Various diagnostic modalities exist to demonstrate blood flow or absence thereof in the vertebral arteries. The gold standard is cerebral angiography (with or without digital subtraction angiography). This involves puncture of a large artery (usually the femoral artery) and advancing an intravascular catheter through the aorta towards the vertebral arteries. At that point, radiocontrast is injected and its downstream flow captured on fluoroscopy (continuous X-ray imaging). The vessel may appear stenotic (narrowed, 41–75%), occluded (blocked, 18–49%), or as an aneurysm (area of dilation, 5–13%). The narrowing may be described as "rat's tail" or "string sign". Cerebral angiography is an invasive procedure, and it requires large volumes of radiocontrast that can cause complications such as kidney damage. Angiography also does not directly demonstrate the blood in the vessel wall, as opposed to more modern modalities. The only remaining use of angiography is when endovascular treatment is contemplated (see below).

More modern methods involve computed tomography (CT angiography) and magnetic resonance imaging (MR angiography). They use smaller amounts of contrast and are not invasive. CT angiography and MR angiography are more or less equivalent when used to diagnose or exclude vertebral artery dissection. CTA has the advantage of showing certain abnormalities earlier, tends to be available outside office hours, and can be performed rapidly. When MR angiography is used, the best results are achieved in the "T" setting using a protocol known as "fat suppression". Doppler ultrasound is less useful as it provides little information about the part of the artery close to the skull base and in the vertebral foramina, and any abnormality detected on ultrasound would still require confirmation with CT or MRI.

The U.S. Preventive Services Task Force (USPSTF) recommends against screening for carotid artery stenosis in those without symptoms.

Vessel restenosis is typically detected by angiography, but can also be detected by duplex ultrasound and other imaging techniques.

Carotid stenosis is usually diagnosed by color flow duplex ultrasound scan of the carotid arteries in the neck. This involves no radiation, no needles and no contrast agents that may cause allergic reactions. This test has moderate sensitivity and specificity, and yields many false-positive results.

Typically duplex ultrasound scan is the only investigation required for decision making in carotid stenosis as it is widely available and rapidly performed. However, further imaging can be required if the stenosis is not near the bifurcation of the carotid artery.

One of several different imaging modalities, such as angiogram, computed tomography angiogram (CTA) or magnetic resonance imaging angiogram (MRA) may be useful. Each imaging modality has its advantages and disadvantages - Magnetic resonance angiography and CT angiography with contrast is contraindicated in patients with renal insufficiency, catheter angioigraphy has a 0.5% to 1.0% risk of stroke, MI, arterial injury or retoperitoneal bleeding. The investigation chosen will depend on the clinical question and the imaging expertise, experience and equipment available.

Prognosis of spontaneous cervical arterial dissection involves neurological and arterial results. The overall functional prognosis of individuals with stroke due to cervical artery dissection does not appear to vary from that of young people with stroke due to other causes. The rate of survival with good outcome (a modified Rankin score of 0–2) is generally about 75%, or possibly slightly better (85.7%) if antiplatelet drugs are used. In studies of anticoagulants and aspirin, the combined mortality with either treatment is 1.8–2.1%.

After the initial episode, 2% may experience a further episode within the first month. After this, there is a 1% annual risk of recurrence. Those with high blood pressure and dissections in multiple arteries may have a higher risk of recurrence. Further episodes of cervical artery dissection are more common in those who are younger, have a family history of cervical artery dissection, or have a diagnosis of Ehlers-Danlos syndrome or fibromuscular dysplasia.

In peripheral procedures, rates are still high. A 2003 study of selective and systematic stenting for limb-threatening ischemia reported restenosis rates at 1 year follow-up in 32.3% of selective stenting patients and 34.7% of systematic stenting patients.

The 2006 SIROCCO trial compared the sirolimus drug-eluting stent with a bare nitinol stent for atherosclerotic lesions of the superficial femoral artery, reporting restenosis at 2 year follow-up was 22.9% and 21.1%, respectively.

A 2009 study compared bare nitinol stents with percutaneous transluminal angioplasty (PTA) in superficial femoral artery disease. At 1 year follow-up, restenosis was reported in 34.4% of stented patients versus 61.1% of PTA patients.

The differentiating presentations are suggestive of FMD being a unique syndrome in respect to the pediatric population. Experienced FMD clinicians warn against relying in the “string of beads” angiography for a diagnosis. In fact, it is suggested that FMD may be both under and over-diagnosed in children with stroke.

70% of patients with carotid arterial dissection are between the ages of 35 and 50, with a mean age of 47 years.

It is the lack of specific symptoms and its potential to appear anywhere that makes FMD a challenge to detect early on. The most accurate diagnosis comes from combining clinical presentation and angiographic imaging. According to the Michigan Outcomes Research and Reporting Program (MCORRP, 2013) the length of time from a patient’s first signs or symptoms to diagnosis is commonly 5 years.

FMD is currently diagnosed through the use of both invasive and non-invasive tests. Non-invasive testing includes duplex ultrasonography, magnetic resonance angiography (MRA), and computed tomographic angiography (CTA). Invasive testing through angiography is the gold standard. However, due to the higher risk of complications this is typically not done early on. Occasionally, FMD is diagnosed asymptomatically after an unrelated x-ray presents the classic ‘string of beads’ appearance of the arteries, or when a practitioner investigates an unexpected bruit found during an exam. When a diagnosis of FMD is considered for a patient thorough medical history, family history as well as vascular examination should be completed.

A definitive diagnosis of FMD can only be made with imaging studies. Catheter-based angiography (with contrast) has proven to be the most accurate imaging technique: this test involves a catheter is inserted into a large artery and advanced until it reaches the vessel of question. The catheter allows practitioners to view and measure the pressure of the artery aiding in the categorization and severity of the FMD diseased artery. According to Olin, “catheter-based angiography is the only imaging modality that can accurately identify the changes of FMD, aneurysm formation, and dissection in the branch vessels.” Practitioners believe it is important to utilize IVUS imaging because stenosis can sometimes only be detected through the methods of pressure gradient or IVUS imaging. In addition, computed tomography angiography and magnetic resonance angiography are commonly used to evaluate arteries in the brain. Doppler ultrasound may be used in both the diagnosis and follow-up of FMD.

Smith (2015) conducted a study that looked into specific biological markers that correlate to Moyamoya disease. Some of the categories of these biomarkers include phenotypes - conditions commonly related to Moyamoya, radiographical markers for the diagnosis of Moyamoya, and proteins as well as cellular changes that occur in cases of Moyamoya.

Similar to Moyamoya Disease, there are conditions that are closely associated with Moyamoya Syndrome. Some of the more common medical conditions that are closely associated with Moyamoya Syndrome include trisomy 21 (Down's Syndrome), sickle cell disease, and neurofibromatosis type 1. There is also evidence that identifies hyperthyroidism and congenital dwarfing syndromes as two of the more loosely associated syndromes that correlate with the possibility of being diagnosed with Moyamoya Disease later in life.

There is also research that has shown that certain radiographic biomarkers that lead to the diagnosis of Moyamoya Disease have been identified. The specific radiographic markers are now considered an acceptable key component to Moyamoya Disease and have been added to the INternational Classification of Diseases (ICD). These biomarkers of Moyamoya are "stenosis of the distal ICA's up to and including the bifurcation, along with segments of the proximal ACA and MCA...dilated basal collateral vessels must be present" Some other common findings that have not been added to the classification index of those with Moyamoya Disease which are found using radiography involve very distinct changes in the vessels of the brain. These changes include newly formed vessels made to compensate for another change noted, ischemia and cerebrovascular reserve, both found on MRI. Functional changes include evidence of ischemia in vessels of the brain (ICA, ACA, MCA, specifically). It is important to also note that the radiographic biomarkers, in order to be classified as Moyamoya Disease, all findings must be bilateral. If this is not the case and the findings are unilateral, it is diagnosed as Moyamoya Syndrome.

There are also several protein biomarkers that have been linked to the Moyamoya Disease diagnosis. Although the sample size of the studies performed are small due to the rarity of the disease, the findings are indicative of a correlation between the disease and several specific protein biomarkers. Other studies have confirmed the correlation of Moyamoya and adhesion molecule 1 (ICAM-1) being increased as compared to normal vascular function counterparts Furthermore, it has been concluded that the localization of inflammatory cells suggests that the inflammation stimulus iteself may be responsible for the proliferation and occlusion in the ICA, ACA, and MCA found in those with Moyamoya Disease.

This is based on MRI scan, magnetic resonance angiography and CT scan. A cerebral digital subtraction angiography (DSA) enhances visualization of the fistula.

- CT scans classically show an enlarged superior ophthalmic vein, cavernous sinus enlargement ipsilateral (same side) as the abnormality and possibly diffuse enlargement of all the extraocular muscles resulting from venous engorgement.

- Selective arteriography is used to evaluate arteriovenous fistulas.

- High resolution digital subtraction angiography may help in classifying CCF into dural and direct type and thus formulate a strategy to treat it either by a balloon or coil or both with or without preservation of parent ipsilateral carotid artery.

The diagnosis of moyamoya is suggested by CT, MRI, or angiogram results. Contrast-enhanced T1-weighted images are better than FLAIR images for depicting the leptomeningeal ivy sign in moyamoya disease. MRI and MRA should be performed for the diagnosis and follow-up of moyamoya disease. Diffusion-weighted imaging can also be used for following the clinical course of children with moyamoya disease, in whom new focal deficits are highly suspicious of new infarcts.

Proliferation of smooth muscle cells in the walls of the Moyamoya affected arteries has been found to be representative of the disease. A study of six autopsies of six patients who died from Moyamoya disease lead to the finding that there is evidence that supports the theory that there is a thickening, or proliferation, of the innermost layer of the vessels affected by Moyamoya. These vessels are the ACA (anterior cerebral artery), MCA (middle cerebral artery), and ICA (internal carotid artery). The occlusion of the ICA results in concomitant diminution of the "puff-of-smoke" collaterals, as they are supplied by the ICA.

Often nuclear medicine studies such as SPECT (single photon emission computerized tomography) are used to demonstrate the decreased blood and oxygen supply to areas of the brain involved with moyamoya disease. Conventional angiography provided the conclusive diagnosis of moyamoya disease in most cases and should be performed before any surgical considerations.

Dr. Darren B. Orbach, MD, PhD explains how the disease progresses as well as the role angiography plays in detecting the progression of Moyamoya in a short video

The goal of treatment is to prevent the development or continuation of neurologic deficits. Treatments include observation, anticoagulation, stent implantation and carotid artery ligation.

The evaluation for VBI starts with a history and physical exam, with great emphasis on the cardiovascular and neurologic exam. It also includes a work-up to exclude benign conditions (such as labyrinthitis, vestibular neuronitis, and benign paroxysmal positional vertigo) that have overlapping signs and symptoms. However, the exact work-up largely depends on the patient’s age and known risk factors. For middle-aged patients, a cardiovascular risk factor evaluation is important. This often includes a cholesterol level, lipid profile (see this to determine what your cholesterol level means), ECG, and echocardiogram. If a person with VBI is under age 45 and has no evidence for atherosclerosis, a work-up for hypercoagulable states (Lupus anticoagulant, anti-cardiolipin antibodies, is indicated. Screening for protein C, protein S, or antithrombin III deficiency is sometimes recommended but these are more usually responsible for venous thrombosis than arterial problems.

Imaging studies are rarely required to diagnose VBI, but sometimes computed tomography (CT) is performed first. The CT is extremely sensitive in detecting hemorrhage. However, magnetic resonance imaging (MRI) is superior to the CT in detecting ischemic changes in the vertebrobasilar distribution. Magnetic resonance angiography (MRA) also can be used to identify vertebrobasilar stenoses or occlusions, but it can often overestimate the degree of stenosis, or wrongly show stenosis as an occlusion. Intracranial MRA is mostly sufficient to evaluate vertebrobasilar arteries, while extracranial vertebral arteries are better diagnosed using contrast-enhanced MRA, which is less dependent on flow phenomena and more accurate in evaluating stenosis.

CT angiography is also highly accurate in evaluation vertebrobasilar vessels, but ionizing radiation and use of nephrotoxic contrast media make it less suitable both in elderly with renal insufficiency and young adults because of radiation exposure. Moreover, vessel wall calcification and beam-hardening artifacts due to dense bones or metal fillings sometimes cause strong CT-image degradation.

In medical pathology, a dissection is a tear within the wall of a blood vessel, which allows blood to separate the wall layers. By separating a portion of the wall of the artery (a layer of the tunica intima or tunica media), a dissection creates two lumens or passages within the vessel, the native or true lumen, and the "false lumen" created by the new space within the wall of the artery.

Median arcuate ligament syndrome is a diagnosis of exclusion. That is, the diagnosis of MALS is generally considered only after patients have undergone an extensive evaluation of their gastrointestinal tract including upper endoscopy, colonoscopy, and evaluation for gallbladder disease and gastroesophageal reflux disease (GERD).

The diagnosis of MALS relies on a combination of clinical features and findings on medical imaging. Clinical features include those signs and symptoms mentioned above; classically, MALS involves a triad of abdominal pain after eating, weight loss, and an abdominal bruit, although the classic triad is found in only a minority of individuals that carry a MALS diagnosis.

Diagnostic imaging for MALS is divided into screening and confirmatory tests. A reasonable screening test for patients with suspected MALS is duplex ultrasonography to measure blood flow through the celiac artery. Peak systolic velocities greater than 200 cm/s are suggestive of celiac artery stenosis associated with MALS.

Further evaluation and confirmation can be obtained via angiography to investigate the anatomy of the celiac artery. Historically, conventional angiography was used, although this has been largely replaced by less invasive techniques such as computed tomography (CT) and magnetic resonance (MR) angiography. Because it provides better visualization of intraabdominal structures, CT angiography is preferred to MR angiography in this setting. The findings of focal narrowing of the proximal celiac artery with poststenotic dilatation, indentation on the superior aspect of the celiac artery, and a hook-shaped contour of the celiac artery support a diagnosis of MALS. These imaging features are exaggerated on expiration, even in normal asymptomatic individuals without the syndrome.

Proximal celiac artery stenosis with poststenotic dilatation can be seen in other conditions affecting the celiac artery. The hook-shaped contour of the celiac artery is characteristic of the anatomy in MALS and helps distinguish it from other causes of celiac artery stenosis such as atherosclerosis. This hooked contour is not entirely specific for MALS however, given that 10-24% of normal asymptomatic individuals have this anatomy.

Examples include:

- Aortic dissection (aorta)

- Coronary artery dissection (coronary artery)

- Carotid artery dissection (carotid artery)

- Vertebral artery dissection (vertebral artery)

Carotid and vertebral artery dissection are grouped together as "cervical artery dissection".

In addition to evaluating the symptoms above, the health care provider may find decreased or no blood pressure in the arm or leg.

Tests to determine any underlying cause for thrombosis or embolism and to confirm presence of the obstruction may include:

- Doppler ultrasound, especially duplex ultrasonography. It may also involve transcranial doppler exam of arteries to the brain

- Echocardiography, sometimes involving more specialized techniques such as Transesophageal echocardiography (TEE) or myocardial contrast echocardiography (MCE) to diagnose myocardial infarction

- Arteriography of the affected extremity or organ Digital subtraction angiography is useful in individuals where administration of radiopaque contrast material must be kept to a minimum.

- Magnetic resonance imaging (MRI)

- Blood tests for measuring elevated enzymes in the blood, including cardiac-specific troponin T and/or troponin I, myoglobins, and creatine kinase isoenzymes. These indicate embolisation to the heart that has caused myocardial infarction. Myoglobins and creatine kinase are also elevated in the blood in embolisation in other locations.

- Blood cultures may be done to identify the organism responsible for any causative infection

- Electrocardiography (ECG) for detecting myocardial infarction

- Angioscopy using a flexible fiberoptic catheter inserted directly into an artery.

In order to treat acute limb ischaemia there are a series of things that can be done to determine where the occlusion is located, the severity, and what the cause was. To find out where the occlusion is located one of the things that can be done is simply a pulse examination to see where the heart rate can be detected and where it stops being sensed. Also there is a lower body temperature below the occlusion as well as paleness. A Doppler evaluation is used to show the extent and severity of the ischaemia by showing flow in smaller arteries. Other diagnostical tools are duplex ultrasonography, computed tomography angiography (CTA), and magnetic resonance angiography (MRA). The CTA and MRA are used most often because the duplex ultrasonography although non-invasive is not precise in planning revascularization. CTA uses radiation and may not pick up on vessels for revascularization that are distal to the occlusion, but it is much quicker than MRA. In treating acute limb ischaemia time is everything.

In the worst cases acute limb ischaemia progresses to critical limb ischaemia, and results in death or limb loss. Early detection and steps towards fixing the problem with limb-sparing techniques can salvage the limb. Compartment syndrome can occur because of acute limb ischaemia because of the biotoxins that accumulate distal to the occlusion resulting in edema.

Heyde's syndrome is now known to be gastrointestinal bleeding from angiodysplasic lesions due to acquired vWD-2A deficiency secondary to aortic stenosis, and the diagnosis is made by confirming the presence of those three things. Gastrointestinal bleeding may present as bloody vomit, dark, tarry stool from metabolized blood, or fresh blood in the stool. In a person presenting with these symptoms, endoscopy, gastroscopy, and/or colonoscopy should be performed to confirm the presence of angiodysplasia. Aortic stenosis can be diagnosed by auscultation for characteristic heart sounds, particularly a crescendo-decrescendo (i.e., 'ejection') murmur, followed by echocardiography to measure aortic valve area (see diagnosis of aortic stenosis). While Heyde's syndrome may exist alone with no other symptoms of aortic stenosis, the person could also present with evidence of heart failure, fainting, or chest pain. Finally, Heyde's syndrome can be confirmed using blood tests for vWD-2A, although traditional blood tests for von Willebrand factor may result in false negatives due to the subtlety of the abnormality. The gold standard for diagnosis is gel electrophoresis; in people with vWD-2A, the large molecular weight von Willebrand factors will be absent from the SDS-agarose electrophoresis plate.

Computed tomography (CT) and MRI scanning will show damaged area in the brain, showing that the symptoms were not caused by a tumor, subdural hematoma or other brain disorder. The blockage will also appear on the angiogram.

Subclavian steal syndrome (SSS), also called subclavian steal phenomenon or subclavian steal steno-occlusive disease, is a constellation of signs and symptoms that arise from retrograde (reversed) blood flow in the vertebral artery or the internal thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the subclavian artery. The arm may be supplied by blood flowing in a retrograde direction down the vertebral artery at the expense of the vertebrobasilar circulation. This is called the "subclavian steal". It is more severe than typical vertebrobasilar insufficiency.

The mainstay of treatment for CCF is endovascular therapy. This may be transarterial (mostly in the case of direct CCF) or transvenous (most commonly in indirect CCF). Occasionally, more direct approaches, such as direct transorbital puncture of the cavernous sinus or cannulation of the draining superior orbital vein are used when conventional approaches are not possible. Spontaneous resolution of indirect fistulae has been reported but is uncommon. Staged manual compression of the ipsilateral carotid has been reported to assist with spontaneous closure in selected cases.

Direct CCF may be treated by occlusion of the affected cavernous sinus (coils, balloon, liquid agents), or by reconstruction of the damaged internal carotid artery (stent, coils or liquid agents).

Indirect CCF may be treated by occlusion of the affected cavernous sinus with coils, liquid agents or a combination of both.

Prevention of atherosclerosis, which is a major risk factor of arterial embolism, can be performed e.g. by dieting, physical exercise and smoking cessation.

In case of high risk for developing thromboembolism, antithrombotic medication such as warfarin or coumadin may be taken prophylactically. Antiplatelet drugs may also be needed.

Diagnosis is based on the demonstration of vascular lesions in large and middle-sized vessels on angiography, CT scan, magnetic resonance angiography or FDG PET. FDG PET can help in diagnosis of active inflammation not just in patients with active Takayasu arteritis prior to treatment but also in addition in relapsing patients receiving immunosuppressive agents.

Contrast angiography has been the gold standard. The earliest detectable lesion is a local narrowing or irregularity of the lumen. This may develop into stenosis and occlusion. The characteristic finding is the presence of "skip lesions," where stenosis or aneurysms alternate with normal vessels. Angiography provides information on vessel anatomy and patency but does not provide information on the degree of inflammation in the wall.

The age at onset helps to differentiate Takayasu's arteritis from other types of large vessel vasculitis. For example, Takaysu's arteritis has an age of onset of 60 years.

Takayasu arteritis is not associated with ANCA, rheumatoid factor, ANA, and anticardiolipin antibodies.