Neuroimaging in Common Neurological Diseases Treated by Anticoagulants

Abstract

Stroke imaging/Cerebral Venous sinus thrombosis/Arterial dissecting disease in Head and Neck regions/Neurocomplication of anticoagulation therapy. Nowsday, anticoagulant drugs are common drugs used in daily practice for patients in neurology clinic. Anticoagulant treatment used for treated symptomatic patients as well as for prophylaxis therapy in asymptomatic patients. The purpose of this chapter based on the review of essential neuroimaging in the most common neurological conditions that benefit from treatment with anticoagulant drugs such as ischemic stroke, cerebral venous sinus thrombosis, and arterial dissecting disease of head and neck arteries and will be enclosed with neuroimaging in case of neurocomplication by anticoagulant therapy.

1. Introduction

Stroke is a neurovascular disease with a high incidence throughout the world; according to the global stroke fact sheet 2019 by World Stroke Organization, stroke is the second leading cause of death and the third leading cause of disability. As up to 13.7 million new cases of stroke each year, globally one in four people over age 25 will have a stroke in his or her lifetime. About 5.5 million people die from stroke annually, and 39% of all who die from stroke are under 70 years old [1]. The burden of stroke is due to widely prevalent risk factors such as hypertension, diabetes, smoking, metabolic syndrome, and behavioral factors. Modification risk factors and administration preventive therapy are the keys to decrease stroke burden. Besides of the systemic disease such as hypertension can cause stroke, a number of cardiac diseases and vascular diseases affected intracranial arteries such as non-valvular atrial fibrillation, prosthetic heart valve, dilated cardiomyopathy, atrial appendage thrombus and atrial myxoma, atherosclerosis disease of aortic arch, neck arteries and intracranial arteries, arterial dissection etc. are the common causes of stroke [2, 3, 4]. Those conditions are prone to cause an embolic stroke (cardioembolic or artery to artery embolism). Antithrombotic agents such as antiplatelet drugs and anticoagulants are the drugs that are efficient in the prevention of embolic stroke. Thus, a majority of patients who have high risk factors in the group of stroke experience and inexperience stroke might have a regular anticoagulant administration. Regular monitoring of prothrombin time and International normalized ratio (INR) to predict the bleeding complications. Because ischemic and hemorrhagic strokes have different causes and effects on the body, both require different treatments. The accurate diagnosis types of strokes as ischemic stroke or hemorrhagic stroke is important. Neuroimaging is the investigate procedure to make a correct diagnosis type of stroke and extension of stroke lesion that take part in triage stroke 2patients for further proper management.

Guideline recommendation for stroke prevention (ischemic stroke/TIA) [5]:

• To evaluate the cause of ischemic stroke.

• Getting rid of all risk factors is important for secondary stroke prevention such as well-controlled DM/hypertension, pause of smoking, and decreased lipid level.

• Changing patients to a healthy diet (low salt, low cholesterol rich diet) and promoting physical activity such as exercise.

• The administration of antithrombolytic therapy in the patients who have no contraindication to antiplatelet or anticoagulant treatment such as combination of antiplatelets and anticoagulation or dual antiplatelet therapy is not recommended in long term treatment. For the short term treatment, dual antiplatelet therapy is recommended in specific patients such as early arriving minor stroke, high risk transient ischemic stroke or severe sympatimatic intracranial stenosis etc.

• Atrial fibrillation remains a common and high-risk condition for second ischemic stroke. Anticoagulation is usually recommended if the patient has no contraindications. Heart rhythm monitoring for occult atrial fibrillation is usually recommended if no other cause of stroke is discovered.

• Extracranial carotid artery disease is an important and treatable cause of stroke. Patients with severe stenosis ipsilateral to a nondisabling stroke or transient ischemic attack who are candidates for intervention should have the stenosis fixed, likely relatively early after their ischemic stroke. The choice between carotid endarterectomy and carotid artery stenting should be driven by specific patient comorbidities and features of their vascular anatomy.

• Patients with severe intracranial stenosis in the vascular territory of ischemic stroke or transient ischemic attack should not receive angioplasty and stenting as first-line therapy for preventing recurrence. Aggressive medical management of risk factors and short-term dual antiplatelet therapy is preferred.

• Patients with embolic stroke of the uncertain source should not be treated empirically with anticoagulants or ticagrelor because it was found to be of no benefit.

Stroke has three major subtypes:

1. Ischemic stroke

2. Hemorrhagic stroke

3. Stroke mimic conditions

Neuroimaging modalities as noninvasive techniques for the diagnosis of stroke are mainly based on computed tomography (CT) or magnetic resonance imaging (MRI) studies such as noncontrast CT study, CT angiography (single-phase or multiphase CTA), CT perfusion (CTP), CT venography (CTV) and dual-energy CT (DECT) or MRI, MR angiography, MR perfusion, etc. invasive study such as digital subtraction catheterized angiography (DSA) is usually preserved for further treatment by endovascular options such as mechanical thrombectomy, coiling aneurysm, etc. Imaging plays a key role in current guidelines for thrombolysis. The knowledge of typical early ischemic signs in nonenhanced computed tomography (CT) is necessary.

Computed Tomography (CT): According to “Time is brain” the patient in stroke condition in the emergency department must be transferred fast and must have a correct diagnosis. Noncontrast CT scan (NCCT) must be performed as soon as possible after an activated stroke. NCCT is preferred in most institutes/centers and used as the gateway in triage patients who have a clinical stroke, which may be caused by an ischemic process or hemorrhagic process or even mimic stroke conditions (e.g., vascular malformation or tumor). If there is a need for further investigation, contrast-enhanced study can be performed such as CTA, CTV, CTP, multiphase CTA, or even regular contrast-enhanced CT brain, etc. Nowadays, the complete CT stroke protocol for triage patients for mechanical thrombectomy is composed of NCCT brain, CTA (multiphases), and CT perfusion, which can be performed in a single examination, which can be completed in 15 minutes.

NCCT: Noncontrast CT interpretation based on knowledge of brain vascular anatomy and basic density on CT scan together with clinical information is needed for correct diagnosis. After noncontrast CT scan can rule out intracranial hemorrhage or stroke mimic conditions, the patient can proceed to have an intravenous thrombolysis drug with a recombinant tissue-type plasminogen activator (r-tPA) for treatment. Exceptional case that have contraindication for IV treatment (Table 1) [6]. CTA and CTP will be further studies for decision-making in management by interventional therapy.

Absolute contraindication

Acute ICH including hemorrhagic infarction

History of ICH (microbleed is not contraindicated)

BP > 185 mmHg, BPs > 110 mmHg

Serious head trauma or stroke < 3 months

Thrombocytopenia (platelet <100,000/mm^3) and coagulopathy (PT > 15, INR > 1.7)

LMWH within 24 hr (38% risk of sICH, 29% risk of death, 33% favorable outcomes, od 0.84 for sICH, od5.3 for death)

DTIs (TT is sensitive to presence of DITs)

Factor Xa inhibitor

Severe hypoglycemia(<50 mg/dl) and hyperglycemia(>400 mg/dl) may be permitted for IVT

Early radiographic ischemic changes(>1/3 MCA)

Relative contraindication

Advanced age (>80 yrs.)

Mild or improving stroke (NIHSS<5)

Severe stroke (IVT should be cautiously administered in NIHSS>25 at 3–4.5 hrs.)

Major surgery within 2 weeks (some 3 months)

Arterial puncture of noncompressible site

Recent GI bleeding or GU bleeding

Seizure at onset

Recent MI within 3 months

Intracranial structure abnormality (axial tumor, AVM, aneurysm)

Dementia

Table 1.

Absolute and relative contraindications to IV rt-PA for acute ischemic stroke [6].

ACUTE stage (onset to 48hrs.): Ischemic stroke pattern composed of two main components as vascular structures and parenchyma changes. The vascular structures CT finding is “hyperdense artery sign, hyperdense vessel sign” which means acute intraluminal clot obstructs in the intracranial arteries such as middle cerebral artery (MCA), internal carotid artery (ICA), basilar artery appears as high density of blood clot by CT along the course of that artery in linear or dot patterns (Figures 1 and 2). However, these findings have high specificity up to 90% but low sensitivity of approximately 30% [7, 8, 9]. Whenever encountered with hyperdense artery sign on NCCT brain, always correlation to clinical information as well as compare to the contralateral side and venous structures, such as transverse sigmoid sinus, superior sagittal sinus to reduce false-positive conditions That cause high density in the arteries, veins such as hemoconcentration condition. The early CT findings in parenchymatous change from ischemic stroke are mainly hypoattenuation area from cytotoxic edema that corresponds to the territory of occluded artery, visible by NCCT within the first few hours. For example, when there is proximal middle cerebral artery occlusion, there may be hypoattenuation area in the following structures: basal ganglia, internal capsule, insular cortex, frontal operculum, temporal operculum, temporal lobe convexity, frontoparietal convexity. Basically, nature of basal ganglia structures (caudate and lentiform nucleus) are gray matter structures which normally slightly high attenuation to nearby white matter as internal capsule, external capsule. Therefore, acute ischemic stroke change in basal ganglia will be hypoattenuation that called “obscuration lentiform nucleus sign” (Figure 3). In the same manner, the insular cortex that locates lateral to basal ganglia and external capsule will be hypodensity and loss of normal cortical lobulated pattern are called as “loss of cortical ribbon sign” (Figure 3). If cortical and subcortical gray-white matter is involved, NCCT will demonstrate loss of gray-white matter differentiation and effacement of cortical gyri (Figure 4). Application of this parenchymatous changes pattern in CT scan of MCA can use in other territories such as ACA, PCA, SCA, AICA and PICA (Figure 5). According to the study by Philip AB, Andrew MD, Jinjin Z, Alastair MB et.al (2000), the Alberta stroke program early CT score (ASPECTS) is widely used due to its simplicity and reliability in predicting functional outcomes and symptomatic intracerebral hemorrhage after intravenous treatment by alteplase [10]. It is a quantitative CT grading system precisely evaluating MCA territory by allotting 10 points in 10 different locations that cover entirely the MCA territory. The normal total score is 10. Each point will be subtracted in any one area of early ischemic change (visible hypodensity abnormality); therefore, the total score is 0 referring to ischemic change in the entire MCA territory. The study suggests that if patient CT ASPECTS is 7 or less, the risk of symptomatic ICH with alteplase is 14 times greater than ASPECTS greater than 7. In patients with scores above 7, the rate of symptomatic intracerebral hemorrhage is 1%. When hemorrhagic transformation develops in the area of cerebral infarction, hyperdensity of acute hemorrhage will be encountered (Figure 6).

Figure 1.

A, B, C, D NCCT brain demonstrates hyperdense artery sign in horizontal segment (M1 segment) of right middle cerebral artery (red arrow, red highlighted in A,B) and Sylvian segment (m2 segment) of right middle cerebral artery (dot sign, white arrow, C). Hyperdensity of blood clot in patient with clinical basilar artery thrombosis (dot sign, black arrow, D).

Figure 2.

A, B, C, D NCCT brain in a 59-year-old patient underlying AF with progressive right hemiplegia demonstrates hyperdense artery sign in horizontal segment (M1 segment) of left middle cerebral artery (A). NCCT brain in a 57-year-old male presenting with right homonymous hemianopia; hyperdense left PCA artery sign is demonstrated (B). NCCT brain in a 79-year-old female with alteration of consciousness; hyperdensity basilar artery sign demonstrates thrombosis (dot sign, C). NCCT brain in a 57-year-old man underlying hypertension and dyslipidemia; hyperdense artery sign is demonstrated at left vertebral artery (D). E,F NCCT brain demonstrates false positive hyperdense artery in horizontal segment (M1 segment) of right middle cerebral artery (white arrow, E) as well as contralateral side left MCA and venous structures such as left transverse sinus (black arrow, E). Normal opacification by contrast medium all arteries and venous structures are demonstrated on contrast enhanced CT scan (F). This patient is dehydrated from high fever and headache with hemoconcentration condition.

Figure 3.

A, B, C, D NCCT brain at level of basal ganglia demonstrates ”loss of insular ribbon sign “ in right insular cortex (white arrow, A and white outline area. B) and obscuration of lentiform nucleus sign” in right lentiform nucleus (white arrow, C) and in left lentiform nucleus (white arrow, D).

Figure 4.

A, B NCCT brain at level of supraganglionic demonstrates hypodensity areas with ”loss of gray-white matter differentiation “ and “ loss of cerebral sulci” in right frontoparietal lobes (black arrow, A and color outlines. B) The right convexity lesion is according to right MCA territory whereas right frontal parasagittal lesion is according to right ACA territory.

Figure 5.

A, B ,C, D NCCT brain at different levels of posterior circulation territories demonstrates hypodensity areas of acute infarction in left occipital lobe according to left distal PCA territory (A), left superior cerebellum according to left superior cerebellar artery (B), left anterior inferior cerebellum according to AICA territory (C) and right posteroinferior cerebellum according to right PICA territory (D).

Figure 6.

A, B NCCT brain in acute stroke of left MCA territory demonstrates ill-defined hypodensity areas of acute infarction in left frontoparietal convexity according to left MCA territory (A), and two weeks follow-up study reveals hyperdensity on top of the infarction area compatible with hemorrhagic transformation in subacute stage (B).

Subacute stage (2 days to 2 weeks): After maximum swelling of hypoxic cell, damage of BBB will increase leakage of intracellular fluid to extracellular fluid space causing vasogenic edema. The infarcted area in subacute stage will be easily detected by NCCT scan due to high-contrast resolution between swelling tissue and adjacent normal tissue. In the early subacute stage of the large territory infarction, increased pressure effect to midline structure, ventricular system may collapse or there may be displacement; therefore,subfalcine herniation or uncal or descending transtentorial herniation may occur. In addition, the high incidence of hemorrhagic transformation in the territory infarction (10–43%) [11] will increase this risk for the patient who has antithrombolytic therapy. If such a circumstance occurs, there is a new high attenuation lesion of the acute hemorrhage within the area of infarction on the follow-up CT scan. In the late subacute stage, the edema will subside with the decreased degree of brain swelling. If the patient is performed contrast enhanced CT scan, gyral enhancement is demonstrated in the subacute stage of cerebral infarction (Figures 6B and 7).

Figure 7.

A, B, C: NCCT brain in subacute stage of left MCA territory infarction (A) increased degree of brain swelling, midline shifted and hemorrhagic transformation developed. Late subacute stage, diminished degree of brain swelling and midline shifted (B). Gyral enhancement along the cortex is demonstrated (C).

Chronic, old stage (2 weeks to 2 months): Further resolution in the degree of brain swelling, as well as degeneration of the dead infarcted brain, is observed. The density of old infarction will be decreased to near CSF density level in some cases. Signs of brain volume loss in the old infarction area may occur as ex vacuo dilatation of ipsilateral ventricle expand toward the old infarction area, retrogradely Wallerian degeneration along ipsilateral corticospinal tract in the lower level to the infarction, etc. (Figure 8).

Figure 8.

A, B, C: NCCT brain in old stage of left MCA territory infarction (A) decreased degree of brain swelling to the near, equal to CSF density level. Ex vacuo dilatation of left lateral ventricle (B). Retrogradely Wallerian degeneration is demonstrated in left cerebral peduncle (C).

CT ANGIOGRAPHY (CTA): It is the noninvasive technique to visualize intracranial arteries by means of noncatheterization technique. In acute ischemic stroke, CTA is increasingly used for imaging the vessel and a combination of NCCT and CTA brain provides sufficient information to determine eligibility for thrombectomy in the first 6 hours. CTA can be performed in single-phase or multiphases during one injection of contrast medium. The outstanding advantage of multiphase (three phases) CTA over a single phase is in the detection of collateral circulation to the area of infarction that assists in decision making for further treatment whether the patient has poor collateral circulation or not due to the high risk of symptomatic ICH after IV Alteplase in acute ischemic stroke with poor collateral circulation [10]. By using multiphase CTA brain, the study can be performed in three contiguous phases of CTA as 1^st phase, 2^nd phase, and 3^rd phase, which can be classified the stroke patients in three groups of collateral circulation: Good, Intermediate, Poor collateral circulation (Figure 9). In some center, CTA protocol in single phase and 1^st phase of multiphase CTA, the coverage of artery extends to aortic arch level to include the origin of three main arteries as the right brachiocephalic trunk, left common carotid artery (CCA), and left subclavian arteries that main trunks from those arteries as bilateral internal carotid artery (ICA) and bilateral vertebral arteries provide bloodstream to intracranial level. CTA brain findings in a patient with acute ischemic stroke by arterial occlusion are abrupt disappearance of contrast medium opacification at the thrombus site as “artery cut off sign”. Distal to the thrombus, the distal run-off arteries can be variable case by case reconstitute by collateral circulation. In addition, CTA provides information on the arteries’ status such as intracranial arteriosclerosis disease, vasculopathy, dissecting artery, intracranial aneurysm, cerebral AVM, dural AVM, assessment degree of arterial stenosis, and screening whole axis blood supplied intracranial system from aortic arch to vertex.

Figure 9.

A-I Multiphases CTA brain in three patients, 1st row (A, B, C) 1st case left proximal MCA occlusion with good collateral score, 2nd row (D, E, F) 2nd case right proximal MCA occlusion with fair collateral score and 3rd row (G,H, I) 3rd case left proximal MCA occlusion with poor collateral score.

CT Perfusion (CTP): It is performed by monitoring only the first pass of an iodinated contrast agent bolus through the cerebral circulation. This principle is used to generate time-attenuation curves for an arterial ROI, a venous ROI, and each pixel. use a semiautomatic option, which consists of first manually tracing a large ROI around the vessel and then letting the software automatically select an accurate ROI. The arterial ROI is optimally selected in one unaffected vessel that is perpendicular to the acquisition plane, either one of the anterior cerebral arteries (ACAs) or the contralateral MCA. In emergency settings, we prefer to select an ACA as the default arterial input function for simplicity because it has been shown to be adequate. The venous ROI is placed over the superior sagittal sinus or torcular Herophili. The software will generate color images of cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT). In the emergency settings, the quick interpretation of CTP is first seen MTT images for the area of increased MTT, if the area of image match to the clinical setting, then further analysis to CBF, CBV in the same area match to MTT image. If CBF and CBV are matched decreased, this is all area of the infarct core (no penumbra) but CBF decreased with normal CBV (or increased) will suggest ischemic penumbra (Figure 10).

Figure 10.

A-E CT-CTA-CTP: Case Acute ischemic stroke presents with right hemiparesis, NCCT brain demonstrated hyperdense clot sign at left M1 segment (A) and early ill-defined hypodensity areas in left basal ganglia and left frontotemporoparietal lobes (B). CTA brain (C) complete occlusion of left proximal MCA. CTP brain (D,E) mismatch defect (CBF-CBV map) in left cerebral hemisphere.

Summary Findings: CT Brain in Stroke

Acute Stroke (Day 0 to Day2)

Vascular Changes: - Hyperdense artery sign

Parenchymatous Changes: - Faint hypodensity area/Loss of gray-white matter differentiation/effacement of cerebral, cerebellar sulci/narrowing of subarachnoid spaces. CT signs for middle cerebral artery (MCA) territory infarction-loss of insular ribbon sign, obscuration of the lentiform nucleus may present.

Subacute Stage (Day 3 to 2 weeks):

• Usually no visible intraluminal clot density

• Increased sharpness (well-demarcated area) of hypodensity of the infarcted area

• Increased mass effect from cytotoxic edema

• Potential to hemorrhagic transformation (looking for hyperdensity lesion among the infarcted area)

Chronic Stage (more than 2 weeks)

• Decreased degree of brain edema.

• Hypodensity of the infarction is equal to CSF density.

• Signs of brain volume loss at old infarcted area such as ex vacuo dilatation of adjacent ventricle, widening of adjacent subarachnoid spaces, such as sulci, folia, and fissure dilatation.

• Retrograde Wallerian degeneration along the corticospinal tract may occur at the level of cerebral peduncle and pons.

MRI (Magnetic Resonance Imaging): In stroke imaging, MRI is one of the noninvasive techniques in the diagnosis of ischemic stroke and other types of strokes such as hemorrhage and stroke mimic conditions [12].

The basic principle of MR machine comprises a magnet embedded within the MRI scanner imaging use of radiofrequency (RF) wave to the brain and activate proton in all different tissues in the area scanned to spin, after that the proton is returning to its original state known as precession with release RF wave to the receiver coil. The different tissue types within the brain return at different rates and it allows us to visualize and differentiate tissues in the brain. MRI is superior to CT in terms of lack of radiation, excellent tissue contrast resolution in spatial and temporal resolution between different normal tissues in the brain, and also well discriminate between normal tissue and the abnormalities. Nevertheless, some disadvantages of the MRI study are it is a long duration scan, it needs the cooperation of the patient, it needs close monitoring, it is high cost, and it is not widely available in all hospitals.

MRI Acute stage: Stroke protocol (Axial DWI/ADC map, T2W, T2W_FLAIR, SWI) (Figure 11)

Figure 11.

A-E MRI brain (stroke protocol) composed of Axial DWI/ADC (A,B), T2W_FLAIR (C), T2WSE (D), SWI (E) for basic evaluation of acute infarction, exclusion of hemorrhagic stroke.

Diffusion weighted image (DWI) is a very important pulse sequence for diagnosing acute ischemic stroke, DWI can early detect acute ischemic stroke 80–90% of cases. Restrictive diffusion lesion in DWI is the area of cytotoxic edema that will be bright (hypersignal) and typically together with a low ADC value in the ADC map image (hyposignal) (Figures 11 and 12). The pattern of DWI will differentiate large vessel occlusion, small vessel infarction or cardiac emboli, or border zone infarction.

• T2WSE is for stroke mimic condition.

• T2W_FLAIR looks for the nonmatched area (T2W_FLAIR-DWI) in the acute stage, which probably represents an area of penumbra, evaluates white matter leukoaraiosis, and some time will help in the diagnosis of subarachnoid hemorrhage by MRI study.

• SWI (susceptibility weighted image) uses for the detection whether hemorrhagic transformation in area of infarction and also provides detection of cerebral hemorrhage prior to treatment or follow up after IV thrombosis treatment and also detect cerebral microbleeds (CMBs). The paramagnetic substances in hemorrhage display blooming of hyposignal (dark signal, signal void) lesion which is in contrast to CT scan hemorrhage is hyperdensity (white color).

Figure 12.

A–B MRI brain (ACUTE INFARCTION) DWI and ADC map demonstrates restrictive diffusion lesion (hypersignal in DWI and hyposignal in ADC map) in left body of corpus callosum and left frontoparietal convexity compatible with acute cerebral infarction (left ACA and MCA territory, Figure 11A) and borderzone infarction array punctate restrictive diffusion lesions (hypersignal DWI/ hyposignal ADC) in central of both frontoparietal lobes.

Subacute-chronic stage

On the subacute stage of infarction, there is no longer visualization of the hypersignal restrictive diffusion but hypersignal in T2W_FLAIR and T2WSE are well-delineated (Figure 13) in the early stage of subacute infarction, degree of mass effect from brain edema is still present.

Figure 13.

A, B, C, D: MRI brain (subacute and chronic infarction) Axial T2W_FLAIR (12 A) and Axial T2WSE (12B) reveals hypersignal lesion in left occipital lobe on T2W_FLAIR and T2WSE with pressure effect to compress left occipital horn suggests of subacute cerebral infarction Axial T2W_FLAIR (12 C) and Axial T2WSE (12D) reveals old infarction in right occipital lobe which hyposignal in T2_FLAIR and hypersignal in T2WSE.

Chronic stage of infarction, the infarcted brain tissue will be phagocytosis by macrophage with fluid replaced as old CSF lesion in the brain, therefore, chronic or old infarction will have a signal intensity similar to CSF, hyposignal T2W_FLAIR and hypersignal in T2WSE (Figure 13).

MR Angiography (Figure 14): Similar to CT scan that uses CTA for evaluation of vessel lumen, MR imaging also has 3D time-of-flight (3D-TOF) use of the movement of blood, and the flowing blood that enters the volume imaged will produce a signal for MRA imaging in the assessment of the intracranial and extracranial arteries. The advantage of MRA is that it is a nonradiation and noncontrast medium administration. The interpretation of MRA is almost similar to CTA for diagnosis of stenosis, occlusion, aneurysm, and AVM. The limitations in interpretation of MRA are inability to visualize calcium deposit at blood vessel, slow flow phenomenon, complex flow phenomenon etc. Those circumstances may cause overestimate of occlusion in the noncontrast MRA study. The hypersignal T1 lesion such as subacute hemorrhage will persist in TOF technique of MRA and may influence in MRA analysis. If one needs a definite evaluation of whether it is a true occlusion, true severe stenosis, or merely complex flow phenomenon, contrast enhanced MRA is helpful.

Figure 14.

A–E: MRA brain uses 3D TOF technique, Normal patency arterial lumen have high signal of MRA along course of arteries in source image (A), MIP images in coronal and axial planars (B,C). Disappearance of MRA signal in left ICA, left MCA and bilateral ACAs (D, E) could be due to severe arterial stenosis or occlusion of those arteries.

Cerebral Venous Sinus Thrombosis (CVST) [13, 14, 15, 16, 17]: Stroke on the cerebral venous system is not uncommon condition. The mean age is young adult and two-thirds of patients are women. It is caused by complete or partial occlusion of either cerebral venous system such as dural venous sinus (superior sagittal sinus, inferior sagittal sinus, transverse and sigmoid sinuses), cortical veins, deep venous system (such as thalamostriate vein, internal cerebral vein or basal vein of Rosenthal, vein of Galen and straight sinus) or in combinations. The mainstay challenge in diagnosis of CVST is due to nonspecific clinical symptoms, and widely clinical manifestations often mimicking other acute neurological conditions. Headache is the most common symptom of CVST in about 90% of cases and may be localized or diffuse or migraine-like and aura. Even though, further investigation by neuroimaging for detection CVST is suggested whenever, new onset of headache, persistent, worse on Valsalva, not response to regular medical treatment in the patient with have CVST risk factors. Stroke-like focal neurological symptoms are about 40% of cases with motor symptoms followed by visual impairment and aphasia and some cases with seizures. Nowadays, an increasing concern of this condition leads to increased detection of CVST patients. The patient is suspected of CVST and needs urgent neuroimaging to confirm diagnosis, such as CT and MRI to visualize blood clots or thrombosis in the cranial venous system.

CT brain (NCCT, CECT): It is the investigation modality of choice for the patients who are in the emergency department. NCCT can confirm or exclusion diagnosis by detecting acute thrombosis or blood clot (direct sign) as hyperdensity lesion in the course of dural venous sinuses, cortical vein, or deep venous structures and also evaluation the brain parenchyma for brain edema, intracranial hemorrhage (indirect sign). The density of blood clot is variable in density depend on the stage of thrombus, the acute thrombosis, blood clot is in hyperdensity (average 50–70 HU) in contrast to the brain (30–40 HU). If acute thrombus is along superior sagittal sinus (SSS) on axial CT scan suggests “hyperdense delta sign” (Figure 15A) and whenever along cortical veins on axial CT scan, we can call “cord sign” (Figure 15B) Even though, NCCT is more sensitive in the detection of deep cerebral venous thrombosis and cortical vein thrombosis than dural venous sinus thrombosis.

Figure 15.

A-H: NCCT, CTV in cerebral venous thrombosis NCCT brain (A, B) “hyperdense delta sign” in posterior of superior sagittal sinus (SSS) (A) and “hyperdense cord sign” in right cortical vein (B), bilateral internal cerebral veins (C,D) CT Venography reveals filling defect in SSS (E, F) Volume rendering technique (G, H) normal CTV (G) and nonopacification of contrast in SSS in case of SSS thrombosis (H).

Similar to the evaluation of hyperdense clot sign in acute ischemic stroke, before interpretation of the hyperdensity lesion such as acute thrombus, a complete evaluation of intracranial vascular system density is needed to get rid of the false sign of hyperconcentration blood.

The brain parenchyma changes (Figures 16A and B) such as brain swelling, vasogenic brain edema related to the site of venous occlusion. Intracranial hemorrhage can occur in the brain parenchyma as hemorrhagic venous infarction, or in the extra-axial locations such as subarachnoid hemorrhage, subdural hemorrhage usually relates to the site of venous occlusion.

Figure 16.

A–B Axial NCCT brain reveals cerebral venous sinus thrombosis with “hyperdense delta sign” (white arrow) in right sigmoid sinus with hemorrhagic venous infarction in right temporal lobe, small subdural hemorrhage is noted along right tentorium cerebelli (black arrow).

Contrast enhanced CT brain (CECT): In the case of equivocal in CVT diagnosis and no contraindication for contrast medium, the contrast enhanced CT by intravenously contrast medium administration is suggested either by injector or manually. CT density of intraluminal thrombus is relative lower than density of contrast medium, therefore, appear as filling defect nonopacification by contrast medium in course of thrombosed venous sinuses, veins. If the circumstance occurs in superior sagittal sinus thrombosis on axial CT scan, it was called “empty delta sign” (Figure 15E).

CT venography (CTV): Slightly different to CECT, CT venography used bolus contrast medium injection of 75–100 ml. by injector with an acquisition delay and automated CT study in the venous phase. CTV will provide an accurate detail in the evaluation of cerebral venous system. Before evaluation and interpretation, thin axial section contrast enhanced CT venography will be used to perform post processing rendering techniques such as maximum intensity projection (MIP) (Figure 15F) or surface, shaded displays (SSD) and volume rendering (VR) (Figure 15H) which all acquired from post-processing work station system send into Picture Archiving and Communication System (PACS). Partial or nonopacification of contrast medium in case of incomplete or complete occlusion of sinuses, and veins are demonstrated

Magnetic Resonance Imaging (MRI) brain: It is the noninvasive neuroimaging technique without exposure to the radiation. The patient who has contraindication to CT scan or equivocal diagnosis by CT scan are indicated for MRI study for diagnosis CVT. Similar to CT, the interpretation must be evaluation two main findings such as intraluminal clot sign along cranial venous system and parenchymatous sign, the change of the brain resulting from venous occlusion.

Intraluminal thrombus: Due to variable stage of the intraluminal clot, MRI on T1W and T2W have variable signal of intraluminal thrombus due to alteration in hemoglobin oxygenation and iron oxidation state in the blood clot such as acute stage (less than 7 days) thrombus signal is isosignal T1W and hyposignal T2W, subacute stage 7 days–15 days) T1W is hypersignal (Figure 17A and B) and T2W is iso- to hypersignal and chronic stage (greater than 15 days) T1W is isosignal and T2 W is hypersignal. Thus, the diagnosis of acute thrombus by MRI is difficult due to signal that seems like normal flow void signal in T2W [13]. Susceptibility weighted image (SWI) is pulse sequences that assist in evaluation of hemorrhagic component by blooming susceptibility effect of the hemorrhagic component to be slightly larger than regular size and easily to visualization (Figure 17).

Figure 17.

A–F MRI and MRV brain in patient with deep cerebral vein and dural venous thrombosis. Axial T1W (A) reveals hypersignal T1 of an intraluminal thrombosis in the vein of Galen, Axial SWI (B) demonstrates blooming susceptibility effect of paramagnetic substance(clot) and post contrast enhanced T1W (C) demonstrates filling defect of noncontrast medium opacification. In addition, nonopacification of right transverse sinus is also detected in the same patient (D). 3D CE-MRV (contrast enhanced MRV), MIP images demonstrate filling defect in vein of Galen and noncontrast segment n right transverse sinus. All of findings suggest subacute stage of cerebral venous sinus thrombosis.

After administration of contrast medium, T1W contrast enhances study, there is nonopacification segment of thrombosed sinuses, and veins cause filling defect of those venous structures (Figure 17) such as an empty delta sign.

Parenchymatous changes: These are indirect signs secondary to thrombus such as brain edema in the brain region related to the site of venous occlusion, hemorrhagic venous infarction, subdural hemorrhage, and subarachnoid hemorrhage. The parenchymatous abnormalities are better shown by MRI than CT as the area of hyposignal T1W and hypersignal T2 lesion in the brain parenchyma, usually in vasogenic edema and not followed arterial territory. Diffused weighted image (DWI) is the pulse sequence that allows subclassification of parenchymal abnormalities as either primarily vasogenic edema or primarily cytotoxic edema. The hyposignal on ADC mapping. In contrast with arterial ischemic stroke, many parenchymal abnormalities secondary to venous occlusion are reversible. After administration of contrast medium, on the T1W contrast enhanced images, marked enhancement of the subependymal plexus and the medullary veins that run perpendicular to the wall of the lateral ventricles are demonstrated. Hemorrhagic venous infarction can sometimes be present, cause susceptibility artifacts on T2*WI, SWI, and GRE images as blooming dark signal (Figure 17) in the infarcted area.

MRV (MR Venography) (Figure 17): It is an MRI technique for demonstration of cerebral venous structures. This technique can be performed either by noncontrast enhanced such as time-of-flight (TOF), phase contrast MRV or contrast enhanced study. Usually, we performed with noncontrast technique and normal cerebral venous sinuses will have normal hypersignal of flow along the course of cerebral venous sinuses includes dural venous sinuses, cortical veins, and deep cerebral venous system. If CVT occurs, there is no flow, no MRV hypersignal in the thrombosed venous structures. However, the limitation of noncontrast enhanced study is the flow artifact. To avoid this limitation, the contrast enhanced MRV may be beneficial. Contrast medium signal opacification entirely of the patency cerebral veins.

CVT can result in death or permanent disability, it generally has a favorable prognosis if diagnosed and treated early. CVT is treatable and curable by medical treatment, and the mainstay is prompt anticoagulation with parenteral heparinization.

Craniocervical Arterial Dissection: [18, 19, 20, 21] It is one of the causes of stroke up to 25% of cases. The patients are in young and middle-aged group. An accurate and prompt diagnosis of this condition is crucial because timely and appropriate therapy can significantly reduce the risk of stroke and long-term sequelae. Because of the great diversity in the clinical features of craniocervical artery dissection, imaging plays a primary role in its diagnosis, nowadays by noninvasive diagnostic imaging techniques such as CT angiography and MRI with MR angiography. To achieve an accurate diagnosis of craniocervical artery dissection, it is important to understand pathologic features (intimal tear, intramural hematoma, and dissecting aneurysm) and the spectrum of imaging findings of CT angiography, magnetic resonance (MR) imaging with MR Angiography, and conventional angiography; and potential pitfalls in image interpretation.

The causes of arterial dissection are traumatic and spontaneous in origin. Head and neck trauma or minor trauma as cervical manipulation can trigger in patients with underlying arteriopathy. Connective tissue diseases, such as fibromuscular dysplasia, Ehlers-Danlos syndrome type IV, Marfan syndrome, autosomal dominant polycystic kidney disease, and osteogenesis imperfect are the underlying cause of arteriopathies. When a primary tear occurs in the intima of the arterial wall, the blood stream can penetrate into the depth of the arterial wall, such as tunica media and extends cranially according to the direction of blood stream, then intramural hematoma develops and compression to the arterial lumen. If dissection toward adventitia, it will form dissecting pseudoaneurysm and thromboembolic phenomenon can occur.

Common locations of dissection is the extracranial segment in the cervical level, spontaneous dissection particularly internal carotid artery (ICA) tends to occur at distal to carotid bulb and extends not beyond ICA entry to the petrous bone. For the extracranial vertebral artery (VA) dissection, the most common locations are at V2 segment (foramen transversarium segment) and V3 segment (extravertebral segment). The reason of high incidence in the extracranial arteries dissection is those neck arteries can mobility than intracranial arteries and also trauma against to adjacent bony structures such as styloid process or cervical spines. The most frequent clinical manifestation of carotid territory ischemia (49%–82.5%), whereas dissections without luminal narrowing cause more local signs and symptoms. A completed stroke usually occurs during the first 7 days after the onset of symptoms but can occur up to 1 month later. Local signs and symptoms include head, facial, or neck pain, Horner syndrome, pulsatile tinnitus, and cranial nerve palsy. Headache is frequently the earliest symptom (47%) of patients. The clinical manifestation from vertebral artery dissection is headache or neck pain accompanied or followed by posterior circulation ischemia (57%–84%). Treatment of craniocervical dissection is by medical therapy, anticoagulant drugs are used to prevent thrombosis and embolism caused by extracranial dissection. Endovascular treatment is for the patient who remains symptomatic due to thromboembolic events or subarachnoid hemorrhage from dissecting pseudoaneurysm intracranial location.

Imaging: Even though Digital Subtraction Angiography (DSA) is the gold standard in the diagnosis craniocervical dissection, but noninvasive imaging technique CT Angiography or MR Angiography is widely accepted and used in clinical practice.

CT Angiography (CTA) (Figure 18): CTA study in diagnosis craniocervical artery dissection may study from aortic arch up to cervical and intracranial levels continuously. Normal CTA is complete contrast medium opacification of the arterial lumen from origin to the whole course of arteries. Based on pathophysiology, eccentric narrowing of the arterial lumen with mural wall thickening cause “target sign” in axial CTA scan. Other signs such as short segment arterial stenosis, total occlusion, dissecting aneurysm, filling defect, intimal flap, focal stenosis and dilatation (string and pearl sign), and tapering stenosis (flame sign) may be detected. Please note that intimal flap is a rare finding for craniocervical arterial dissection and is common in carotid dissection. The sensitivity of CTA in the diagnosis of cervical artery dissection is 74%-98% and specificity is 84%-100%.

Figure 18.

A-F CT Angiography of a 50-year-old woman, known case of aortic dissection type A, presented with quadriparesis for 5 hours suspected of carotid dissection. Axial CTA (A–D) demonstrates radiolucency lines in the aortic arch (A), dissection extends to right brachiocephalic artery, left CCA and left subclavian artery (B), bilateral CCAs (C) cause near total occlusion LCCA with eccentric residual lumen (D). MPR in coronal plane (E) with typical string sign and 3D Volume rendering image (F) decreased contrast opacity in the remaining LCCA and LICA.

MRI and MR Angiography (MRA) (Figure 19): Similar to the CTA study, the MRA study may study in the whole axis from the aortic arch to the intracranial level. Whenever suspicious of extracranial arterial dissection, MRI with fat-suppressed T1 weighted image is a recommended pulse sequence in detection intramural thrombus. If intramural thrombus is in the subacute stage (3 days up to 2 months duration of blood clot), the hematoma will give hypersignal in T1W; therefore, the mural thrombus might be demonstrated for diagnosis of arterial dissection. Luminal stenosis, eccentric shaped lumen (mural wall thickening with the displacement of arterial lumen off midline and external diameter enlargement from the summation of mural hematoma are all possible findings that assist in the diagnosis of arterial dissection. MRI and MRA are excellent imaging methods in diagnosis of carotid artery dissecting artery with sensitivity 87%-99% compare to DSA whereas sensitivity is about 60% for vertebral artery (VA) dissection. The detection in vertebral artery dissection is quite lower than in carotid artery are due to small size of vertebral artery and flow related enhancement of paravertebral veins make the diagnosis is difficult. In clinical practice, when equivocal finding in diagnosis VA dissection, CTA is recommended.

Figure 19.

MRA craniocervical artery of a 69-year-old male, source images MRA intracranial level (A, B) 3D-TOF demonstrates hypointense signal of intimal flap in bilateral V4 segments of vertebral arteries. MRA MIP images (C, D) arterial dissection extends up to vertebrobasilar junction. MRA MIP image (E) at cervical level demonstrates normal MRA of all bilateral CCA, cervical ICAs, cervical VAs. DWI images (F, G) demonstrate restrictive diffusion areas of acute infarction in pons, cerebellum and midbrain from thromboembolism.

Recommendation, when clinical suspicious of carotid artery dissection, we can use either CTA or MRA with similar results, whenever, suspicious of VA dissection, CTA may be superior to MRA.

2. Neurological complication of anticoagulation therapy

The most common intracranial complication during regular treatment by anticoagulant drugs is intracerebral hemorrhage (ICH) [22, 23, 24, 25]. Basically, the cause of ICH is classified into two groups as primary cause due to spontaneous rupture of small vessels or amyloid angiopathy as a majority of the patients about 78%-88% and secondary cause associated with tumor, impaired coagulopathy as a minority group. Even though small in number but significant risk factors with ICH such as hemophilia or acute leukemia with thrombocytopenia or patient during treatment by anticoagulant drugs, massive intracranial hemorrhage is often cause of death.

2.1 Cause of intracranial hemorrhage (ICH)

ACQUIRED:

Iatrogenic coagulopathy

• ICH related to aspirin

• ICH related to anticoagulation, heparin, and Coumadin

• ICH related to thrombolytic treatment

Neoplastic coagulopathy

• ICH related to leukemia

• SDH in cancer patient

Rare cause of ICH

• Drug-induced thrombocytopenia

• Uremia

• Alcohol

• Liver transplantation

CONGENITAL:

• Hemophilia

2.2 Physiology of hemostasis

Two important mechanisms against bleeding are blood coagulation and platelet-mediated hemostasis. The coagulation cascade is triggered as soon as blood contacts the injured endothelial lining. The combination of both coagulation cascade and active formation of the platelet plug is effective autoregulation mechanisms in occlusion of a vascular lesion. Coagulation cascade mechanism have its own two main pathways: 1) intrinsic pathway by physical-chemical activation which its role is not well understanding and 2) extrinsic pathway activated by tissue factor released from the damaged cell.

Extrinsic Pathway: When blood vessel wall injuries exposed plasma to tissue factor, then, Factor VII is a plasma protein bind to tissue factor and activated to factor VIIa, this complex will activate factor IX, X to factor IXa, Xa. Factor Xa and its cofactor Va form a phospholipid-bound complex called the prothrombinase complex, which is highly activated on the surface of platelets and cleaves prothrombin (factor II) to thrombin (factor IIa). Thrombin cleaves fibrinogen (factor I) to fibrin (factor Ia), which is covalently cross-linked by factor XIIIa into fibrin strands. Factor VIII binds to vWF (an adhesive protein important for the generation of the initial platelet plug). Thrombin feedback is important to the entire system. Thrombin, one generated is powerful procoagulant further conversion factor V, VIII to factor Va, VIIIa and covert more prothrombin to thrombin. Thrombin will further accelerate the entire cascade in the formation of a large amount of fibrin.

Regulatory mechanism of the coagulation cascade, such as tissue factor pathway inhibitor, antithrombin III, activated protein C and protein S, thrombomodulin, and fibrinolytic system, is to limit the amount of fibrin clot avoiding tissue ischemia and to prevent widespread thrombosis.

2.3 Pathophysiology of bleeding disorders

Coagulopathies leading to intracranial hemorrhage mostly from acquired caused. Iatrogenic coagulopathy from aspirin, anticoagulants, and thrombolytic agent treatment.

Antiplatelet drugs: Aspirin is the most common antiplatelet drug that is used daily in clinical practice such as acute MI and arterial occlusive cardiovascular disease. Its mechanism is to inactivation enzyme cyclooxygenase result in decreased platelet aggregant thromboxane A2. Incidence of intracranial hemorrhage due to aspirin In the 1991 Swedish Aspirin Low-Dose Trial investigators of patients with a history of TIA or minor stroke reported that the prevalence of intracranial hemorrhage was 1.5%. Finally, in 1997, the International Stroke Trial Collaborative Group concluded that administration of 300 mg aspirin daily compared with placebo following acute stroke pre-vented 1.2 ischemic strokes per 100 treated patients but caused in excess of 0.41 ICHs. Aspirin therapy for primary or secondary stroke prevention and primary MI prevention may slightly increase the low baseline risk of ICH but the increased risk is usually outweighed by the benefits of aspirin. Other antiplatelet agents: clopidogrel (Plavix), abciximab (Reopro), etc. act as glycoprotein IIb/IIIa inhibitors. The incidence of ICH in the clopidogrel group was 0.33%, whereas it was 0.47% in the aspirin group. The newer antiplatelet agents seem to be associated with an ICH risk profile similar to that of aspirin.

Anticoagulant drugs: Warfarin, heparin, and enoxaparin are the most common anticoagulants in routine clinical practice.

• Warfarin is an oral anticoagulant that interfere with vitamin K metabolism in the liver and cause impairment synthesis functional coagulation factors II, VII, IX, X and protein C, protein S. Therefore, Warfarin administration can prolong prothrombin time (PT), INR.

• Heparin is administered parenterally and inhibits action of antithrombin III cause prolong of the partial.

• Thromboplastin time (PTT).

• Enoxaparin, low molecular weight heparin, similar action to heparin with a longer half-life time (4.5 hrs.)

Anticoagulant therapy related ICH is about 10%-20% and ICH is the most dreaded and least treatable complication. The mortality rate is about 46%-68%. The distribution of intracranial hemorrhage related to anticoagulant therapy is in the brain parenchyma, intracerebral hemorrhage (ICH) about 70% followed by subdural hemorrhage (SDH). There is no specific predilection in the brain. Risk factors such as hypertension, increasing age, and previous cerebral infarction. The mechanism of spontaneous ICH developing during anticoagulants is not clearly understood. Postulate that patients with underlying hypertension with hemorrhage derived from small vessel vasculopathy, usually have normal hemostatic mechanisms but fail when anticoagulant.

Thrombolytic agent: Fibrinolytic agents have been used in clinical practice, such as acute MI and acute stroke. The examples of drugs in this group are the exogenous substances streptokinase, urokinase, and endogenous tPA. The mechanism in action is to activate the body’s fibrinolytic system by converting plasminogen to plasmin. Plasmin binds to fresh fibrin clots, dissolving them and generating fibrinogen degradation products. Intracranial hemorrhage cause by the thrombolytic agent is in lobar hemorrhage 70%–90% and multiple locations in almost one-third of patients. ICH related to rtPA tended to have fluid levels in the hematomas (suggesting continuing or repeated hemorrhages), multiple parenchymal hemorrhages, and blood in multiple compartments (intraventricular, subarachnoid, subdural, and parenchymal). Patients with post-rtPA ICH also tended to suffer a catastrophic clinical course, with dying or ending up in a persistent vegetative state within hours of hemorrhage onset. Thus, in the case of acute ischemic stroke, there is a summary of absolute and relative contraindication to IV rtPA [6].

Absolute and relative contraindications to IV rt-PA for acute ischemic stroke.

Absolute contraindication

• Acute ICH including hemorrhagic infarction.

• History of ICH (microbleed is not contraindicated).

• BP>185mmHg, BPs>110mmHg.

• Serious head trauma or stroke < 3months.

• Thrombocytopenia (platelet <100,000/mm3) and coagulopathy (PT>15, INR>1.7).

• LMWH within 24 hr (38% risk of sICH, 29% risk of death, 33% favorable outcomes, od 0.84 for sICH, od5.3 for death).

• DTIs (TT is sensitive to the presence of DITs).

• Factor Xa inhibitor.

• Severe hypoglycemia(<50mg/dl) and hyperglycemia(>400mg/dl) may be permitted for IVT.

• Early radiographic ischemic changes (>1/3 MCA).

Relative contraindication

• Advanced age (>80yrs.)

• Mild or improving stroke (NIHSS<5)

• Severe stroke (IVT should be cautiously administered in NIHSS>25 at 3–4.5 hrs.)

• Major surgery within 2 weeks (some 3 months)

• Arterial puncture of noncompressible site

• Recent GI bleeding or GU bleeding

• Seizure at onset

• Recent MI within 3 months

• Intracranial structure abnormality (axial tumor, AVM, aneurysm)

• Dementia

CT brain (Figures 20–22): Noncontrast CT brain is the investigation modality of choice for the patient who had a neurological disorder and was suspected of coagulopathy related symptoms. The most common finding is intracerebral hematoma (ICH), followed by SDH. The CT pattern that raises suspicious of coagulopathy related intracranial hemorrhage is multicompartments hemorrhage such as bleed in the parenchymatous and also in subarachnoid space and in subdural space at the time of initial CT study, which leads to suspicion of hemorrhage related to coagulopathy. The density pattern of hemorrhage is varying case by case as homogenous hyperdensity either or heterogeneous hyperdensity, fluid-hemorrhage level. The density of the hyperdensity portion is 60–80 HU.

Figure 20.

A,B,C Axial NCCT brain of patient with history of acute aortic dissection type A S/P modified Bentall operation with hemiarch replacement with right carotid artery bypass and resternotomy with clot removal and CABG, on heparin and develops alteration of consciousness. Spontaneous intracranial hemorrhage mainly in subarachnoid space (SAH) (black arrow) with small fluid –level ICH (white arrow) in right frontal lobe.

Figure 21.

A,B,C Axial NCCT brain of a patient with congenital heart disease postsurgery (on warfarin), presented with alteration of consciousness. Spontaneous intracranial hemorrhage mainly in subarachnoid space (SAH) (black arrow) and ICH (white arrow) in left frontal lobe.

Figure 22.

A-F A 53-year-old man, with history of DM and HT presented with right hemiparesis and right facial palsy. Acute ischemic stroke was diagnosed at outside hospital. Treatment was giving rTPA at 9.20 p.m. At referred hospital, Axial NCCT at 0.10 a.m. (A, B) reveals ill-defined hypodensity area in left lentiform nucleus, left insular cortex and left high cortical frontal lobe. AI ASPECT score=8 (neuroradiologist reading score=7) Further treatment with mechanical thrombectomy (Figure 20D, E) was performed with completely reopening of left MCA and no immediate complication. Axial NCCT brain (07.33 a.m. the day after thrombectomy) reveals ICH in left basal ganglia with IVH.

3. Summary

Neuroimaging is a noninvasive investigation tool that is essential not only to confirm the diagnosis of emergency neurological diseases such as stroke but also to play a role in triage patients into receiving proper medical treatment, surgical treatment, or intervention treatment. Basic interpretation of CT brain and MRI brain in stroke, CVT, dissection, hemorrhage warrants the understanding of density (CT) or signal intensity (MRI) changes of affected brain tissue in stroke and intraluminal thrombus in each stage of the disease. Further using of advanced neuroimaging investigation such as CTA, multiphase CTA, CTV, and CTP aimed for more specific conditions of the artery disease such as arterial thrombosis, arterial dissection, venous disease such as venous sinus thrombosis, yet, also reduced the need for more invasive investigation such as digital subtraction angiography.