NeuroSurgery Flashcards
(100 cards)
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).