NeuroSurgery Flashcards
A 54-year-old female was taken to an emergency
room after collapsing at work. She was alert and communicative, with a severe headache, photophobia, nuchal rigidity,
and blurry vision. Computed tomography (CT) of the brain
revealed diffuse subarachnoid blood in the basal cisterns,
mild hydrocephalus, and no intraparenchymal hematoma.
Her angiogram is depicted below. What is the clinical Hunt and Hess grade of this patient?
A. Grade I
B. Grade II
C. Grade III
D. Grade IV
E. Grade V
A. Grade I
**B. Grade II **
C. Grade III
D. Grade IV
E. Grade V
Patients with
posterior communicating artery (PComA) aneurysms typically present with subarachnoid hemorrhage (SAl-I) and
partial or complete third nerve palsies (ptosis, dilated pupil,
extraocular muscle abnormalities) due to cOIl1pression of the
third nerve by the aneurysm . . Another common presentation
of PComA aneurysms is the development of a third nerve
deficit in the absence of SAl-I. The appearance of an enlarged
pupil with or without involvement of other third nerve ftmctions should be taken as diagnostic of a PComA aneurysm
until proven otherwise. After the aneurysm is clipped, it
should be punctured not only to ensure complete obliteration but also to achieve maximal decompression of the third
nerve. Most patients with third nerve palsies improve within
6 months and frequently sooner. Some PComA aneurysms
will not produce any oculomotor nerve deficit. Special care
must be taken in interpreting the angiograms of these
patients, since the aneurysms often project laterally onto the
medial edge of the temporal lobe rather than in more common posterolateral or downward directions. This is relevant
during operative planning, since early re traction of the
temporal lobe may result in premature aneurysmal rupture.
A 54-year-old female was taken to an emergency
room after collapsing at work. She was alert and communicative, with a severe headache, photophobia, nuchal rigidity,
and blurry vision. Computed tomography (CT) of the brain
revealed diffuse subarachnoid blood in the basal cisterns,
mild hydrocephalus, and no intraparenchymal hematoma.
Her angiogram is depicted below. Some posterior communicating artery (PComA) aneurysms
do not produce any third nerve deficit. Why should special
attention be given to the angiogram in these cases?
A. If the aneurysm is projecting posterolaterally rather
than in a more common medial position, there is an
increased risk of injuring the perforating vessels from
the PComA during microdissection
B. An aneurysm projecting laterally onto the medial edge
of the temporal lobe argues against premature retraction of the temporal lobe
C. The angiogram may reveal a ventral carotid wall
aneurysm instead of a PComA lesion, which is often
better managed with coiling
D. To look for any other associated aneurysms and/or
vasospasm
E. It may help with surgical planning, as medially projecting lesions are better approached through the carotidoculomotor triangle
A. If the aneurysm is projecting posterolaterally rather
than in a more common medial position, there is an
increased risk of injuring the perforating vessels from
the PComA during microdissection
**B. An aneurysm projecting laterally onto the medial edge
of the temporal lobe argues against premature retraction of the temporal lobe **
C. The angiogram may reveal a ventral carotid wall
aneurysm instead of a PComA lesion, which is often
better managed with coiling
D. To look for any other associated aneurysms and/or
vasospasm
E. It may help with surgical planning, as medially projecting lesions are better approached through the carotidoculomotor triangle
Patients with
posterior communicating artery (PComA) aneurysms typically present with subarachnoid hemorrhage (SAl-I) and
partial or complete third nerve palsies (ptosis, dilated pupil,
extraocular muscle abnormalities) due to cOIl1pression of the
third nerve by the aneurysm . . Another common presentation
of PComA aneurysms is the development of a third nerve
deficit in the absence of SAl-I. The appearance of an enlarged
pupil with or without involvement of other third nerve ftmctions should be taken as diagnostic of a PComA aneurysm
until proven otherwise. After the aneurysm is clipped, it
should be punctured not only to ensure complete obliteration but also to achieve maximal decompression of the third
nerve. Most patients with third nerve palsies improve within
6 months and frequently sooner. Some PComA aneurysms
will not produce any oculomotor nerve deficit. Special care
must be taken in interpreting the angiograms of these
patients, since the aneurysms often project laterally onto the
medial edge of the temporal lobe rather than in more common posterolateral or downward directions. This is relevant
during operative planning, since early re traction of the
temporal lobe may result in premature aneurysmal rupture.
A 54-year-old female was taken to an emergency
room after collapsing at work. She was alert and communicative, with a severe headache, photophobia, nuchal rigidity,
and blurry vision. Computed tomography (CT) of the brain
revealed diffuse subarachnoid blood in the basal cisterns,
mild hydrocephalus, and no intraparenchymal hematoma.
Her angiogram is depicted below.
The patient is taken to the operating room for aneurysm
clipping. Proximal and distal control of the internal carotid
artery is obtained with temporary clip placement prior to
aneurysmal neck dissection. Despite this maneuver, the
aneurysm ruptures during microdissection and significant
bleeding is encountered, which significantly hinders visualization. ‘Vhat preventative maneuver could have been
employed prior to aneurysmal rupture to deCl’ease the
amount of intraoperative bleeding?
A. Blunt surgical microdissection
B. Obtaining proximal control of the internal carotid
artery in the neck
C. ReleaSing the dome of the aneurysm from the temporal
lobe prior to temporary clip placement to prevent traction on the fundus
D. Identifying the distal posterior communicating artery
medial to the internal carotid artery for temporary clip
placement if possible
E. Temporary clip placement on the ophthalmic artery to
prevent retrograde bleeding from the orbit
A. Blunt surgical microdissection
B. Obtaining proximal control of the internal carotid
artery in the neck
C. ReleaSing the dome of the aneurysm from the temporal
lobe prior to temporary clip placement to prevent traction on the fundus
**D. Identifying the distal posterior communicating artery
medial to the internal carotid artery for temporary clip
placement if possible **
E. Temporary clip placement on the ophthalmic artery to
prevent retrograde bleeding from the orbit
Patients with
posterior communicating artery (PComA) aneurysms typically present with subarachnoid hemorrhage (SAl-I) and
partial or complete third nerve palsies (ptosis, dilated pupil,
extraocular muscle abnormalities) due to cOIl1pression of the
third nerve by the aneurysm . . Another common presentation
of PComA aneurysms is the development of a third nerve
deficit in the absence of SAl-I. The appearance of an enlarged
pupil with or without involvement of other third nerve ftmctions should be taken as diagnostic of a PComA aneurysm
until proven otherwise. After the aneurysm is clipped, it
should be punctured not only to ensure complete obliteration but also to achieve maximal decompression of the third
nerve. Most patients with third nerve palsies improve within
6 months and frequently sooner. Some PComA aneurysms
will not produce any oculomotor nerve deficit. Special care
must be taken in interpreting the angiograms of these
patients, since the aneurysms often project laterally onto the
medial edge of the temporal lobe rather than in more common posterolateral or downward directions. This is relevant
during operative planning, since early re traction of the
temporal lobe may result in premature aneurysmal rupture.
A 54-year-old female was taken to an emergency
room after collapsing at work. She was alert and communicative, with a severe headache, photophobia, nuchal rigidity,
and blurry vision. Computed tomography (CT) of the brain
revealed diffuse subarachnoid blood in the basal cisterns,
mild hydrocephalus, and no intraparenchymal hematoma.
Her angiogram is depicted below
Postoperatively, the patient wakes up with contralateral
wealmess, numbness, and homonymous hemianopia. A CT
scan of the brain shows an infarct in the posterior limb of the
internal capsule and in the adjacent white matter (above the
temporal horn of the lateral ventricle). This complication
might possibly have been avoided by
A. Identifying the anterior choroidal artery prior to
aneurysm clipping in order to prevent damage or
incorporation of this vessel into the clip construct
B. Increasing temporary occlusion time to prevent hasty
microdissection
C. Limiting the sylvian fissure dissection to the sphenoidal portion in order to prevent unnecessary
dissection adjacent to PComA artery perforators,
which supply the posterior limb of the internal capsule
D. Obtaining an intraoperative angiogram to confirm
proper clip placement
E. Identifying and preserving the recurrent artery of
Heubner
**A. Identifying the anterior choroidal artery prior to
aneurysm clipping in order to prevent damage or
incorporation of this vessel into the clip construct **
B. Increasing temporary occlusion time to prevent hasty
microdissection
C. Limiting the sylvian fissure dissection to the sphenoidal portion in order to prevent unnecessary
dissection adjacent to PComA artery perforators,
which supply the posterior limb of the internal capsule
D. Obtaining an intraoperative angiogram to confirm
proper clip placement
E. Identifying and preserving the recurrent artery of
Heubner
Patients with
posterior communicating artery (PComA) aneurysms typically present with subarachnoid hemorrhage (SAl-I) and
partial or complete third nerve palsies (ptosis, dilated pupil,
extraocular muscle abnormalities) due to cOIl1pression of the
third nerve by the aneurysm . . Another common presentation
of PComA aneurysms is the development of a third nerve
deficit in the absence of SAl-I. The appearance of an enlarged
pupil with or without involvement of other third nerve ftmctions should be taken as diagnostic of a PComA aneurysm
until proven otherwise. After the aneurysm is clipped, it
should be punctured not only to ensure complete obliteration but also to achieve maximal decompression of the third
nerve. Most patients with third nerve palsies improve within
6 months and frequently sooner. Some PComA aneurysms
will not produce any oculomotor nerve deficit. Special care
must be taken in interpreting the angiograms of these
patients, since the aneurysms often project laterally onto the
medial edge of the temporal lobe rather than in more common posterolateral or downward directions. This is relevant
during operative planning, since early re traction of the
temporal lobe may result in premature aneurysmal rupture.
A 54-year-old female was taken to an emergency
room after collapsing at work. She was alert and communicative, with a severe headache, photophobia, nuchal rigidity,
and blurry vision. Computed tomography (CT) of the brain
revealed diffuse subarachnoid blood in the basal cisterns,
mild hydrocephalus, and no intraparenchymal hematoma.
Her angiogram is depicted below
Postoperatively, the patient sustained damage to the
frontal branch of the facial nerve. What is the most likely
reason for the frontal branch facial nerve injury?
A. The supraorbital nerve was not identified in detaching
the scalp from the supraorbital rim
B. The incision was started less than 1 cm anterior to the
tragus
C. ·There was nerve neuropraxia from postoperative
swelling
D. The nerve in the subgaleal fat pad was injured during
surgical dissection
E. The nerve between the superficial and deep layers of
the temporalis fascia was injured with monopolar
cautery
A. The supraorbital nerve was not identified in detaching
the scalp from the supraorbital rim
B. The incision was started less than 1 cm anterior to the
tragus
C. ·There was nerve neuropraxia from postoperative
swelling
**D. The nerve in the subgaleal fat pad was injured during
surgical dissection **
E. The nerve between the superficial and deep layers of
the temporalis fascia was injured with monopolar
cautery
Patients with
posterior communicating artery (PComA) aneurysms typically present with subarachnoid hemorrhage (SAl-I) and
partial or complete third nerve palsies (ptosis, dilated pupil,
extraocular muscle abnormalities) due to cOIl1pression of the
third nerve by the aneurysm . . Another common presentation
of PComA aneurysms is the development of a third nerve
deficit in the absence of SAl-I. The appearance of an enlarged
pupil with or without involvement of other third nerve ftmctions should be taken as diagnostic of a PComA aneurysm
until proven otherwise. After the aneurysm is clipped, it
should be punctured not only to ensure complete obliteration but also to achieve maximal decompression of the third
nerve. Most patients with third nerve palsies improve within
6 months and frequently sooner. Some PComA aneurysms
will not produce any oculomotor nerve deficit. Special care
must be taken in interpreting the angiograms of these
patients, since the aneurysms often project laterally onto the
medial edge of the temporal lobe rather than in more common posterolateral or downward directions. This is relevant
during operative planning, since early re traction of the
temporal lobe may result in premature aneurysmal rupture.
A 28-year-old male was involved in a motorcycle
accident. About 1 week after being discharged from the
hospital he began experiencing fevers, severe retroorbital
headaches, diplopia, and left eye proptosis, which prompted
a visit to the emergency department. A computed tomography
(CT) scan of the brain showed a ‘ resolving 2- by 3-cm left
frontal contusion underlying a minimally displaced frontal
bone fracture, which was sustained at the time of initial
injury. His erythrocyte sedimentation rate (ESR) and Creactive protein (CRP) were mildly elevated. The angiogram
is depicted below
What is the most likely diagnosis?
A. Superior orbital fissure syndrome
B. Incidental meningioma originating fro111 the medial
aspect of the sphenoid ridge
C. Arterial-venous fistula
D. Occlusion of the internal carotid artery proximal to the
ophthalmic artery ol:igin
E. Cavernous sinus thrombosis
A. Superior orbital fissure syndrome
B. Incidental meningioma originating fro111 the medial
aspect of the sphenoid ridge
**C. Arterial-venous fistula **
D. Occlusion of the internal carotid artery proximal to the
ophthalmic artery ol:igin
E. Cavernous sinus thrombosis
Carotid-cavernous fistulas (CCFs) can be
divided into posttraumatic and spontaneous types. They are
direct shunts between the ICA or ECA and cavernous sinus
and usually occur after trauma or spontaneous aneurysmal
rupture. Traumatic CCFs often present in a delayed fashion ;
like spontaneous fistulas, they often present with retro-orbital
199
200 Intensive Neurosurgery Board Review
pain, chemosis, pulsatile proptosis, ocular or cranial bruit,
decreased visual acuity, diplopia, and rarely epistaxis and
subarachnoid hemorrhage. The symptoms depend on the
direction of venous flow and quantity of blood flow through
the fistula. There are four types of CCFs: type A is a direct,
high-flow shunt between the ICA and cavernous sinus (as
in this case), and types B to D are low-flow shunts between
the cavernous sinus and meningeal branches of the internal
carotid artery, external carotid artery, or both, respectively. Approximately 50% of low-flow fistulas spontaneously
thrombose without treatment. The main treatment option
has traditionally included transarterial balloon embolization
through the ICA for type A fistulas, although accessing the
fistula transvenously (Le., inferior petrosal sinus) is also
commonly performed, especially for indirect types B to D.
A direct surgical approach is indicated if transarterial or
transvenous approaches fail. Radiosurgery has been proposed as an option for some of the low-flow fistulas, although
it would not be the best strategy for the high-flow symptomatic fistula seen in this patient. Figure A depicts nearly
complete capture of the blood from the internal carotid
artery, and fistulous drainage primarily from the superior
ophthalmic and superior petrosal veins. Figure B depicts a
later venous run with superior petrosal vein drainage into the
transverse-sigmoid sinus junction as well as some venous
drainage into the superior sagittal sinus (Kaye and Blacl~,
pp. 1132; Greenberg, pp. 811- 812; Youmans, pp. 2341-
2352; Will~ins, pp. 2529- 2535).
A 28-year-old male was involved in a motorcycle
accident. About 1 week after being discharged from the
hospital he began experiencing fevers, severe retroorbital
headaches, diplopia, and left eye proptosis, which prompted
a visit to the emergency department. A computed tomography
(CT) scan of the brain showed a ‘ resolving 2- by 3-cm left
frontal contusion underlying a minimally displaced frontal
bone fracture, which was sustained at the time of initial
injury. His erythrocyte sedimentation rate (ESR) and Creactive protein (CRP) were mildly elevated. The angiogram
is depicted below
The signs/symptoms of this disease process depend
mostly upon
A. The size and location of the tumor relative to the optic
nerve
B. The direction of venous drainage and rate of blood flow
through the shunt
C. The extent of the inflammatory reaction adjacent to
the cavernous sinus
D. The extent of the inflammatory reaction adjacent to
the superior orbital fissure
E. The extent of collateral flow from the opposite internal
carotid artery and external meningeal feeders
A. The size and location of the tumor relative to the optic
nerve
B. The direction of venous drainage and rate of blood flow
through the shunt
C. The extent of the inflammatory reaction adjacent to
the cavernous sinus
D. The extent of the inflammatory reaction adjacent to
the superior orbital fissure
E. The extent of collateral flow from the opposite internal
carotid artery and external meningeal feeders
Carotid-cavernous fistulas (CCFs) can be
divided into posttraumatic and spontaneous types. They are
direct shunts between the ICA or ECA and cavernous sinus
and usually occur after trauma or spontaneous aneurysmal
rupture. Traumatic CCFs often present in a delayed fashion ;
like spontaneous fistulas, they often present with retro-orbital
199
200 Intensive Neurosurgery Board Review
pain, chemosis, pulsatile proptosis, ocular or cranial bruit,
decreased visual acuity, diplopia, and rarely epistaxis and
subarachnoid hemorrhage. The symptoms depend on the
direction of venous flow and quantity of blood flow through
the fistula. There are four types of CCFs: type A is a direct,
high-flow shunt between the ICA and cavernous sinus (as
in this case), and types B to D are low-flow shunts between
the cavernous sinus and meningeal branches of the internal
carotid artery, external carotid artery, or both, respectively. Approximately 50% of low-flow fistulas spontaneously
thrombose without treatment. The main treatment option
has traditionally included transarterial balloon embolization
through the ICA for type A fistulas, although accessing the
fistula transvenously (Le., inferior petrosal sinus) is also
commonly performed, especially for indirect types B to D.
A direct surgical approach is indicated if transarterial or
transvenous approaches fail. Radiosurgery has been proposed as an option for some of the low-flow fistulas, although
it would not be the best strategy for the high-flow symptomatic fistula seen in this patient. Figure A depicts nearly
complete capture of the blood from the internal carotid
artery, and fistulous drainage primarily from the superior
ophthalmic and superior petrosal veins. Figure B depicts a
later venous run with superior petrosal vein drainage into the
transverse-sigmoid sinus junction as well as some venous
drainage into the superior sagittal sinus (Kaye and Blacl~,
pp. 1132; Greenberg, pp. 811- 812; Youmans, pp. 2341-
2352; Will~ins, pp. 2529- 2535).
A 28-year-old male was involved in a motorcycle
accident. About 1 week after being discharged from the
hospital he began experiencing fevers, severe retroorbital
headaches, diplopia, and left eye proptosis, which prompted
a visit to the emergency department. A computed tomography
(CT) scan of the brain showed a ‘ resolving 2- by 3-cm left
frontal contusion underlying a minimally displaced frontal
bone fracture, which was sustained at the time of initial
injury. His erythrocyte sedimentation rate (ESR) and Creactive protein (CRP) were mildly elevated. The angiogram
is depicted below
What should be the initial treatment of choice for this
patient?
A. Six weeks of antibiotics followed by repeat angiography
B. Glue embolization of major arterial feeders followed by
tumor resection
C. Carotid artery sacrifice
D. Transarterial detachable balloon embolization
E. Heparin infusion
A. Six weeks of antibiotics followed by repeat angiography
B. Glue embolization of major arterial feeders followed by
tumor resection
C. Carotid artery sacrifice
**D. Transarterial detachable balloon embolization **
E. Heparin infusion
Carotid-cavernous fistulas (CCFs) can be
divided into posttraumatic and spontaneous types. They are
direct shunts between the ICA or ECA and cavernous sinus
and usually occur after trauma or spontaneous aneurysmal
rupture. Traumatic CCFs often present in a delayed fashion ;
like spontaneous fistulas, they often present with retro-orbital
199
200 Intensive Neurosurgery Board Review
pain, chemosis, pulsatile proptosis, ocular or cranial bruit,
decreased visual acuity, diplopia, and rarely epistaxis and
subarachnoid hemorrhage. The symptoms depend on the
direction of venous flow and quantity of blood flow through
the fistula. There are four types of CCFs: type A is a direct,
high-flow shunt between the ICA and cavernous sinus (as
in this case), and types B to D are low-flow shunts between
the cavernous sinus and meningeal branches of the internal
carotid artery, external carotid artery, or both, respectively. Approximately 50% of low-flow fistulas spontaneously
thrombose without treatment. The main treatment option
has traditionally included transarterial balloon embolization
through the ICA for type A fistulas, although accessing the
fistula transvenously (Le., inferior petrosal sinus) is also
commonly performed, especially for indirect types B to D.
A direct surgical approach is indicated if transarterial or
transvenous approaches fail. Radiosurgery has been proposed as an option for some of the low-flow fistulas, although
it would not be the best strategy for the high-flow symptomatic fistula seen in this patient. Figure A depicts nearly
complete capture of the blood from the internal carotid
artery, and fistulous drainage primarily from the superior
ophthalmic and superior petrosal veins. Figure B depicts a
later venous run with superior petrosal vein drainage into the
transverse-sigmoid sinus junction as well as some venous
drainage into the superior sagittal sinus (Kaye and Blacl~,
pp. 1132; Greenberg, pp. 811- 812; Youmans, pp. 2341-
2352; Will~ins, pp. 2529- 2535).
A 28-year-old male was involved in a motorcycle
accident. About 1 week after being discharged from the
hospital he began experiencing fevers, severe retroorbital
headaches, diplopia, and left eye proptosis, which prompted
a visit to the emergency department. A computed tomography
(CT) scan of the brain showed a ‘ resolving 2- by 3-cm left
frontal contusion underlying a minimally displaced frontal
bone fracture, which was sustained at the time of initial
injury. His erythrocyte sedimentation rate (ESR) and Creactive protein (CRP) were mildly elevated. The angiogram
is depicted below
If the desired treatment strategy fails, what would be
another potential treatment option?
1. Surgical debridement of the infection
2. Direct surgical packing of the cavernous sinus with
either Gelfoam, Surgicel, platinum coils, or strands of
cotton
3. Preoperative glue embolization of arterial feeders
followed by tumor resection
4. Endovascular procedure for internal carotid artery
sacrifice
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. 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
Carotid-cavernous fistulas (CCFs) can be
divided into posttraumatic and spontaneous types. They are
direct shunts between the ICA or ECA and cavernous sinus
and usually occur after trauma or spontaneous aneurysmal
rupture. Traumatic CCFs often present in a delayed fashion ;
like spontaneous fistulas, they often present with retro-orbital
199
200 Intensive Neurosurgery Board Review
pain, chemosis, pulsatile proptosis, ocular or cranial bruit,
decreased visual acuity, diplopia, and rarely epistaxis and
subarachnoid hemorrhage. The symptoms depend on the
direction of venous flow and quantity of blood flow through
the fistula. There are four types of CCFs: type A is a direct,
high-flow shunt between the ICA and cavernous sinus (as
in this case), and types B to D are low-flow shunts between
the cavernous sinus and meningeal branches of the internal
carotid artery, external carotid artery, or both, respectively. Approximately 50% of low-flow fistulas spontaneously
thrombose without treatment. The main treatment option
has traditionally included transarterial balloon embolization
through the ICA for type A fistulas, although accessing the
fistula transvenously (Le., inferior petrosal sinus) is also
commonly performed, especially for indirect types B to D.
A direct surgical approach is indicated if transarterial or
transvenous approaches fail. Radiosurgery has been proposed as an option for some of the low-flow fistulas, although
it would not be the best strategy for the high-flow symptomatic fistula seen in this patient. Figure A depicts nearly
complete capture of the blood from the internal carotid
artery, and fistulous drainage primarily from the superior
ophthalmic and superior petrosal veins. Figure B depicts a
later venous run with superior petrosal vein drainage into the
transverse-sigmoid sinus junction as well as some venous
drainage into the superior sagittal sinus (Kaye and Blacl~,
pp. 1132; Greenberg, pp. 811- 812; Youmans, pp. 2341-
2352; Will~ins, pp. 2529- 2535).
‘Vhat finding in the pathologic process depicted by
the angiogram below (Figure 6.10Q) would mandate urgent
treatment?
A. Retrograde cortical venous drainage
B. J’vlultiple meningeal artery feeders
C. Dual internal and external carotid artery supply
D. Embolic stroke
E. Venous sinus occlusion
**A. Retrograde cortical venous drainage **
B. J’vlultiple meningeal artery feeders
C. Dual internal and external carotid artery supply
D. Embolic stroke
E. Venous sinus occlusion
The natural history of DAVF is variable and includes
spontaneous resolution, recruitment of meningeal arterial
feeders, and the development of intracranial hypertension.
DAVF can present with pulsatile tinnitus, visual symptoms,
papilledema , hydrocephalus, and intracranial hemorrhage.
The presence of retrograde cortical venous drainage indicates
the potential for intracranial hemorrhage and mandates
urgent treatment of the DAVF. Intracranial hemorrhage from
a DA VF in the absence of retrograde cortical venous drainage
has not been reported. Hemorrhage from a DA VF is associated with a high morbidity and mortality (approximately
30%). Ectatic dilation or venous occlusion of the involved
sinus, multiple or dual ICiVECA arterial feeders, or embolic
stroke, in the absence of retrograde cortical venous drainage
has not been reported to increase hemorrhage rates of
DAVFs (Kaye and Blaci<, pp. 1125-1135; Greenberg, p. 811;
Youmans, pp. 2171- 2173; Will~ins, pp. 2523-2527).
A 67-year-old male with a history of diabetes
mellitus and hypertension presents to the emergency department with right arm wealmess and numbness. He is found to
have> 90% stenosis of the left internal carotid artery and
restricted MR diffusion in portions of the brain supplied by
the left middle cerebral artery. He elects to proceed with
surgery for his carotid stenosis but is found to have a highriding carotid artery bifurcation.
Surgical maneuvers that may increase surgical exposure
of a high-riding carotid artery bifurcation during carotid
endarterectomy include all of the following EXCEPT?
A. Medial mobilization of the ansa cervicalis
B. Dividing the posterior belly of the digastric muscle
C. l’vIandibular osteotomy or disarticulation of the mandible
at the temporomandibular joint
D. Judicious cautery and ligation of select vessels (occipital
artery, common facial vein) hindering exposure
E. Transverse sectioning of the clavicular head of the
sternocleidomastoid muscle at the level of the hyoid
bone for better visualization of the carotid artery
lateral to the jugular vein
A. Medial mobilization of the ansa cervicalis
B. Dividing the posterior belly of the digastric muscle
C. l’vIandibular osteotomy or disarticulation of the mandible
at the temporomandibular joint
D. Judicious cautery and ligation of select vessels (occipital
artery, common facial vein) hindering exposure
**E. Transverse sectioning of the clavicular head of the
sternocleidomastoid muscle at the level of the hyoid
bone for better visualization of the carotid artery
lateral to the jugular vein
**
Attempts to gain additional
exposure for a high-riding carotid artery bifurcation include
mobilization of the ansa cervicalis, sectioning the posterior
belly of the digastric muscle , cautery and ligation of the
occipital artery, and mandibular osteotomy or disarticulation of the jaw at the temporomandibular joint. This type
of exposure places the hypoglossal nerve at particular risk,
although segments of cranial nerves VII, DC, X, and Xl can also be injured during carotid endarterectomy (CEA).
Patients who become hypotensive and bradycardic during
surgery often do so as a result of manipulation of the nerve of
Hering near the carotid bulb. This is not uncommon with
CEA and can often be addressed with lidocaine infusion adjacent to the carotid bulb. Placing the clamps on the internal
carotid artery first, followed by the common and then the
external carotid artery often ensures that the clot will pass
through the external carotid artery instead of the internal
carotid artery. The order for clamp removal should be just
the opposite, as this should again ensure that any accumulated blood clot will be more likely to pass through the
external rather than internal carotid circulation. It is not
uncommon during CEA to have some backbleeding into the
surgical field by the ascending pharyngeal artery after clamp
placement on the major vessels. If the extent of bleeding is
severe and hinders the operation, identification, clamping
(aneurysm clip), or. ligation of this vessel may drastically
improve visibility. A patient who awakens with a major
neurologic deficit is likely to have suffered thrombosis at the
arteriotomy site, which usually warrants immediate attention (surgical exploration) rather than time-consuming
diagnostic studies, as some case reports describe a significant neurologic improvement if flow is re-established
within 45 minutes. For later-onset deficits, workup (Le. ,
CT, angiogram) may be indicated. CT may help to identify
hemorrhage and an angiogram may reveal whether the ICA
is occluded or if the deficit is from another cause (emboli)
that would not necessarily require surgical re-exploration
(Kaye and Blacl~, pp. 1179- 1187; Greenberg, pp. 837-841;
Youmans, pp. 1631-1645; Will~ins, pp. 2113- 2114).
A 67-year-old male with a history of diabetes
mellitus and hypertension presents to the emergency department with right arm wealmess and numbness. He is found to
have> 90% stenosis of the left internal carotid artery and
restricted MR diffusion in portions of the brain supplied by
the left middle cerebral artery. He elects to proceed with
surgery for his carotid stenosis but is found to have a highriding carotid artery bifurcation.
What cranial nerve is at most risk of injury when exposing a high-riding carotid artery bifurcation?
A. VII
B. IX
C. X
D. XI
E. XII
A. VII
B. IX
C. X
D. XI
E. XII
Attempts to gain additional
exposure for a high-riding carotid artery bifurcation include
mobilization of the ansa cervicalis, sectioning the posterior
belly of the digastric muscle , cautery and ligation of the
occipital artery, and mandibular osteotomy or disarticulation of the jaw at the temporomandibular joint. This type
of exposure places the hypoglossal nerve at particular risk,
although segments of cranial nerves VII, DC, X, and Xl can also be injured during carotid endarterectomy (CEA).
Patients who become hypotensive and bradycardic during
surgery often do so as a result of manipulation of the nerve of
Hering near the carotid bulb. This is not uncommon with
CEA and can often be addressed with lidocaine infusion adjacent to the carotid bulb. Placing the clamps on the internal
carotid artery first, followed by the common and then the
external carotid artery often ensures that the clot will pass
through the external carotid artery instead of the internal
carotid artery. The order for clamp removal should be just
the opposite, as this should again ensure that any accumulated blood clot will be more likely to pass through the
external rather than internal carotid circulation. It is not
uncommon during CEA to have some backbleeding into the
surgical field by the ascending pharyngeal artery after clamp
placement on the major vessels. If the extent of bleeding is
severe and hinders the operation, identification, clamping
(aneurysm clip), or. ligation of this vessel may drastically
improve visibility. A patient who awakens with a major
neurologic deficit is likely to have suffered thrombosis at the
arteriotomy site, which usually warrants immediate attention (surgical exploration) rather than time-consuming
diagnostic studies, as some case reports describe a significant neurologic improvement if flow is re-established
within 45 minutes. For later-onset deficits, workup (Le. ,
CT, angiogram) may be indicated. CT may help to identify
hemorrhage and an angiogram may reveal whether the ICA
is occluded or if the deficit is from another cause (emboli)
that would not necessarily require surgical re-exploration
(Kaye and Blacl~, pp. 1179- 1187; Greenberg, pp. 837-841;
Youmans, pp. 1631-1645; Will~ins, pp. 2113- 2114).
A 67-year-old male with a history of diabetes
mellitus and hypertension presents to the emergency department with right arm wealmess and numbness. He is found to
have> 90% stenosis of the left internal carotid artery and
restricted MR diffusion in portions of the brain supplied by
the left middle cerebral artery. He elects to proceed with
surgery for his carotid stenosis but is found to have a highriding carotid artery bifurcation.
What is the order of clamp placement on the arteries
during carotid endarterectomy?
A. External, internal, common
B. Internal, common, external
C. External, common, internal
D. Common, external, internal
E. Common, internal, external
A. External, internal, common
**B. Internal, common, external **
C. External, common, internal
D. Common, external, internal
E. Common, internal, external
Attempts to gain additional
exposure for a high-riding carotid artery bifurcation include
mobilization of the ansa cervicalis, sectioning the posterior
belly of the digastric muscle , cautery and ligation of the
occipital artery, and mandibular osteotomy or disarticulation of the jaw at the temporomandibular joint. This type
of exposure places the hypoglossal nerve at particular risk,
although segments of cranial nerves VII, DC, X, and Xl can also be injured during carotid endarterectomy (CEA).
Patients who become hypotensive and bradycardic during
surgery often do so as a result of manipulation of the nerve of
Hering near the carotid bulb. This is not uncommon with
CEA and can often be addressed with lidocaine infusion adjacent to the carotid bulb. Placing the clamps on the internal
carotid artery first, followed by the common and then the
external carotid artery often ensures that the clot will pass
through the external carotid artery instead of the internal
carotid artery. The order for clamp removal should be just
the opposite, as this should again ensure that any accumulated blood clot will be more likely to pass through the
external rather than internal carotid circulation. It is not
uncommon during CEA to have some backbleeding into the
surgical field by the ascending pharyngeal artery after clamp
placement on the major vessels. If the extent of bleeding is
severe and hinders the operation, identification, clamping
(aneurysm clip), or. ligation of this vessel may drastically
improve visibility. A patient who awakens with a major
neurologic deficit is likely to have suffered thrombosis at the
arteriotomy site, which usually warrants immediate attention (surgical exploration) rather than time-consuming
diagnostic studies, as some case reports describe a significant neurologic improvement if flow is re-established
within 45 minutes. For later-onset deficits, workup (Le. ,
CT, angiogram) may be indicated. CT may help to identify
hemorrhage and an angiogram may reveal whether the ICA
is occluded or if the deficit is from another cause (emboli)
that would not necessarily require surgical re-exploration
(Kaye and Blacl~, pp. 1179- 1187; Greenberg, pp. 837-841;
Youmans, pp. 1631-1645; Will~ins, pp. 2113- 2114).
A 67-year-old male with a history of diabetes
mellitus and hypertension presents to the emergency department with right arm wealmess and numbness. He is found to
have> 90% stenosis of the left internal carotid artery and
restricted MR diffusion in portions of the brain supplied by
the left middle cerebral artery. He elects to proceed with
surgery for his carotid stenosis but is found to have a highriding carotid artery bifurcation.
After clamp placement and arteriotomy, the surgeon
notices continued bleeding from the back wall of the carotid
artery, which severely hinders visualization during the
surgical procedure. What is the most likely reason for the
continued bleeding?
A. Incomplete clamping of the common carotid artery
B. Backbleeding from the superficial temporal artery
C. Backbleeding from the ascending pharyngeal artery
D. Venous bleeding from the adventitia of the internal
carotid artery
E. Clotting abnormality from heparin inhlsion
A. Incomplete clamping of the common carotid artery
B. Backbleeding from the superficial temporal artery
**C. Backbleeding from the ascending pharyngeal artery **
D. Venous bleeding from the adventitia of the internal
carotid artery
E. Clotting abnormality from heparin inhlsion
Attempts to gain additional
exposure for a high-riding carotid artery bifurcation include
mobilization of the ansa cervicalis, sectioning the posterior
belly of the digastric muscle , cautery and ligation of the
occipital artery, and mandibular osteotomy or disarticulation of the jaw at the temporomandibular joint. This type
of exposure places the hypoglossal nerve at particular risk,
although segments of cranial nerves VII, DC, X, and Xl can also be injured during carotid endarterectomy (CEA).
Patients who become hypotensive and bradycardic during
surgery often do so as a result of manipulation of the nerve of
Hering near the carotid bulb. This is not uncommon with
CEA and can often be addressed with lidocaine infusion adjacent to the carotid bulb. Placing the clamps on the internal
carotid artery first, followed by the common and then the
external carotid artery often ensures that the clot will pass
through the external carotid artery instead of the internal
carotid artery. The order for clamp removal should be just
the opposite, as this should again ensure that any accumulated blood clot will be more likely to pass through the
external rather than internal carotid circulation. It is not
uncommon during CEA to have some backbleeding into the
surgical field by the ascending pharyngeal artery after clamp
placement on the major vessels. If the extent of bleeding is
severe and hinders the operation, identification, clamping
(aneurysm clip), or. ligation of this vessel may drastically
improve visibility. A patient who awakens with a major
neurologic deficit is likely to have suffered thrombosis at the
arteriotomy site, which usually warrants immediate attention (surgical exploration) rather than time-consuming
diagnostic studies, as some case reports describe a significant neurologic improvement if flow is re-established
within 45 minutes. For later-onset deficits, workup (Le. ,
CT, angiogram) may be indicated. CT may help to identify
hemorrhage and an angiogram may reveal whether the ICA
is occluded or if the deficit is from another cause (emboli)
that would not necessarily require surgical re-exploration
(Kaye and Blacl~, pp. 1179- 1187; Greenberg, pp. 837-841;
Youmans, pp. 1631-1645; Will~ins, pp. 2113- 2114).
A 67-year-old male with a history of diabetes
mellitus and hypertension presents to the emergency department with right arm wealmess and numbness. He is found to
have> 90% stenosis of the left internal carotid artery and
restricted MR diffusion in portions of the brain supplied by
the left middle cerebral artery. He elects to proceed with
surgery for his carotid stenosis but is found to have a highriding carotid artery bifurcation.
During surgical dissection adjacent to the carotid
artery, the anesthesiologist notices that the patient becomes
hypotensive and bradycardic. The next course of management should include
A. Obtain an immediate arterial blood gas (ABG) to
determine if the patient is suffering from a pulmonary
embolus
B. Check cardiac enzymes, as the patient is likely suffering from an anterior myocardial wall infarction
C. The nerve to the carotid sinus (nerve of Hering) should
be anesthetized with 0.5 mL of 2% lidocaine
D. Begin dobutamine , check central venous pressures,
and obtain a lactate level, as the patient is likely to be
volume-depleted
E. 100 IV/kg of heparin should be infused intravenously
to prevent further emboli
A. Obtain an immediate arterial blood gas (ABG) to
determine if the patient is suffering from a pulmonary
embolus
B. Check cardiac enzymes, as the patient is likely suffering from an anterior myocardial wall infarction
**C. The nerve to the carotid sinus (nerve of Hering) should
be anesthetized with 0.5 mL of 2% lidocaine **
D. Begin dobutamine , check central venous pressures,
and obtain a lactate level, as the patient is likely to be
volume-depleted
E. 100 IV/kg of heparin should be infused intravenously
to prevent further emboli
Attempts to gain additional
exposure for a high-riding carotid artery bifurcation include
mobilization of the ansa cervicalis, sectioning the posterior
belly of the digastric muscle , cautery and ligation of the
occipital artery, and mandibular osteotomy or disarticulation of the jaw at the temporomandibular joint. This type
of exposure places the hypoglossal nerve at particular risk,
although segments of cranial nerves VII, DC, X, and Xl can also be injured during carotid endarterectomy (CEA).
Patients who become hypotensive and bradycardic during
surgery often do so as a result of manipulation of the nerve of
Hering near the carotid bulb. This is not uncommon with
CEA and can often be addressed with lidocaine infusion adjacent to the carotid bulb. Placing the clamps on the internal
carotid artery first, followed by the common and then the
external carotid artery often ensures that the clot will pass
through the external carotid artery instead of the internal
carotid artery. The order for clamp removal should be just
the opposite, as this should again ensure that any accumulated blood clot will be more likely to pass through the
external rather than internal carotid circulation. It is not
uncommon during CEA to have some backbleeding into the
surgical field by the ascending pharyngeal artery after clamp
placement on the major vessels. If the extent of bleeding is
severe and hinders the operation, identification, clamping
(aneurysm clip), or. ligation of this vessel may drastically
improve visibility. A patient who awakens with a major
neurologic deficit is likely to have suffered thrombosis at the
arteriotomy site, which usually warrants immediate attention (surgical exploration) rather than time-consuming
diagnostic studies, as some case reports describe a significant neurologic improvement if flow is re-established
within 45 minutes. For later-onset deficits, workup (Le. ,
CT, angiogram) may be indicated. CT may help to identify
hemorrhage and an angiogram may reveal whether the ICA
is occluded or if the deficit is from another cause (emboli)
that would not necessarily require surgical re-exploration
(Kaye and Blacl~, pp. 1179- 1187; Greenberg, pp. 837-841;
Youmans, pp. 1631-1645; Will~ins, pp. 2113- 2114).
A 67-year-old male with a history of diabetes
mellitus and hypertension presents to the emergency department with right arm wealmess and numbness. He is found to
have> 90% stenosis of the left internal carotid artery and
restricted MR diffusion in portions of the brain supplied by
the left middle cerebral artery. He elects to proceed with
surgery for his carotid stenosis but is found to have a highriding carotid artery bifurcation.
Postoperatively, the patient awoke with right-sided
hemiplegia and lethargy. The next logical course of management should include
A. Immediate CT angiography to assess the patency of the
right carotid artery
B. Immediate selective angiography of the right carotid
artery
C. Antiplatelet therapy for 1 week, followed by repeat
angiography
D. Stent placement across the arteriotomy site to reinforce the closure
E. Immediate surgical reexploration for thrombectomy
A. Immediate CT angiography to assess the patency of the
right carotid artery
B. Immediate selective angiography of the right carotid
artery
C. Antiplatelet therapy for 1 week, followed by repeat
angiography
D. Stent placement across the arteriotomy site to reinforce the closure
E. Immediate surgical reexploration for thrombectomy
Attempts to gain additional
exposure for a high-riding carotid artery bifurcation include
mobilization of the ansa cervicalis, sectioning the posterior
belly of the digastric muscle , cautery and ligation of the
occipital artery, and mandibular osteotomy or disarticulation of the jaw at the temporomandibular joint. This type
of exposure places the hypoglossal nerve at particular risk,
although segments of cranial nerves VII, DC, X, and Xl can also be injured during carotid endarterectomy (CEA).
Patients who become hypotensive and bradycardic during
surgery often do so as a result of manipulation of the nerve of
Hering near the carotid bulb. This is not uncommon with
CEA and can often be addressed with lidocaine infusion adjacent to the carotid bulb. Placing the clamps on the internal
carotid artery first, followed by the common and then the
external carotid artery often ensures that the clot will pass
through the external carotid artery instead of the internal
carotid artery. The order for clamp removal should be just
the opposite, as this should again ensure that any accumulated blood clot will be more likely to pass through the
external rather than internal carotid circulation. It is not
uncommon during CEA to have some backbleeding into the
surgical field by the ascending pharyngeal artery after clamp
placement on the major vessels. If the extent of bleeding is
severe and hinders the operation, identification, clamping
(aneurysm clip), or. ligation of this vessel may drastically
improve visibility. A patient who awakens with a major
neurologic deficit is likely to have suffered thrombosis at the
arteriotomy site, which usually warrants immediate attention (surgical exploration) rather than time-consuming
diagnostic studies, as some case reports describe a significant neurologic improvement if flow is re-established
within 45 minutes. For later-onset deficits, workup (Le. ,
CT, angiogram) may be indicated. CT may help to identify
hemorrhage and an angiogram may reveal whether the ICA
is occluded or if the deficit is from another cause (emboli)
that would not necessarily require surgical re-exploration
(Kaye and Blacl~, pp. 1179- 1187; Greenberg, pp. 837-841;
Youmans, pp. 1631-1645; Will~ins, pp. 2113- 2114).
A lS-year-old female undergoes uncomplicated resection of
the lesion depicted below (Figure 6.17-6.18Q). Four days
later she develops lethargy, fever, meningismus, and photophobia. A cerebrospinal fluid (CSF) sample reveals a protein
level of 86 mg/dL (reference range, 12 to 60 mg/dL), a glucose level of 61 mg/dL (reference range , 40 to 70 mg/dL),
16 red blood cells/mL, and 126 white blood celis/mL with a
differential of 11% neutrophils, 82% lymphocytes, and 7%
histiocytes. Gram stain and culture of CSF were sterile and
remained so for the presence of organisms.
Wha t is the most likely diagnosis ?
A. Bacterial meningitis
B. Aseptic meningitis
C. Hydrocephalus
D. Postmeningitis syndrome
E. Viral encephalitis
A. Bacterial meningitis
**B. Aseptic meningitis **
C. Hydrocephalus
D. Postmeningitis syndrome
E. Viral encephalitis
AseptiC meningitis (AM) is a well-recognized
complication after posterior fossa surgery but is typically
self-limited and requires no treatment. It has generally been
attributed to one or more irritants released into the subarachnoid space during surgery, including blood breakdown
products, tumor, muscle , and brain. Lowering of intracranial
pressure with lumbar puncture and dexamethasone is the
mainstay of treatment in certain patients with continued ,
problems. Bacterial meningitis and postmeningitic syndrome are unlikely, considering that an organism was not
isolated from the CSF, although this is not always the case.
lVloreover, the CSF profile was more consistent with aseptic
meningi tis than bacterial meningitis. Hydrocephalus is
unlikely, since fever, meningismus, and photophobia rarely
accompany this diagnosis, and encephalitis would be very
uncommon in this situation (Carmel et ai., pp. 276-280;
Youmans, pp. 3645, 3659; Kaye and Blacl~, p. 868; Will~ins,
p.3965).
A lS-year-old female undergoes uncomplicated resection of
the lesion depicted below (Figure 6.17-6.18Q). Four days
later she develops lethargy, fever, meningismus, and photophobia. A cerebrospinal fluid (CSF) sample reveals a protein
level of 86 mg/dL (reference range, 12 to 60 mg/dL), a glucose level of 61 mg/dL (reference range , 40 to 70 mg/dL),
16 red blood cells/mL, and 126 white blood celis/mL with a
differential of 11% neutrophils, 82% lymphocytes, and 7%
histiocytes. Gram stain and culture of CSF were sterile and
remained so for the presence of organisms.
What is the natural history of this problem?
A. Requires a 10-day course of antibiotics despite negative
cultures to cover for slow-growing bacterial species
B. Patients frequently require steroid therapy followed
by repeat lumbar punctures
C. Usually self-limited and requires no treatment
D. Patients show drastic improvement with shunting
E. Usually favorable once any synthetic material placed
during surgery (e.g., dural graft) is removed
A. Requires a 10-day course of antibiotics despite negative
cultures to cover for slow-growing bacterial species
B. Patients frequently require steroid therapy followed
by repeat lumbar punctures
C. Usually self-limited and requires no treatment
D. Patients show drastic improvement with shunting
E. Usually favorable once any synthetic material placed
during surgery (e.g., dural graft) is removed
AseptiC meningitis (AM) is a well-recognized
complication after posterior fossa surgery but is typically
self-limited and requires no treatment. It has generally been
attributed to one or more irritants released into the subarachnoid space during surgery, including blood breakdown
products, tumor, muscle , and brain. Lowering of intracranial
pressure with lumbar puncture and dexamethasone is the
mainstay of treatment in certain patients with continued ,
problems. Bacterial meningitis and postmeningitic syndrome are unlikely, considering that an organism was not
isolated from the CSF, although this is not always the case.
lVloreover, the CSF profile was more consistent with aseptic
meningi tis than bacterial meningitis. Hydrocephalus is
unlikely, since fever, meningismus, and photophobia rarely
accompany this diagnosis, and encephalitis would be very
uncommon in this situation (Carmel et ai., pp. 276-280;
Youmans, pp. 3645, 3659; Kaye and Blacl~, p. 868; Will~ins,
p.3965).
A 62-year-old female undergoes microvascular decompression for hemifacial spasm. Postoperatively, she has complete ipsilateral deafness but no other neurologic deficits.
The most likely cause of this deficit was injury to one of the
blood vessels that originated from which artery?
A. Posterior cerebral artery (PCA)
B. Superior cerebellar artery (SCA)
C. Anterior inferior cerebellar artery (AICA)
D. Posterior inferior cerebellar artery (PICA)
E. Vertebral artery
A. Posterior cerebral artery (PCA)
B. Superior cerebellar artery (SCA)
**C. Anterior inferior cerebellar artery (AICA) **
D. Posterior inferior cerebellar artery (PICA)
E. Vertebral artery
Complications of microvascular decompression for
hemifacial spasm include CSF leak, facial weakness, facial
anesthesia, corneal anesthesia, intracranial hemorrhage,
and infarction. Complete ipsilateral deafness is associated
with disruption or coagulation of the labyrinthine artery,
which is most commonly a branch of either the AlCA
(45%), SCA (25%), or basilar artery (16%) (Kaye and Black,
pp. 1652-1653; Osborne DN, p. 186; Greenberg, pp. 358-
360; Youmans, pp. 3013-3014; Wil~<ins, pp. 3227-3233).
A 14-year-old girl with progressive loss of vision in her
right eye was recently diagnosed with a 2.0- by 3.5-cm right
optic nerve glioma extending to the optic chiasm. During
surgery, the portion of the tumor on the optic nerve was
successfully resected, but the tumor adjacent to the optic
chiasm was left behind. What is the maximal dose of singlefraction radiosurgery that can safely be employed to the
optic chiasm?
A. 4 to 7 Gy
B. 9 to 10 Gy
C. 11 to 13 Gy
D. 14 to 16 Gy
E. 21 Gy
A. 4 to 7 Gy
**B. 9 to 10 Gy **
C. 11 to 13 Gy
D. 14 to 16 Gy
E. 21 Gy
The maximal safe dose of Single-shot radiosurgelY
that the optic chiasm can tolerate is approximately 9 to
10 Gy (Alexander, p. 171).
A surgeon decides to utilize an infratentorialsupra cerebellar corridor to approach a pineal region mass.
What blood vessel is frequently cauterized and divided
for better exposure of the posterior surface of the tumor
during this approach?
A. Vein of Galen
B. Ipsilateral basal vein of Rosenthal
C. Posterior cerebral artery (PCA)
D. Precentral cerebellar vein
E. Superior petrosal sinus
A. Vein of Galen
B. Ipsilateral basal vein of Rosenthal
C. Posterior cerebral artery (PCA)
**D. Precentral cerebellar vein **
E. Superior petrosal sinus
Cauterizing and dividing the precentral cerebellar
vein will often expose the posterior surface of pineal region
tumors. The veins of Galen and Rosenthal should be preserved during this operation, as well as the vennian vein,
which often can be spared in this approach. The choroidal
arteries may supply feeders to the tumor but rarely need to
be cauterized and ligated for adequate tumor resection (Kaye
and Black, pp. 815-824; Youmans; pp. 1017- 1021, Will<ins,
p.l029).
During translabyrinthine exposure for acoustic neuroma
resection, surgeons find themselves exposing Trautmann’s
triangle. All of the following structures delineate this area
EXCEPT?
A. A triangular patch of dura on the posterior aspect of
the temporal bone facing the cei’ebellopontine angle
B. The sigmoid sinus laterally
C. The superior petrosal sinus above
D. The jugular bulb below
E. The foramen magnum medially
A. A triangular patch of dura on the posterior aspect of
the temporal bone facing the cei’ebellopontine angle
B. The sigmoid sinus laterally
C. The superior petrosal sinus above
D. The jugular bulb below
**E. The foramen magnum medially **
There are two goals of the translabyrinthine approach
for acoustic neuroma resection that may help achieve m~’dmal tumor resection. The first is to remove enough bone
to identify the nerves lateral to the tumor as they course
through the lAC, and the second is to expose the dura of the
posterior aspect of the temporal bone that faces the cerebellopontine angle (CPA). This triangular patch of dura facing
the CPA is called Trautmann’s triangle and extends from
the sigmoid sinus laterally, the superior petrosal sinus
above, and the jugular bulb below. The foramen magnum
is not included in Trautmann’s triangle (Kaye and Black,
pp. 851-860; Youmans, pp. 1155- 1156; Wilkins, pp. 1067-
1071).
One of the earliest procedures performed for Parkinson’s
disease was ligation of what blood vessel ?
A. Anterior choroidal artery
B. Medial posterior choroidal artery
C. Recurrent artery of Heubner
D. Tentorial artery of Bernasconi and Cassarini
E. Medial lenticulostriate artery
A. Anterior choroidal artery
B. Medial posterior choroidal artery
C. Recurrent artery of Heubner
D. Tentorial artery of Bernasconi and Cassarini
E. Medial lenticulostriate artery
Neurosurgical therapies for Parkinson’s disease (PD)
have been utilized in patients with progressive disease
despite maximal medical therapy. An early procedure performed for PD was ligation of the anterior choroidal artery,
with subsequent infarction of the pallidum. Due to the variable distribution of this vessel outside the confines of the pallidum, results were too unpredictable and this procedure lost
favor. In the 1950s, anterodorsal pallidotomy became an
accepted procedure, but the long-term benefits were mostly
for rigidity, while tremor and dyskinesia did not improve.
Subsequently, the ventrolateral thalamus became the preferred target for lesioning, but this procedure also lost
favor, as patients were often still left with bradykinesia
and/or rigidity. Moreover, this procedure reduced tremor
only in the contralateral half of the body, and bilateral thalamotomies were not recommended due to an unacceptably
high risk of postoperative dysarthria and gait disturbances.
Thalamotomy procedures fell off dramatically in the late
1960s with the introduction of L-DOPA.
J\·Iore recently, dramatic and beneficial effects of both
subthalamic nucleus (STN) and globus pallidus interna (Gpi) deep brain stimulation (DBS) have been consistently
observed. Both interventions appear to result in significant
improvements in both motor fluctuations and dyskinesias.
The DBS study group, in a large multicenter study, reported
that on time without dyskinesia during the walling hours
increased from 25 to 30% at baseline to 65 to 75% 6 months
postoperatively. In a complementary fashion , these procedures also markedly decreased off time and on time without
dyskinesia. Although some preliminary studies suggest STN
DBS may be a superior intervention, no large randomized
controlled trial comparing STN and Gpi DBS has been conducted to compare the efficacy of these treatments. The most
consistent finding has been the reduction in antiparkinson
medication following STN DBS compared to Gpi DBS.
(Greenberg, p. 751; Tarsy, p. 191).
Vagal nerve stimulation is reserved for select patients
with epilepsy. Why is it performed on the left side?
A. To avoid injuring the recurrent laryngeal nerve, which
follows a more torturous route on the right
B. To avoid damage to the dominant superior laryngeal
nerve on the right
C. To avoid damage to cranial nerve X, which supplies the
heart mainly from the right
D. To avoid injuring the thoracic duct
E. Less chance of vocal cord paralysis and hoarseness
from the left
A. To avoid injuring the recurrent laryngeal nerve, which
follows a more torturous route on the right
B. To avoid damage to the dominant superior laryngeal
nerve on the right
C. To avoid damage to cranial nerve X, which supplies the
heart mainly from the right
D. To avoid injuring the thoracic duct
E. Less chance of vocal cord paralysis and hoarseness
from the left
Vagal nerve stimulation must be performed on the left
side so that the cardiac innervation of CN X is unaffected
(Youmans, pp. 2644-2645).
What is the treatment of choice for chronic, intractable
brachial plexus avulsion injury?
A. Cordotomy
B. Dorsal root entry zone (DREZ) lesioning
C. Morphine pump placement
D. Midline myelotomy
E. Ventroposterior lateral (VPL) thalamic deep brain
stimulation
A. Cordotomy
**B. Dorsal root entry zone (DREZ) lesioning **
C. Morphine pump placement
D. Midline myelotomy
E. Ventroposterior lateral (VPL) thalamic deep brain
stimulation
Dorsal root entry zone (DREZ) lesioning involves
radiofrequency ablation along the dorsolateral sulcus of the
spinal cord. The DREZ procedure is most effective in the
treatment of brachial and lumbar plexus avulsion pain.
Direct sectioning of the spinothalamiC tract (cordotomy) is
very effective for unilateral pain below the upper chest
region; however, it is associa ted wi th many complica tions
and is usually performed only in terminally ill patients.
Complications of cordotomy include hemiparesis, respiratory depreSSion (“Ondine’s curse” with bilateral procedures),
and dysesthesias. Midline mye!otomies can also be performed
to interrupt the decussating fibers of the spinothalamic tract,
and this can be quite effective in the treatment of chronic
pelvic pain secondary to cancer. Intrathecal narcotic administration is typically used for the treatment of chronic pain
associated with malignancy or failed low back syndrome.
Deep brain stimulation of the VPL and VPM nuclei of the
thalamus as well as the periaqueductal gray have been performed in the treatment of thalamic pain states, postherpetic
neuralgia, and causalgia. Chronic low-threshold stimulation
of the motor cortex is also utilized in the treatment of thalamic pain syndromes; it is thought to work by retrograde
thalamic stimulation pathways (Kaye and Blacl<, pp. 1521-
1537; Greenberg, pp. 365-370; Youmans, pp. 3025- 3030,
3045-3048, 3068- 3070, 3101, 3125, 3128-3129; Will<ins,
pp. 4036-4038, 4055- 4059)
What basal cistern(s) contain portions of the vein of
Rosenthal?
1. Crural
2. Quadrigeminal
3. Ambient
4. Quadrigeminal
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
**B. 1 and 3 are correct **
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above
The ambient and crural cisterns contain portions of
the basal vein of Rosenthal (Youmans, pp. 36- 39).
A 3-month-old boy is brought to your office for an
abnormally shaped head. The child is noted to have a flat
occiput on the left, a left ear that is anterior to the right, and
a prominent forehead and malar eminence on the left. ‘Vhat
is the most likely etiology of this deformity?
A. Left lambdoid synostosis
B. Right lambdoid synostosis
C. Sagittal suture synostosis
D. Skull molding
E. Right coronal suture synostosis
A. Left lambdoid synostosis
B. Right lambdoid synostosis
C. Sagittal suture synostosis
**D. Skull molding **
E. Right coronal suture synostosis
Lambdoid synostosis is among the rarest forms of
suture synostosis, while sagittal synostosis is the most common. After the American Academy of Pediatrics published its
recommendations that all children sleep on their back, the
incidence of skull molding increased. Most infants sleep on
their backs and spend the rest of the day sitting in a car seat
or infant seat. Children with this condition are often noted to
have a flat occiput, one ear that is anterior to the other in
an axial plane, and a prominent forehead and malar eminence. Many infants may also have a mild torticollis due to a
shortened sternocleidomastoid muscle on one side, as well as
decreased range of motion in the neck. The skull deformity
usually responds very well to behavioral modification, which
includes having the parents turn the infant or child from side
to side during sleep and reducing the amount of time spent in
a car seat. If this is unsuccessful, a molding helmet or band
is often helpful. For nonresponders, a variety of occipital
remolding surgical procedures are available (Committee on
Education in Neurological Surgery, pp. 43, 137; Pattisapu,
pp.178- 179)
All of the following are suboptimal conditions for placement of an odontoid screw EXCEPT
A. Old fractures (> 6 weeks)
B. Diagonal fractures through the odontoid process
C. Barrel-chested patient
D. Odontoid fracture that is displaced anteriorly
E. An intact transverse ligament
A. Old fractures (> 6 weeks)
B. Diagonal fractures through the odontoid process
C. Barrel-chested patient
D. Odontoid fracture that is displaced anteriorly
E. An intact transverse ligament
An intact transverse ligament must be confirmed
preoperatively prior to placement of an odontoid screw. Old
fractures in which a nonunion has already formed, diagonal
fractures through the odontoid process, and comminuted
odontoid fractures do not aUow for proper odontoid screw
placement due to suboptimal arthrodesis rates and inadequate screw purchase and compression effects (Kaye and
Blacl<, pp. 2048-2050; Youmans, pp. 4943- 4945; Benzel,
pp.225- 228).
A 56-year-old female underwent clipping of the
aneurysm depicted on the angiogram below (Figure 6.29Q).
Upon awakening from surgery, she was noted to have greater
wealmess in her left arm than in her left leg. What is the most
likely reason for this new deficit?
A. Injury of a blood vessel originating from the A2 segment of the anterior cerebral artery
B. Venous infarct from excessive frontal lobe retraction
C. Injury to the small perforating blood vessels originating from the anterior communicating artery
D. Posterior internal capsule infarction from microemboli
originating from the internal carotid artery
E. Mesial temporal lobe retraction
**A. Injury of a blood vessel originating from the A2 segment of the anterior cerebral artery **
B. Venous infarct from excessive frontal lobe retraction
C. Injury to the small perforating blood vessels originating from the anterior communicating artery
D. Posterior internal capsule infarction from microemboli
originating from the internal carotid artery
E. Mesial temporal lobe retraction
A. The recurrent artery of Heubner usually originates
from the A2 segment of the anterior cerebral artery (ACA).
Injury of this vessel during surgery is generally witnessed on
the first postoperative day, as evidenced by a hypodensity on
CT scan. Although injury to this vessel during surgery often
presents with arm wealmess greater than leg wealmess on
the nondominant side and cognitive deficits from injury on
the dominant Side, a percentage of patients do not have
any adverse neurologic sequelae after injury of this vessel.
Identifying this vessel early in the dissection may prevent
later injury (Greenberg, pp. 103-104).
Basilar skull fractures can be associated with cranial
nerve palsies, bilateral periorbital ecchymosis, mastoid
ecchymosis, hemotympanum, and rhinorrhea. Nasal
drainage that is not clearly CSF can be assayed for
____ , which is unique to CSF and ____ _
A. a-Fetoprotein, saliva
B. Transferrin, vitreous fluid of the eye
C. ~2- Transferrin, tears
D. Hypoglycorrhachia, nasal secretions
E. Sodium, peritoneal fluid
A. a-Fetoprotein, saliva
**B. Transferrin, vitreous fluid of the eye **
C. ~2- Transferrin, tears
D. Hypoglycorrhachia, nasal secretions
E. Sodium, peritoneal fluid
Prtransferrin is present in the CSF but absent in the
tears, saliva, peritoneal fluid , nasal exudates, and serum
(except for newborns or those with liver disease). The
only other source is the vitreous humor of the eye. Other
commonly employed tests include measuring the glucose
level of the fluid (CSF glucose> 30 mg %, whereas lacrimal and
mucous secretions are < 5 mg%) or placing the fluid on a
piece of linen (bed sheet, pillowcase) and seeing whether a
ring of blood surrounded by a larger concentric ring of clear
fluid develops (“ring” or “halo” sign) (Greenberg, pp. 168-
169).
A 4-month-old male fell from his crib and suffered a
growing skull fracture . All of the following are true of this
disease entity EXCEPT?
A. May be assoc iated with late neurologic deficits
B. A dural laceration is always present
C. There may be ongoing damage to underlying brain
from continued herniation of brain through the defect
D. CSF diversion is often the only treatment required for
this fracture pattern
E. May be associated with leptomeningeal cyst development
A. May be assoc iated with late neurologic deficits
B. A dural laceration is always present
C. There may be ongoing damage to underlying brain
from continued herniation of brain through the defect
**D. CSF diversion is often the only treatment required for
this fracture pattern **
E. May be associated with leptomeningeal cyst development
Growing skull fractures occur in children, are always
associated with underlying dural lacerations, and almost
always require surgical treatment. Early surgical correction
of growing fractures is often necessary because these types of
fractures almost never heal spontaneously and late neuro logic deterioration can occur. The pathophysiology requires
a fracture with enough force to cause a tear in the dura
(which is always present) and an underlying constant
force such as a growing brain, leptomeningeal cyst, hydrocephalus, or porencephaly. The precise etiology of late
neurologic deficits remains unclear but is believed to occur
by one of two mechanisms. There may be ongoing brain
damage from brain herniation and pulsations of the brain
against the bone edges. Alternatively, some have proposed
that there may be vascular compromise of blood vessels at
the bone edges. Although some authors have recommended a
CSF diversion procedure for growing skull fractures, direct
repair of the fracture is the definitive treatment (Youmans,
pp. 3468-3469; Will<ins, pp. 2757- 2761)
A 54-year-old female completed radiation therapy for
breast cancer. She has been complaining of wealmess in
her left arm over the past 3 months and is concerned there
may be recurrence of her cancer. How can her physician
distinguish between radiation-induced plexopathy and
cancerous invasion of the brachial plexus ?
A. Radiation-induced plexopathy is frequently accompanied by pain and lack of edema
B. Cancerous invasion of the brachial plexus is accompanied by lymphedema, painless wealmess, and
sensory loss
C. Radiation-induced plexopathy is frequently reversible
D. l’vlyokymia on EMG favors radiation-induced plexopathy
E. Prolonged I-I latency is typically seen only with brachial
plexopathy secondary to radiation damage
A. Radiation-induced plexopathy is frequently accompanied by pain and lack of edema
B. Cancerous invasion of the brachial plexus is accompanied by lymphedema, painless wealmess, and
sensory loss
C. Radiation-induced plexopathy is frequently reversible
**D. l’vlyokymia on EMG favors radiation-induced plexopathy **
E. Prolonged I-I latency is typically seen only with brachial
plexopathy secondary to radiation damage
Myokymia (quivering of muscles) on EMG strongly
favors radiation-induced changes of the brachial plexus.
Lymphedema, painless paresis, and numbness suggest
radiation-induced injury (irreversible), whereas pain and
lack of edema suggest recurrent tumor. When ancillary
studies are inconclusive, surgical exploration of the plexus
may have to be considered (Merritt, p. 459)
A 42-year-old male falls 25 feet while at work and
arrives at the emergency department with a Glasgow Coma
Scale (GCS) score of 5, a dilated and nonreactive right
pupil, and a mean arterial blood pressure of 80. IVter airway
management and fluid resuscitation, his GCS improves to 7,
but his right hemiparesis and nonreactive pupil remain
unchanged. The patient also sustained a pelvic fracture, a left
humeral fracture , splenic and liver lacerations, and multiple
fractures of the cervical spine.
Initial management of this patient should include
1. Begin hyperventilation to decrease the pC02
2. Administer mannitol on arrival to the emergency
department because of clinical evidence of an asymmetric exam
3. Complete the primary survey, obtain cervical spine filins
and chest x-ray, and then move directly to CT scan
4. The patient should be started on pentobarbital for
elevated intracranial pressure immediately after
completion of the primary survey if no mass lesion
is found on CT
A. 1,2, and3 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, and3 are correct
**B. 1 and 3 are correct **
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above
Current head injury research guidelines suggest that mannitol and hyperventilation may
exacerbate cerebral ischemia after head injury. However,
mannitol and hyperventilation are recommended for those
patients with acute head injury as a temporary measure
to control elevated intracranial pressure. Hyperventilation
may be commenced immediately, but mannitol should be
withheld until the primary survey is complete and adequate
intravascular volume and urine output are realized. The
mechanism of action of mannitol is still debated, but it is
believed to have the follOWing beneficial effects. First, it acts
to immediately expand the plasma by reducing hematocrit
and blood viscosity (improved rheology), which improves
CBF and O2 delivery. This reduces ICP very quicldy, which is
most marked in patients with CPP < 70 mm r-rg. Second, it
draws edema from the adjacent cerebral parenchyma into
the intravascular compartment (osmotic effect), an effect
that may last up to 6 hours. And last, it is a possible freeradical scavenger. Despite these short-lived but beneficial
effects, the administration of mannitol is not without risks. It
opens the blood-brain barrier and can potentially draw fluid
into the CNS and aggravate vasogenic cerebral edema. It
should also be used cautiously with concomitant administration of steroids and phenytoin (Dilantin), as it may cause a
nonketotic hyperosmolar state, with high mortality. With
overuse, it can also result in hypertension and increased
CBF if cerebral autoregulation is defective . . And last, high
doses carry a significant risk for the development of acute
renal failure , especially with coexisting sepsis, concomitant nephrotoxic drug use, serum osmolarity> 320, or preexisting kidney disease. Some patients with mass lesions on
one side may not uniformly develop contralateral hemiparesis
A 42-year-old male falls 25 feet while at work and
arrives at the emergency department with a Glasgow Coma
Scale (GCS) score of 5, a dilated and nonreactive right
pupil, and a mean arterial blood pressure of 80. IVter airway
management and fluid resuscitation, his GCS improves to 7,
but his right hemiparesis and nonreactive pupil remain
unchanged. The patient also sustained a pelvic fracture, a left
humeral fracture , splenic and liver lacerations, and multiple
fractures of the cervical spine.
The CT scan of the brain is depicted below (Figure
6.34Q). Why did this patient develop hemiparesis on the
same side as the hematoma ?
A. Shift of the brainstem away frol11 the mass producing
compression of the contralateral cerebral peduncle
against the tentorium
B. The patient lil{ely suffered a Duret hemorrhage
C. There was likely a contusion in the underlying motor
cortex on the contralateral side that was not detected
on the initial CT scan
D. The patient likely had a left internal ca rotid artery
dissection that subsequently showered emboli to the
distal vasculature
E. There was an associated fracture of the transverse
foramen on the left, which produced a vertebral artery
dissection and small infarct in the ventral pons
**A. Shift of the brainstem away frol11 the mass producing
compression of the contralateral cerebral peduncle
against the tentorium **
B. The patient lil{ely suffered a Duret hemorrhage
C. There was likely a contusion in the underlying motor
cortex on the contralateral side that was not detected
on the initial CT scan
D. The patient likely had a left internal ca rotid artery
dissection that subsequently showered emboli to the
distal vasculature
E. There was an associated fracture of the transverse
foramen on the left, which produced a vertebral artery
dissection and small infarct in the ventral pons
Current head injury research guidelines suggest that mannitol and hyperventilation may
exacerbate cerebral ischemia after head injury. However,
mannitol and hyperventilation are recommended for those
patients with acute head injury as a temporary measure
to control elevated intracranial pressure. Hyperventilation
may be commenced immediately, but mannitol should be
withheld until the primary survey is complete and adequate
intravascular volume and urine output are realized. The
mechanism of action of mannitol is still debated, but it is
believed to have the follOWing beneficial effects. First, it acts
to immediately expand the plasma by reducing hematocrit
and blood viscosity (improved rheology), which improves
CBF and O2 delivery. This reduces ICP very quicldy, which is
most marked in patients with CPP < 70 mm r-rg. Second, it
draws edema from the adjacent cerebral parenchyma into
the intravascular compartment (osmotic effect), an effect
that may last up to 6 hours. And last, it is a possible freeradical scavenger. Despite these short-lived but beneficial
effects, the administration of mannitol is not without risks. It
opens the blood-brain barrier and can potentially draw fluid
into the CNS and aggravate vasogenic cerebral edema. It
should also be used cautiously with concomitant administration of steroids and phenytoin (Dilantin), as it may cause a
nonketotic hyperosmolar state, with high mortality. With
overuse, it can also result in hypertension and increased
CBF if cerebral autoregulation is defective . . And last, high
doses carry a significant risk for the development of acute
renal failure , especially with coexisting sepsis, concomitant nephrotoxic drug use, serum osmolarity> 320, or preexisting kidney disease. Some patients with mass lesions on
one side may not uniformly develop contralateral hemiparesis
A 42-year-old male falls 25 feet while at work and
arrives at the emergency department with a Glasgow Coma
Scale (GCS) score of 5, a dilated and nonreactive right
pupil, and a mean arterial blood pressure of 80. IVter airway
management and fluid resuscitation, his GCS improves to 7,
but his right hemiparesis and nonreactive pupil remain
unchanged. The patient also sustained a pelvic fracture, a left
humeral fracture , splenic and liver lacerations, and multiple
fractures of the cervical spine.
‘Vhich of the following are possible complications of
mannitol administration?
1. Aggravation of vasogenic edema
2. Development of a hyperosmolar nonketotic state
3. Acute tubular necrosis
4. Hypotension
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
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
**E. All of the above **
Current head injury research guidelines suggest that mannitol and hyperventilation may
exacerbate cerebral ischemia after head injury. However,
mannitol and hyperventilation are recommended for those
patients with acute head injury as a temporary measure
to control elevated intracranial pressure. Hyperventilation
may be commenced immediately, but mannitol should be
withheld until the primary survey is complete and adequate
intravascular volume and urine output are realized. The
mechanism of action of mannitol is still debated, but it is
believed to have the follOWing beneficial effects. First, it acts
to immediately expand the plasma by reducing hematocrit
and blood viscosity (improved rheology), which improves
CBF and O2 delivery. This reduces ICP very quicldy, which is
most marked in patients with CPP < 70 mm r-rg. Second, it
draws edema from the adjacent cerebral parenchyma into
the intravascular compartment (osmotic effect), an effect
that may last up to 6 hours. And last, it is a possible freeradical scavenger. Despite these short-lived but beneficial
effects, the administration of mannitol is not without risks. It
opens the blood-brain barrier and can potentially draw fluid
into the CNS and aggravate vasogenic cerebral edema. It
should also be used cautiously with concomitant administration of steroids and phenytoin (Dilantin), as it may cause a
nonketotic hyperosmolar state, with high mortality. With
overuse, it can also result in hypertension and increased
CBF if cerebral autoregulation is defective . . And last, high
doses carry a significant risk for the development of acute
renal failure , especially with coexisting sepsis, concomitant nephrotoxic drug use, serum osmolarity> 320, or preexisting kidney disease. Some patients with mass lesions on
one side may not uniformly develop contralateral hemiparesis
A 42-year-old male falls 25 feet while at work and
arrives at the emergency department with a Glasgow Coma
Scale (GCS) score of 5, a dilated and nonreactive right
pupil, and a mean arterial blood pressure of 80. IVter airway
management and fluid resuscitation, his GCS improves to 7,
but his right hemiparesis and nonreactive pupil remain
unchanged. The patient also sustained a pelvic fracture, a left
humeral fracture , splenic and liver lacerations, and multiple
fractures of the cervical spine.
After surgery for evacuation of the right subdural
hematoma, CT angiogram was obtained to rule out a vertebral artery injury because of the multiple fractures of the
cervical spine extending through the transverse foramina .
The study was inconclusive, and a follow-up angiogram (Figure 6.36Q) was obtained later that evening after hematoma
evacuation. What would be the most reasonable treatment
strategy at this point for this multisystem trauma patient?
Consider that the patient adequately fills the posterior circulation from the right vertebral artery.
1. Commencement of a heparin infusion with a goal of
keeping the PTT approximately two times the normal
level
2. Antiplatelet therapy
3. Intravenous t-PA
4. Endovascular sacrifice of the occluded vertebral artery
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
B. 1 and 3 are correct
**C. 2 and 4 are correct **
D. Only 4 is correct
E. All of the above
Current head injury research guidelines suggest that mannitol and hyperventilation may
exacerbate cerebral ischemia after head injury. However,
mannitol and hyperventilation are recommended for those
patients with acute head injury as a temporary measure
to control elevated intracranial pressure. Hyperventilation
may be commenced immediately, but mannitol should be
withheld until the primary survey is complete and adequate
intravascular volume and urine output are realized. The
mechanism of action of mannitol is still debated, but it is
believed to have the follOWing beneficial effects. First, it acts
to immediately expand the plasma by reducing hematocrit
and blood viscosity (improved rheology), which improves
CBF and O2 delivery. This reduces ICP very quicldy, which is
most marked in patients with CPP < 70 mm r-rg. Second, it
draws edema from the adjacent cerebral parenchyma into
the intravascular compartment (osmotic effect), an effect
that may last up to 6 hours. And last, it is a possible freeradical scavenger. Despite these short-lived but beneficial
effects, the administration of mannitol is not without risks. It
opens the blood-brain barrier and can potentially draw fluid
into the CNS and aggravate vasogenic cerebral edema. It
should also be used cautiously with concomitant administration of steroids and phenytoin (Dilantin), as it may cause a
nonketotic hyperosmolar state, with high mortality. With
overuse, it can also result in hypertension and increased
CBF if cerebral autoregulation is defective . . And last, high
doses carry a significant risk for the development of acute
renal failure , especially with coexisting sepsis, concomitant nephrotoxic drug use, serum osmolarity> 320, or preexisting kidney disease. Some patients with mass lesions on
one side may not uniformly develop contralateral hemiparesis
A 45-year-old male presents to an emergency
room with fever, nausea, vomiting, and severe headache.
CT of the brain is normal. Lumbar puncture reveals slightly
elevated red blood cells, but normal protein, glucose, white
blood cell count, and no xanthochromia. His angiogram is
depicted below.
What is the most likely etiology of the abnormality
depicted in the angiogram below?
A. Head trauma
B. Infection
C. Genetic predisposition
D. Collagen vascular disease
E. Hypertension
A. Head trauma
**B. Infection **
C. Genetic predisposition
D. Collagen vascular disease
E. Hypertension
Mycotic or infective aneurysms account for
about 4% of intracranial aneurysms and are most commonly
found along the distribution of the distal middle cerebral
artery (MCA). Patients with head trauma also are at risk of
developing aneurysms, although these are most frequently
located along the distal anterior cerebral artery distribution.
Mycotic aneurysms occur in about 3 to 15% of patients with
subacute bacte rial endoca rditis (SBE), and the most com1110n organism isolated from the blood is Streptococclis
viTidans species. Patients that are IV drug abusers or
immunodeficient (HIV) are at increased risk of developing
A 45-year-old male presents to an emergency
room with fever, nausea, vomiting, and severe headache.
CT of the brain is normal. Lumbar puncture reveals slightly
elevated red blood cells, but normal protein, glucose, white
blood cell count, and no xanthochromia. His angiogram is
depicted below.
This finding occurs most frequently in what condition?
A. Alcoholism
B. Ehlers-Danlos disease
C. Subacute bacterial endocarditis
D. Marfan’s syndrome
E. Polycystic kidney disease
A. Alcoholism
B. Ehlers-Danlos disease
C. Subacute bacterial endocarditis
D. Marfan’s syndrome
E. Polycystic kidney disease
Mycotic or infective aneurysms account for
about 4% of intracranial aneurysms and are most commonly
found along the distribution of the distal middle cerebral
artery (MCA). Patients with head trauma also are at risk of
developing aneurysms, although these are most frequently
located along the distal anterior cerebral artery distribution.
Mycotic aneurysms occur in about 3 to 15% of patients with
subacute bacte rial endoca rditis (SBE), and the most com1110n organism isolated from the blood is Streptococclis
viTidans species. Patients that are IV drug abusers or
immunodeficient (HIV) are at increased risk of developing
A 45-year-old male presents to an emergency
room with fever, nausea, vomiting, and severe headache.
CT of the brain is normal. Lumbar puncture reveals slightly
elevated red blood cells, but normal protein, glucose, white
blood cell count, and no xanthochromia. His angiogram is
depicted below.
How should this problem be treated?
A. Observation followed by repeat angiography in 6 months
B. Antibiotics followed by repeat angiography
C. Emergent surgery
D. Stentlcoiling followed by blood pressure control
E. Steroids
A. Observation followed by repeat angiography in 6 months
**B. Antibiotics followed by repeat angiography **
C. Emergent surgery
D. Stentlcoiling followed by blood pressure control
E. Steroids
Mycotic or infective aneurysms account for
about 4% of intracranial aneurysms and are most commonly
found along the distribution of the distal middle cerebral
artery (MCA). Patients with head trauma also are at risk of
developing aneurysms, although these are most frequently
located along the distal anterior cerebral artery distribution.
Mycotic aneurysms occur in about 3 to 15% of patients with
subacute bacte rial endoca rditis (SBE), and the most com1110n organism isolated from the blood is Streptococclis
viTidans species. Patients that are IV drug abusers or
immunodeficient (HIV) are at increased risk of developing
A lS-month-old girl was brought to the emergency
department for lethargy, nausea, and vomiting and was found
to have aqueductal stenosis on brain MRI.
What is the best treatment strategy for this patient?
A. Observation
B. Placement of a subgaleal shunt
C. Placement of a ventriculoperitoneal shunt followed
by endoscopic third ventriculostomy if shunting fails
D. EndoscopiC third ventriculostomy
E. EndoscopiC third ventriculostomy followed by septostomy
A. Observation
B. Placement of a subgaleal shunt
C. Placement of a ventriculoperitoneal shunt followed
by endoscopic third ventriculostomy if shunting fails
**D. EndoscopiC third ventriculostomy **
E. EndoscopiC third ventriculostomy followed by septostomy
ETV is a commonly performed procedure for patients with aqueductal stenosis (AS). Although
there is some controversy about the age at which this
procedure should first be employed, results indicate high
success rates for properly selected patients. Complications of
shunting may include slit ventricle syndrome, intracranial
hypotension, subdural hematomas, craniosynostosis, microcephaly, and overdrainage, which are typically not noted
after endoscopy. The precise location to fenestrate the floor
of the third ventricle may vary on a case-by-case baSiS, but
perforating the floor anterior to the mamillary bodies and
posterior to the infundibulum seems to a popular approach .
Performing a septostomy in conjunction to a third ventriculostomy does not improve results in patients with AS, as
the obstruction is downstream to the foramen of Monro. A
patient with scarring or a cyst obstructing one foramen of
Monro would likely benefit from this ancillary procedure.
Predicting the success rate of ETV by preoperative imaging
studies has proven to be very difficult, although identifying
relevant anatomy (thickness of the floor of the third
ventricle, location of basilar artery) to help guide the operation has proven to be effective (Kaye and Blacl~, pp. 789- 797;
Youmans, pp. 3429- 3430; Will~ins, pp. 541-542).