Oct. 04, 2021
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Cerebral arteriovenous malformations are congenital vascular malformations in the brain that are the underlying cause of 1% to 2% of all strokes, 3% of strokes in young adults, and around 10% of all subarachnoid hemorrhages (02; 38). They occur in about 0.1% of the population and represent one tenth of all intracranial aneurysms (38). Though mostly asymptomatic, these lesions come to clinical attention with a variety of neurologic presentations, including headaches, seizures, progressive neurologic deficits, or by incidental discovery (Derdeyn et al 2017). Short-term morbidity and mortality associated with arteriovenous malformations are low, but patients may do poorly in the long-term given the cumulative risk of hemorrhage. In determining the need for intervention, key morphologic and clinical characteristics are considered, such as age, size, location, vascular features, and most importantly, the risk of hemorrhage (04). In 2013, the first large-scale randomized clinical trial comparing medical and interventional management of unruptured brain arteriovenous malformations, the ARUBA trial, was published, showing that medical management alone remained superior to interventional therapy for the prevention of death or symptomatic stroke, even up to 5 years out (37). The purpose of this article is to discuss the clinical manifestations, pathophysiology, diagnosis, prognosis, and management of cerebral arteriovenous malformations.
• Cerebral arteriovenous malformations are congenital vascular malformations in the brain that result in direct connections between arteries and veins, without intervening capillary beds.
• They are an uncommon, but notable, cause of strokes and hemorrhages, especially in younger adults.
• Most cerebral arteriovenous malformations are asymptomatic and are discovered incidentally with neuroimaging.
• Cerebral arteriovenous malformations are reliably identified by CT and MR angiography, but conventional angiography remains the definitive diagnostic modality.
• Interventions for cerebral arteriovenous malformations include surgical resection, stereotactic radiation, and endovascular embolization.
Vascular malformations of the central nervous system (CNS) have been described in the literature dating back to the 19th century. With advances in imaging modalities and microsurgical techniques, the understanding of and treatment options for these lesions have since grown. Modern categorization and nomenclature of CNS vascular malformations was established by McCormick in 1966, using histopathologic features to classify each lesion as a venous angioma, cavernous malformation, capillary telangiectasia, or arteriovenous malformation. The Spetzler-Martin grading system (Table 1) for cerebral arteriovenous malformations takes into account major factors influencing the risk of surgical resection and hemorrhage (55). It is the most commonly used grading system, helping clinicians make treatment decisions and offering a standardized classification terminology. A supplementary scoring system was published in 2010 taking into account additional components: age at resection, hemorrhage before resection, and diffuseness of the arteriovenous malformations nidus. This supplementary grading scale (also known as the Lawton-Young Grading System) was found to be more accurate at predicting neurologic patient outcome than the Spetzler-Martin system alone and further clarified surgical risk stratification (39). It was further validated and found to hold true, even with higher proportion of high-grade arteriovenous malformations; however, perforators play important role on the outcome (23).
Number of points assigned
Size of arteriovenous malformation
Pattern of venous drainage
Score = sum of all categories, with lesions graded 1 to 5 based on total sum (eg, 1 point = grade 1).
• Most cerebral arteriovenous malformations are asymptomatic and discovered incidentally.
• Neurologic presentations of cerebral arteriovenous malformations vary, ranging from seizures to headaches to hemorrhage.
• The annual hemorrhage rate of cerebral arteriovenous malformations ranges from 1% to 3%.
Most cerebral arteriovenous malformations (cAVMs) are asymptomatic and are discovered as an incidental radiographic finding. They are usually diagnosed between the first and fourth decade of life, but have a bimodal peak: one in childhood and again at age 30 to 50 (20; Derdeyn et al 2017). If symptoms are present, they vary based on age, size, vascular features, and lesion morphology location (36). Symptoms include hemorrhage, seizures, headaches, or focal neurologic manifestations. The most dreaded complication and presentation of cerebral arteriovenous malformations is intracranial hemorrhage (36; Derdeyn et al 2017).
A large metaanalyses (n = 3923) summarizing the natural history of cerebral arteriovenous malformations reported an annual hemorrhage rate of 3% (21). Earlier studies reported the average annual mortality in patients with untreated cerebral arteriovenous malformations from 0.7% to 1% (45; 06). Another patient-level metaanalysis published in 2014 found an overall annual rate of intracranial hemorrhage of 2% (31).
Due to the variability of locations in cerebral arteriovenous malformation-related hemorrhage, clinical presentation can vary considerably. Cerebral arteriovenous malformations are generally located in the brain parenchyma, resulting in parenchymal hemorrhages. However, secondary subarachnoid, intraventricular, or subdural extension may occur. More superficially located arteriovenous malformations may exhibit a pattern of hemorrhage that masquerades as aneurysmal hemorrhage. Moreover, arteriovenous malformations that have deep draining systems can lead to primary intraventricular hemorrhage. Hemorrhages may be clinically silent and can be incidentally discovered on subsequent imaging.
Numerous risk factors affect the risk of hemorrhage. According to one of the largest systemic reviews, the annual rate of hemorrhage is 2.2% for unruptured arteriovenous malformations and 4.5% for ruptured arteriovenous malformations (21). Children were not at higher risk for subsequent hemorrhage after initial hemorrhage compared to adults (19). However, clinically silent hemorrhage visualized on neuroimaging is a risk factor for subsequent hemorrhage (22). Certain anatomical features, such the presence of an associated aneurysm, exclusively deep venous drainage and deep subcortical brain location, all confer increased risk of hemorrhage (30; 09; 57; 10; 22). Arteriovenous malformation size does not appear to influence the risk of hemorrhage but does influence the surgical risk associated with treatment. Pregnancy and puerperium are not risk factors for hemorrhage according to the current literature (27; 33), though conflicting data in a North American cohort demonstrate an increase in intraventricular hemorrhage up to 6% in pregnant women (49).
Brain arteriovenous malformations often present with seizures. Though the etiology is not entirely clear, mechanisms include increased venous back pressure related to outflow obstruction, periarteriovenous malformation nidus gliosis, and cortical irritation from prior hemorrhage (17; 20). The majority of seizures are simple partial or complex partial seizures; however, the rate of generalized tonic-clonic seizures ranges from 27% to 35% (46; 26). Superficially temporal or frontal lesion locations correlates with clinical seizure presentation (20). According to a prospective population-based study in Scotland (n = 229 patients) with arteriovenous malformations, the 5-year risk of first-ever seizure after presentation was higher when presenting with intracranial hemorrhage or focal neurologic deficit than for incidental arteriovenous malformations (23% vs. 8%). Moreover, 58% of these patients were at a higher risk of developing subsequent epilepsy (28).
Headaches are also commonly encountered as a presenting symptom of cerebral arteriovenous malformation. Estimates of the incidence of headaches in these patients have been difficult to obtain, but in one study, 0.2% of patients with headache and normal neurologic examinations were found to have incidental arteriovenous malformations (16; 36).
Focal neurologic deficits can be seen in patients with cerebral arteriovenous malformations; however, the incidence is unknown. Its significance depends on the lesion’s location. It has been hypothesized that a vascular steal syndrome may be related to focal deficits, as well as more obvious effects from hemorrhage or post ictal (36).
The prognosis of intracerebral hemorrhage due to arteriovenous malformations is more favorable than other etiologies (40). The rate of rebleeding is considered low, approximately 6% in the first year, and the risk of vasospasm in the acute setting is rare. Mortality associated with the initial bleed is low, ranging from 1.5% to 9%. One study with arteriovenous malformation-related intracerebral hemorrhage (34 out of 342 total intracerebral hemorrhage patients) reported that patients with ruptured arteriovenous malformations had higher odds of ambulatory independence at discharge (OR 4.4) compared to patients with other causes of intracerebral hemorrhage (40). However, given the yearly cumulative risk of hemorrhage with arteriovenous malformations, the long-term outlook tends to be less favorable. Recurrent hemorrhage is estimated to be around 1% in 4 to 7 years and 2% annually after the first year of hemorrhage. It is well known that with repeated hemorrhages, morbidity and mortality rise substantially (36).
Patients with intracerebral hemorrhage secondary to cerebral arteriovenous malformations rupture tend to be younger, with lower pre-stroke and admission blood pressures and higher admission Glasgow Coma Scale (GCS) scores. They are more likely to have lobar location of intracerebral hemorrhage compared to all patients with spontaneous intracerebral hemorrhage (38). The ruptured brain arteriovenous malformations prognostic (RAP) score was proposed to help to stratify the risk of poor long-term outcome after cerebral arteriovenous malformation rupture. The RAP score was a stronger predictor of a poor long-term outcome and inpatient mortality than the intracerebral hemorrhage score. For a RAP score 6 or higher, sensitivity and specificity for predicting poor outcome were 76.8% and 90.8%, respectively (53); however, more studies are needed for further validation of this score.
Other prognostic factors associated with development of intracerebral hemorrhage in patients with arteriovenous malformations include older age, exclusively deep venous drainage and location, and associated arterial vasculature. However, validated risk prediction models have not been produced (Derdeyn 2017). Patients presenting with progressively worsening neurologic deficits have the worst prognosis as these symptoms indicate a large arteriovenous malformation that is difficult to manage and treat.
A 32-year-old man with no significant past medical history presented with a bilaterally throbbing headache. He denied any focal neurologic deficits. However, he did note that in his early 20s, he would get the “jitters” when he felt a warm sensation in his lips and tongue that spread into his right hand. These occurred sporadically over the next several years, but then dissipated. His neurologic exam was normal. Noncontrasted brain MRI showed a large group of tortuous veins adjacent to the left sylvian fissure, without evidence of hemorrhage. The patient was informed and encouraged to maintain proper blood pressure and glycemic control.
A scheduled 1-year follow up MRI showed no progression or hemorrhage, and he was scheduled for another MRI in 1 year. However, after several months, he developed a severe, diffuse headache. In the emergency room, he was noted to be nauseous and agitated, but other than a right extensor plantar response, his neurologic exam was normal. Noncontrast head CT showed a small amount of subarachnoid blood in the right parietal region. CT with contrast elucidated the known arteriovenous malformation, but the draining veins now appeared larger and more tortuous. The patient was stabilized and underwent catheter-based embolization the following week, with no complications. He was discharged without any deficits and was scheduled for outpatient follow-up in 6 months, followed by annual visits.
Arteriovenous malformations were traditionally considered sporadic congenital vascular malformations of the nervous system; however, there are reports of de novo arteriovenous malformation formation. Although dysregulated vasculogenesis may result in congenital appearance, it is now possible that this may occur in childhood or even adulthood (11). Some rare cases of familial arteriovenous malformations have been reported in the literature, but it is unclear if they reflect a clear genetic connection or pure coincidence (59).
Some genetic syndromes are associated with arteriovenous malformations, with the most common being hereditary hemorrhagic telangiectasias, also known as Osler-Weber-Rendu syndrome. The presence of numerous cerebral arteriovenous malformations, otherwise uncommon, is highly predictive of hemorrhagic telangiectasias (05). Studies have supported the notion that some arteriovenous malformations may actually be acquired and not congenital. Studies have shown that malformations develop as a result of KRAS-induced activation of the MAPK-ERK signaling pathway in brain endothelial cells (42). Ongoing work involving next generation sequencing is currently aiming to detect a molecular basis and pathogenic mechanisms involving angiogenesis as an etiology for sporadic cases of arteriovenous malformations (52).
Arteriovenous malformations have unique hemodynamics with direct connections between arteries and veins, without intervening capillary beds. These connections contain the nidus; a tangle of abnormal dilated channels that are neither arterial nor venous. Arterial blood is shunted through the nidus with elevated flow in both ends and pressure on the venous end, predisponsing the vessel towards inflammation and thrombosis (Derdeyn et al 2017). The arterial supply or venous drainage may be composed of single or multiple vessels. Surrounding gliotic brain tissue is usually admixed with the vascular tangle, along with occasional micro or macrocalcifications (Derdeyn et al 2017).
In cerebral arteriovenous malformations, although draining veins are large and easily recognizable on imaging, the arteries feeding them can be small, sometimes referred to as “cryptic” (51). These feeding arteries have medial hypertrophy and endothelial thickening, narrowing their lumen, which can then become stenotic and even occluded (44). The arteries within the cerebral arteriovenous malformations are usually deficient in the muscularis layer. Arteries within the lesion can also be large, but lined with thin walls, due to poorly developed internal elastic lamina and media. Examination of adjacent and intralesional parenchyma reveals abnormal gliosis (35). Angiographic findings indicate that the arterial portions of arteriovenous malformations shunt blood directly toward the venous components. This rapid shunting of blood into large, dilated, draining veins increases blood flow, promoting the formation of aneurysms.
Arteriovenous malformations tend to grow slowly after initial formation. The feeding arteries and draining veins grow in caliber, recruiting adjacent vessels into its architecture. One theory as to why arteriovenous malformations grow is the inability of the abnormal vessel group to accommodate arterial pressure (35). Other important anatomic features associated with hemorrhagic presentation include the presence of drainage into the galenic system, venous outflow obstruction, and deep or infratentorial location (01).
Cerebral arteriovenous malformations can also cause small recurrent intracerebral hemorrhages. These bleeds cause loss of adjacent brain parenchyma as hematoma and necrotic tissue are reabsorbed. The space created by this process may allow room for an arteriovenous malformation to abut and grow. Pulsation of the arteriovenous malformation is also thought to slowly damage surrounding tissue (36).
• Cerebral arteriovenous malformations occur rarely, in about 0.1% of the population, but account for at least 1% to 2% of strokes, and up to 9% of all nontraumatic subarachnoid hemorrhages.
Brain arteriovenous malformations occur in about 0.1% of the population, or one tenth the incidence of intracranial aneurysms. Ninety percent of cerebral arteriovenous malformations are supratentorial with the rest located in the posterior fossa (36). Brain arteriovenous malformations account for 1% to 2% of all strokes, 3% of strokes in young adults, and 9% of all nontraumatic subarachnoid hemorrhages (02).
As cerebral arteriovenous malformations are thought to be due to sporadic genetic mutations, no information is available at this time for prevention. For family members of patients with hereditary hemorrhagic telangiectasias, screening is indicated, but otherwise, there is no role for routine screening of the general population (59).
Arteriovenous malformations fall under a larger group of vascular malformations, including venous angiomas, cavernous angiomas (cavernomas), complex intracranial aneurysms, and capillary telangiectasias.
Venous angiomas are composed of a group of anomalous veins, usually separated from normal brain parenchyma. These vessels do not fill during the arterial phase of cerebral angiography, differentiating them from arteriovenous malformations.
Cavernous angiomas are well-encapsulated masses of sinusoidal vessels separate from brain parenchyma. These lesions do not opacify during the arterial phase of cerebral angiography, differentiating them from arteriovenous malformations. Cavernous angiomas are usually sporadic, but some familial cases have also been reported (CCM1, CCM2, and CCM3 genetic loci) (15; Laberge-le et al 1999; 60).
Capillary telangiectasias are small lesions in which capillaries are separated from each other by normal brain parenchyma commonly located in the pons and brainstem. These lesions are multiple and quite small compared to arteriovenous malformations, and they do not fill on contrast angiography (08).
• Cerebral arteriovenous malformations are reliably identified by CT and MR angiography.
• Digital subtraction angiography remains the gold standard for diagnosis.
Arteriovenous malformations are typically diagnosed by neuroimaging and are most often incidental findings. Arteriovenous malformations are reliably identified by CT and MRI, including angiographic imaging (CTA and MRA). Digital subtraction angiography is currently used for a definitive diagnosis (Derdeyn et al 2017).
Noncontrast CT is limited in detecting arteriovenous malformations, but it can show certain characteristics supporting a diagnosis. Enlarged or calcified vessels along the margin of the hemorrhage or regions of increased density around the nidus, indicating an underlying vascular anomaly, can be seen (Delgado et al 2009). The overwhelming majority of patients with indeterminate results undergo CT angiography. Advances in adapting temporal coding into CT angiography techniques now permit better delineation of arterial, nidal, and venous components (Derdeyn et 2017).
Advances in MR and MR angiography technology now make it comparable to CT and CTA in terms of accuracy of detecting arteriovenous malformations in intracerebral hemorrhage. Both CT and MR imaging provide information about the arteriovenous malformation as well as adjacent brain tissue, which is essential in determining treatment plans (Derdeyn et 2017).
Adjunctive imaging studies, such as transcranial color duplex and regular doppler, have been studied extensively and can be helpful in analyzing the hemodynamic changes occurring pre- and postnidus, and can be used to assess for changes following treatment (07).
The gold standard for diagnosing arteriovenous malformations is digital subtraction angiography (DSA), which is often pursued after CT or MR angiography identifies a suspicious lesion. Digital subtraction angiography is additionally used to help with treatment planning and follow-up.
• The aim in arteriovenous malformation treatment is to completely eliminate the nidus and the shunt.
• The primary treatment modalities used are surgical excision, stereotactic radiosurgery, and endovascular embolization.
• Multimodality approaches are often used in a stage-wise process.
• The ARUBA trial (2013) compared conservative (nonsurgical) management to surgical intervention in unruptured aneurysms, and even in a 5-year follow up, it found better outcomes (prevention of stroke or death) with conservative management.
The goal of arteriovenous malformation treatment is completely eliminating the nidus and arteriovenous malformation shunt, along with reducing morbidity and mortality associated with the natural course of these lesions. Following diagnosis and evaluation of an arteriovenous malformation, 3 treatment modalities are currently accepted: microsurgery or macro-surgery, stereotactic radiosurgery, and endovascular embolization. Endovascular embolization can be performed before microsurgery and stereotactic radiosurgery to reduce bleeding risks and nidal volumes (Derdeyn et al 2017).
For ruptured arteriovenous malformations, intervention is indicated. Cerebral arteriovenous malformations with angiographic features suggesting an increased risk of recurrent hemorrhage, such as an associated aneurysm, are treated acutely, whereas other arteriovenous malformations are generally treated 4 to 6 weeks after the hemorrhage, as absorption of the hematoma and resolution of any surrounding edema improve access to the arteriovenous malformation for future intervention (04).
Surgical excision. Open surgical excision has a well-established history of use in the treatment of arteriovenous malformations and offers the best chance for immediate cure (04). However, the surgery is often complicated and requires complex planning with angiographic review of the microarchitecture. Surgical risks associated with surgery include intraoperative hemorrhage and damage to adjacent cerebral and vascular structures. Successful surgery completely removes the rupture-prone malformed vessels and obliterates feeding and draining vessels. This modality results in immediate elimination of hemorrhage risk and complete eradication of the nidus. The introduction of surgical adjuncts, such as functional MRI and diffusion tensor imaging-based tractography, as well as stereotactic neuro-navigational systems, allows for more accurate intervention and minimization of postoperative morbidity risk (Derdeyn et al 2017).
As discussed, the Spetzler-Martin scale is commonly used to establish surgical intervention risk. Arteriovenous malformations of larger size, deep venous drainage patterns, and near eloquent cortex have higher surgical risks and may require adjunctive presurgical interventions. An analysis of surgical outcomes based on the Spetzler-Martin scale showed permanent neurologic deficits at rates of 0% for grades I to III, 21.9% for grade IV, and 16.7% for grade V (24). Smaller arteriovenous malformations, not in a deep location, and have a single feeding artery and drainage into a cortical vein can be well managed with surgical resection alone. For grade IV to V lesions, treatment is more selective, and surgery alone is not recommended due to the significantly higher risk of resection (43).
Stereotactic radiosurgery. Stereotactic radiosurgery is another treatment modality for arteriovenous malformations. It is particularly helpful for small lesions (less than 3 cm max diameter with volume less than 12 cm3), lesions near eloquent cortex that could be damaged by surgery, or lesions deemed too risky due to anatomical or medical reasons (14). Targeted radiation is delivered over a period of years. Patients who undergo successful radiosurgery are protected from future hemorrhage once complete obliteration is achieved. Therefore, patients still undergoing radiotherapy, called the latency period, are still at risk of hemorrhage until the treatment is complete (Pollock et al 2003). Recommended radiation fraction doses and delivery schedules vary in the literature, as do the reported rates of success with stereotactic radiosurgery. Radiation doses and arteriovenous malformation volumes can predict obliteration rates (29). Radiosurgery alone is efficacious in obliterating smaller arteriovenous malformations, whereas larger lesions require additional therapies. Neurologic function after stereotactic radiosurgery appears preserved or improved in the vast majority of patients with arteriovenous malformations (58). However, there are risks associated with this treatment modality, including new deficits, seizures, cranial nerve palsies, headaches, cyst formation, and radiation-induced necrosis, which can occur in to 8% to 12% of patients (34; 18; 54). Some factors that may contribute to complications from stereotactic surgery include lesion location, target volume, and radiation dose to surrounding normal tissue (Derdeyn 2017).
Endovascular embolization. Endovascular treatment modalities utilize microcatheters to deliver microparticles or embolizing agents to obliterate feeding vessels in the target lesion (50). Despite the initial optimism with the use of this modality, embolization alone rarely results in lesion eradication and is often used in conjunction with other treatment approaches to reduce the nidus size or intraoperative risk of hemorrhage and rupture (56). Smaller cerebral arteriovenous malformations can be completely obliterated with embolization alone if less than 1 cm in diameter and has a single feeding vessel. Palliative endovascular treatment may also be used to reduce vascular steal symptoms. Morbidity and mortality rates for attempted surgical resection alone of grade V arteriovenous malformations approaches 50%, but this risk is significantly reduced with staged presurgical embolization (50). An embolized arteriovenous malformation may also have a similar or improved ease of resection if at least 50% size reduction is achieved (24). The use of EVOH (ethylene vinyl alcohol copolymer; Onyx) as an embolic agent has increased total obliteration rates to as high as 51% among all arteriovenous malformations and up to 96% for lesions with simple angiographic features. Endovascular surgery itself carries risks and should be used when it can significantly reduce the overall risk. Possible complications include new neurologic deficits, intraoperative and postembolization hemorrhage, and subsequent ischemic stroke (Derdeyn et al 2017).
Multimodality treatment strategies are often utilized for large or complex lesions. Combining different techniques reduces the risk of subsequent interventions, lowering overall treatment risk. Using the Spetzler-Martin grading scale as a guide, endovascular embolization can be followed by surgery, or it can be followed by stereotactic radiosurgery. The intention of multimodality intervention is complete lesion obliteration as partial obliteration increases hemorrhage risk (41). Several institutions have reported applying this model with radiographic obliteration rates of 38% to 83% and permanent neurologic morbidity rates of 4% to 14% (Derdeyn 2017). When undergoing multiple treatments, the risk of complications from each individual procedure should still be considered, as higher rates of new neurologic deficit in staged endovascular and surgical therapy was found compared to surgery alone (25). The benefit of staged embolization before surgery for large arteriovenous malformations has been established (56; 47), but not all combination therapies are beneficial. Andrade-Souza and colleagues showed significantly decreased obliteration rate with embolization before radiosurgery compared to radiosurgery alone (03).
Conservative medical management (observation). To date, the ARUBA trial (A Randomized trial of Unruptured Brain Arteriovenous malformations) is the only randomized clinical trial that compared medical (conservative) versus surgical (interventional surgery, microsurgery, or endovascular) treatment in unruptured cerebral arteriovenous malformations (38). Patients with unruptured cerebral arteriovenous malformations were assigned to medical versus interventional treatment, including surgery, radiotherapy, or endovascular therapy. In 2013, after collecting outcome data on 223 patients followed for a mean of 33 months, randomization was halted early. Composite rates of symptomatic stroke (ischemic and hemorrhagic) and death were higher in the interventional compared to medical treatment group (31% vs. 10%). Rates of neurologic disability were also lower in conservatively treated patients. Deaths occurred in 2% of patients in both groups. The trial was planned to continue for another 5 years, but with initial results halting randomization, all patients will continue to be followed without further intervention in an observational phase that is still underway. Criticism surrounding the study includes the variable nonstandardized approaches used in the interventional treatment arm, a small sample size, and a relatively short follow-up period. This was remedied with a 5-year follow up study finally done, which found that after a mean follow-up of 50 months, medical management still remained superior to medical management with interventional therapy for the prevention of death or symptomatic stroke in patients with an unruptured cerebral arteriovenous malformation (37).
Literature discussing the association between cerebral arteriovenous malformations and pregnancy is sparse. Previously, it has been speculated that fluctuating hormone levels in pregnancy may play a role in arteriovenous malformation-related intracranial hemorrhage during and after pregnancy. However, in one study (n = 774) of female patients 18 to 40 years of age with cerebral arteriovenous malformations with or without ICH, with 452 pregnancies reported, the investigators found no increased risk (OR, 0.71) of hemorrhage in pregnancy or puerperium (33). Another retrospective analysis of 451 women with cerebral arteriovenous malformations found that the hemorrhage rates in pregnant women was no different than their nonpregnant counterpart (27), though conflicting data in a North American cohort demonstrate an increase in intracerebral hemorrhage up to 6% in pregnant women (49).
Steven R Levine MD
Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.See Profile
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