GENERAL INFORMATION

• It is an expectation that all patients receive care/services from a licensed clinician. All appropriate supporting documentation, including recent pertinent office visit notes, laboratory data, and results of any special testing must be provided. If applicable: All prior relevant imaging results and the reason that alternative imaging cannot be performed must be included in the documentation submitted. 
• Where a specific clinical indication is not directly addressed in this guideline, medical necessity determination will be made based on widely accepted standard of care criteria. These criteria are supported by evidence-based or peer-reviewed sources such as medical literature, societal guidelines and state/national recommendations.

INDICATIONS FOR BRAIN (HEAD) MR Angiography/MR Venography
Brain MRI/MRA are not approvable simultaneously unless they meet the criteria described below in the Indications for Brain MRI/Brain MRA combination studies section. If there is a combination request* for an overlapping body part, either requested at the same time or sequentially (within the past 3 months) the results of the prior study should be:

• Inconclusive or show a need for additional or follow up imaging evaluation OR 
• The office notes should clearly document an indication why overlapping imaging is needed and how it will change management for the patient.

(*Unless approvable in the combination section as noted in the guidelines)

For evaluation of suspected intracranial vascular disease^{1, 2}

• Aneurysm screening
  • Screening for intracranial aneurysm if two or more first-degree family members (parent brother, sister, or child) with history of intracranial aneurysm
    • Repeat study is recommended every 5 years³
  • For one first degree relative with aneurysm, asymptomatic screening is not indicated -would require a neurological sign or symptom supporting clinical concern for aneurysm.^4-6
  • Screening for aneurysm in polycystic kidney disease (in adults), Loeys-Dietz syndrome*, fibromuscular dysplasia, spontaneous coronary arteries dissection (SCAD), or known aortic coarctation (after age 10)^7-15

*For Loeys-Dietz imaging should be repeated at least every two years

• Vascular abnormalities 
  • Suspected vascular malformation (arteriovenous malformation (AVM) or dural arteriovenous fistula) in patient with previous or indeterminate imaging study
  • Thunderclap headache with continued concern for underlying vascular abnormality (i.e. aneurysm or reversible cerebral vasoconstriction syndrome) after initial negative brain imaging ¹⁶

Note: Negative brain CT < 6 hours after headache onset excludes subarachnoid hemorrhage in neurologically intact patients. MRI lacks sensitivity in excluding subarachnoid hemorrhage less than 24 hours after headache onset.^17,18

• Headache associated with exercise, exertion, Valsalva, or sexual activity¹⁸
• Isolated third nerve palsy (oculomotor) with pupil involvement to evaluate for aneurysm¹⁹
• Pulsatile tinnitus to identify a suspected arterial vascular etiology^20,21

Note: MRI is the study of choice for detecting cavernomas, developmental venous anomalies and capillary telangiectasia (see background)²²

• Cerebrovascular Disease
  • Ischemic
    • Recent ischemic stroke or transient ischemic attack (See background)^23,24

Note: For remote strokes with no prior vascular imaging, imaging can be considered based on location/type of stroke and documented potential to change management 

• Known or suspected vertebrobasilar insufficiency (VBI) in patients with symptoms such as dizziness, vertigo, headaches, diplopia, blindness, vomiting, ataxia, weakness in both sides of the body, or abnormal speech^{19, 25-27}

• Hemorrhagic
  • Known subarachnoid hemorrhage (SAH) – CTA is favored over MRA 
  • Known cerebral intraparenchymal hemorrhage with concern for underlying vascular abnormality
• Venous-MRV^†
  • Suspected central venous thrombosis (dural sinus thrombosis)^{28, 29}
  • Distinguishing benign intracranial hypertension (pseudotumor cerebri) from dural sinus thrombosis^{30, 31}
• Sickle cells disease (ischemic and/or hemorrhagic)^{32, 33}
  • Neurological signs or symptoms in sickle cell patients 
  • High stroke risk in sickle cell patients (2 – 16 years of age) with a transcranial doppler velocity > 200
• Vasculitis with initial laboratory workup (such as ESR, CRP, serology)³⁴
  • Suspected secondary CNS vasculitis based on neurological sign or symptoms in the setting of an underlying systemic disease with abnormal inflammatory markers or autoimmune antibodies
  • Suspected primary CNS vasculitis based on neurological signs and symptoms with completed infectious/inflammatory lab work-up^{35, 36}
  • Giant cell arteritis with suspected intracranial involvement^37-40
• Other intracranial vascular disease
  • Suspected Moyomoya disease^{41, 42}
  • Suspected reversible cerebral vasoconstriction syndrome⁴³

For evaluation of known intracranial vascular disease^{1, 2}

• Known intracranial aneurysm, treated aneurysm, or known vascular malformation (i.e., AVM or dural arteriovenous fistula)
• Known vertebrobasilar insufficiency with new or worsening signs or symptoms^{25, 27}
• Known vasculitis, reversible cerebral vasoconstriction syndrome or Moyomoya disease^{35, 41-44}

Pre-operative/procedural evaluation for brain/skull surgery

• Pre-operative evaluation for a planned surgery or procedure
• Refractory trigeminal neuralgia when done for surgical planning⁴⁵

Post-operative/procedural evaluation^{46, 47}

• A follow-up study may be needed to help evaluate a patient’s progress after treatment, procedure, intervention, or surgery. Documentation requires a medical reason that clearly indicates why additional imaging is needed for the type and area(s) requested 

Further evaluation of indeterminate or questionable findings on prior imaging: 

• For initial evaluation of an inconclusive finding on a prior imaging report that requires further clarification. 
• One follow-up exam of a prior indeterminate MR/CT finding to ensure no suspicious interval change has occurred. (No further surveillance unless specified as highly suspicious or change was found on last follow-up exam)

Indications for Brain MRA/Neck MRA combination studies^{1, 2}

• Recent ischemic stroke or transient ischemic attack (TIA)24 (also in combo section) 
• Note: For remote strokes with no prior vascular imaging, imaging can be considered based on location/type of stroke and documented potential to change management 
• Known or suspected vertebrobasilar insufficiency (VBI) in patients with symptoms such as dizziness, vertigo, headaches, diplopia, blindness, vomiting, ataxia, weakness in both sides of the body, or abnormal speech^25-27
• Suspected carotid or vertebral artery dissection; secondary to trauma or spontaneous due to weakness of vessel wall^{48, 49}
• Follow-up of known carotid or vertebral artery dissection within 3-6 months for evaluation of recanalization and/or to guide anticoagulation treatment^50-52
• Asymptomatic patients with an abnormal ultrasound of the neck or carotid duplex imaging (e.g., carotid stenosis ≥ 70%, technically limited study, aberrant direction of flow in the carotid or vertebral arteries) and patient is surgery or angioplasty candidate^53-55
• Symptomatic patients with an abnormal ultrasound of the neck or carotid duplex imaging (e.g., carotid stenosis ≥ 50%, technically limited study, aberrant direction of flow in the carotid or vertebral arteries) and patient is surgery or angioplasty candidate^{53, 56}
• Pulsatile tinnitus to identify a suspected arterial vascular etiology^{20, 21}

Indications for Brain MRI/Brain MRA combination studies^{1, 2}

• Recent ischemic stroke or transient ischemic attack (TIA)
• Thunderclap headache with continued concern for underlying vascular abnormality (i.e., aneurysm or reversible cerebral vasoconstriction syndrome) after initial negative brain imaging¹⁶

Note: Negative brain CT < 6 hours after headache onset excludes subarachnoid hemorrhage in neurologically intact patients. MRI lacks sensitivity in excluding subarachnoid hemorrhage less than 24 hours after headache onset.^{17, 18}

• Acute, sudden onset of headache with personal history of a vascular abnormality or first-degree family history of aneurysm
• Headache associated with exercise, exertion, Valsalva or sexual activity¹⁸
• Suspected venous thrombosis (dural sinus thrombosis) — MRI/MRV^†
• Neurological signs or symptoms in sickle cell patients 
• High stroke risk in sickle cell patients (2 – 16 years of age) with a transcranial doppler velocity > 200

Indications for Brain MRI/Brain MRA/Neck MRA combination studies

• Recent ischemic stroke or transient ischemic attack (TIA)^{1, 2, 57}
• Approved indications as noted above and being performed in a child under 8 years of age who will need anesthesia for the procedure and there is a suspicion of concurrent intracranial pathology⁵⁸

Any Combination of Brain MRA/Neck MRA/Brain MRI with IAC

• Pulsatile tinnitus with concern for a suspected arterial vascular and/or intracranial etiology^{20, 57}

*Note: CTA and MRA are generally comparable noninvasive imaging alternatives each with their own advantages and disadvantages. Brain MRI can be combined with Brain CTA/Neck CTA.

Rationale
Magnetic resonance angiography (MRA) or magnetic resonance venography (MRV) can be used as a first-line investigation of intracranial vascular disease. It is an alternative to invasive intra-catheter angiography that was once the mainstay for the investigation of intracranial vascular disease. MRA/MRV may use a contrast agent, gadolinium, which is non-iodine-based, for better visualization. It can be used in patients who have history of contrast allergy and who are at high risk of kidney failure. A single authorization covers both MRA and MRV.

The three different techniques of MRA/MRV include time of flight (both 2D and 3D TOF), phase contrast (PC), and contrast-enhanced angiography. Time of flight MRA takes advantage of the phenomena of flow-related enhancement and is the preferred MRA technique due to the speed at which the exam can be acquired. 

MRA and Cerebral Aneurysms — Studies that compared MRA with catheter angiography in detecting aneurysms found that MRA could find 77% – 94% of the aneurysms previously diagnosed by catheter angiography that were larger than 5 mm. For aneurysms smaller than 5 mm, MRI detected only 10% – 60% of those detected with catheter angiography. On the other hand, aneurysms that were missed by catheter angiography in patients with acute subarachnoid hemorrhage were detected with MRA due to 
the much larger number of projections available with MRA.⁵⁹ The decrease in specificity, when compared with CTA, is reported to have false-positive cases related to normal vascular variants of infundibular origin of vessels and vessel loops. Limitations of MRA head include required safety screening and relatively long acquisition time in urgent clinical scenario.

MRA and PCKD^{13-15, 60}
Screening imaging every 5 years, and annual follow-up imaging in patients in with a known intracranial aneurysm is recommended. The current literature recommends initial screening by the age of 30 yearsand earlier if there is a strong family history of intracranial aneurysm. Screening is generally not recommended is the pediatric population (less than 18 years). No upper age limit for screening patients with ADPKD has been recommended.

MRA and Cerebral Arteriovenous Malformations (AVM) — Brain arteriovenous malformation (AVM) may cause intracranial hemorrhage and is usually treated by surgery. 3D TOF-MRA is commonly used during the planning of radiosurgery to delineate the AVM nidus, but it is not highly specific for the detection of a small residual AVM after radiosurgery. There is no evidence to support screening of first-degree relatives for AVMs⁶¹. The risk of having an AVM may be higher than in the general population, but absolute risk is low.

MRA and non-aneurysmal vascular malformations — Non-aneurysmal vascular malformations can be divided in low flow vascular malformations and high flow vascular malformations. Low flow vascular malformations include dural venous anomalies (DVA), cavernomas, and capillary telangiectasias. High flow vascular malformations include AVM and dural arteriovenous fistulas (dAVF). For low flow malformations, MRI is the study of choice. There is limited medical literature to support vascular imagining (CTA or MRA). CTA plays a limited role in the assessment of cavernoma but may be used to demonstrate a DVA. MRA is not usually helpful in the assessment of cavernoma, capillary 
telangiectasia, and DVA. Vascular imaging is indicated in high flow vascular malformations.^{1, 2, 22}

MRA vs CTA for CVA — Preferred vascular imaging of the head and neck includes non-contrast head MRA and contrast-enhanced neck MRA. MRA may not be able to be performed in patients with claustrophobia, morbid obesity, or implanted device, but it can be useful in patients with renal failure or contrast allergies. For acute stroke, CTA is preferred after CT (to rule out hemorrhage) and to look for thrombus/possible intervention that is time sensitive.⁶²

MRA and recent stroke or transient ischemic attack — A stroke or central nervous system infarction is defined as “brain, spinal cord, or retinal cell death attributable to ischemia, based on neuropathological, neuroimaging, and/or clinical evidence of permanent injury. … Ischemic stroke specifically refers to central nervous system infarction accompanied by overt symptoms, whereas silent infarction causes no known symptoms.”⁶³ If imaging or pathology is not available, a clinical stroke is diagnosed by symptoms persisting for more than 24 hours. Ischemic stroke can be further classified by the type and location of ischemia and the presumed etiology of the brain injury. These include large-artery atherosclerotic occlusion (extracranial or intracranial), cardiac embolism, small-vessel disease and less commonly dissection, hypercoagulable states, sickle cell disease and undetermined causes.⁶⁴ TIAs in contrast, “are a brief episode of neurological dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction on imaging.” ⁶⁵ On average, the annual risk of future ischemic stroke after a TIA or initial ischemic stroke is 3 – 4%, with an incidence as high as 11% over the next 7 days and 24–29% over the following 5 years. This has significantly decreased in the last half century due to advances in secondary prevention.⁶⁶

Therefore, when revascularization therapy is not indicated or available in patients with an ischemic stroke or TIA, the focus of the work-up is on secondary prevention. This includes noninvasive vascular imaging to identify the underlying etiology, assess immediate complications and risk of future stroke. The majority of stroke evaluations take place in the inpatient setting. Admitting TIA patients is reasonable if they present within 72 hours and have an ABCD(2) score ≥ 3, indicating high risk of early recurrence, or the evaluation cannot be rapidly completed on an outpatient basis (Easton, 2009). Minimally, both stroke and TIA should have an evaluation for high-risk modifiable factors, such as carotid stenosis atrial fibrillation, as the cause of ischemic symptoms.⁶⁴ Diagnostic recommendations include neuroimaging evaluation as soon as possible, preferably with magnetic resonance imaging, including DWI; noninvasive imaging of the extracranial vessels should be performed, and noninvasive imaging of intracranial vessels is reasonable.²³

Patients with a history of stroke and recent workup with new signs or symptoms indicating progression or complications of the initial CVA should have repeat brain imaging as an initial study. Patients with remote or silent strokes discovered on imaging should be evaluated for high-risk modifiable risk factors based on the location and type of the presumed etiology of the brain injury.

MRA and Intracerebral Hemorrhage — MRA is useful as a screening tool for an underlying vascular abnormality⁶⁷ in the evaluation of spontaneous intracerebral hemorrhage (ICH). Etiologies of spontaneous ICH include tumor, vascular malformation, aneurysm, hypertensive arteriopathy, cerebral amyloid angiopathy, venous thrombosis, vasculitis, RCVS, drug-induced vasospasm, venous sinus thrombosis, Moyomoya disease, anticoagulant use and hemorrhagic transformation of an ischemic infarct. History can help point to a specific etiology. Possible risk factors for the presence of underlying vascular abnormalities include age younger than 65, female, lobar or intraventricular location, and the absence of hypertension or impaired coagulation.

MRV — A pitfall of the TOF technique, particularly 3D TOF, is that in areas of slowly flowing blood, turbulence, or blood which flows in the imaging plane there can be regions of absent or diminished signal. The signal loss can be confused with vascular occlusion or thrombi. To avoid this pitfall, MRA performed after the intravenous administration of gadolinium-based contrast agents is utilized at many facilities. 

Intracranial magnetic resonance venography (MRV) is used primarily to evaluate the patency of the venous sinuses. The study can be performed with TOF, Phase contrast and IV contrast-enhanced techniques. Delayed images to allow for enhancement of the venous system are required to obtain images when intravenous gadolinium-enhanced studies are undertaken.

Saturation pulses are utilized in studies not undertaken with intravenous contrast to help eliminate flow-related signal in a specified direction and thus display the desired arterial or venous structures on their own. In cranial applications, saturation pulses applied at the inferior margin of the imaging field eliminate signal from arterial flow in order to visualize the veins. Conversely, superior saturation pulses are used to eliminate venous flow-related enhancement when evaluation of the arterial structures is desired.⁶⁸

†MRV and Central Venous Thrombosis — a MR Venogram is indicated for the evaluation of a central venous thrombosis/dural sinus thrombosis. The most frequent presentations are isolated headache, intracranial hypertension syndrome (headache, nausea/vomiting, transient visual obscurations, pulsatile tinnitus, CN VI palsy, papilledema),⁶⁹ seizures, focal neurological deficits, and encephalopathy. Risk factors are hypercoagulable states inducing genetic prothrombotic conditions, antiphospholipid syndrome and other acquired prothrombotic diseases (such as cancer), oral contraceptives, pregnancy, puerperium (6 weeks postpartum), infections, and trauma. COVID-19 infection is associated with hypercoagulability, a thromboinflammatory response, and an increased incidence of venous thromboembolic events (VTE).^{70, 71} Since venous thrombosis can cause SAH, infarctions, and hemorrhage, parenchymal imaging with MRI/CT is also appropriate.^72-74

Combination MRI/MRA of the Brain — This is one of the most misused combination studies and other than what is indicated above these examinations should be ordered in sequence, not together. Vascular abnormalities can be visualized on the brain MRI. 

Patients presenting with a new migraine with aura (especially an atypical or complex aura) can mimic a transient ischemic attack or an acute stroke. If there is a new neurologic deficit, imaging should be guided by concern for cerebrovascular disease, not that the patient has a headache.¹⁶

MRA and dissection — Craniocervical dissections can be spontaneous or traumatic. Patients with blunt head or neck trauma who meet Denver Screening criteria should be assessed for cerebrovascular injury (although about 20% will not meet criteria). The criteria include focal or lateralizing neurological deficits (not explained by head CT); infarct on head CT; face, basilar skull, or cervical spine fractures;cervical hematomas that are not expanding; Glasgow coma score less than 8 without CT findings; massive epistaxis; cervical bruit or thrill.^{48, 75-77} Spontaneous dissection presents with headache, neck pain with neurological signs or symptoms. There is often minor trauma or precipitating factor (i.e., exercise, neck manipulation). Dissection is thought to occur due to weakness of the vessel wall, and there may be an underlying connective tissue disorder. Dissection of the extracranial vessels can extend intracranially and/or lead to thrombus which can migrate into the intracranial circulation, causing ischemia. Therefore, MRA of the head and neck is warranted.^{49, 78}

References   

1. Robertson RL, Palasis S, Rivkin MJ, et al. ACR Appropriateness Criteria® Cerebrovascular Disease-Child. J Am Coll Radiol. May 2020;17(5s):S36-s54. doi:10.1016/j.jacr.2020.01.036
2. Salmela MB, Mortazavi S, Jagadeesan BD, et al. ACR Appropriateness Criteria(®) Cerebrovascular Disease. J Am Coll Radiol. May 2017;14(5s):S34-s61. doi:10.1016/j.jacr.2017.01.051
3. Chalouhi N, Chitale R, Jabbour P, et al. The case for family screening for intracranial aneurysms. Neurosurg Focus. Dec 2011;31(6):E8. doi:10.3171/2011.9.Focus11210
4. Rinkel GJ, Ruigrok YM. Preventive screening for intracranial aneurysms. Int J Stroke. Jan 2022;17(1):30-36. doi:10.1177/17474930211024584
5. Risks and benefits of screening for intracranial aneurysms in first-degree relatives of patients with sporadic subarachnoid hemorrhage. N Engl J Med. Oct 28 1999;341(18):1344-50. doi:10.1056/nejm199910283411803
6. Brown RD, Jr., Huston J, Hornung R, et al. Screening for brain aneurysm in the Familial Intracranial Aneurysm study: frequency and predictors of lesion detection. J Neurosurg. Jun 2008;108(6):1132-8. doi:10.3171/jns/2008/108/6/1132
7. Hayes SN, Kim ESH, Saw J, et al. Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association. Circulation. May 8 2018;137(19):e523-e557. doi:10.1161/cir.0000000000000564
8. Hitchcock E, Gibson WT. A Review of the Genetics of Intracranial Berry Aneurysms and Implications for Genetic Counseling. J Genet Couns. Feb 2017;26(1):21-31. doi:10.1007/s10897-016-0029-8
9. Jung WS, Kim JH, Ahn SJ, et al. Prevalence of Intracranial Aneurysms in Patients with Aortic Dissection. AJNR Am J Neuroradiol. Nov 2017;38(11):2089-2093. doi:10.3174/ajnr.A5359
10. Egbe AC, Padang R, Brown RD, et al. Prevalence and predictors of intracranial aneurysms in patients with bicuspid aortic valve. Heart. Oct 2017;103(19):1508-1514. doi:10.1136/heartjnl-2016-311076
11. Rouchaud A, Brandt MD, Rydberg AM, et al. Prevalence of Intracranial Aneurysms in Patients with Aortic Aneurysms. AJNR Am J Neuroradiol. Sep 2016;37(9):1664-8. doi:10.3174/ajnr.A4827
12. Pickard SS, Prakash A, Newburger JW, Malek AM, Wong JB. Screening for Intracranial Aneurysms in Coarctation of the Aorta: A Decision and Cost-Effectiveness Analysis. Circ Cardiovasc Qual Outcomes. Aug 2020;13(8):e006406. doi:10.1161/circoutcomes.119.006406
13. Xu HW, Yu SQ, Mei CL, Li MH. Screening for intracranial aneurysm in 355 patients with autosomal-dominant polycystic kidney disease. Stroke. Jan 2011;42(1):204-6. doi:10.1161/strokeaha.110.578740
14. Malhotra A, Wu X, Matouk CC, Forman HP, Gandhi D, Sanelli P. MR Angiography Screening and Surveillance for Intracranial Aneurysms in Autosomal Dominant Polycystic Kidney Disease: A Cost-effectiveness Analysis. Radiology. May 2019;291(2):400-408. doi:10.1148/radiol.2019181399
15. Flahault A, Joly D. Screening for Intracranial Aneurysms in Patients with Autosomal Dominant Polycystic Kidney Disease. Clin J Am Soc Nephrol. Aug 7 2019;14(8):1242-1244. doi:10.2215/cjn.02100219
16. Whitehead MT, Cardenas AM, Corey AS, et al. ACR Appropriateness Criteria® Headache. J Am Coll Radiol. Nov 2019;16(11s):S364-s377. doi:10.1016/j.jacr.2019.05.030
17. Marcolini E, Hine J. Approach to the Diagnosis and Management of Subarachnoid Hemorrhage. West J Emerg Med. Mar 2019;20(2):203-211. doi:10.5811/westjem.2019.1.37352
18. Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition. Cephalalgia. Jan 2018;38(1):1-211. doi:10.1177/0333102417738202
19. Pula JH, Kwan K, Yuen CA, Kattah JC. Update on the evaluation of transient vision loss. Clin Ophthalmol. 2016;10:297-303. doi:10.2147/opth.S94971
20. Pegge SAH, Steens SCA, Kunst HPM, Meijer FJA. Pulsatile Tinnitus: Differential Diagnosis and Radiological Work-Up. Curr Radiol Rep. 2017;5(1):5. doi:10.1007/s40134-017-0199-7
21. Hofmann E, Behr R, Neumann-Haefelin T, Schwager K. Pulsatile tinnitus: imaging and differential diagnosis. Dtsch Arztebl Int. Jun 2013;110(26):451-8. doi:10.3238/arztebl.2013.0451
22. Lee M, Kim MS. Image findings in brain developmental venous anomalies. J Cerebrovasc Endovasc Neurosurg. Mar 2012;14(1):37-43. doi:10.7461/jcen.2012.14.1.37
23. Wintermark M, Sanelli PC, Albers GW, et al. Imaging recommendations for acute stroke and transient ischemic attack patients: A joint statement by the American Society of Neuroradiology, the American College of Radiology, and the Society of NeuroInterventional Surgery. AJNR Am J Neuroradiol. Nov-Dec 2013;34(11):E117-27. doi:10.3174/ajnr.A3690
24. Sanelli PC, Sykes JB, Ford AL, Lee JM, Vo KD, Hallam DK. Imaging and treatment of patients with acute stroke: an evidence-based review. AJNR Am J Neuroradiol. Jun 2014;35(6):1045-51. doi:10.3174/ajnr.A3518
25. Lima Neto AC, Bittar R, Gattas GS, et al. Pathophysiology and Diagnosis of Vertebrobasilar Insufficiency: A Review of the Literature. Int Arch Otorhinolaryngol. Jul 2017;21(3):302-307. doi:10.1055/s-0036-1593448
26. Pirau L, Lui F. Vertebrobasilar Insufficiency. StatPearls Publishing Updated July 18, 2022. Accessed January 29, 2023. https://www.ncbi.nlm.nih.gov/books/NBK482259/
27. Searls DE, Pazdera L, Korbel E, Vysata O, Caplan LR. Symptoms and signs of posterior circulation ischemia in the new England medical center posterior circulation registry. Arch Neurol. Mar 2012;69(3):346-51. doi:10.1001/archneurol.2011.2083
28. Ferro JM, Bousser MG, Canhão P, et al. European Stroke Organization guideline for the diagnosis and treatment of cerebral venous thrombosis - Endorsed by the European Academy of Neurology. Eur Stroke J. Sep 2017;2(3):195-221. doi:10.1177/2396987317719364
29. Saposnik G, Barinagarrementeria F, Brown RD, Jr., et al. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. Apr 2011;42(4):1158-92. doi:10.1161/STR.0b013e31820a8364
30. Agarwal P, Kumar M, Arora V. Clinical profile of cerebral venous sinus thrombosis and the role of imaging in its diagnosis in patients with presumed idiopathic intracranial hypertension. Indian J Ophthalmol. Mar-Apr 2010;58(2):153-5. doi:10.4103/0301-4738.60092
31. Aldossary NM. Value of double - track sign in differentiating primary from thrombosed transverse sinus stenosis in patients presumed to have idiopathic intracranial hypertension. eNeurologicalSci. Mar 2018;10:22-25. doi:10.1016/j.ensci.2018.01.006
32. Thust SC, Burke C, Siddiqui A. Neuroimaging findings in sickle cell disease. Br J Radiol. Aug 2014;87(1040):20130699. doi:10.1259/bjr.20130699
33. Abboud MR, Cure J, Granger S, et al. Magnetic resonance angiography in children with sickle cell disease and abnormal transcranial Doppler ultrasonography findings enrolled in the STOP study. Blood. Apr 1 2004;103(7):2822-6. doi:10.1182/blood-2003-06-1972
34. Berlit P, Kraemer M. Cerebral vasculitis in adults: what are the steps in order to establish the diagnosis? Red flags and pitfalls. Clin Exp Immunol. Mar 2014;175(3):419-24. doi:10.1111/cei.12221
35. Godasi R, Pang G, Chauhan S, Bollu PC. Primary Central Nervous System Vasculitis. StatPearls Publishing. Updated October 12, 2022. Accessed January 23, 2023. https://www.ncbi.nlm.nih.gov/books/NBK482476/
36. Zuccoli G, Pipitone N, Haldipur A, Brown RD, Jr., Hunder G, Salvarani C. Imaging findings in primary central nervous system vasculitis. Clin Exp Rheumatol. Jan-Feb 2011;29(1 Suppl 64):S104-9. 
37. Abdel Razek AA, Alvarez H, Bagg S, Refaat S, Castillo M. Imaging spectrum of CNS vasculitis. Radiographics. Jul-Aug 2014;34(4):873-94. doi:10.1148/rg.344135028
38. Halbach C, McClelland CM, Chen J, Li S, Lee MS. Use of Noninvasive Imaging in Giant Cell Arteritis. Asia Pac J Ophthalmol (Phila). Jul-Aug 2018;7(4):260-264. doi:10.22608/apo.2018133
39. Khan A, Dasgupta B. Imaging in Giant Cell Arteritis. Curr Rheumatol Rep. Aug 2015;17(8):52. doi:10.1007/s11926-015-0527-y
40. Koster MJ, Matteson EL, Warrington KJ. Large-vessel giant cell arteritis: diagnosis, monitoring and management. Rheumatology (Oxford). Feb 1 2018;57(suppl_2):ii32-ii42. doi:10.1093/rheumatology/kex424
41. Ancelet C, Boulouis G, Blauwblomme T, et al. [Imaging Moya-Moya disease]. Rev Neurol (Paris). Jan 2015;171(1):45-57. Imagerie du Moya-Moya. doi:10.1016/j.neurol.2014.11.004
42. Tarasów E, Kułakowska A, Lukasiewicz A, et al. Moyamoya disease: Diagnostic imaging. Pol J Radiol. Jan 2011;76(1):73-9. 
43. Singhal AB, Topcuoglu MA, Fok JW, et al. Reversible cerebral vasoconstriction syndromes and primary angiitis of the central nervous system: clinical, imaging, and angiographic comparison. Ann Neurol. Jun 2016;79(6):882-94. doi:10.1002/ana.24652
44. Obusez EC, Hui F, Hajj-Ali RA, et al. High-resolution MRI vessel wall imaging: spatial and temporal patterns of reversible cerebral vasoconstriction syndrome and central nervous system vasculitis. AJNR Am J Neuroradiol. Aug 2014;35(8):1527-32. doi:10.3174/ajnr.A3909
45. Leal PR, Hermier M, Froment JC, Souza MA, Cristino-Filho G, Sindou M. Preoperative demonstration of the neurovascular compression characteristics with special emphasis on the degree of compression, using high-resolution magnetic resonance imaging: a prospective study, with comparison to surgical findings, in 100 consecutive patients who underwent microvascular decompression for trigeminal neuralgia. Acta Neurochir (Wien). May 2010;152(5):817-25. doi:10.1007/s00701-009-0588-7
46. Lee CC, Reardon MA, Ball BZ, et al. The predictive value of magnetic resonance imaging in evaluating intracranial arteriovenous malformation obliteration after stereotactic radiosurgery. J Neurosurg. Jul 2015;123(1):136-44. doi:10.3171/2014.10.Jns141565
47. Serafin Z, Strześniewski P, Lasek W, Beuth W. Follow-up after embolization of ruptured intracranial aneurysms: a prospective comparison of two-dimensional digital subtraction angiography, three-dimensional digital subtraction angiography, and time-of-flight magnetic resonance angiography. Neuroradiology. Nov 2012;54(11):1253-60. doi:10.1007/s00234-012-1030-z
48. Franz RW, Willette PA, Wood MJ, Wright ML, Hartman JF. A systematic review and meta-analysis of diagnostic screening criteria for blunt cerebrovascular injuries. J Am Coll Surg. Mar 2012;214(3):313-27. doi:10.1016/j.jamcollsurg.2011.11.012
49. Shakir HJ, Davies JM, Shallwani H, Siddiqui AH, Levy EI. Carotid and Vertebral Dissection Imaging. Curr Pain Headache Rep. Dec 2016;20(12):68. doi:10.1007/s11916-016-0593-5
50. Larsson SC, King A, Madigan J, Levi C, Norris JW, Markus HS. Prognosis of carotid dissecting aneurysms: Results from CADISS and a systematic review. Neurology. Feb 14 2017;88(7):646-652. doi:10.1212/wnl.0000000000003617
51. Patel SD, Haynes R, Staff I, Tunguturi A, Elmoursi S, Nouh A. Recanalization of cervicocephalic artery dissection. Brain Circ. Jul-Sep 2020;6(3):175-180. doi:10.4103/bc.bc_19_20
52. Saposnik G, Barinagarrementeria F, Brown RD, et al. Diagnosis and Management of Cerebral Venous Thrombosis. Stroke. 2011;42(4):1158-1192.  doi:doi:10.1161/STR.0b013e31820a8364
53. Brott TG, Halperin JL, Abbara S, et al. 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease: executive summary. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American Stroke Association, American Association of Neuroscience Nurses, American Association of Neurological Surgeons, American College of Radiology, American Society of Neuroradiology, Congress of Neurological Surgeons, Society of Atherosclerosis Imaging and Prevention, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of NeuroInterventional Surgery, Society for Vascular Medicine, and Society for Vascular Surgery. Circulation. Jul 26 2011;124(4):489-532. doi:10.1161/CIR.0b013e31820d8d78
54. DaCosta M, Tadi P, Surowiec SM. Carotid Endarterectomy. StatPearls Publishing Updated July 25, 2022. Accessed January 29, 2023. https://www.ncbi.nlm.nih.gov/books/NBK470582/
55. Marquardt L, Geraghty OC, Mehta Z, Rothwell PM. Low risk of ipsilateral stroke in patients with asymptomatic carotid stenosis on best medical treatment: a prospective, population-based study. Stroke. Jan 2010;41(1):e11-7. doi:10.1161/strokeaha.109.561837
56. Rerkasem K, Rothwell PM. Carotid endarterectomy for symptomatic carotid stenosis. Cochrane Database Syst Rev. Apr 13 2011;(4):Cd001081. doi:10.1002/14651858.CD001081.pub2
57. Yew KS. Diagnostic approach to patients with tinnitus. Am Fam Physician. Jan 15 2014;89(2):106-13. 
58. Lawson GR. Controversy: Sedation of children for magnetic resonance imaging. Arch Dis Child. Feb 2000;82(2):150-3. doi:10.1136/adc.82.2.150
59. Chen X, Liu Y, Tong H, et al. Meta-analysis of computed tomography angiography versus magnetic resonance angiography for intracranial aneurysm. Medicine (Baltimore). May 2018;97(20):e10771. doi:10.1097/md.0000000000010771
60. Walker EYX, Marlais M. Should we screen for intracranial aneurysms in children with autosomal dominant polycystic kidney disease? Pediatr Nephrol. Jan 2023;38(1):77-85. doi:10.1007/s00467-022-05432-5
61. van Beijnum J, van der Worp HB, Algra A, et al. Prevalence of brain arteriovenous malformations in first-degree relatives of patients with a brain arteriovenous malformation. Stroke. Nov 2014;45(11):3231-5. doi:10.1161/strokeaha.114.005442
62. American College of Radiology. ACR Appropriateness Criteria®Cerebrovascular Disease. American College of Radiology (ACR). Updated 2016. Accessed January 29, 2023. https://acsearch.acr.org/docs/69478/Narrative/
63. Sacco RL, Kasner SE, Broderick JP, et al. An updated definition of stroke for the 21st century: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. Jul 2013;44(7):2064-89. doi:10.1161/STR.0b013e318296aeca
64. Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. Jul 2014;45(7):2160-236. doi:10.1161/str.0000000000000024
65. Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. Jun 2009;40(6):2276-93. doi:10.1161/strokeaha.108.192218
66. Hong KS, Yegiaian S, Lee M, Lee J, Saver JL. Declining stroke and vascular event recurrence rates in secondary prevention trials over the past 50 years and consequences for current trial design. Circulation. May 17 2011;123(19):2111-9. doi:10.1161/circulationaha.109.934786
67. Bekelis K, Desai A, Zhao W, et al. Computed tomography angiography: improving diagnostic yield and cost effectiveness in the initial evaluation of spontaneous nonsubarachnoid intracerebral hemorrhage. J Neurosurg. Oct 2012;117(4):761-6. doi:10.3171/2012.7.Jns12281
68. Ayanzen RH, Bird CR, Keller PJ, McCully FJ, Theobald MR, Heiserman JE. Cerebral MR venography: normal anatomy and potential diagnostic pitfalls. AJNR Am J Neuroradiol. Jan 2000;21(1):74-8. 
69. Jensen RH, Radojicic A, Yri H. The diagnosis and management of idiopathic intracranial hypertension and the associated headache. Ther Adv Neurol Disord. Jul 2016;9(4):317-26. doi:10.1177/1756285616635987
70. Connors JM, Levy JH. Thromboinflammation and the hypercoagulability of COVID-19. J Thromb Haemost. Jul 2020;18(7):1559-1561. doi:10.1111/jth.14849
71. Tu TM, Goh C, Tan YK, et al. Cerebral Venous Thrombosis in Patients with COVID-19 Infection: a Case Series and Systematic Review. J Stroke Cerebrovasc Dis. Dec 2020;29(12):105379. doi:10.1016/j.jstrokecerebrovasdis.2020.105379
72. Bushnell C, Saposnik G. Evaluation and management of cerebral venous thrombosis. Continuum (Minneap Minn). Apr 2014;20(2 Cerebrovascular Disease):335-51. doi:10.1212/01.CON.0000446105.67173.a8
73. Coutinho JM. Cerebral venous thrombosis. J Thromb Haemost. Jun 2015;13 Suppl 1:S238-44. doi:10.1111/jth.12945
74. Ferro JM, Canhão P, Aguiar de Sousa D. Cerebral venous thrombosis. Presse Med. Dec 2016;45(12 Pt 2):e429-e450. doi:10.1016/j.lpm.2016.10.007
75. Liang T, Tso DK, Chiu RY, Nicolaou S. Imaging of blunt vascular neck injuries: a review of screening and imaging modalities. AJR Am J Roentgenol. Oct 2013;201(4):884-92. doi:10.2214/ajr.12.9664
76. Simon LV, Nassar AK, Mohseni M. Vertebral Artery Injury. StatPearls Publishing Updated July 18, 2022. Accessed January 29, 2023. https://www.ncbi.nlm.nih.gov/books/NBK470363/
77. Mundinger GS, Dorafshar AH, Gilson MM, Mithani SK, Manson PN, Rodriguez ED. Blunt-mechanism facial fracture patterns associated with internal carotid artery injuries: recommendations for additional screening criteria based on analysis of 4,398 patients. J Oral Maxillofac Surg. Dec 2013;71(12):2092-100. doi:10.1016/j.joms.2013.07.005
78. Nash M, Rafay MF. Craniocervical Arterial Dissection in Children: Pathophysiology and Management. Pediatr Neurol. Jun 2019;95:9-18.  doi:10.1016/j.pediatrneurol.2019.01.020

Coding Section 

Procedure and diagnosis codes on Medical Policy documents are included only as a general reference tool for each policy. They may not be all-inclusive. 

This medical policy was developed through consideration of peer-reviewed medical literature generally recognized by the relevant medical community, U.S. FDA approval status, nationally accepted standards of medical practice and accepted standards of medical practice in this community,  and other nonaffiliated technology evaluation centers, reference to federal regulations, other plan medical policies, and accredited national guidelines.

"Current Procedural Terminology © American Medical Association. All Rights Reserved" 

History From 2020 Forward