).
What amount of C1 lateral l11ass excursion beyond the
axis indicates transverse ligament disruption ?
A. 4111111
B. 5 111111
C. 6 111m
**D. 7 nUll **
E. 9 nun
**D. 7 nUll **
The fracture-pattern (Jefferson fracture)
depicted on this axial CT scan most often results from an
axial load on a neutral neck. These patients are usually neurologically intact due to the large diameter of the spinal canal
at this level. If the sum of overhang of both lateral masses on
C2 is :2: 7 mm, the transverse ligament is probably disrupted,
which requires rigid immobilization (usually with a halo
vest) or surgical n.xation if additional fractures are present
(Greenberg, pp. 702-703).
What is the most likely mechanism of injury of the
abnormality depicted below (Figure 8.133-8.134Q)?
A. Hyperextension and ax ial loading
B. Ax.ialload on a neutral neck
C. A .. ‘tial loading on a laterally bent neck
D. Severe hyperflexion and axial loading
E. Hyperextension and distraction
**A. Hyperextension and axial loading **
The mechanism of most modern hangman’s
fractures results from hyperextension and axial loading
(diving and motor vehicle aCCidents), while judicial hangings
often resulted in hyperextension and distractive forces from
submeatal Imot placement. Patients rarely require surgical
intervention for this type of fracture, which is typically
reserved for irreducible fractures, failure of external immobilization, traumatic C2-3 disc herniation (with canal compromise and progressive neurologic deficit), and established
nonunion. All fusion techniques typically involve fusing C2
to C3, although the majority of patients can be successfully
treated with a cervical collar, SOMI brace, or halo vest (most
common) (Greenberg, pp. 704-706).
Therapeutic options may include all of the following
EXCEPT?
A. Cervical collar
B. Halo vest immobilization
C. Open reduc tion with internal n….:ation (C2 to C3)
D. Odontoid screw
E. SOMI brace
**D. Odontoid screw **
The mechanism of most modern hangman’s
fractures results from hyperextension and axial loading
(diving and motor vehicle aCCidents), while judicial hangings
often resulted in hyperextension and distractive forces from
submeatal Imot placement. Patients rarely require surgical
intervention for this type of fracture, which is typically
reserved for irreducible fractures, failure of external immobilization, traumatic C2-3 disc herniation (with canal compromise and progressive neurologic deficit), and established
nonunion. All fusion techniques typically involve fusing C2
to C3, although the majority of patients can be successfully
treated with a cervical collar, SOMI brace, or halo vest (most
common) (Greenberg, pp. 704-706).
Match the disorder (mucopolysaccharidosis)
with the enzyme abnormality, using each answer once, more
than once, or not at all
Sulfatase B
A. I-Iurler
B. Hunter
C. Sanfilippo A
D. Sanfilippo B
E. MorquioA
F. Morquio B
G. Maroteaux-Lamy
H. Sly
I. None of the above
**G. Maroteaux-Lamy **
Match the disorder (mucopolysaccharidosis)
with the enzyme abnormality, using each answer once, more
than once, or not at all
p-Galactosidase
A. I-Iurler
B. Hunter
C. Sanfilippo A
D. Sanfilippo B
E. MorquioA
F. Morquio B
G. Maroteaux-Lamy
H. Sly
I. None of the above
**F. Morquio B **
Match the disorder (mucopolysaccharidosis)
with the enzyme abnormality, using each answer once, more
than once, or not at all
Sulfamidase
A. I-Iurler
B. Hunter
C. Sanfilippo A
D. Sanfilippo B
E. MorquioA
F. Morquio B
G. Maroteaux-Lamy
H. Sly
I. None of the above
**C. Sanfilippo A **
Match the disorder (mucopolysaccharidosis)
with the enzyme abnormality, using each answer once, more
than once, or not at all
Galactose-6-sulfate sulfatase
A. I-Iurler
B. Hunter
C. Sanfilippo A
D. Sanfilippo B
E. MorquioA
F. Morquio B
G. Maroteaux-Lamy
H. Sly
I. None of the above
**E. MorquioA **
Match the disorder (mucopolysaccharidosis)
with the enzyme abnormality, using each answer once, more
than once, or not at all
Iduronate-2-sulfate sulfatase
A. I-Iurler
B. Hunter
C. Sanfilippo A
D. Sanfilippo B
E. MorquioA
F. Morquio B
G. Maroteaux-Lamy
H. Sly
I. None of the above
**B. Hunter **
Match the disorder (mucopolysaccharidosis)
with the enzyme abnormality, using each answer once, more
than once, or not at all
a-L-Iduronidase
A. I-Iurler
B. Hunter
C. Sanfilippo A
D. Sanfilippo B
E. MorquioA
F. Morquio B
G. Maroteaux-Lamy
H. Sly
I. None of the above
**A. I-Iurler **
What is the most ill,ely diagnosis?
A. Toxoplasmosis
B. Alzheimer’s disease
C. Neurocysticercosis
D. Echinococctls
E. Spinal cord injury
**B. Alzheimer’s disease **
Note the prominent diffuse plaques traversed by
neuronal processes in this patient with Alzheimer’s disease .
Diffuse amyloid plaques are extracellular, ill-defined focal
aggregates of amyloid and preamyloid material and are
approximately 60 to 300 mm in diameter. Neuronal cell
processes traversing the plaque typically appear normal
and do not contain tau protein (Ellison, pp. 553- 557).
What is depicted in the photomicrograph below
(Figure 8.165Q)?
A. Choroid plexus papilloma
B. Ependymoma
C. Adaman tinomatous craniopharyngioma
D. Chordoma
E. Angiomatous meningioma
**C. Adaman tinomatous craniopharyngioma **
Note the squamous cells, peripheral palisading of
nuclei, and nodules of wet keratin in this adamantinomatous
craniopharyngioma (Ellison, pp. 724-727; WHO, pp. 244-
246).
A wedding singer from your town presents to your office
with a I-week history of necl( pain and slight left ann and
hand numbness. His IvIRI is depicted below (Figure 8.168-
8.169Q). What is the most likely diagnosis ?
A. Synovial cyst
B. Juxtafacet cyst
C. Hypertrophy of the ligamentum f1avum
D. Disc herniation
E. Ossification of the posterior longitudinal ligament
(OPLL)
**D. Disc herniation **
Depicted here is an axial and parasagittal MIU
showing a soft (mainly disc material) posterolateral disc
herniation of the cervical spine that is eccentric to the left.
Considering that this disc herniation is not purely central , it
may be runenable to a posterolateral procedure in an attempt
to preserve vocal cord function (posterior keyhole laminotomy) in this wedding singer. Over 90% of patients with
acute cervical radiculopathy will improve with nonsurgical
therapy including adequate pain medication and antiinllammatories. Surgery is indicated for those who fail to
improve or develop progressive neurologic deficits while
undergoing nonsurgical therapy. A number of large series
have reported good or excellent results in 90 to 96% of
patients who underwent a posterior approach for such disc
herniations (Greenberg, pp. 310-314).
The patient’s symptomatology does not improve after 8 weeks of nonsurgical therapy. He returns to your office to explore surgical options. You inform him that the best surgical option for him should include what procedure, if possible?
A. Anterior cervical discectomy and fusion
B. Posterior cervical laminectomy
C. Posterior keyhole laminotomy
D. Anterior cervical corpectomy and fusion
E. Costotransversectomy
C. Posterior keyhole laminotomy
Depicted here is an axial and parasagittal MIU showing a soft (mainly disc material) posterolateral disc herniation of the cervical spine that is eccentric to the left. Considering that this disc herniation is not purely central, it may be runenable to a posterolateral procedure in an attempt
to preserve vocal cord function (posterior keyhole laminotomy) in this wedding singer. Over 90% of patients with acute cervical radiculopathy will improve with nonsurgical therapy including adequate pain medication and antiinllammatories. Surgery is indicated for those who fail to
improve or develop progressive neurologic deficits while
undergoing nonsurgical therapy. A number of large series
have reported good or excellent results in 90 to 96% of
patients who underwent a posterior approach for such disc
herniations (Greenberg, pp. 310-314).
What is depicted in Figure 8.173Q?
A. Pleomorphic xanthoactrocytoma
B. Ependymoma
C. Choriocarcinoma
D. Medulloblastoma
E. Adenohypophysis
E. Adenohypophysis
Note the prominent lobules of cells with an intervening vascular network of sinusoids in this photomicrograph of
a normal adenohypophysis (Ellison, p. 716).
A 54-year-old male presents to the emergency department with a ge ne ralized tonic-clonic seizure and a 6-month
history of behavioral changes. His lateral angiogram is
depicted below (Figure 8.180- 8.181Q). What is the most
likely diagnosis ?
A. IIydrocephalus from a third ventricular tumor
obstructing the foramen of Monro
B. Glioblastoma
C. Olfactory groove meningioma
D. Craniopharyngioma
E. Arterial-venous malformation
**C. Olfactory groove meningioma **
Note that the anterior cerebral arteries are
being pushed upward on this lateral angiogram, depicting
an olfactory groove meningioma. These lesions often grow
insidiously, causing gradual compression of the frontal lobes;
thus they are quite large and bilateral by the time of presentation. Common signs/symptoms may include headaches,
personality changes, visual loss, anosmia, and seizures. A
bifrontal transbasal approach is frequently used in resecting
these tumors, although a unilateral subfrontal or frontotemporal (pterional) craniotomy can also be used. The anterior
and posterior ethmoid arteries typically supply olfactory
groove meningiomas (Kaye and Blacl(, pp. 523-532;
Youmans, pp. 1115-1115).
The most common blood supply to this lesion originates
from what blood vessel(s) ?
A. Superior hypophyseal artery
B. Anterior meningeal branches from the maxillary
artery
C. Superficial temporal artery
D. Anterior meningeal branches from the cavernous
internal carotid artery
E. The anterior and posterior ethmoidal arteries
**E. The anterior and posterior ethmoidal arteries **
Note that the anterior cerebral arteries are
being pushed upward on this lateral angiogram, depicting
an olfactory groove meningioma. These lesions often grow
insidiously, causing gradual compression of the frontal lobes;
thus they are quite large and bilateral by the time of presentation. Common signs/symptoms may include headaches,
personality changes, visual loss, anosmia, and seizures. A
bifrontal transbasal approach is frequently used in resecting
these tumors, although a unilateral subfrontal or frontotemporal (pterional) craniotomy can also be used. The anterior
and posterior ethmoid arteries typically supply olfactory
groove meningiomas (Kaye and Blacl(, pp. 523-532;
Youmans, pp. 1115-1115).
What is the diagnosis of the lesion depicted in this
photomicrograph (Figure 8.190-8.192Q)?
A. Oysembryoplastic neuroepithelial tumor (ONT)
B. Central neurocytoma
C. Pleomorphic xanthoastrocytoma (PXA)
D. Giant cell astrocytoma (GCA)
E. Chordoid glioma of the third ventricle
A. Oysembryoplastic neuroepithelial tumor (ONT)
This lesion is most consistent with a DNT
(WIIO grade I). Patients usually present with long-standing
drug-resistant partial seizures that begin before the age of 20.
They are usually found in the temporal lobe or other supratentorial location and typically encompass the cerebral
cortex. On occasion, they appear to deform the overlying calvarium, a finding that furthe r supports the diagnosis of DNT.
The histologic hallmark of this tumor is the glioneuronal
element, which is shown here to consist of a free-floating
neuron in a microcyst surrounded by oligodendroglia I-like
cells (Ellison, pp. 659- 661; WHO, pp. 103-106).
What is the histologic hallmark of this lesion?
A. Rosenthal fibers
B. Alzheimer I! astrocytes
C. Glioneuronal element
D. Synaptophysin reactivity
E. Bizarre-appearing nuclea ted cells
**C. Glioneuronal element **
This lesion is most consistent with a DNT
(WIIO grade I). Patients usually present with long-standing
drug-resistant partial seizures that begin before the age of 20.
They are usually found in the temporal lobe or other supratentorial location and typically encompass the cerebral
cortex. On occasion, they appear to deform the overlying calvarium, a finding that furthe r supports the diagnosis of DNT.
The histologic hallmark of this tumor is the glioneuronal
element, which is shown here to consist of a free-floating
neuron in a microcyst surrounded by oligodendroglia I-like
cells (Ellison, pp. 659- 661; WHO, pp. 103-106).
Patients harboring this lesion typically present with
A. Meningitis
B. Seizures
C. Hemorrhage
D. Leptomeningeal dissemination
E. Hydrocephalus
**B. Seizures **
This lesion is most consistent with a DNT
(WIIO grade I). Patients usually present with long-standing
drug-resistant partial seizures that begin before the age of 20.
They are usually found in the temporal lobe or other supratentorial location and typically encompass the cerebral
cortex. On occasion, they appear to deform the overlying calvarium, a finding that furthe r supports the diagnosis of DNT.
The histologic hallmark of this tumor is the glioneuronal
element, which is shown here to consist of a free-floating
neuron in a microcyst surrounded by oligodendroglia I-like
cells (Ellison, pp. 659- 661; WHO, pp. 103-106).
This axial CT scan (Figure 8.201Q) demonstrates
A. Arachnoiditis
B. Hypertrophy of the ligamentulll f1avulll
C. Synovial cyst
D. Laminar fracture
E. Hemangioma
**A. Arachnoiditis **
Note the multiple prominent irregularities and
loculations located circumferentially around the margins of
the dura on this CT myelogram, which is most consistent
with arachnoiditis (Ramsey, pp. 739-741).
The EEG below (Figure 8.203Q) is most consistent
with?
A. 1, 2, and3 are correct
B. 1 and3 are correct
C. 2 and4 are correct
D. Only 4 is correct
E. All of the above
A. Alcohol intoxication
B. Left frontal lobe mass
C. A lethal closed head injury
D. Hepatic encephalopathy
E. Delta rhythm
Electrocerebral inactivity is consistent with brain
death in the setting of a detailed brain death exam. It is
defined as no cerebral electrical potentials greater than 2 ~IV.
It is not required to pronounce brain death and is used as an
ancillary test when the diagnosis is not clear. Drug intoxication (e.g., phenobarbital) and hypothermia may result in
reversible electrocerebral inactivity (Greenberg, p. 130).
What abnormality is depicted on the ECG below (Figure
8.204Q)?
9.A. Torsades de polites
B. Hyperkalemia
C. Digoxin toxicity
D. First-degree heart block
E. Multifocal atrial tachycardia
A. Torsades de polites
B. Hyperkalemia
C. Digoxin toxicity
D. First-degree heart block
E. Multifocal atrial tachycardia
The most potentially serious complication of hyperkalemia is slowing of electrical heart conduction. The ECG
begins to change when the serum K+ reaches approximately
6.0 mEq/L and is always abnormal when it is > 8.0 mEq/L.
The earliest ECG abnormality is a tall, tapering l’ wave that is
most evident in the precordial leads V2 and V”. As W levels
increase further, the P-wave amplitude decreases and the PR
interval lengthens. The P waves may eventually disappear
and the QRS complex widen . The final event is ventricular
asystole (Marino, pp. 654- 655).
Match the visual field cut (Figure 8.20S-8.209Q)
with the most likely lesion site
Temporallobe
E
Occlusion of the anterior
choroidal artery causes a homonymous defect in the upper and lower quadrants, with sparing of the horizontal sector
(quadruple sectoranopia, B), which is usually characteristic
of a lateral geniculate body infarct that is supplied by the
anterior choroidal artery. The central portion of the lateral
geniculate body receives blood flow primarily from the lateral posterior choroidal artery. Interruption of this vessel
causes a horizontal homonymous sector defect (wedgeshaped, D). Superior homonymous quadran tic defects (“piein the sky, “ E) may result from a lesion along i-Ieyer’s loop
(after temporal lobectomy) or along the inferior bank of
the calcarine fissure . The anterior chiasm or junctional
syndrome results in a unilateral optic nerve defect of one
eye and a superior temporal defect in the other eye (A) due
to the loop made by the inferonasal retina of the other eye
(\Villebrand’s knee). Lesions located in the most anterior
portion of the calcarine cortex cause a crescent-shaped
defect restricted to the temporal field of the contralateral eye
(monocular temporal crescent, C). This is the only retrochiasmatic lesion that may result in a strictly unilateral visual
field defect (Bralis, pp. 132-140).
Match the visual field cut (Figure 8.20S-8.209Q)
with the most likely lesion site
Lateral posterior choroidal artery
D
Occlusion of the anterior
choroidal artery causes a homonymous defect in the upper and lower quadrants, with sparing of the horizontal sector
(quadruple sectoranopia, B), which is usually characteristic
of a lateral geniculate body infarct that is supplied by the
anterior choroidal artery. The central portion of the lateral
geniculate body receives blood flow primarily from the lateral posterior choroidal artery. Interruption of this vessel
causes a horizontal homonymous sector defect (wedgeshaped, D). Superior homonymous quadran tic defects (“piein the sky, “ E) may result from a lesion along i-Ieyer’s loop
(after temporal lobectomy) or along the inferior bank of
the calcarine fissure . The anterior chiasm or junctional
syndrome results in a unilateral optic nerve defect of one
eye and a superior temporal defect in the other eye (A) due
to the loop made by the inferonasal retina of the other eye
(\Villebrand’s knee). Lesions located in the most anterior
portion of the calcarine cortex cause a crescent-shaped
defect restricted to the temporal field of the contralateral eye
(monocular temporal crescent, C). This is the only retrochiasmatic lesion that may result in a strictly unilateral visual
field defect (Bralis, pp. 132-140).
Match the visual field cut (Figure 8.20S-8.209Q)
with the most likely lesion site
Anterior chiasm
A
Occlusion of the anterior
choroidal artery causes a homonymous defect in the upper and lower quadrants, with sparing of the horizontal sector
(quadruple sectoranopia, B), which is usually characteristic
of a lateral geniculate body infarct that is supplied by the
anterior choroidal artery. The central portion of the lateral
geniculate body receives blood flow primarily from the lateral posterior choroidal artery. Interruption of this vessel
causes a horizontal homonymous sector defect (wedgeshaped, D). Superior homonymous quadran tic defects (“piein the sky, “ E) may result from a lesion along i-Ieyer’s loop
(after temporal lobectomy) or along the inferior bank of
the calcarine fissure . The anterior chiasm or junctional
syndrome results in a unilateral optic nerve defect of one
eye and a superior temporal defect in the other eye (A) due
to the loop made by the inferonasal retina of the other eye
(\Villebrand’s knee). Lesions located in the most anterior
portion of the calcarine cortex cause a crescent-shaped
defect restricted to the temporal field of the contralateral eye
(monocular temporal crescent, C). This is the only retrochiasmatic lesion that may result in a strictly unilateral visual
field defect (Bralis, pp. 132-140).
Match the visual field cut (Figure 8.20S-8.209Q)
with the most likely lesion site
Anterior calcarine cortex
C
Occlusion of the anterior
choroidal artery causes a homonymous defect in the upper and lower quadrants, with sparing of the horizontal sector
(quadruple sectoranopia, B), which is usually characteristic
of a lateral geniculate body infarct that is supplied by the
anterior choroidal artery. The central portion of the lateral
geniculate body receives blood flow primarily from the lateral posterior choroidal artery. Interruption of this vessel
causes a horizontal homonymous sector defect (wedgeshaped, D). Superior homonymous quadran tic defects (“piein the sky, “ E) may result from a lesion along i-Ieyer’s loop
(after temporal lobectomy) or along the inferior bank of
the calcarine fissure . The anterior chiasm or junctional
syndrome results in a unilateral optic nerve defect of one
eye and a superior temporal defect in the other eye (A) due
to the loop made by the inferonasal retina of the other eye
(\Villebrand’s knee). Lesions located in the most anterior
portion of the calcarine cortex cause a crescent-shaped
defect restricted to the temporal field of the contralateral eye
(monocular temporal crescent, C). This is the only retrochiasmatic lesion that may result in a strictly unilateral visual
field defect (Bralis, pp. 132-140).
Match the visual field cut (Figure 8.20S-8.209Q)
with the most likely lesion site
Anterior choroidal artery
B
Occlusion of the anterior
choroidal artery causes a homonymous defect in the upper and lower quadrants, with sparing of the horizontal sector
(quadruple sectoranopia, B), which is usually characteristic
of a lateral geniculate body infarct that is supplied by the
anterior choroidal artery. The central portion of the lateral
geniculate body receives blood flow primarily from the lateral posterior choroidal artery. Interruption of this vessel
causes a horizontal homonymous sector defect (wedgeshaped, D). Superior homonymous quadran tic defects (“piein the sky, “ E) may result from a lesion along i-Ieyer’s loop
(after temporal lobectomy) or along the inferior bank of
the calcarine fissure . The anterior chiasm or junctional
syndrome results in a unilateral optic nerve defect of one
eye and a superior temporal defect in the other eye (A) due
to the loop made by the inferonasal retina of the other eye
(\Villebrand’s knee). Lesions located in the most anterior
portion of the calcarine cortex cause a crescent-shaped
defect restricted to the temporal field of the contralateral eye
(monocular temporal crescent, C). This is the only retrochiasmatic lesion that may result in a strictly unilateral visual
field defect (Bralis, pp. 132-140).
What is the diagnosis ?
A. j\lobar holoprosencephaly
B. Lobar holoprosencephaly
C. Hydranencephaly
D. Severe hydrocephalus
E . Anencephaly
A. j\lobar holoprosencephaly
B. Lobar holoprosencephaly
**C. Hydranencephaly **
D. Severe hydrocephalus
E * . Anencephaly
Hydranencephaly describes a brain replaced by
CSF rather than compressed by expansion of the ventricles,
as in severe hydrocephalus. Moreover, with severe hydrocephalus, there is usually a thin mantle of brain, which is
absent in hydranencephaly. The absel1ce of a cortical mantle
with hydranencephaly is most often associated with angiographic evidence of supra clinoid occlusion of the carotid
arteries, which strongly suggests a vascular pathogenesis.
The posterior fossa and thalami are often preserved due to
preserved posterior circulation. The craniulll of afilicted
children usually fails to grow and remains small. The
incidence is estimated to be 1 in 6000, and affected infants
rarely live longer than a yea r (Albright, pp. 155- 156).
What is the most likely etiology of this finding?
A. Obstl’l1ctive hydrocephalus
B. Failure of disjunction
C. Disorder of cellular migration
D. Bilateral in utero disl’l1ption of the anterior circulation
E. Failure of neural tube closure
A. Obstl’l1ctive hydrocephalus
B. Failure of disjunction
**C. Disorder of cellular migration **
D. Bilateral in utero disl’l1ption of the anterior circulation
E. Failure of neural tube closure
Hydranencephaly describes a brain replaced by
CSF rather than compressed by expansion of the ventricles,
as in severe hydrocephalus. Moreover, with severe hydrocephalus, there is usually a thin mantle of brain, which is
absent in hydranencephaly. The absel1ce of a cortical mantle
with hydranencephaly is most often associated with angiographic evidence of supra clinoid occlusion of the carotid
arteries, which strongly suggests a vascular pathogenesis.
The posterior fossa and thalami are often preserved due to
preserved posterior circulation. The craniulll of afilicted
children usually fails to grow and remains small. The
incidence is estimated to be 1 in 6000, and affected infants
rarely live longer than a yea r (Albright, pp. 155- 156).
What is depicted by the photomicrograph below (Figure 8.215Q)?
A. Gemistocytic astrocytoma
B. I-Iemangioblastoma
C. Chordoma
D. Clear cell meningioma
E. Desmoplastic medulloblastoma
**A. Gemistocytic astrocytoma **
B. I-Iemangioblastoma
C. Chordoma
D. Clear cell meningioma
E. Desmoplastic medulloblastoma
Note the large, glassy eosinophilic cell bodies with
an angular shape on this photomicrograph, which depicts a
gemistocytic astrocytoma (Ellison, p. 627; WHO, p. 25).
A 35-year-old male with the photomicrograph depicted
below (Figure 8.218Q) presents with fever, chills, and a
seizure. What is the diagnosis?
A. Creutzfeldt-Jakob disease
B. Herpes encephalitis
C. Malaria
D. Ganglioglioma
E. Lymphoma
A. Creutzfeldt-Jakob disease
B. Herpes encephalitis
**C. Malaria **
D. Ganglioglioma
E. Lymphoma
Note the occlusion of the blood vessel, which is
due to the presence of many ghost-like red blood cells
that contain parasites on this I-I & E section depicting
malaria. Patients with this disease can present with seizures,
headache, somnolence, confUSion, photophobia, and almost
any focal neurologic deficit. Without urgent treatment, these
patients usually progress to coma and brain death (Ellison,
pp. 653- 656).
The lesion depicted below (Figure 8.219Q) is most often
associated with what other abnormality?
A. Castleman’s syndrome
B. Tuberous sclerosis
C. Temporal lobe epilepsy
D. Cafe aulait spots
E. Cobblestone skin pattern
A. Castleman’s syndrome
**B. Tuberous sclerosis **
C. Temporal lobe epilepsy
D. Cafe aulait spots
E. Cobblestone skin pattern
This photomicrograph depicts a subependymal giant
cell astrocytoma. This lesion is usually located adjacent
to the foramen of ~'Ionro and is associated with tuberous
sclerosis (dominant mutation in TSC 1 on 9p or TSC 2 on
16p). It usually resembles gemistocytic astrocytoma, but
is not infiltrative. Note the abundant cytoplasm, abundant
perivascular fibrillar zone, and prominent nucleolus in this
section. The nuclei are eccentric, which distinguishes this
from gemistocytic astrocytoma (Ell ison, pp. 637-639).
The EEG below (Figure 8.225Q) is most consistent with
what diagnosis?
A. Right frontal tumor
B. Left occipital tumor
C. Uremia
D. Sleep
E. Large hemispheric insult
A. Right frontal tumor
B. Left occipital tumor
C. Uremia
D. Sleep
E. Large hemispheric insult
The seizure spikes are over a fairly wide area of the
right parasagittal region (ma.ximal F4, C4) consistent with a
right frontal onset corresponding with a right parasagittal
meningioma. In order to localize seizure foci, it is imperative
for clinicians to memorize standard electrode placement and
designations. Note that by convention, electrodes designated
with odd numbers are on the left, while with even numbers
on the right. The standard electrode designations are as
follows: Fpl/Fp2 = frontopolar or prefrontal; F3/F4 = midfrontal; C3/C4 = central (roughly over central sulcus); P3/P4
= parietal; 01/02 = OCCipital; F7/F8 = inferior frontal (sometimes called anterior frontal); T3/T4 = mid temporal (records
activity over anterior and midtemporal activity, important
for temporal lobe epilepsy); 1’5/1’6 = posterior temporal; Fz,
Cz, pz = midline electrodes in frontal and parietal regions
(record mesial surfaces of hemispheres); AlIA2 = ear reference electrodes (while used for references also record
mid temporal activity); TI/T2 = so-called true anterior temporal electrodes; Spl/Sp2 = sphenoidal electrodes (record activity from inferomesial surface of the temporal lobes)
(Rowan, pp. 4- 7).
The following is a schematic diagram through the
pallidofugal fiber system in a coronal plane. Match the fibers
(numbered items) with the appropriate letterhead (Figure
8.226-8.231Q), using each answer either once, more than
once, or not at all.
Ansa lenticularis
D
Fibers of the ansa
lenticularis (D) leave the outer part of the medial globus
pallidus, pass around the internal capsule, and enter the prerubral field (field H of Forel, not labeled) prior to merging
with the lenticular fasciculus (H2). Fibers of the lenticular
fasciculus originate from the inner part of the medial globus
pallidus, traverse the posterior limb of the anterior capsule,
and pass medially, dorsal to the subthalamic nucleus, to also
enter the prerubral field. The ansa lenticularis and lenticular
fasciculus then travel together dorsal to the zona incerta as
components of the thalamic fasciculus (A). The subthalamic
fasciculus (C) is comprised of pallidosubthalamic fibers
originating from the lateral or external pallidal segment and
subthalamopallidal fibers that terminate in the medullary
lamina of both pallidal segments. Both components of the
subthalamic fasciculus cross the internal capsule. Thalamostriate fibers from the centromedian nucleus project to the
putamen (E) (Carpenter, pp. 337- 345).
The following is a schematic diagram through the
pallidofugal fiber system in a coronal plane. Match the fibers
(numbered items) with the appropriate letterhead (Figure
8.226-8.231Q), using each answer either once, more than
once, or not at all.
Thalamostriate fibers
E
Fibers of the ansa
lenticularis (D) leave the outer part of the medial globus
pallidus, pass around the internal capsule, and enter the prerubral field (field H of Forel, not labeled) prior to merging
with the lenticular fasciculus (H2). Fibers of the lenticular
fasciculus originate from the inner part of the medial globus
pallidus, traverse the posterior limb of the anterior capsule,
and pass medially, dorsal to the subthalamic nucleus, to also
enter the prerubral field. The ansa lenticularis and lenticular
fasciculus then travel together dorsal to the zona incerta as
components of the thalamic fasciculus (A). The subthalamic
fasciculus (C) is comprised of pallidosubthalamic fibers
originating from the lateral or external pallidal segment and
subthalamopallidal fibers that terminate in the medullary
lamina of both pallidal segments. Both components of the
subthalamic fasciculus cross the internal capsule. Thalamostriate fibers from the centromedian nucleus project to the
putamen (E) (Carpenter, pp. 337- 345).
The following is a schematic diagram through the
pallidofugal fiber system in a coronal plane. Match the fibers
(numbered items) with the appropriate letterhead (Figure
8.226-8.231Q), using each answer either once, more than
once, or not at all.
Optic tract
F
Fibers of the ansa
lenticularis (D) leave the outer part of the medial globus
pallidus, pass around the internal capsule, and enter the prerubral field (field H of Forel, not labeled) prior to merging
with the lenticular fasciculus (H2). Fibers of the lenticular
fasciculus originate from the inner part of the medial globus
pallidus, traverse the posterior limb of the anterior capsule,
and pass medially, dorsal to the subthalamic nucleus, to also
enter the prerubral field. The ansa lenticularis and lenticular
fasciculus then travel together dorsal to the zona incerta as
components of the thalamic fasciculus (A). The subthalamic
fasciculus (C) is comprised of pallidosubthalamic fibers
originating from the lateral or external pallidal segment and
subthalamopallidal fibers that terminate in the medullary
lamina of both pallidal segments. Both components of the
subthalamic fasciculus cross the internal capsule. Thalamostriate fibers from the centromedian nucleus project to the
putamen (E) (Carpenter, pp. 337- 345).
The following is a schematic diagram through the
pallidofugal fiber system in a coronal plane. Match the fibers
(numbered items) with the appropriate letterhead (Figure
8.226-8.231Q), using each answer either once, more than
once, or not at all.
Subthalamic fasciculus
C
Fibers of the ansa
lenticularis (D) leave the outer part of the medial globus
pallidus, pass around the internal capsule, and enter the prerubral field (field H of Forel, not labeled) prior to merging
with the lenticular fasciculus (H2). Fibers of the lenticular
fasciculus originate from the inner part of the medial globus
pallidus, traverse the posterior limb of the anterior capsule,
and pass medially, dorsal to the subthalamic nucleus, to also
enter the prerubral field. The ansa lenticularis and lenticular
fasciculus then travel together dorsal to the zona incerta as
components of the thalamic fasciculus (A). The subthalamic
fasciculus (C) is comprised of pallidosubthalamic fibers
originating from the lateral or external pallidal segment and
subthalamopallidal fibers that terminate in the medullary
lamina of both pallidal segments. Both components of the
subthalamic fasciculus cross the internal capsule. Thalamostriate fibers from the centromedian nucleus project to the
putamen (E) (Carpenter, pp. 337- 345).
The following is a schematic diagram through the
pallidofugal fiber system in a coronal plane. Match the fibers
(numbered items) with the appropriate letterhead (Figure
8.226-8.231Q), using each answer either once, more than
once, or not at all.
Thalamic fasciculus (HI)
A
Fibers of the ansa
lenticularis (D) leave the outer part of the medial globus
pallidus, pass around the internal capsule, and enter the prerubral field (field H of Forel, not labeled) prior to merging
with the lenticular fasciculus (H2). Fibers of the lenticular
fasciculus originate from the inner part of the medial globus
pallidus, traverse the posterior limb of the anterior capsule,
and pass medially, dorsal to the subthalamic nucleus, to also
enter the prerubral field. The ansa lenticularis and lenticular
fasciculus then travel together dorsal to the zona incerta as
components of the thalamic fasciculus (A). The subthalamic
fasciculus (C) is comprised of pallidosubthalamic fibers
originating from the lateral or external pallidal segment and
subthalamopallidal fibers that terminate in the medullary
lamina of both pallidal segments. Both components of the
subthalamic fasciculus cross the internal capsule. Thalamostriate fibers from the centromedian nucleus project to the
putamen (E) (Carpenter, pp. 337- 345).
The following is a schematic diagram through the
pallidofugal fiber system in a coronal plane. Match the fibers
(numbered items) with the appropriate letterhead (Figure
8.226-8.231Q), using each answer either once, more than
once, or not at all.
Lenticular fasciculus (H2)
B
Fibers of the ansa
lenticularis (D) leave the outer part of the medial globus
pallidus, pass around the internal capsule, and enter the prerubral field (field H of Forel, not labeled) prior to merging
with the lenticular fasciculus (H2). Fibers of the lenticular
fasciculus originate from the inner part of the medial globus
pallidus, traverse the posterior limb of the anterior capsule,
and pass medially, dorsal to the subthalamic nucleus, to also
enter the prerubral field. The ansa lenticularis and lenticular
fasciculus then travel together dorsal to the zona incerta as
components of the thalamic fasciculus (A). The subthalamic
fasciculus (C) is comprised of pallidosubthalamic fibers
originating from the lateral or external pallidal segment and
subthalamopallidal fibers that terminate in the medullary
lamina of both pallidal segments. Both components of the
subthalamic fasciculus cross the internal capsule. Thalamostriate fibers from the centromedian nucleus project to the
putamen (E) (Carpenter, pp. 337- 345).
A 31-year-old immunocompromised male with a history of intravenous drug abuse presents with back pain. His
sagittal postcontrasted Tl-weighted MRI is depicted below
(Figure 8.232Q). What is the most likely diagnosis?
A. Leukemia
B. Lymphoma
C. Epidural abscess
D. Epidural lipomatosis
E. IIemangioblastoma
A. Leukemia
B. Lymphoma
**C. Epidural abscess **
D. Epidural lipomatosis
E. IIemangioblastoma
Note the prominent ring enhancement of this spinal
epidural abscess, with compression of the adjacent spinal
cord . The most lil{ely causative organism in a patient with a
history of intravenous drug abuse is Staph. aU1”eliS (Ramsey,
pp.498- 502)
What is the most likely
diagnosis of this patient?
A. Sphenoid wing meningioma
B. Chondrosarcoma
C. Fibrous dysplasia
D. Esthenioblastoma
E. Osteochondroma
A. Sphenoid wing meningioma
B. Chondrosarcoma
C. Fibrous dysplasia
D. Esthenioblastoma
E. Osteochondroma
Note the expansion of bone (sphenoid) and
“ground glass appearance” on this noncontrasted CT scan in
a patient with fibrous dysplasia. Malignant degeneration,
usually to osteosarcoma, has been reported to occur in
approximately 0.5% of patients with fibrous dysplasia
(Albright, pp. 456- 457).
Malignant degeneration of this lesion is most likely to
produce what type of neoplasm?
A. Osteochondroma
B. Osteoblastoma
C. Chloroma
D. Osteosarcoma
E. Neuroblastoma
A. Osteochondroma
B. Osteoblastoma
C. Chloroma
**D. Osteosarcoma **
E. Neuroblastoma
Note the expansion of bone (sphenoid) and
“ground glass appearance” on this noncontrasted CT scan in
a patient with fibrous dysplasia. Malignant degeneration,
usually to osteosarcoma, has been reported to occur in
approximately 0.5% of patients with fibrous dysplasia
(Albright, pp. 456- 457).
An 18-year-old male presents to the emergency department with morning headaches associated with nausea and
right arm numbness; his CT scan showed a low-density area
in the left parietal region. The angiogram is depicted below
(Figure 8.244Q). What is the most likely diagnosis ?
A. Atherosclerosis
B. Malignant brain tumor
C. Fibromuscular dysplasia
D. lvloyamoya disease
E. Embolic infarct
A. Atherosclerosis
B. Malignant brain tumor
C. Fibromuscular dysplasia
**D. lvloyamoya disease **
E. Embolic infarct
Note the paucity of blood flow in the distal internal
carotid and cerebral artery vasculature and the presence
of prominent collaterals that resemble a “puff of smoke” on
this lateral angiogram, which depicts moyamoya (Albright,
pp. 1053- 1069).
A 67-year-old male underwent an anterior cervical
fusion in the remote past and presents with a 3-month history of new-onset neck pain and deltoid wealmess on the
right. His sagittal T2-weighted .MRJ is depicted on the next
page (Figure 8.2S0Q). What is shown on this sagittal MRJ
scan that may account for this new clinical picture?
A. Pseudoarthrosis
B. Osteomyelitis
C. End-fusion degenerative changes
D. Spondylolysis
E. Subsidence
A. Pseudoarthrosis
B. Osteomyelitis
**C. End-fusion degenerative changes **
D. Spondylolysis
E. Subsidence
The acquisition of bony spinal fusion increases
motion and stress at adjacent Illation segments, which can
accelerate degenerative changes. This process is further
enhanced by failure to repair sagittal balance during surgery.
Although not the ideal study to evaluate bony fUSion, this
MRl does not demonstrate pseudoarthrosis at the prior fusion site, subsidence, basilar invagination , or osteomyelitis.
It shows end-fusion degenerative changes and loss of the
normal lordotic curve of the cervical spine, which may be
contributing to this patients’ new clinical problems (Benzel,
p.130).
Figure 8.251-8.257Q depicts the right internal
auditory canal and surrounding petrous temporal bone .
l'latch the following anatomic structures with the appropriate letterhead, using each answer only once.
Superior division of vestibular nerve
B
This diagram
shows the structures that traverse the internal auditory
canal (lAC). The facial nerve (A) and nervus intermedius are
separated from the superior vestibular nerve by a vertical
crest of bone known as Bill’s bar (F). Bill’s bar arises from the
transverse crest (G) within the lateral aspect of the lAC.
The cochlear nerve (C) and inferior vestibular nerve enter
the lAC inferior to the transverse crest, as depicted in the
diagram (Will<ins, pp. 1063-1071, 1101- 1114).
Figure 8.251-8.257Q depicts the right internal
auditory canal and surrounding petrous temporal bone .
l'latch the following anatomic structures with the appropriate letterhead, using each answer only once.
Cochlear nerve
C
This diagram
shows the structures that traverse the internal auditory
canal (lAC). The facial nerve (A) and nervus intermedius are
separated from the superior vestibular nerve by a vertical
crest of bone known as Bill’s bar (F). Bill’s bar arises from the
transverse crest (G) within the lateral aspect of the lAC.
The cochlear nerve (C) and inferior vestibular nerve enter
the lAC inferior to the transverse crest, as depicted in the
diagram (Will<ins, pp. 1063-1071, 1101- 1114).
Figure 8.251-8.257Q depicts the right internal
auditory canal and surrounding petrous temporal bone .
l'latch the following anatomic structures with the appropriate letterhead, using each answer only once.
Inferior division of vestibular nerve
D
This diagram
shows the structures that traverse the internal auditory
canal (lAC). The facial nerve (A) and nervus intermedius are
separated from the superior vestibular nerve by a vertical
crest of bone known as Bill’s bar (F). Bill’s bar arises from the
transverse crest (G) within the lateral aspect of the lAC.
The cochlear nerve (C) and inferior vestibular nerve enter
the lAC inferior to the transverse crest, as depicted in the
diagram (Will<ins, pp. 1063-1071, 1101- 1114).
Figure 8.251-8.257Q depicts the right internal
auditory canal and surrounding petrous temporal bone .
l'latch the following anatomic structures with the appropriate letterhead, using each answer only once.
Facial nerve
A
This diagram
shows the structures that traverse the internal auditory
canal (lAC). The facial nerve (A) and nervus intermedius are
separated from the superior vestibular nerve by a vertical
crest of bone known as Bill’s bar (F). Bill’s bar arises from the
transverse crest (G) within the lateral aspect of the lAC.
The cochlear nerve (C) and inferior vestibular nerve enter
the lAC inferior to the transverse crest, as depicted in the
diagram (Will<ins, pp. 1063-1071, 1101- 1114).
Figure 8.251-8.257Q depicts the right internal
auditory canal and surrounding petrous temporal bone .
l'latch the following anatomic structures with the appropriate letterhead, using each answer only once.
Nervous intermedius
E
This diagram
shows the structures that traverse the internal auditory
canal (lAC). The facial nerve (A) and nervus intermedius are
separated from the superior vestibular nerve by a vertical
crest of bone known as Bill’s bar (F). Bill’s bar arises from the
transverse crest (G) within the lateral aspect of the lAC.
The cochlear nerve (C) and inferior vestibular nerve enter
the lAC inferior to the transverse crest, as depicted in the
diagram (Will<ins, pp. 1063-1071, 1101- 1114).
Figure 8.251-8.257Q depicts the right internal
auditory canal and surrounding petrous temporal bone .
l'latch the following anatomic structures with the appropriate letterhead, using each answer only once.
Bill’s bar
F
This diagram
shows the structures that traverse the internal auditory
canal (lAC). The facial nerve (A) and nervus intermedius are
separated from the superior vestibular nerve by a vertical
crest of bone known as Bill’s bar (F). Bill’s bar arises from the
transverse crest (G) within the lateral aspect of the lAC.
The cochlear nerve (C) and inferior vestibular nerve enter
the lAC inferior to the transverse crest, as depicted in the
diagram (Will<ins, pp. 1063-1071, 1101- 1114).
Figure 8.251-8.257Q depicts the right internal
auditory canal and surrounding petrous temporal bone .
l'latch the following anatomic structures with the appropriate letterhead, using each answer only once.
Transverse crest
G
This diagram
shows the structures that traverse the internal auditory
canal (lAC). The facial nerve (A) and nervus intermedius are
separated from the superior vestibular nerve by a vertical
crest of bone known as Bill’s bar (F). Bill’s bar arises from the
transverse crest (G) within the lateral aspect of the lAC.
The cochlear nerve (C) and inferior vestibular nerve enter
the lAC inferior to the transverse crest, as depicted in the
diagram (Will<ins, pp. 1063-1071, 1101- 1114).
A 77-year-old male presents to your office with a
4-month history of unilateral epistaxis and nasal discharge.
His MRI is depicted below (Figure 8.264Q). Histopathologic
analysis of the tumor revealed un i form small cells with round
nuclei, scant cytoplasm, a prominent reticular core, and
scattered Homer-Wright rosettes. Immunohistochemistry
was positive for neuron-specific enolase and S-100 but was
cytokeratin, CD20, and CD79a negative. What is the most
likely diagnosis?
A. Lymphoma
B. Squamous cell carcinoma
C. Esthesioneuroblastoma
D. Adenocarcinoma
E. Rl1abdomyosarcoma
A. Lymphoma
B. Squamous cell carcinoma
**C. Esthesioneuroblastoma **
D. Adenocarcinoma
E. Rl1abdomyosarcoma
The clinical history of this patient and destructive
MRI appearance of tIllS lesion are highly suggestive of a
malignant neoplasm involVing the paranasal sinuses. The
histologic and immunohistochemical markers are most
consistent with esthesioneuroblastoma (Kaye and Laws,
pp. 885- 889).
The observation of various adverse effects during deep brain stimulation (DES) often characterizes the
extent of current spread to adjacent structures. For each
stimulation-induced adverse effect, match the associated
direction of current spread, using each answer once, more
than once, or not at all
Flushing and perspiration after STN DES
A. Anterior
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
**A. Anterior **
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
The observation of various adverse effects during deep brain stimulation (DES) often characterizes the
extent of current spread to adjacent structures. For each
stimulation-induced adverse effect, match the associated
direction of current spread, using each answer once, more
than once, or not at all
Dysarthria after STN DES
A. Anterior
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
A. Anterior
B. Posterior
C. Medial
**D. Lateral **
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
The observation of various adverse effects during deep brain stimulation (DES) often characterizes the
extent of current spread to adjacent structures. For each
stimulation-induced adverse effect, match the associated
direction of current spread, using each answer once, more
than once, or not at all
Paresthesias after GPi DES
A. Anterior
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
A. Anterior
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
**G. Posterior and medial **
H. None of the above
The observation of various adverse effects during deep brain stimulation (DES) often characterizes the
extent of current spread to adjacent structures. For each
stimulation-induced adverse effect, match the associated
direction of current spread, using each answer once, more
than once, or not at all
Photopsia and nausea after Gpi DES
A. Anterior
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
**A. Anterior **
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
The observation of various adverse effects during deep brain stimulation (DES) often characterizes the
extent of current spread to adjacent structures. For each
stimulation-induced adverse effect, match the associated
direction of current spread, using each answer once, more
than once, or not at all
Diplopia after STN DES
A. Anterior
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
**F. Inferior and medial **
G. Posterior and medial
H. None of the above
The observation of various adverse effects during deep brain stimulation (DES) often characterizes the
extent of current spread to adjacent structures. For each
stimulation-induced adverse effect, match the associated
direction of current spread, using each answer once, more
than once, or not at all
Tonic contraction after Vim DBS
A. Anterior
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
A. Anterior
B. Posterior
C. Medial
**D. Lateral **
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
The observation of various adverse effects during deep brain stimulation (DES) often characterizes the
extent of current spread to adjacent structures. For each
stimulation-induced adverse effect, match the associated
direction of current spread, using each answer once, more
than once, or not at all
Blepharospasm after STN DES
A. Anterior
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
A. Anterior
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
The observation of various adverse effects during deep brain stimulation (DES) often characterizes the
extent of current spread to adjacent structures. For each
stimulation-induced adverse effect, match the associated
direction of current spread, using each answer once, more
than once, or not at all
Dysequilibrium and gait ataxia (without limb at<uia)
after STN DES
A. Anterior
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
A. Anterior
B. Posterior
**C. Medial **
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
The observation of various adverse effects during deep brain stimulation (DES) often characterizes the
extent of current spread to adjacent structures. For each
stimulation-induced adverse effect, match the associated
direction of current spread, using each answer once, more
than once, or not at all
Tonic contraction after STN DBS
A. Anterior
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
A. Anterior
B. Posterior
C. Medial
D. Lateral
**E. Anterior and lateral **
F. Inferior and medial
G. Posterior and medial
H. None of the above
The observation of various adverse effects during deep brain stimulation (DES) often characterizes the
extent of current spread to adjacent structures. For each
stimulation-induced adverse effect, match the associated
direction of current spread, using each answer once, more
than once, or not at all
Paresthesias after Vim DBS
A. Anterior
B. Posterior
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
A. Anterior
**B. Posterior **
C. Medial
D. Lateral
E. Anterior and lateral
F. Inferior and medial
G. Posterior and medial
H. None of the above
The photomicrograph depicted below (Figure 8.278Q)
is most consistent with what diagnosis ?
A. Tuberculosis
B. Chronic infarct
C. Multiple sclerosis
D. Histoplasmosis
E. Pilocytic astrocytoma
**A. Tuberculosis **
B. Chronic infarct
C. Multiple sclerosis
D. Histoplasmosis
E. Pilocytic astrocytoma
Within this tuberculoma, note the prominent region
of caseating necrosis (left), in which no cellular detail can be
ascertained. A peripheral rim of lymphocytes and a fibrous
capsule surround the granuloma, and an occasional histiocyte is observed (Ellison, pp. 339- 342).
The gross specimen depicted below (Figure 8.279Q)
reveals ?
A. Neurocysticercosis
B. Third ventricular tumor
C. Metastatic disease
D. Toxoplasmosis
E. Multiple sclerosis
A. Neurocysticercosis
B. Third ventricular tumor
**C. Metastatic disease **
D. Toxoplasmosis
E. Multiple sclerosis
Note the multiple lesions at the gray-white junction,
which is most consistent with metastatic disease (Ellison,
pp.743-750).
What is depicted on the CT scan below (Figure 8.297Q)?
A. Evidence of posterior interhemispheric blood after
head trauma
B. Empty delta sign of superior sagittal thrombosis associated with a cystic tumor
C. Pineocytoma
D. A hyperdense MCA sign
E. A left posterior temporal infarct
A. Evidence of posterior interhemispheric blood after
head trauma
**B. Empty delta sign of superior sagittal thrombosis associated with a cystic tumor **
C. Pineocytoma
D. A hyperdense MCA sign
E. A left posterior temporal infarct
Note the empty delta sign, representing an occluded
superior sagittal sinus. This abnormality may be associated
with pregnancy, dehydration , infections, hypercoagulable
states, and tumors (as in this case) (Merritt, pp. 269-
271).
