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5. VASCULAR NEUROSURGERY Thomas Leipzig ascular neurosurgery has long been one of the focal points of neurosurgical practice, and the topic is routinely included in the Oral Board Examination process. Each case involves clinical and diagnostic acumen, a solid grasp of the natural history and treatment risks, consideration of operative approaches, alternative treatment options, and the management of potentially catastrophic complications as a result of what we have done or what we failed to do. Similar to the evolution seen in spinal neurosurgery, there have been dramatic advances in the way we have managed neurovascular patients over the past two decades. The International Study of Unruptured Intracranial Aneurysms (ISUIA) and the International Subarachnoid Aneurysm T rial (ISA T), along with the development and rapid growth of endovascular neurosurgery, have led to a paradigm shift in the management of intracranial aneurysms. CASE 1 HISTORY AND PHYSICAL EXAMINA TION A 35- year- old right- handed woman experienced an explo sive onset of headache during sexual intercourse. She has a history of “borderline” hypertension and smokes one pack of cigarettes daily. This was the worst headache she had ever experienced. She also developed nausea, vomiting, and photophobia. Her blood pressure is 170/ 85 mm Hg. She has no focal neurological deficits but is disoriented to year and location. She is uncomfortable. She has moderate nuchal rigidity. IMAGING STUDIES The patient undergoes a computed tomography (CT) scan (Figure 5.1) and subsequent four- vessel cerebral angiogra phy. The angiogram demonstrates a left ophthalmic artery (OA) aneurysm and a left middle cerebral artery (MCA) aneurysm (Figure 5.2). ANALYSIS OF CASE AND TREA TMENT PLAN Aneurysmal subarachnoid hemorrhage (aSAH) is a pres entation that has a very high probability of being one of the cases presented during the Oral Board Examination. It represents a quintessential neurosurgical problem that addresses multiple issues regarding diagnostic evaluation, understanding of the disease process, general patient man agement, and technical skills. Case- fatality rates in the United States remain high. Roughly 50% of survivors are left with some neurological deficit, and rates of persistent dependence are between 8% and 20%. Global cognitive impairments are present in approximately 20% of aSAH patients. Misdiagnosis of aSAH still occurs in approximately 10% of cases. In any patient presenting to you with head ache, it is absolutely critical to ascertain the nature of its onset. A  sentinel hemorrhage or “warning leak” may not produce such an alarming headache that either the patient or medical professional may not realize the need for urgent hospitalization. However, it is potentially catastrophic to miss this prelude, which typically occurs 2 to 8 weeks before overt aSAH. This case demonstrates a classical presentation of SAH. The incidence is higher in women, and this patient has the risk factors of hypertension and cigarette smoking. Other risk factors to inquire about include high alcohol con sumption, very low body mass index, use of sympathomi metic drugs, family history of aSAH, and certain genetic syndromes (autosomal dominant polycystic kidney disease, Ehlers- Danlos type IV syndrome, Marfan syndrome, and several other less common disorders). This patient is somewhat young. The average age of onset for aSAH in adults is typically 50 years or older.

athomi metic drugs, family history of aSAH, and certain genetic syndromes (autosomal dominant polycystic kidney disease, Ehlers- Danlos type IV syndrome, Marfan syndrome, and several other less common disorders). This patient is somewhat young. The average age of onset for aSAH in adults is typically 50 years or older. Although aSAH is not nec essarily related to activity, the occurrence during sexual

athomi metic drugs, family history of aSAH, and certain genetic syndromes (autosomal dominant polycystic kidney disease, Ehlers- Danlos type IV syndrome, Marfan syndrome, and several other less common disorders). This patient is somewhat young. The average age of onset for aSAH in adults is typically 50 years or older. Although aSAH is not nec essarily related to activity, the occurrence during sexual 26 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW intercourse or V alsalva maneuver is not an uncommon history. Her W orld Federation of Neurological Surgeons (WFNS) grade is 2. In any acute presentation such as this, assessment of airway, breathing, and circulation (ABCs), routine laboratory testing (e.g., complete blood count, chemistry profile, coagulation studies), and medications can be quickly acknowl edged. Do not belabor this evaluation during the oral examination. The examiners will apprise you of any signif icant issues. In aSAH, early management of blood pressure before aneurysm obliteration is beneficial to balance the risk for stroke, hypertension- related rebleeding, and the maintenance of cerebral perfusion pressure. A  titrat able medication is preferable, and nicardipine may give smoother blood pressure control than either labetalol or sodium nitroprusside. A reasonable goal is to keep the systolic blood pressure below 160 mm Hg. If tolerated, a systolic blood pressure of less than 140  mm Hg may be advisable in higher grade patients (Hunt and Hess grade 1- 3). The patient’s initial CT scan demonstrates a Fisher grade 3 SAH. The sensitivity of CT scan in diagnosing aSAH in the first 3 days is nearly 100%. However, after 5 to 7  days, the rate of negative CT scan findings rises sig nificantly. If the CT scan is negative and there is clinical suspicion for a possible aSAH, the patient should undergo lumbar puncture to check for blood, xanthochromia, and opening pressure. The minimal amount of cerebrospinal fluid (CSF) should be withdrawn to avoid decompression of the aneurysmal dome and possible rebleed. Certain magnetic resonance imaging (MRI) sequences (fluid- attenuated inversion recovery, gradient- echo sequence, and proton density) may diagnose SAH when the initial CT scan is negative. However, nondiagnostic MRI would still require CSF analysis. Figure 5.1 Representative cut of non– contrast- enhanced computed tomography of the brain demonstrates a diffuse subarachnoid hemorrhage, more prominent on the left side (Fisher grade 3). The temporal horns are slightly prominent. There was very mild ventricular enlargement on the other cuts. Figure 5.2 Cerebral angiogram, anteroposterior (A) and oblique (B) projections. The left internal carotid artery (ICA) angiogram demonstrates an ophthalmic aneurysm and a slightly larger, lobulated middle cerebral artery (MCA) aneurysm.

slightly prominent. There was very mild ventricular enlargement on the other cuts. Figure 5.2 Cerebral angiogram, anteroposterior (A) and oblique (B) projections. The left internal carotid artery (ICA) angiogram demonstrates an ophthalmic aneurysm and a slightly larger, lobulated middle cerebral artery (MCA) aneurysm. v ASCULAR N EUROSURGERY • 27 Three- dimensional rotational digital subtraction angi ography (DSA) remains the “gold standard” for cerebro vascular imaging. Currently, because of ease and safety, computed tomographic angiography (CT A) is being used more frequently in the initial workup of SAH. However, aneurysms smaller than 3  mm may not be detected on either CT A or magnetic resonance angiography (MRA). In the face of spontaneous SAH and a negative CT A, formal three- dimensional DSA is warranted. In any patient presenting with a higher Hunt and Hess grade (4– 5) or progressively worsening level of con sciousness, consideration needs to be given to treating any associated hydrocephalus. Acute hydrocephalus has been reported to occur in 15% to 87% patients after aSAH. Often, in poor grade patients, the diversion of CSF will lead to marked clinical improvement over the course of 12 to 24 hours. Care needs to be taken to avoid rapid reduction in size of the ventricle because this may precipi tate recurrent hemorrhage from the aneurysm by allevi ating the tamponade effect on the dome. CSF diversion may be accomplished by placement of either an external ventricular drain (EVD) or a lumbar drain. If an anterior circulation aneurysm has been visualized, it will be conve nient to place the drain on the side opposite an anticipated surgical approach, unless it is going to be placed intraoperatively. If coiling is the expected treatment, the drain should be placed on the side of the nondominant hemisphere. In the case of elevated intracranial pressure (ICP), controlled CSF drainage is used to bring the ICP to a level of 15 to 20 mm Hg. When the diagnosis of aSAH has been established, oral nimodipine therapy should be instituted. Therapy should be started within 96 hours of an aSAH and continued for up to 21 days. The typical dose is 60 mg every 4 hours. In patients who develop significant hypotension after admin istration of the medication, we change the dosage to 30 mg every 2 hours. Nimodipine has been shown to improve neurological outcomes despite having no effect on angio graphic cerebral vasospasm. Seizures may occur in up to 10% to 20% of patients after aSAH, often immediately following the ictus and usually in the first 24 hours after hemorrhage. Seizures are more commonly associated with hypertension, MCA and anterior communicating artery aneurysms, and intracerebral hemorrhage. In patients who have not experienced a seizure, one should carefully consider the prophylactic use of an anti epileptic drug (AED) until the aneurysm has been secured. The extended use of prophylactic AEDs in aSAH should be avoided. AEDs have been associated with neurological worsening, delayed fever, and poor outcome. Antifibrinolytic therapy has been shown to decrease the incidence of rebleeding and can be considered for use if there is going to be an unavoidable delay in treating the ruptured aneurysm. The short- term use of antifibrinolytics (<72 hours) in patients without compelling contraindica tions has not increased the risk for delayed cerebral isch emia. The short- term use of antifibrinolytic therapy is not standardly advised and represents an individual practitio ner’s choice in the management of an unsecured, ruptured aneurysm. T ranexamic acid and epsilon- aminocaproic acid have not been officially approved by the US Food and Drug Administration for the prevention of aneurysmal rebleeding.

tifibrinolytic therapy is not standardly advised and represents an individual practitio ner’s choice in the management of an unsecured, ruptured aneurysm. T ranexamic acid and epsilon- aminocaproic acid have not been officially approved by the US Food and Drug Administration for the prevention of aneurysmal rebleeding. After the patient has undergone initial stabilization and diagnostic assessment, attention should quickly turn to eliminating the ruptured aneurysm. Recurrent hemorrhage from a ruptured aneurysm is associated with a very high mortality rate and significantly worsens the chance for a reasonable functional recovery in those who survive. The risk for rebleeding is greatest in the first 24 hours, with reported rates of 4% to 13.6%. The risk may be highest in the first 6 to 12 hours. Ideally, treatment should be performed as soon as logistically possible in the context of the technical and personnel demands that the procedure will entail. This case involves a young patient with an aSAH from either an OA or MCA aneurysm. It highlights several important issues in the decision process on how to treat her. Currently, the two main treatment considerations for securing an acutely ruptured aneurysm are endovascular coiling and microsurgical clip ligation. Because of the need for aggressive antiplatelet therapy, the use of stents to assist with coiling or the use of flow- diverting stents are not typically advised in the acute period following aSAH. Microsurgical clip ligation had been the mainstay of aneurysm treatment, with progressive technical and man agement advances especially throughout the 1970s to mid- 1990s. With the development of electrolytically detachable coils by Guglielmi (GDC) in 1991 for the endovascular treatment of cerebral aneurysms, the door opened on a novel treatment method that subsequently has been met with research and development funding unparalleled in the open surgical arena. This has led to resultant improvements in endovascular capabilities and results. The initial debate between the merits of microsurgi cal clip ligation and endovascular coiling was intense and led to the initiation of the ISA T. ISA T is a randomized study on the treatment of ruptured intracranial aneu rysms that was conducted in 42 neurosurgical centers primarily in the United Kingdom and Europe. It was ini tially published in 2002. The public press and nonsurgical

n and endovascular coiling was intense and led to the initiation of the ISA T. ISA T is a randomized study on the treatment of ruptured intracranial aneu rysms that was conducted in 42 neurosurgical centers primarily in the United Kingdom and Europe. It was ini tially published in 2002. The public press and nonsurgical 28 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW medical practitioners quickly became enamored with the endovascular option. The primary outcome assessment of death or dependent living at 1 year strongly favored treat ment by endovascular means. Death and disability rates in the microsurgical group were 31% versus 24% with endovascular therapy (7% absolute and 23% relative risk reduction). This difference was principally fueled by a diminished rate of disability at 1  year in endovascularly treated patients. The trend toward primary endovascular treatment for any ruptured aneurysm continues to grow, even among neurosurgeons. Growing apprehension with surgical comfort in light of diminishing volumes raises concerns that this will become a self- fulfilling prophecy. However, the best decision for each patient must be care fully evaluated on an individual basis. The examiners will scrutinize your choice. In this case, the patient has both OA and MCA aneu rysms on her left side. Determining which aneurysm has bled often has significance in the management of a patient with aSAH who has multiple intracranial aneurysms, and this knowledge may dictate the modality for treatment. Usually, the pattern of hemorrhage (based on intracere bral hemorrhage, the thickness and distribution of blood in the subarachnoid spaces) and the characteristics of the aneurysm (size, shape, and presence of daughter blisters) can lead to a ready determination of which aneurysm was the cause of the SAH. In this case, it would be very difficult to definitively identify which aneurysm bled based on the CT pattern of SAH. The larger size and irregularity of the MCA aneurysm may favor it as the source. In ISA T, only the patients with ruptured aneurysms that were thought to be comparably suitable for either treatment modality were randomized. Thus, only about 22% of more than 9500 patients with aSAH were randomized. In nearly 80% of patients, there was a clear recommendation between the interventionalist and surgeon that the aneurysm should be treated by one modality preferentially. Although tech nology has evolved over the years, most MCA aneurysms, such as in this patient, are currently considered for primary microsurgical treatment. There are continued concerns regarding the durabil ity of treatment with GDC coils and the potential need for additional treatment. In ISA T, early retreatment (attributable to incomplete or failed primary treatment) was performed in 8.8% of coil patients compared with 2.9% of surgical patients. Late retreatments (>3  months post- GDC, >1  month postsurgery) were considered a surrogate for aneurysm recurrence. Nine percent of endo vascularly treated patients and 0.9% of surgically treated patients underwent late retreatment. Retreatment was also more common in the endovascular patients in the Barrow Ruptured Aneurysm T rial (BRA T). In a follow- up analysis of the ISA T data, it was noted that the 1- year poor outcome rates were dependent on age of patients treated with coil embolization. Based on the findings that there is a higher rate of rebleeding after coil embolization compared with surgery and that the differ ence in the rates for poor outcome between the two treat ment groups is much smaller for younger patients, Mitchell and colleagues (2008) concluded that the advantage of coil embolization over clip ligation for ruptured intracranial aneurysms cannot be assumed for patients younger than 40 years.

ery and that the differ ence in the rates for poor outcome between the two treat ment groups is much smaller for younger patients, Mitchell and colleagues (2008) concluded that the advantage of coil embolization over clip ligation for ruptured intracranial aneurysms cannot be assumed for patients younger than 40 years. Long- term analysis (>5  years) in ISA T demonstrated an increased rebleed rate for endovascularly treated aneu rysms over all time periods studied. Similarly, the Cerebral Aneurysm Rerupture After T reatment (CARA T) study also demonstrated more rebleeds in the coiled group (3.4%) compared with the surgical group (1.3%). The risk for rebleeding in ISA T and CARA T diminished over time, but it did not disappear. However, in the more recent BRA T, there were no noted episodes of rebleeding in the patients treated with endovascular coiling, although the need for retreatment was still more common. In general, with current technology, morphologic fea tures of the aneurysm typically dictate its amenability to treatment with GDC coils. Incomplete occlusion and sub sequent risk for recurrence are related to neck diameter, dome size, and the aspect ratio. Also, it may be difficult to achieve complete obliteration in very small aneurysms (<3  mm). Partial volume averaging phenomena on CT A may artificially widen the aneurysm neck, which could alter the decision- making process. In this patient, the OA aneurysm is potentially amena ble to primary GDC treatment. Again, in the acute setting, stent- assisted coiling or deployment of a flow- diverting stent is not an option because of the need for antiplatelet therapy. Because of the inability to know with certainty which aneurysm bled, treatment of the MCA aneurysm directs us toward surgical intervention. Furthermore, the patient’s young age tips the scale toward clip ligation. Surgery is arranged as expediently as possible. Both aneurysms should be treated. The pertinent surgical risks include possible infection, extraaxial or intraaxial clot, aneurysmal rebleed, stroke symptoms possibly involving the patient’s language and right side, left- sided blindness, and death. Standard neuroanesthetic techniques are employed. In general, the use of intraoperative hypotension should be minimized during aneurysm surgery. There has not

n, extraaxial or intraaxial clot, aneurysmal rebleed, stroke symptoms possibly involving the patient’s language and right side, left- sided blindness, and death. Standard neuroanesthetic techniques are employed. In general, the use of intraoperative hypotension should be minimized during aneurysm surgery. There has not v ASCULAR N EUROSURGERY • 29 been strong evidence supporting the use of hypothermia, although some surgeons still employ it. Standard posi tioning in a pin- fixation headrest for an anterior circula tion aneurysm is employed with the head rotated 25 to 45 degrees, depending on aneurysm location, and with the malar eminence elevated to facilitate atraumatic subfrontal exposure. V arious additional measures, such as an intraoperative electroencephalogram (EEG), DSA, cerebral blood flow monitoring, and navigation, should only be mentioned if you are familiar with them and consider using them rou tinely. Be ready to provide the rationale for why you choose to use such measures. The concept of proximal control is essential in any aneurysm case. In this particular patient with an ophthalmic artery aneurysm, it is absolutely critical to note that the left side of the neck, as well as the head, will be prepared for surgery. The femoral region may also be prepared for possible intraoperative angiography. The omission of dissecting out the carotid vessels in the neck for proximal control through temporary occlusion can be a lethal error on the Oral Board Examination. Surgical exposure of the cervical carotid vasculature and placement of vascular loops must be completed before the craniotomy is accomplished. Y ou must have proximal control for the ophthalmic aneurysm. (Y ou can be guaranteed that the examiners will tell you that the ophthalmic aneu rysm has reruptured prematurely if you do not first have the cervical vessels exposed.) A standard left, retro- hairline, pterional craniotomy is then completed. For an ophthal mic aneurysm, the anterior clinoid process almost always needs to be removed. This can be accomplished from either an extradural or an intradural approach. Again, choose the method that you would use based on your experience or knowledge. With dural opening, further brain relaxation can be initiated. This could include various means, such as CSF drainage, mild hyperventilation, or osmotic diuresis. If an EVD is already in place, additional drainage of CSF fol lowing dural opening can be accomplished easily. If there is not an EVD, intraoperative ventricular canalization can be used to gain enough brain relaxation to allow dissection to proceed. T ypically, the drain is inserted perpendicularly through a frontal gyrus at the apex of a medially directed, 3- cm equilateral triangle based on the exposed sylvian fis sure starting at the dural surface. Alternatively, a separate bur hole or twist drill can be used to place a frontal EVD in standard fashion. In a “tight brain, ” this may be neces sary before attempting to place the frontal retractor along the pterion. Opening the carotid and chiasmatic cisterns may allow for further relaxation. Care must be taken in the presence of a potentially ruptured OA aneurysm. Routine fenestration of the lamina terminalis has not proved useful for reducing the rate of shunt- dependent hydrocephalus. There is a strong rationale to deal with the OA aneu rysm initially. Placement of the frontal retractor along the pterional route must be done with extreme caution. The aneurysm may distort the optic nerve superomedially as it projects up from the internal carotid artery (ICA). Initial dissection of the proximal stem of the left sylvian fissure and along the lateral aspect of the carotid cistern may be advis able early on.

ong the pterional route must be done with extreme caution. The aneurysm may distort the optic nerve superomedially as it projects up from the internal carotid artery (ICA). Initial dissection of the proximal stem of the left sylvian fissure and along the lateral aspect of the carotid cistern may be advis able early on. The chiasmatic cistern over the left optic nerve may be opened somewhat distally so that the arachnoid over the aneurysm remains relatively undisturbed until it is time to dissect the base of the aneurysm. Generally, the nature of the subarachnoid blood and the consistency of the clot around the aneurysm give clear indication as to which aneurysm ruptured. Depending on the aneurysmal anatomy, the elective use of temporary occlusion of the ICA (and possibly also the external carotid artery [ECA]) may assist in the final dis section of the aneurysm. Certainly, if there is an intraop erative rupture, placement of temporary occluding clips on the cervical ICA and ECA will help stanch the hemorrhage and allow continuation of controlled dissection around the aneurysm neck. It is inadvisable to quickly apply clips to the bleeding aneurysm if dissection has not been completed. Maneuvers performed in a panicked state may lead to additional catastrophes. If proximal temporary occlusion does not stop or diminish the bleeding, trapping the aneurysm by additionally placing a temporary occluding clip on the supraclinoid ICA distal to the aneurysm may be helpful. Obviously, the shortest duration of temporary occlusion is desirable. Burst suppression of the EEG during the time of temporary occlusion has been employed as a protective measure, and it is often accomplished with the titrated administration of either etomidate or propofol. Induced hypertension may be considered when the duration of temporary occlusion is anticipated to be longer than 2 minutes. Adenosine- induced flow arrest has also been used to con trol bleeding from intraoperative aneurysm rupture, but its use has not been validated by any controlled studies. It is critical to identify the ophthalmic artery in an effort preserve it. Often, a side- angled clip is the best choice for obtaining optimal obliteration of this aneurysm at the skull base. After the ophthalmic aneurysm has been secured, attention can be directed to the MCA aneurysm. The sylvian fissure needs to be opened and the M1 and M2 segments of the left MCA identified. Often, the base of an MCA aneurysm will incorporate the origin of either the temporal or frontal trunk, or both. Reconstructing the

After the ophthalmic aneurysm has been secured, attention can be directed to the MCA aneurysm. The sylvian fissure needs to be opened and the M1 and M2 segments of the left MCA identified. Often, the base of an MCA aneurysm will incorporate the origin of either the temporal or frontal trunk, or both. Reconstructing the 30 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW bifurcation can be difficult, especially with larger or ath erosclerotic aneurysms. T emporary proximal occlusion of the M1 segment or trapping of the aneurysm by the place ment of multiple temporary clips may facilitate dissection or clip application in selected circumstances. With larger or atherosclerotic aneurysms, the clip may “slip” down the neck of the aneurysm and occlude or significantly stenose one of the trunks. Placing another clip above the first clip, and then removing the initial clip, may lead to a better result. After occlusion of the aneurysm, a micro- Doppler or similar tool can be used to check for the presence of flow in all involved arteries as well as for the absence of flow in the aneurysm. Indocyanine green fluorescent angiography visualized through the microscope is a quick and noninva sive tool to ensure adequate clip ligation of the aneurysm. However, only the structures visualized in the microscopic field of vision can be analyzed. If visualization is not opti mal, as may be the case more frequently in anterior com municating artery aneurysms, intraoperative DSA should be considered. The American Heart Association/ American Stroke Association (AHA/ ASA) guidelines recommend that endovascular coiling be considered when the ruptured aneurysm is judged to be technically amenable to both endovascular coiling and microsurgical clip ligation. Microsurgical clipping should receive increased consideration in MCA aneurysms, those with larger intraparenchymal hematomas (>50 mL), and possibly younger patients. There should be increased consideration for coiling in elderly patients (>70 years of age), poor grade patients, and those with basilar aneurysms. Delayed imaging following either clip liga tion or coiling of a ruptured aneurysm should be obtained to confirm occlusion of the aneurysm. With coiling, longterm assessment ( ≥5  years) is needed because there is a higher risk for coil compaction or recanalization of the treated aneurysm. As a reminder, most aneurysms do not have equipoise with regard to the option of either coiling or clipping. Y ou should not routinely choose one technique over the other. COMPLICA TIONS The general complications associated with craniotomy for clip ligation of a ruptured aneurysm were outlined in the prior discussion on surgical risks. One of the more frequent complications associated with aSAH is the development of an altered level of consciousness during the course of the hospitalization. The nurses report that this patient is significantly more confused and somewhat obtunded on the fifth morning after her aSAH. She has developed a right- sided pronator drift. This should trigger several actions. First, remember to clinically examine the patient yourself. Assess the degree of obtundation and look for additional focal neurological deficits (dysphasia, a central facial palsy, paresis, or anisocoria). Second, check her vital signs. Look for fever, developing hypertension (which may be associated with vasospasm), or hypotension. Fever is a common source of altered mental status in neurosurgical patients and should be managed aggressively. Third, review the patient’s laboratory data. Significant anemia may diminish oxygen delivery to the brain. A marked rise in her white blood cell count (especially the neutrophil count) may indicate an underlying infectious process.

e of altered mental status in neurosurgical patients and should be managed aggressively. Third, review the patient’s laboratory data. Significant anemia may diminish oxygen delivery to the brain. A marked rise in her white blood cell count (especially the neutrophil count) may indicate an underlying infectious process. Hyponatremia occurs in 10% to 30% of patients, often corresponding to the onset of clinical vasospasm. T ypically, hyponatremia in this setting is secondary to cerebral salt wasting rather than the syndrome of inappropriate antidiuretic hormone. T reatment of cerebral salt wasting involves aggressive volume resuscitation, usually with a hypertonic saline solution. Fludrocortisone, a mineralocorticoid, has also been used with some effectiveness for both the sodium and fluid balance. Fourth, review her medication list. See if she is receiv ing any medications that could potentially alter her men tal status (including narcotic analgesics, phenothiazines, and AEDs). If she is taking an AED such as phenytoin or carbamazepine, a drug level should be checked for toxicity or subtherapeutic dosing. Whether or not she is taking an AED, keep in mind the possibility that she could be postictal from an unwitnessed seizure. Fifth, a non– contrast- enhanced CT scan should be checked for postoperative hemorrhage or ventriculomegaly. Usually, a symptomatic hemorrhage will be detected earlier in the postoperative period. If an EVD is in place, occasionally more aggressive CSF drainage will be needed to treat underlying hydrocephalus. Sixth, assuming no significant findings were detected in the previous survey, investigate for possible vasospasm. Cerebral vasospasm following aSAH typically occurs between the 4th and 21st day after the ictus and generally peaks between the 7th to 10th days. The combined risk for all morbidity and mortality due to vasospasm is 10% to 15%. Serial transcranial Doppler (TCD) study is employed in many centers as a noninvasive method to assess for large vessel vasospasm. TCD is most accurate for assessing vasospasm in the MCA M1 segment. Mean flow velocity of more than 200 cm/ second is indicative of severe spasm. With TCD, mean flow velocities of less than 120  cm/ second or more

pler (TCD) study is employed in many centers as a noninvasive method to assess for large vessel vasospasm. TCD is most accurate for assessing vasospasm in the MCA M1 segment. Mean flow velocity of more than 200 cm/ second is indicative of severe spasm. With TCD, mean flow velocities of less than 120  cm/ second or more v ASCULAR N EUROSURGERY • 31 than 200 cm/ second are most useful to gauge the presence or absence of spasm. The Lindegaard ratio can help distin guish between vasospasm and hyperemia. This is the ratio of the mean flow velocities in the MCA to the cervical ICA. Large, serial elevation of mean flow velocity on daily TCD studies may be a harbinger of the development of severe vasospasm. In a patient with a good Hunt and Hess grade (1– 3), serial neurological examinations are generally the element guiding the evaluation and treatment of vasospasm. Delayed cerebral ischemia (DCI) is not always associated with angiographically confirmed vasospasm. Generally, DCI can be correlated to the degree of large vessel narrowing identified on the study. However, patients may have severe angiographic vasospasm without any ischemic symptoms. Conversely, patients with modest angiographic findings may develop significant symptomatic ischemia and cerebral infarction. A  variety of mechanisms have been postulated to contribute to the phenomena of DCI. The improvement in neurological outcomes with nimodipine despite its lack of effect on large vessel spasm is attributed to its effect on these other processes. The initial treatment for DCI is “triple- H therapy” (hypertension, hypervolemia, and hemodilution), and this has empirically shown benefit for most of these patients. Active hemodilution has essentially been abandoned because most patients in this setting undergo a passive hemodilution. More recently, there has been some shift away from the induction of hypervolemia to treatment with induced hypertension and the maintenance of euvolemia. If there is no response to the initiation of triple- H therapy, balloon angioplasty for the proximal vessels and infu sion of vasodilators for distal vessels should be employed (Figure 5.3). Currently, papaverine is being used less fre quently than calcium channel blockers. Infusion of nitric oxide donors has also been used, but it has only been reported in small series. The effect of balloon angioplasty is durable, whereas the effect of vasodilator therapy is shortlived and often requires serial treatment. Hemodynamic augmentation should be maintained even after an interventional procedure is completed until it is clear that the symptomatic vasospasm process is subsiding. Diagnosis and treatment of vasospasm are more com plex in a poor grade patient (Hunt and Hess grade 4- 5). Significant elevation in mean flow velocities on TCD and angiographic vasospasm may, or may not, be correlated with DCI. It appears that the perfusion imaging is emerg ing as a more accurate way to detect areas of hypoperfusion. However, the ability to do this testing on a serial basis is limited. Statin agents are commonly employed for the prophylactic management of DCI from aSAH, but the results are mixed, Figure 5.3 Left internal carotid artery (ICA) angiogram. A: The angiogram demonstrates intense vasospasm affecting the supraclinoid ICA, anterior cerebral, and M1 segments. The aneurysms are no longer visualized. B: Postangioplasty study demonstrates significant improvement, especially in the ICA and middle cerebral artery (MCA) distributions.

carotid artery (ICA) angiogram. A: The angiogram demonstrates intense vasospasm affecting the supraclinoid ICA, anterior cerebral, and M1 segments. The aneurysms are no longer visualized. B: Postangioplasty study demonstrates significant improvement, especially in the ICA and middle cerebral artery (MCA) distributions. 32 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW and a larger phase 3 trial is currently underway. Clazosentan (an endothelin- 1 antagonist) and magnesium sulfate have not shown benefit so far. Prophylactic angioplasty and prophylactic antiplatelet therapy have not reduced morbidity and are not recommended. The current AHA/ ASA guidelines also do not recommend the prophylactic use of hypervolemia. Newer methods of treatment are being evaluated. The previous discussion represents a relatively large overview of the issues involved in the management of aSAH. Be aware of the various options and issues if they come up as points of discussion. It is best to manage the patient on the Oral Board Examination as you would manage the patient in your practice and facility. It is better not to guess what you think the examiners may do. This may take you down an unfamiliar path and lead to more issues being raised. Be cautious in suggesting cutting- edge or novel treatments and therapies. The examination is about meeting and practicing the currently accepted standard of care. PEARLS • In nontraumatic SAH, DSA should be performed if noninvasive studies (CT A or MRA) are negative. • In only about 20% of cases will there be true equipoise between the options of endovascular or microsurgical treatment. Most aneurysms are best treated by one technique. Currently, for the Oral Board Examination, this likely involves the surgical option. • With microsurgical clipping, establish proximal control early in the approach. • Develop an algorithm to investigate a delayed neurological decline. CASE 2 HISTORY AND PHYSICAL EXAMINA TION A 20- year- old, right- handed, male college student experi enced a grand mal seizure. By the time he was evaluated in the emergency department, he had returned to normal. His neurological examination was unremarkable. There was no papilledema. The toxicology screen and blood alcohol level were negative. IMAGING STUDIES CT scan showed a hyperdensity in the right frontal lobe without evidence of acute hemorrhage. MRI was then obtained (Figure 5.4) and demonstrated a probable arte riovenous malformation (AVM). Subsequently, a formal angiogram was performed (Figure 5.5). ANALYSIS OF CASE AND TREA TMENT PLAN The patient suffered a seizure, most likely related to the AVM. Fifteen to 35% of patients with an AVM will pres ent with seizure. T reatment with an AED and standard, new- onset seizure- related precautions are initiated in this young man. The diagnosis of AVM was essentially confirmed by the MRI. MRI is a critical part of the evaluation for an AVM. The MRI can better demonstrate evidence of prior hemorrhage. It also provides valuable anatomic information on the location and size of the AVM, which may significantly affect treatment decisions. A formal angiogram is the next diagnostic step. Generally, all intracranial and extracranial vasculature should be analyzed. MRA or CT A cannot currently provide the detail and dynamic circulatory information provided by a formal angiographic study. Currently, such studies add very little to the investigation of an AVM and usually are not obtained. In managing any patient with an unruptured vascular lesion, the key consideration regarding the advisability of treatment is relatively simple. The decision to treat is based on the known natural history of the lesion balanced against the risks involved in its treatment.

tigation of an AVM and usually are not obtained. In managing any patient with an unruptured vascular lesion, the key consideration regarding the advisability of treatment is relatively simple. The decision to treat is based on the known natural history of the lesion balanced against the risks involved in its treatment. Although issues such as epilepsy, vascular steal, or rarely mass effect related to an AVM may become possible considerations for treatment, Figure 5.4 Magnetic resonance imaging demonstrates a compact area of flow void in the right frontal region. No evidence of prior hemorrhage is detected.

tigation of an AVM and usually are not obtained. In managing any patient with an unruptured vascular lesion, the key consideration regarding the advisability of treatment is relatively simple. The decision to treat is based on the known natural history of the lesion balanced against the risks involved in its treatment. Although issues such as epilepsy, vascular steal, or rarely mass effect related to an AVM may become possible considerations for treatment, Figure 5.4 Magnetic resonance imaging demonstrates a compact area of flow void in the right frontal region. No evidence of prior hemorrhage is detected. v ASCULAR N EUROSURGERY • 33 the primary issue generally involves the potential risk for hemorrhage. Hemorrhage, typically intracerebral hemorrhage (ICH), is the most common presenting sign of an AVM. It occurs in approximately 50% of patients, almost double the rate of seizure at presentation. Patients are most likely to pres ent with hemorrhage between the ages of 20 and 40 years. AVMs account for 38% of hemorrhages in patients between 15 and 45  years old. Long- term neurological impairment and mortality from the initial AVM hemorrhage are each reported to be 10% to 30%. The risk for an initial hemorrhage from a previously unruptured brain AVM is about 2% to 3% per year. The rate of hemorrhage for a previously ruptured AVM is about 4% per year. The lifetime risk for hemorrhage is determined by the following calculation: 1  – Risk for no bleeding (in decimal) remaining years of expected life Based on an annual estimated risk for hemorrhage of 3%, the following formula can be used to approximate the risk for this patient: Lifetime risk for hemorrhage from AVM  =  105  – patient age in years. Thus, at the age of 20  years, this patient has a potentially high risk for rupture of his AVM over the course of his lifetime. Each AVM is truly a distinct and unique lesion. Factors that have been reported to be associated with an increased risk for hemorrhage from an AVM include the presence of aneurysms (feeding artery, intranidal, or venous), exclusive drainage into the deep venous system, deep location (basal ganglia, internal capsule, thalamus, or corpus callosum), small size, a single draining vein, venous stasis or stenosis, and prior evidence of hemorrhage. Methods of treatment include microsurgical excision, stereotactic radiosurgery (SRS), embolization, or any com bination of these three modalities. The risk for surgical treatment has been stratified by the Spetzler- Martin grading system. This grading scheme is based on AVM size, eloquence, and deep venous drainage (T able 5.1). This young man has a Spetzler- Martin grade 1 AVM (size = 1, location  =  0, deep venous drainage  =  0). Microsurgical treatment for Spetzler- Martin grades 1 and 2 AVM can be performed with relatively low risk and a high expectation of a favorable outcome in high- volume treatment centers. The risk for treatment increases substantially for each additional grade while the probability of a good outcome diminishes. SRS offers another potential option for treatment of an AVM. Calculated obliteration rates range from 68% to 92% and are generally dependent on the size of the lesion. For lesions less than 10 cm3 in volume or less than 3 cm in diameter, the reported cure rates are higher than 80%. However, this rate drops to less than 70% for larger lesions. There is a latency period until obliteration occurs, which is typically 2  years or longer. There may be up to a 9% rate of symp tomatic complications, which usually are transient. The risk for permanent neurological deficit secondary to radiation necrosis is reported to be about 3%. Embolization for AVM is typically used as an adjunc tive measure. There is limited benefit to its adjunctive use in grades 1 and 2 AVM. The rate of cure with emboliza tion has traditionally been low and is estimated at about 5%, although rates of 20% have been reported in some series. Complication rates with embolization range from AB C Figure 5.5 Right internal carotid artery (ICA) angiogram.

imited benefit to its adjunctive use in grades 1 and 2 AVM. The rate of cure with emboliza tion has traditionally been low and is estimated at about 5%, although rates of 20% have been reported in some series. Complication rates with embolization range from AB C Figure 5.5 Right internal carotid artery (ICA) angiogram. A: Anteroposterior projection in early arterial phase demonstrates the right frontal arteriovenous malformation (AVM). B: Anteroposterior projection in late arterial phase demonstrates the AVM nidus and the early draining veins coursing to the sagittal, transverse, and cavernous sinuses. C: Lateral right ICA projection in late arterial phase again demonstrates the compact nidus located in the frontal lobe and the early draining veins.

B: Anteroposterior projection in late arterial phase demonstrates the AVM nidus and the early draining veins coursing to the sagittal, transverse, and cavernous sinuses. C: Lateral right ICA projection in late arterial phase again demonstrates the compact nidus located in the frontal lobe and the early draining veins. 34 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW 6% to 14%. Most are minor problems. However, there is an approximate morbidity of 5% and a 1% mortality rate from embolization. In 2013, the results of ARUBA (A Randomized T rial of Unruptured Brain Arteriovenous Malformations) were released. This study randomized patients with AVMs to medical management alone or medical management with interventional therapy. The trial followed 223 patients (114 patients assigned to interventional therapy and 109 patients assigned to medical management). The National Institute of Neurological Disorders and Stroke halted randomiza tion in 2013. The primary composite endpoint of death or symptomatic stroke was reached in 11 (10.1%) in the medical management group and 35 (30.7%) in the interventional group. An additional 5 years of follow- up are planned to see if the disparity persists. Superficially, ARUBA would seem to indicate that patients do not benefit from treatment of their AVM. It is important to note that the accrual rate was very slow and the initial number of patients to be studied was drastically reduced as time went on. Patients enrolled in ARUBA had Spetzler- Martin grades from 1 to 4. Sixty- two percent were grade 1 or 2. In the interventional arm, 53 patients were in the process of ongoing treatment at the time random ization was stopped, and 20 patients had not yet initiated treatment. Of those treated, only 5 patients had microsur gery alone, 12 had embolization plus surgery, and 1 had treatment with all three modalities. On the other hand, 30 patients were treated solely with embolization, and 31 were treated solely with radiosurgery. Fifteen patients had SRS and embolization. The number of patients who received surgical treat ment in ARUBA was very small. In 2014, Bervini and col leagues carefully analyzed their results in 377 patients with an unruptured brain AVM and concluded that the results of surgical intervention for grades 1 and 2 patients were quickly superior to the natural history. The results for treatment in grade 3 patients are less certain, and the authors concluded that grades 4 and 5 patients fare better without treatment. As such, in this 20- year- old patient with an unrup tured cerebral AVM, we recommend surgical treatment. SRS is part of the treatment discussion and would be rec ommended if he declined surgical treatment. The primary goal in treating an AVM is complete obliteration of the lesion. He is young and faces a lifelong risk for hemorrhage. Excision of this grade 1 AVM can be accomplished with relatively low risk and a greater than 90% chance of a favorable outcome. Similar to the tenet of proximal control in aneurysm surgery, there are several standard principles involved in the microsurgical resection of an AVM. The cranial exposure for an AVM should involve a generous bone flap, which allows adequate visualization of the superficial feeding arteries and draining veins along with the ability to dissect the involved vasculature, which may be traveling deeper in the sulci. In this patient, complete excision can be accomplished through a standard, retro- hairline, pterional craniotomy without the use of preoperative embolization. Initially, it is best to eliminate the larger feeding arteries close to the nidus. This maneuver will greatly facilitate the remainder of the case. Microsurgical dissection is typically accom plished in a circumferential pattern around the nidus.

rline, pterional craniotomy without the use of preoperative embolization. Initially, it is best to eliminate the larger feeding arteries close to the nidus. This maneuver will greatly facilitate the remainder of the case. Microsurgical dissection is typically accom plished in a circumferential pattern around the nidus. Care should be taken to preserve the draining veins until the end, when the nidus has been devascularized. Occasionally, a smaller draining vein may need to be amputated slightly earlier to be able to better mobilize the nidus for continued dissection. COMPLICA TIONS T wenty- one percent of complications are not directly related to the resection of the AVM itself (e.g., infection, pulmo nary complications). Any patient can develop a postop erative extraaxial hematoma (subdural or epidural) related directly to having undergone a craniotomy. One of the most feared complications related to AVM surgery is malignant brain edema and hemorrhage. Although hemorrhage may result from residual nidus, this etiology has been seen less frequently when intraoperative or immediate postoperative DSA is used. The more typical etiology of malignant brain edema and hemorrhage associated with AVM resection is arterial- capillary- venous hypertension (ACVH). This has also been called normal perfusion pressure breakthrough . It T able 5.1 SPETZLER- MARTIN GRADING SYSTEM* SIZE <3 CM 3– 6 CM >6 CM 1 2 3 Eloquence† Ye s No 0 1 Deep venous drainage None Present 0 1 *The grade (1– 4) is determined by adding the score from each category (size, eloquence, and deep venous drainage). †Eloquent locations include sensorimotor, language, or visual cortices and hypothalamus, thalamus, brainstem, and cerebellar nuclei.

6 CM 1 2 3 Eloquence† Ye s No 0 1 Deep venous drainage None Present 0 1 *The grade (1– 4) is determined by adding the score from each category (size, eloquence, and deep venous drainage). †Eloquent locations include sensorimotor, language, or visual cortices and hypothalamus, thalamus, brainstem, and cerebellar nuclei. v ASCULAR N EUROSURGERY • 35 occurs in about 3% of operated cases. The risk for ACVH is greatest when treating an AVM with a nidus more than 4 cm in diameter. It is thought to be secondary to auto regulatory failure in the relatively ischemic bed surround ing the AVM. Another hypothesis for the etiology of this potentially catastrophic event is occlusive hyperemia. This is caused by stagnation or obstruction in the arterial inflow and venous outflow pathways. Often, the draining veins are markedly redundant. Malignant brain edema and hemorrhage may occur immediately or in a delayed fashion. Although 83% of new postoperative deficits are seen on emergence from anesthesia (for several possible reasons, including ACVH, clot, or ischemic stroke), 17% are delayed and may develop during the first postoperative week. PEARLS • Complete obliteration of the AVM is the absolute goal with treatment. Subtotal therapy does not protect from hemorrhage. • Microsurgical excision should be primarily considered for a young patient with a Spetzler- Martin grade 1 or 2 AVM. • Embolization should be employed sparingly for low- grade AVMs and only when it is thought to facilitate resection of the AVM. • SRS represents a good alternative for patients with grades 1 and 2 AVMs who decline surgery or are not good surgical candidates. • The draining veins should be preserved until the nidus has been devascularized. • The decision to treat patients with unruptured Spetzler- Martin grade 3 AVMs needs to be made on a case- by- case basis. Patients with unruptured grades 4 and 5 lesions appear to fare better with medical management. CASE 3 HISTORY AND PHYSICAL EXAMINA TION A 53- year- old woman was found unconscious at home. She is taking amlodipine besylate/ benazepril HCl for hypertension and warfarin for atrial fibrillation. Her international normalized ratio (INR) is 3.8. The patient is intubated. Her blood pressure is 208/ 102 mm Hg. Her left pupil is large and sluggishly reactive. She is purposeful on her left and barely withdraws on the right. She has bilateral Babinski responses. Her Glasgow Coma Scale score is 7 T (E1,V1T, M5). IMAGING STUDIES The initial non– contrast enhanced CT scan demonstrates a large left occipitotemporal ICH with intraventricular hemorrhage (IVH) and midline shift (Figure 5.6). No underlying vascular abnormality is identified on the CT A (Figure 5.7). ANALYSIS OF CASE AND TREA TMENT PLAN Spontaneous ICH is a common problem generating a neurosurgical evaluation. Most patients have small ICHs that are not life- threatening and are readily managed medically. The typical basal ganglionic hemorrhage in a patient with known hypertension usually does not merit further inves tigation. Similarly, a lobar hemorrhage in an elderly patient with mild dementia probably is due to amyloid angiopathy. Most other forms of spontaneous ICH merit some type of additional investigation for an underlying medical condition such as a coagulopathic process or a structural lesion such as an underlying tumor or vascular abnormality. Risk factors for an underlying vascular abnormality are age younger than 65 years, female sex, lobar ICH, nonsmoker, intraventricular extension, and absence of hypertension or coagulopathy. Although this patient is taking anticoagula tion medications, we thought that a CT A was warranted before surgical intervention. The ICH score can be used to stratify risk for the patient.

e younger than 65 years, female sex, lobar ICH, nonsmoker, intraventricular extension, and absence of hypertension or coagulopathy. Although this patient is taking anticoagula tion medications, we thought that a CT A was warranted before surgical intervention. The ICH score can be used to stratify risk for the patient. The 30- day mortality steadily increases with higher ICH scores. In the original study, there were no survivors in patients with an ICH score of 5. The ICH score for this patient is 3 (T able 5.2). Her ICH needs to be evacuated. With the focus on rapid intervention for ischemic stroke, prehospital management of an ICH patient should be similar to that of a stroke patient. Primary attention is directed toward airway and cardiovascular assessment as well as history of onset. Excessive hypertension (systolic blood pressure >220 mm Hg), vomiting, rapid progression of symptoms, and decreased level of consciousness or coma point toward ICH as the etiology. Early deterioration following ICH is common, both in the prehospital interval and in the first few hours of hospi talization. Of patients who had a CT scan within several hours of their ictus, ICH expansion is seen in approxi mately one third on follow- up imaging. The presence of a “spot sign” on a contrast- enhanced CT scan is a potential harbinger of hematoma expansion.

e prehospital interval and in the first few hours of hospi talization. Of patients who had a CT scan within several hours of their ictus, ICH expansion is seen in approxi mately one third on follow- up imaging. The presence of a “spot sign” on a contrast- enhanced CT scan is a potential harbinger of hematoma expansion. 36 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW The AHA/ ASA guidelines for the management of spontaneous ICH recommend lowering systolic blood pressure to less than 140  mm Hg. The acute lowering of systolic blood pressure to this target has been shown to be safe in multiple studies. It appears to have a modest effect on achieving a better recovery. There are no specific recommendations on the method of antihypertensive treatment. However, patients with significant hypertension may be better served with a continuous intravenous agent. Given the patient’s large hemorrhage and increased intracranial pressure, a presurgical goal of less than 160 mm Hg may be reasonable. Up to 20% of patients with an ICH are taking an oral anticoagulant. It is important to inquire about the use of Figure 5.6 Non– contrast- enhanced computed tomography of the brain demonstrating A: A large left intracranial hemorrhageB: With intraventricular extension and midline shift. Figure 5.7 Computed tomographic angiogram A: Lateral and B: Anteroposterior reconstructions. No underlying vascular malformation is identified in relation to this large occipitotemporal intracranial hemorrhage.

in demonstrating A: A large left intracranial hemorrhageB: With intraventricular extension and midline shift. Figure 5.7 Computed tomographic angiogram A: Lateral and B: Anteroposterior reconstructions. No underlying vascular malformation is identified in relation to this large occipitotemporal intracranial hemorrhage. v ASCULAR N EUROSURGERY • 37 these medications or platelet- inhibiting agents. This patient is taking warfarin, which is the most commonly used vita min K antagonist. Her INR is significantly elevated, so reversal is initiated. She receive10 mg of vitamin K intra venously. However, its onset of action is not immediate, and it takes up to 24 hours to achieve full effect in most circumstances. Fresh frozen plasma (FFP) has been used for more rapid reversal. However, FFP is associated with a higher rate of transfusion- related acute lung injury, and the volume of FFP required can create cardiopulmonary difficulties. W e also administered prothrombin complex concen trate (PCC). PCC and activated PCC are being used more frequently for rapid reversal of warfarin- induced coagulopathy. PCCs are overwhelmingly more successful at produc ing a normalized INR (<1.3) within 30 minutes than FFP. Furthermore, they are easier to use. They do not require a cross- match. They are administered in a small volume, and infectious agents are inactivated. PCCs have a significant effect on the INR within minutes. There are three- factor (factors II, IX, and X) and four- factor (factors II, VII, IX, and X) PCCs. The use of recombinant activated factor VII (rFVIIa) is not routinely recommended for reversal of warfarininduced coagulopathy because it does not replenish the other vitamin K– dependent factors (II, IX, and X) and may not be as efficacious as PCC. At this time, there is no clear indication for use of rFVIIa in patients with an ICH unless it is secondary to factor VII deficiency. Reversal of the newer, novel oral anticoagulants and their parenteral counterparts is much more problematic. These agents include factor Xa inhibitors and direct thrombin inhibitors (T able 5.3). Specific reversal strategies and antidotes are being developed and evaluated. Emergency consultation with a hematologist may be most appropri ate if surgical intervention is anticipated for patients taking these newer agents. If a patient is taking an oral antiplatelet agent, transfu sion of platelets will override the inhibitory effects. Platelets and cryoprecipitate may be needed to counteract the T able 5.2 INTRACEREBRAL HEMA TOMA SCORE* Glasgow Coma Scale score 3– 4 2 5– 12 1 13– 15 0 Intracerebral hematoma (ICH) volume ≥30 mL 1 <30 mL 0 Intraventricular hemorrhage Ye s 1 No 0 Infratentorial origin of ICH Ye s 1 No 0 Age ≥80 yr 1 <80 yr 0 *The total score is determined by totalling the points from each category. T able 5.3 CURRENT ANTIPLA TELET AND ANTICOAGULANT AGENTS* Antiplatelet agents Oral Intravenous • release dypridimole and aspirin (Aggrenox) abciximab (ReoPro) prasugrel (Effient) eptifibatide (Integrelin) Aspirin tirofabin (Aggrastat) clopedigrel (Plavix) ticagrelar (Brilinta) cilostazol (Pletal) Heparins Heparin Low- molecular- weight heparins Enoxaparin (Lovenox) Dalteparin (f ragmin) Tinzaparin (Innohep) W arfarin (vitamin K antagonists) FactorXa inhibitors Oral Subcutaneous apixaban (Eliquis) fondaparinux (Arixtra) rivaroxaban (xarelto) Direct thrombin inhibitors Oral Intravenous dabigatrin (Pradaxa) bivalirudin (Angiomax) argatroban (Novastan) Recombinant tissue plasminogen activator (r- tP A) *As of 2015.

(Innohep) W arfarin (vitamin K antagonists) FactorXa inhibitors Oral Subcutaneous apixaban (Eliquis) fondaparinux (Arixtra) rivaroxaban (xarelto) Direct thrombin inhibitors Oral Intravenous dabigatrin (Pradaxa) bivalirudin (Angiomax) argatroban (Novastan) Recombinant tissue plasminogen activator (r- tP A) *As of 2015. 38 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW various intravenous antiplatelet agents (see T able 5.3). For recombinant tissue plasminogen activator (r- tPA), transfusion with platelets, cryoprecipitate, and possibly plasma has been recommended. Also, be aware that the low- molecularweight heparins do not reverse as readily as heparin with the administration of protamine sulfate. The prophylactic use of AEDs has not been shown to be beneficial, and it is not recommended in the manage ment of spontaneous ICH. Most seizures related to an ICH occur soon after the ictus or within the first week. The risk for seizure is higher when there is involvement of the cortex. The use of corticosteroids in ICH should also be avoided. These agents increase the risk for complications and have not demonstrated any significant benefit. The use of ICP monitoring has not been well studied. There is a relatively uniform agreement that patients with a large (>3  cm) cerebellar hemorrhage who are neu rologically compromised from brainstem compression or hydrocephalus should undergo surgical decompression. Attempted management of a patient with a large cerebel lar clot by an EVD alone is suboptimal and may actually be harmful. There also is general agreement that a clearly lifethreatening ICH in a potentially salvageable patient should be evacuated. The benefits of a decompressive craniectomy have not yet been clearly defined. After initial control of her blood pressure and the administration of vitamin K and PCC, this patient underwent a standard craniotomy for clot evacuation. On the other hand, the benefits from surgery for non– life- threatening supratentorial ICH are less clear. The Surgical T reatment for Ischemic Heart Failure (STICH) studies did not demonstrate a significant advantage with respect to mortality or neurological outcome with early surgical intervention over medical management in these patients. Recent ongoing trials, including the Minimally Invasive Surgery Plus rt- PA for Intracerebral Hemorrhage Evacuation (MISTIE) III and Clot Lysis:  Evaluating Accelerated Resolution of Intraventricular Hemorrhage Phase III (CLEAR III) trials, are evaluating the effective ness of minimally invasive approaches for the treatment of ICH and IVH. COMPLICA TIONS Postoperatively, the patient’s level of alertness initially improves, but after several days, she becomes much less responsive. As outlined in the earlier discussion on postoperative worsening following treatment of a ruptured aneu rysm, you should have a mental checklist to address this issue of delayed worsening. There are no metabolic issues identified. Repeat CT demonstrates evacuation of the ICH, no new hemorrhage, and significant improvement in the mass effect. Continuous EEG monitoring is instituted and demonstrates epileptiform activity. With appropriate AED therapy, the patient’s condition improves, and she continues to make a good recovery. PEARLS • For most patients with ICH, systolic blood pressure can be safely lowered to less than 140 mm Hg. Do not use corticosteroids. In general, do not use prophylactic AEDs. • Surgery is indicated for life- threatening ICH. • Surgery is indicated for any patient with a large (>3 cm) cerebellar hemorrhage who is neurologically compromised. • Any coagulopathy should be aggressively reversed before surgery.

than 140 mm Hg. Do not use corticosteroids. In general, do not use prophylactic AEDs. • Surgery is indicated for life- threatening ICH. • Surgery is indicated for any patient with a large (>3 cm) cerebellar hemorrhage who is neurologically compromised. • Any coagulopathy should be aggressively reversed before surgery. CASE 4 HISTORY AND PHYSICAL EXAMINA TION A healthy, 72- year- old man presented to his primary care physician with a history of progressive difficulty with walking and paresthetic sensations in his legs. Symptoms worsened with fast- paced walking and occasionally with bowel movements. He had an associated dull pain in the low back with radiation into the legs, more prominently on his right side. Resting improved symptoms within sev eral minutes. His primary care physician obtained standard radio graphs, which demonstrated a minimal spondylolisthesis at L3- L4. He did not respond to nonnarcotic analgesics and physical therapy. After several months of continuing symptoms, MRI of the lumbar spine was obtained (Figure 5.8). Spinal stenosis was reported, and the patient underwent two epidural steroid injections with questionable benefit. Over time, he periodically began using a cane or walker. He was also started on tamsulosin because of difficulty with urination. He was referred for decompression. His examination revealed 4/ 5 strength in the distal lower extremities, which was worse in his right leg. There was diminished pinprick perception in both legs in a patchy distribution without a distinct level. The reflexes in the upper extremities were 1+, the knees 2+ to 3+, and the ankles 2+. There was no Babinski response, but there were several beats of clonus at the right ankle. T one was slightly increased in both lower extremities. MRI of the thoracic spine is obtained.

a patchy distribution without a distinct level. The reflexes in the upper extremities were 1+, the knees 2+ to 3+, and the ankles 2+. There was no Babinski response, but there were several beats of clonus at the right ankle. T one was slightly increased in both lower extremities. MRI of the thoracic spine is obtained. v ASCULAR N EUROSURGERY • 39 IMAGING STUDIES The initial MRI of the lumbar spine demonstrates only mild spondylostenosis and does not account for the patient’s progressive leg symptoms (see Figure 5.8). Flexion- extension views of the lumbar spine did not show any instability. The sagittal T2- weighted MRI of the thoracic spine demon strates signal abnormality in the lower thoracic cord and conus medullaris. There is also dilation of the perimedul lary veins (Figure 5.9). Subsequent spinal angiography (Figure 5.10) reveals a dural arteriovenous fistula (dAVF) at the L3 level on the right side. ANALYSIS OF CASE AND TREA TMENT PLAN There are several potential pitfalls that can be encountered if the history, physical examination, and imaging studies are not methodically assessed. Spinal dAVF is an uncommon disorder with initially nonspecific symptoms. Misdiagnoses are frequent, and inappropriate surgical interventions may precede definitive treatment. Cases at the Oral Board Examination are presented in a random order; keep this in the back of your mind for a spinal stenosis case in which everything is not adding up correctly. Although the patient was referred with a diagnosis of degenerative lumbar stenosis, the MRI findings in his lumbar spine were quite underwhelming. The disproportionate symptoms and mild myelopathic findings on his physical examination should absolutely detour any thoughts of a decompressive lumbar procedure. The T2 signal abnormality could potentially repre sent demyelination, inflammation, or tumor. His age and progressive symptoms make demyelination an unlikely etiology. Patients such as this have undergone surgery for exploration and biopsy or resection. The surgeon quickly aborts the case when engorged and arterialized vessels are encountered on dural opening. The clinical presentation of a middle- aged to older man with gradually progres sive pain, motor, or sensory symptoms accompanied by sphincter disturbance should alert the physician to the possibility of a spinal dAVF . Assessing the T2- weighted sagittal images for enlarged perimedullary veins is critical and often will confirm the need to proceed with spinal angiography. Selective angiography allows precise local ization of the fistula, typically at the dural nerve root sleeve. T reatment to obliterate the fistula is advised because of the inexorable progression of symptoms related to the venous congestion and hypertension in the spinal cord. Although hemorrhage from a spinal dAVF is exceedingly rare, the neurological deficits become irreversible as time elapses. Dorsal spinal dAVFs are predominantly located on the left side, usually from the lower thoracic and lumbar vertebral segmental arteries. T wo to 3% of patients will have Figure 5.8 Sagittal and axial T2- weighted magnetic resonance images of the lumbar spine. There is a minimal spondylolisthesis at L3- L4. There is no significant foraminal, lateral recess, or canal stenosis identified on either the sagittal (A) or axial (B) images at L3- L4.

l arteries. T wo to 3% of patients will have Figure 5.8 Sagittal and axial T2- weighted magnetic resonance images of the lumbar spine. There is a minimal spondylolisthesis at L3- L4. There is no significant foraminal, lateral recess, or canal stenosis identified on either the sagittal (A) or axial (B) images at L3- L4. 40 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW multiple dAVFs. Current treatment options include endovascular therapy and microsurgical obliteration. Endovascular therapy with polyvinyl alcohol was plagued by initially low rates of complete obliteration and high rates of recurrence. There has been more success recently with the use of liquid adhesive embolic agents, which allow deeper penetration of the material into the proximal vein. Still, the rate of recurrence of the dAVF is higher with embolization therapy. A  spinal medullary artery arising from the segmental artery supplying the dAVF is a contraindication to endovascular treatment. Navigating tortuous radicular arteries in this older popula tion and the inability to deposit embolic material into the vein proximally are some of the more technically problem atic challenges. On the other hand, surgical obliteration of a spinal dAVF carries a very low rate of morbidity and provides an extremely high rate of occlusion, which is durable. Surgery requires precise intraoperative localization of the correct level. Marking the skin under radiographic guidance preoperatively can lead to navigational error because the skin may translate when the patient is placed in the prone position. This patient was positioned on a Jackson table to facilitate intraoperative imaging. Catheterization of the femoral artery with an extended sheath is completed before turn ing the patient prone if intraoperative angiography is used. Alternatively, angiography performed in the prone position by accessing the popliteal artery has also been described. When the patient is positioned, the location is confirmed radiographically, and a limited laminectomy is completed. After dural opening, the arterialized vein is easily identified and traced to the dura of the root sleeve. Hypervascularity of the dura in this region may be appreciated. Classically, a clip is placed on the arterialized vein at the dura, occluding the fistulous connection. Because the presence of the clip may complicate dural closure, coagulation and division of the fistulous venous segment can be considered as an alter native (Figure 5.11). Confirmation of obliteration of the dAVF can be achieved through intraoperative or postoperative angiography. The successful use of indocyanine green fluorescent angiography has also been reported and may further enhance this elegantly simple procedure. Fusion is not required unless there are preexisting concerns about instability at the level of treatment. After successful surgical or endovascular obliteration of the dAVF, most patients will experience stabilization or improvement in their neurological symptoms. Motor symptoms tend to improve more readily than sensory or sphincter disturbances. The more advanced the symptoms, Figure 5.9 T2- weighted sagittal magnetic resonance imaging of thoracic spine. The gold arrow points to signal alteration in the lower thoracic spinal cord and conus medullaris. The white arrows point to engorged perimedullary veins on the dorsal spinal surface. Figure 5.10 Spinal angiogram, right L3 segmental artery, right anterior oblique projection. The enlarged medullary vein is identified as it flows in retrograde manner to the dilated coronal venous plexus.

nal cord and conus medullaris. The white arrows point to engorged perimedullary veins on the dorsal spinal surface. Figure 5.10 Spinal angiogram, right L3 segmental artery, right anterior oblique projection. The enlarged medullary vein is identified as it flows in retrograde manner to the dilated coronal venous plexus. v ASCULAR N EUROSURGERY • 41 the less likely there will be clinical improvement. This makes earlier and timely diagnosis of a spinal dAVF critical. COMPLICA TIONS Infection is a standard risk. Instability is an unlikely com plication. The bony exposure for a spinal dAVF does not require an extensive facetectomy on the side of the fistula, let alone the contralateral side. There is a risk for CSF leakage following any spinal intradural operation. W atertight dural closure should be attempted. It may be covered with collagen sponge and tissue glue. Use of a wound drain with a suction device is a personal preference. Some surgeons avoid this because of concerns about facilitating a possible CSF leak. The patient’s initial postoperative neurological exami nations are stable. However, when he begins to ambulate after the period of flat bed rest, he notices worsened weak ness in his legs with more difficulty walking and a greater sense of numbness in his feet. Proprioception and pin prick perception are preserved. Although he may not have improvement following obliteration of the fistula, dete rioration would be an unusual finding. With a worsened neurological status, postoperative MRI is warranted. The MRI reveals a sizable postoperative hematoma, and the most prudent solution is to return to the operating room for evacuation of the clot (Figure 5.12). If the MRI were unremarkable, then follow- up angiography would have been completed. Neurological worsening months or years after oblitera tion merits repeat imaging studies and spinal angiography to look for a recurrence of the dAVF, especially if it was closed interventionally. PEARLS • Misdiagnosis or delay in diagnosis is not uncommon. If the history, examination, and imaging studies do not add up, consider investigating for a spinal dAVF. Figure 5.11 Intraoperative images after a partial L2- L3 laminectomy. A: The enlarged, arterialized vein is identified as it arises from the fistula located at the dural root sleeve. B: Classically, a clip is placed across the medullary vein at the fistula. Change in caliber is already noted. C: The fistulous vein can be coagulated and then divided to allow removal of the clip. This may facilitate dural closure. Note the darker coloration of the remaining medullary venous segment. Figure 5.12 Axial T2- weighted image at L3 level. The hyperintense epidural hematoma is seen compressing the thecal sac.

noted. C: The fistulous vein can be coagulated and then divided to allow removal of the clip. This may facilitate dural closure. Note the darker coloration of the remaining medullary venous segment. Figure 5.12 Axial T2- weighted image at L3 level. The hyperintense epidural hematoma is seen compressing the thecal sac. 42 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW • Symptoms will progress if not treated. Motor symptoms tend to respond the best. • Although a spinal dAVF potentially can be treated endovascularly, surgery is simple, safe, and durable. CASE 5 HISTORY AND PHYSICAL EXAMINA TION A 70- year- old right- handed man experienced a 15- minute episode of nausea, dizziness, left eye blindness, and right arm flaccidity. He continued to have mild expressive dys phasia for another 2 hours. He has a history of hypertension and smokes 1 pack of cigarettes daily. His blood pressure is 157/ 90 mm Hg, and there is a left carotid bruit. Neurological examination is now normal. IMAGING STUDIES The initial CT scan of the brain and the brain perfusion study are normal. MRI demonstrates small infarcts (Figure 5.13). Duplex ultrasound reveals 30% stenosis on the right and 80% on the left. CT A reveals significant carotid Figure 5.13 Axial (A, B) and coronal (C, D) apparent diffusion coefficient images. Small areas of acute stroke are identified in the frontal region, consistent with embolic infarcts.

s small infarcts (Figure 5.13). Duplex ultrasound reveals 30% stenosis on the right and 80% on the left. CT A reveals significant carotid Figure 5.13 Axial (A, B) and coronal (C, D) apparent diffusion coefficient images. Small areas of acute stroke are identified in the frontal region, consistent with embolic infarcts. v ASCULAR N EUROSURGERY • 43 stenosis on the left (Figure 5.14, Figure  5.15, and Figure 5.16). Intracranial CT A shows a patent circle of Willis. ANALYSIS OF CASE AND TREA TMENT PLAN This patient presented with a classical transient isch emic attack (TIA) secondary to his carotid stenosis. Hemodynamic TIAs tend to resolve within minutes, whereas embolic TIAs usually last for several hours. About one third of patients who experience a TIA eventually suffer a stroke. After experiencing a TIA, the risk for stroke is 5% during the first month and 12% during the subsequent year. Extracranial atherosclerotic disease of the carotid arteries and aortic arch account for more than 50% of all strokes. Disease at the carotid bifurcation is associated with 20% to 30% of all strokes. The incidence of stroke may be further increased as associated ulceration in the plaque becomes more complex. Modifiable risk factors for stroke include hyperten sion, heavy alcohol use, and smoking. This patient has two of three risk factors. Diabetes mellitus is another risk fac tor, but it is uncertain whether tight control significantly alters the risk for stroke. The patient also has a cervical bruit, which is the most common physical sign of extracra nial vascular disease. However, this finding has a very broad differential diagnosis, and up to 50% of patients with sig nificant stenosis may not have a bruit. A bruit can be con sidered as a general sign of atherosclerotic disease. Careful preoperative cardiac evaluation is important because many of these patients have associated cardiac disease. The patient is started on low- dose acetylsalicylic acid (ASA; 81– 325 mg) and a “statin.” Hepatic hydroxymethyl glutaryl coenzyme A reductase inhibitors have been shown to lower the risk for stroke in patients with carotid athero sclerosis by 19% to 32%. Duplex ultrasound and CT A showed significant carotid stenosis. Duplex ultrasound may be more accurate than angiography in demonstrating ulceration, but it tends to underestimate the degree of stenosis. There is generally good correlation between angiography and MRA, but MRA tends to overestimate the degree of narrowing and may give a false impression of occlusion. Currently, CT A seems to be supplanting formal angiography for the assess ment of carotid atherosclerotic disease given its low risk profile and high degree of accuracy. W e routinely perform an intracranial CT A to look for tandem lesions and to the assess patency of the circle of Willis. There is compelling evidence to treat this patient’s symptomatic carotid stenosis. In the North American Symptomatic Carotid Endarterectomy T rial (NASCET), carotid stenosis of 70% or greater was associated with a 26% incidence of stroke after 2 years with medical management compared with 9% with carotid endarterectomy (CEA), resulting in a relative risk reduction of 65%. The absolute Figure 5.14 Coronal reformatted computed tomographic angiography of the neck. Mild stenosis is identified on the right (A), and there is significant stenosis of the left carotid artery (B). Calcification in the plaque is also detected. Figure 5.15 Sagittal reformatted computed tomographic angiography of the left cervical carotid artery. The significant stenosis is again noted.

raphy of the neck. Mild stenosis is identified on the right (A), and there is significant stenosis of the left carotid artery (B). Calcification in the plaque is also detected. Figure 5.15 Sagittal reformatted computed tomographic angiography of the left cervical carotid artery. The significant stenosis is again noted. 44 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW risk reduction from CEA was 16% at 5 years. For symptomatic carotid stenosis of 50% to 69%, the benefit of CEA is smaller (absolute risk reduction of 4.6% at 5 years). Pooled data from the European Carotid Surgery T rial (ECST), the V eterans Affairs Cooperative Study, and NASCET show benefit from CEA. W e recommend expeditious treatment for this patient because CEA within 2 weeks following the last symptom atic event (TIA or nondisabling stroke) is associated with better results. Currently, for a patient like this, the question has moved from whether to treat to how to treat: CEA or carotid angioplasty and stent (CAS). In 2010, the Carotid Revascularization Endarterectomy V ersus Stenting T rial (CREST) showed no significant difference in the primary composite outcome of stroke, myocardial infarction (MI), or death for CEA and CAS. However, in the periprocedural period, there was a higher risk for stroke with CAS and a higher risk for MI with CEA. Stroke had a greater adverse effect on quality of life than did MI. Y ounger patients (<70 years) had slightly better outcomes with CAS, and older patients (>69 years) had better outcomes with CEA. The worse outcome in elderly patients with CAS may be secondary to vascular tortuosity and calcifications. An abnormally high carotid bifurcation, previous radiation, or prior neck surgery may favor CAS. Given this patient’s age and lack of anatomic risk fac tors, the decision was made to perform a CEA. Cardiac evaluation and the perioperative use of ASA are important to minimize the cardiac risk. CEA can be performed under local or general anesthesia. The carotid bifurcation is usually located at the level of the thyroid cartilage. The belly of the omohyoid muscle usually demarcates the inferior margin of dissection of the common carotid artery (CCA). Superiorly, dissection is carried over the lateral CCA to the bifurcation and origin of the ICA, and it is extended beyond the end of the plaque. The CCA courses posteromedially to the internal jugular vein. Often, the common facial vein must be ligated and divided near the bifurcation. The ansa cervicalis is kept medial, and it leads to the hypoglossal nerve. Occasionally, the supe rior division of the ansa cervicalis needs to be divided as it descends from the hypoglossal nerve to gain better access to the carotid artery. It is important to keep the medial blades of the self- retaining retractor superficial to the trachea to avoid injury to the trachea and its nerve supply. Before cross- clamping, a fixed dose (5,000U) or a weight- based dose of heparin is administered intravenously. The ICA, CCA, ECA, and superior thyroid artery are cross- clamped or occluded in sequential order (“I- C- E”). At this time, hemodynamic, electrophysiologic, transcra nial Doppler or clinical monitoring is used to check for potential hemispheric cerebral ischemia. Stump pressure below a mean blood pressure of less than 20 to 25 mm Hg, EEG slowing, significant reduction in MCA mean flow velocity, or the development of neurological signs when surgery is performed under local anesthesia may indicate significant ischemia. Inducing moderate hypertension to help increase collateral flow is the first maneuver to employ, but a shunt may ultimately be needed. The use of a shunt can create some technical difficulties with the CEA and can be a source for emboli or intimal injury.

formed under local anesthesia may indicate significant ischemia. Inducing moderate hypertension to help increase collateral flow is the first maneuver to employ, but a shunt may ultimately be needed. The use of a shunt can create some technical difficulties with the CEA and can be a source for emboli or intimal injury. Some surgeons simply employ pharmacological EEG burst suppression or the routine use of a shunt during the period of cross- clamping. Y ou will need to have your personal algorithm prepared for the examination. The arteriotomy is started below and lateral to the carotid bifurcation and extends rostrally along the cen tral aspect of the ICA. The plaque- media interface is dis sected, and the plaque is excised. The proximal and distal Figure 5.16 Three- dimensional reconstruction computed tomographic angiography of the neck. Again, the severe carotid stenosis is identified. The maximal constriction at the distal portion of the left internal carotid artery is a result of plaque.

erface is dis sected, and the plaque is excised. The proximal and distal Figure 5.16 Three- dimensional reconstruction computed tomographic angiography of the neck. Again, the severe carotid stenosis is identified. The maximal constriction at the distal portion of the left internal carotid artery is a result of plaque. v ASCULAR N EUROSURGERY • 45 ends of the endarterectomy are inspected for any filaments of plaque or intimal flaps. Closure is initiated, and then debris and air bubbles are expelled by backbleeding from each vessel. Removal of the clip on the superior thyroid artery allows continuous backbleeding during placement of the final few sutures. The ECA is then reopened. The CCA is temporarily reopened to flush debris into the ECA system, followed by temporarily reopening the ICA to flush into the ECA. Finally, the clamps are permanently removed from the CCA and then the ICA (reverse “I- C- E” order). The heparin is allowed to dissipate without protamine reversal. If there is bleeding from the arteriotomy closure, this is usually controlled by the application of a hemostatic sponge. Low- dose ASA (81– 325 mg) is recommended before and for at least 3 months after surgery to reduce the risk for stroke, MI, and death. Unless contraindicated, it should be used indefinitely. Blood pressure is strictly con trolled throughout the postoperative period. COMPLICA TIONS After CAS and CEA, cerebral hyperperfusion can develop in 1% to 2% of patients, respectively. It develops more quickly following CAS. Cerebral hyperperfusion is characterized by unilateral headache, face and eye pain, seizures, and focal neurological symptoms. There can be cerebral edema. ICH occurs in less than 1%. The development of ICH after endarterectomy is avoided by tight blood pressure control. On the other hand, SAH is more common following CAS and is not correlated to blood pressure management. The risk for perioperative MI remains 2% to 3%. W ound hematoma is seen in about 5% of cases. A variety of nerve injuries can be seen with CEA. Most of these are stretch injuries and resolve within 3 to 6  months. Injury to the mandibular branch of the facial nerve at the inferior margin of the parotid gland can affect the lip depressor. Injury to the recurrent laryngeal nerve has been reported in 6%, and this risk is lessened by keeping the medial blade of the retractor at or above the level of the trachea. Superior laryngeal nerve injury can be disabling owing to difficulty swallowing and sensing food. It can be injured during high dissection medial to the ICA and ECA. Injury to the spinal accessory nerve coursing under sterno cleidomastoid paralyzes the ipsilateral trapezius and sternocleidomastoid muscles. Hypoglossal nerve injury occurs in about 5% of cases. The risk for restenosis of about 50% by duplex ultra sound is 8% to 12% at 2 years following CEA. It is symp tomatic in only 10% to 20%. There is no increased risk for TIA, stroke, or death compared with patients without recurrent disease. PEARLS • CEA is an extremely effective surgery. It should be performed within 2 weeks following a TIA or minor stroke. It is associated with a higher risk for MI compared with CAS. Older patients had fewer events with CEA than CAS. Low- dose ASA should be used preoperatively and for a minimum of 3 months after surgery. • CAS has been shown not to be inferior to CEA. Y ounger patients had slightly fewer events after CAS compared with CEA. CAS is associated with a higher risk for stroke than for MI and thus more adversely affects quality of life. • In CEA, cross- clamps are applied using the I- C- E order and removed in reverse sequence. BIBLIOGRAPHY 1. Adamczyk P, Amar AP, Mack WJ, Larsen DW. Recurrence of “cured” dural arteriovenous fistulas after Onyx embolization. Neurosurg Focus.

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