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Slide 5 Q: What type of imaging modalities are used to evaluate patients presenting with acute stroke? A: Nonenhanced CT head vs. MRI.A large part of our discussion today will involve appropriate ordering of imaging studies for specific clinical indications. The American College of Radiology has devised ACR appropriateness criteria to provide guidance to physicians when deciding what type of imaging examination to select for the work-up of their patient. These can be found on-line at acr.org

Slide 6 This is an example of what a normal noncontrast CT head looks like.

Slide 7 Q: Here is an example of a normal MRI. Can you identify the different sequences here? A: T1, T2, FLAIR (left to right)Q: What things allow you to distinguish T1 and T2? A: CSF is dark on T1 and bright on T2.• How can we distinguish T1 from FLAIR? A. It is difficult when just

beginning. Look at gray matter. On FLAIR, it is slightly hyperintense to white matter; on T1 it is slightly hypointense to white matter. FLAIR images are T2 weighted but the CSF signal is nulled. This makes edema in the parenchyma stand out, particularly when the abnormality is adjacent to CSF since the CSF is also bright on T2.

*Recognizing a FLAIR sequence is considered more advanced and not part of the stated learning objectives for this workshop.

Slide 8 Q: What is the most sensitive method of detection of acute ischemia? A: DWI on MRI. The sequences here are from the same patient and are DWI (left) and the ADC map (right). These are the images we use when we are looking for acute ischemia. Areas of infarct will look bright on DWI and are called “restricted diffusion.” Areas of infarct will look dark on the ADC. When there is matching bright signal on DWI and dark signal on ADC, that represents restricted diffusion, which is what we would expect to see in the setting of ischemic infarct.

Slide 9 Q: Describe factors which influence which modality is chosen. A: Nonenhanced CT should be the first exam for patients who are candidates for the administration of TPA. In the emergent setting, the availability, shorter imaging time, ease of performing on patients who are unable to cooperate, and high sensitivity for detection of ICH, make CT the best initial exam for a patient with acute neurologic deficits. Patient who have evidence of ICH on nonenhanced CT head are excluded from receiving tpa. Patients must be within a window of 3 hours (many stroke centers use 4.5 hrs now) from onset of stroke symptoms to be considered for intravenous tpa. Patients who present outside of this window are considered to have greater risk of developing ICH after tpa administration and thus are excluded.While MRI is more sensitive for detection of acute ischemia, its decreased accessibility makes it difficult for all patients who have signs and symptoms of stroke to be imaged immediately with MRI. In addition, studies which have determined who will benefit from tpa have not been based on findings seen on NECT head, NOT MRI findings.

Slide 10 Q: What modalities can be used to evaluate the cerebral vasculature? A: MRA, CTA and DSA/convention/catheter based angiography can be used to evaluated the cerebral arterial vasculature.

Slide 11 Let’s discuss the advantages and disadvantages to each of these modalities that are used to study the cerebral vasculature. Consider having students break into three small groups. Each group is assigned one of the modalities from the above three rows and then needs to come up with pros and cons of that particular exam. After a few minutes (no more than 5), a representative from each group should state the answers that their group gave. Answers appear on next slide where chart is filled in.

Slide 12 Most recent literature suggests that the gap between sensitivity of MRA vs. CTA in detection of aneurysm has closed when MRA performed on 3T with optimized technique. The caveat here is that 3T and optimized technique are not as widely available as MDCT with >/= 16 detectors. >/= 16 MDCT approach DSA aneurysm detection for aneurysm > 3 mm. For aneurysm <3 mm, DSA is superior to both CTA and MRA.

Slide 13 Lets take this opportunity to review the normal anatomy of the intracranial circulation.Q. What kind of exam is this? A: MRA of the intracranial circulation, frontal projection.Q: Label the normal anatomy of the cerebral vasculature. First anterior - ICA, ACA, MCA; and then posterior: – vertobasilar and branches and PCA.

If you are using an Ipad for this workshop, the next few images you can have the students draw the labels on the images

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Slide 15 Q: Now label normal vasculature on in lateral projection: anterior circ – ICA and ACA; posterior circ – verts, basilar and PCA.

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Slide 17 Q: What vessel connects the anterior and posterior circulation? A: Posterior communicating artery.Q. Can you draw where you would see it? A: see labeled version on next slide

Slide 18 The yellow line represent where the posterior communicating artery would be found. We do not always see it on MRA because of its small caliber.

Slide 19 Q: In what clinical scenarios should a clinician order an MRA? A: MRA is an excellent choice for a noninvasive screening exam for aneurysm or as an exam to follow up an aneurysm that is being managed conservatively. This is because no XRT and no administration of contrast (no gad). MRA is also often done in the setting of acute stroke in conjunction with MRI to evaluate for high grade stenosis in the intracranial circulation.

Slide 20 We will now also review normal anatomy of the major venous sinuses. Q: What sort of exam is this? A: MR venogram. Facilitator should mention that we do not need contrast (gad) for this exam. Have student identify some of the normal venous anatomy (superior sagittal, straight, transverse, sigmoid sinuses, jugular veins, internal cerebral veins, vein of Galen) Q: When is MR venography utilized ? A: Clinical settings when venous thrombosis occurs (hypercoagulable states, pregnancy, dehydration, etc) and presentation with headache, seizure of neurologic deficit.

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Slide 22 This is a 78 yo male who came in to the ED. Q. How do you think he may have presented? A. Abrupt onset of left sided hemiparesis, sensory loss on left side of body.

Slide 23 Q. This study was obtained 24 hours after the onset of symptoms. How would you describe the findings? A. There is a wedge shaped hypodense/hypoattenuating area with mild mass effect resulting is some effacement of the sulci and mild compression of the right frontal horn. Q: What is responsible for this appearance. A: Edema caused by ischemic infarct

Slide 24 This is same patient as on previous slide.Q: What type of images are these? A: DWI (left); ADC map (right)Q: What do these images tell us? A: That the infarct in acute. Bright signal on the diffusion weighted image with corresponding low signal on the ADC map represents restricted diffusion. In the clinical setting of stroke, the restricted diffusion represents an acute infarct. [if students ask, the simplest way to explain the ADC map, is that it takes away the element of T2 weighting that is present on DWI]

Slide 25 YOU MAY USE THIS SLIDE TO HELP STUDENTS UNDERSTAND HOW DWI BECOMES POSITIVE. THE BIOCHEMISTRY DISCUSSED HERE, HOWEVER, IS NOT INCLUDED IN THE LEARNING OBJECTIVES AND CAN BE SKIPPED IF WISH-DWI (diffusion weighted imaging) represents the degree of free movement of water molecules.-Normal neurons (upper row) have intact ATP powered Na+/K+ pumps in their cell walls that maintain active transport that translates into normal cell volume and normal constituency of extracellular fluid space (the space between adjacent cells).-With ischemia severe enough to infarct tissue, the Na+/K+ pumps are irreversibly destroyed. Active transport across neurons ceases and the osmotic gradient is lost. As a result, simple osmosis causes extracellular fluid to enter the neurons with no resistance.-The uncontrolled influx of extracellular fluid causes marked cellular swelling. This swelling results in “cytotoxic edema” that accompanies infarction. As the neurons and glial cells swell, the extracellular space surrounding the cells is markedly reduced and thus, the free movement of water molecules is limited/restricted = restricted diffusion.-At baseline, there is relatively less water diffusion in the intracellular compartment relative to the extracellular compartment, and thus flux of water into the intracellular space also contributed to restricted diffusion.

Slide 26 Q: At what point after the onset of stroke like symptoms does DWI become positive? A: As early as 30 minutes and up to 2 hours.Student often ask if the DWI will remain positive thereafter. We do not expect students to know this but, when the question comes up, DWI typically normalizes after 2 weeks. This means that the bright signal in the infarcted area will no longer be bright on DWI.

Slide 27 55 yo female with new right hemiparesis, right neglect and expressive aphasia.Q: What type of studies are displayed here? Be specific. A: Nonenhanced CT head (left) and DWI from MRI (right).Q: The head CT was called normal and here is a select slice through the normal head CT. We also show diffusion weighted images from the same level. What do the diffusion weighted images tell us? A: Restricted diffusion in the left MCA distribution compatible with left MCA infarct.

Slide 28 The NECT head was obtained 1.5 hours after onset of sx. The MRI was obtained within 45 minutes after the NECT head, thus 2.25 hours after onset of sx.Q: How can you explain the discordance in the findings between these two studies obtained in such a short interval? A: In the setting of acute stroke, DWI can become positive within 15 to 30 minutes. CT takes a minimum of 6 hours before signs of early ischemia can be detected. Thus, in the setting of acute stroke, it certainly possible to have a negative CT and MRI with positive signs of acute ischemia on DWI.

Slide 29 Q: What is in your differential diagnosis? A: Stroke, hemorrhage, recreational drugs, demyelinating disease.

Slide 30 Q: What imaging test would you order? A: NECT.Q: Why? A: The patient’s symptoms began 2 hours ago and if he is having a stroke, he is in the window for receiving iv tpa. Before giving iv tpa the following needed to be excluded on the NECT head: 1. ICH 2. evidence of infarct on imaging that involves > 1/3 of arterial distribution involved 3. intracranial mass lesionQ: Why not MRI first since we know that DWI is the best method for detection of acute ischemia? A: We are trying to make sure that it is safe for this patient to receive tpa as quickly as possible. Studies performed to determine whether or not patients should receive tpa, were based on findings on NECT, not MRI.

Slide 31 Q: What type of study is this? A: NECT headQ: What is/are the findings? A: Hyperdensity in the left MCA which is compatible with thrombus. Have a student circle it.

Slide 32 Same patient 5 days later.Q: What has happened in the interval? A: Infarction has progressed, with increased edema (edema peaks at 2-5 days) and development of hemorrhagic transformation.Q: What is the major risk incurred by hemorrhagic transformation? A: Increased mass effect that can result in herniation.

Slide 33 Q: What are the signs of mass effect? A: Increased effacement of sulci, increased compression of left lateral ventricle, subfalcine herniation.

Slide 34 Q: How does hemorrhagic transformation of ischemic infarct occur? A: Reperfusion into the ischemically injured vessels can result in extravasation of blood through the damaged blood-brain barrier. Complicates about 15-20% of ischemic infarcts.

Slide 35 Here is the 67 yo male who suffered a left MCA infarct with hemorrhagic transformation, 2 months later.Q: What has happened to the blood products? A: Blood products have broken down and no longer hyperdense to brain.Q: What has happened to the edema? A: With infarcts, edema peaks at 2-5 days. This infarct is 2 months old and thus the edema has resolved.Q: How can we differentiate this chronic infarct from an acute one? A: We no longer see the signs of mass effect (effacement of sulci, compression of the ventricles, midline shift), but instead, see signs of volume loss (the left lateral ventricle is dilated, the adjacent sulci are widened).

Slide 36 This patient has new onset of acute hemiparesis and sensory loss.Q: Can you identify the acute and chronic infarcts shown here and discuss the differences? A: There is a large wedge shaped area of restricted diffusion in the left MCA distribution (bright signal on DWI and dark signal on ADC). This is the patient’s acute infarct and explains the abrupt onset of new neurologic deficits. There is corresponding increased signal on the T2 image because edema is bright on T2. The wedge shaped area of even brighter increased T2 signal in the right parietal lobe represents a chronic infarct. It is bright because of the loss of brain tissue in this region allowing some CSF signal to be seen and also scarring which occurs in the brain (gliosis) after an infarct is bright on T2. Clues that this is chronic are the signs of volume loss/negative mass effect in the right parietal lobe and there is no bright signal on the DWI images in this region.

Slide 37 Q: What is your differential dx? A: venous sinus thrombosis, arterial infarct (unusual to have h/a with arterial infarct), isolated intracranial HTN/pseudotumor cerebri.

Slide 38 Q: What type of imaging examination should be ordered? A: Given the abnormal neurologic exam, we are concerned about infarct. Venous infarcts are more common in children and young adults than in older population. OCPs are known to have a prothrombotic effect. While, it would not be wrong to obtain a noncontrast head CT in this situation, particularly given that venous infarcts often bleed, the best exam is MRI/MRV given the 3 day history (this patient would not be a candidate for tpa), our concern for venous sinus thrombosis (this is an MR diagnosis) and sensitivity of DWI for ischemia.

Slide 39 While MRI/MRV is the best examination given the concern for venous thrombosis and ischemia, nonenhanced CT head is still frequently obtained first, when patients come through the ED simply because of ease, rapidity and sensitivity for ICH.Q: Why are venous infarcts often associated with ICH? A: The arterial supply to the infarcted tissue is not compromised and thus hemorrhage within this tissue is common.

Slide 40 Q: What Study is this? A: MRVQ: Compare patient’s study to normal, what vessels are not identified on our patient? A: Sup Sag Sinus, bilateral transverse sinuses, bilateral sigmoid sinuses are not visualized.Q: What does this make you concerned for? A: thrombosis of the dural venous sinuses.

Slide 41 Q: What are patient’s risk factor(s)? A: Oral contraceptive agents are known to have a prothrombotic effect.

Slide 42 Q: What are some other risk factors for venous sinus thrombosis? A: dehydration, pregnancy, trauma, infection, malignancy, malnutrition, chemotherapy, indwelling catheters.

Slide 43 Q: Now let us turn to patient’s MRI. What do we expect to see on the DWI? A: Bright signal on DWI, which is compatible with acute ischemia/infarct.

Slide 44 Q: What sequences do we have here? A: axial DWI and axial T2Q: Do you think this patient has evidence of ischemia/infarct? A: Yes, there is bright signal on the DWI sequence indicating restricted diffusion, c/w acute infarct. The bright signal on the T2 sequence represent edema. The dark areas within the restricted diffusion and edema represent blood products. This patient has a bleed as was already seen on NECT head.

Slide 45 Our last patient had both severe headache and neurologic deficits and would be considered to have a secondary type of headache. Let’s take this opportunity to transition into discussion of imaging of headaches.Q: Can you give examples of other secondary headaches?A: -head and/or neck trauma (e.g., intraaxial and extraaxial hemorrhage, dissection)-cranial or cervical vascular disorder (e.g., Giant cell arteritis, CADASIL, MELAS. C-reactive peptide, ESR may be relevant tests)-non-vascular intracranial disorder (e.g., Mass effect from tumors)-substance abuse or its withdrawal (e.g., opioids, anabolic steroids, ethanol, marijuana, cocaine)-Infection (e.g., HIV, Lyme’s disease due to Borrelia burgdorferi, meningitis)-disorder of homeostasis (e.g., hypoxia, hypercapnia, pheochromocytoma, hypertensive disorders of pregnancy, hypothyroidism)-disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cranial structures (e.g. skull disease, sinonasal infection/inflammation, dental or orbital infection/inflammation)-psychiatric disorderWith secondary headaches, imaging may be used to focus more on identifying and distinguishing among the secondary types that may account for the patient’s complaints.

Slide 46 Q: What are examples of primary headaches?A: migraine, tension-type, cluster Headaches (chronic in nature). Primary headaches do not require imaging.

Slide 47 Q: What should be done next for this patient? A: Non enhanced CT head. You must exclude SAH in this patient and CT is considered superior for detection of SAH.

Slide 48 Q: When should a noncontrast CT head be ordered in the clinical setting of headache?A: Patients who: 1. present with “worst headache of life.”, need to exclude SAH

2. Present with sudden severe “thunderclap” headache.

3. exclude herniation prior to LP4. evaluate for hydrocephalus.

Slide 49 Q: What is the abnormality? A: subarachnoid hemorrhage in the left sylvian fissure and parasagittal frontal sulci.Q: What are you concerned is the underlying etiology of the SAH? A: aneurysm

Slide 50 Q: What imaging examination would be performed next? A: CT angiogram.Q: Why is CTA preferable to catheter angio or MRA? A: immediately available, quick, minimally invasive, high diagnostic yield per radiation dose, and typically more finally conclusive than MRA (unless done on 3T with optimized parameters). Also MRA requires sick patient to hold very still for longer period of time in order to obtain a high quality exam.

Slide 51 Q: What if CTA is negative? A: catheter angiogram is the next appropriate step in a patient with nontraumatic cisternal subarachnoid hemorrhage. Learner needs to know that a ruptured aneurysm is a high stakes “can’t miss” diagnosis with a dismal natural history if left undiagnosed and untreated due to high rates of fatal rebleeding, etc)

Slide 52 The image is a 3D reformat of the catheter angiogram, showing a paraophthalmic left internal carotid artery aneurysm.Q: What are the treatment options for ruptured aneurysm? A: Endovascular coil embolization and surgical clipping.

Slide 53 Q: What are advantages and disadvantages to each? A: Endovascular coil embolization is less invasive, thus shorter hospital stay, quicker recovery time. Endovascular coiling has a higher rate of aneurysm recurrence. However, it has not been shown that the higher angiographic rate of recurrence equates with a higher risk of rebleeding. Surgical clipping is more invasive, thus longer hospital day and longer recovery time; lower rate of aneurysm recurrence. Risk of stroke or death is about equal for the two (Raja et al 2008)

Slide 54 This is an example of a large aneurysm arising from the tip of the basilar artery (left) which was coiled. Plain radiography of skull (left) and axial CT image (bone window) on right demonstrate what a coil pack looks like after an aneurysm has been coiled. The coil pack is metallic density.

Slide 55 Q: What are the most common location location of intracranial berry aneurysms? A: (1) a comm (2) p comm (3) mca tri/bifurcation.Intracranial aneurysms tend to occur at vessel branch points/bifurcations because normal laminar flow is disrupted. The turbulent flow weakens the wall of the vessels and a saccular dilatation can develop (aneurysm). Apply LaPlace’s Law to aneurysms - as radius increases, wall tension increases which makes rupture more likely. Instructors may want to use analogy of blowing up a balloon that will eventually burst when wall tension too high.

Slide 56 Q: How do aneurysms cause headaches? A: When aneurysms rupture, the hemorrhage in the SAH space irritates the meninges and results in severe h/a. Some patients (10-30% reported in the literature) will present with headache couple weeks to couple hours prior to rupture caused by sentinel hemorrhage. Occasionally patient may present with focal neurologic deficit or headache due to expansion of aneurysm causing increased pressure.MOST COMMON EXAMPLE = enlarging p. comm aneurysm resulting in retroorbital h/a and oculomotor nerve palsy.

Slide 57 Q: What examinations can be used to detect aneurysms? A: CTA, MRA can both be used for detection of intracranial aneurysm with excellent sensitivity. Conventional angiography is gold standard but is invasive and thus carries with it associated risks (transient neurologic deficit in 1%, permanent neurologic deficit in 0.5%). CTA used over MRA in setting of rupture due to increased accessibility, ease and speed of exam.

Slide 58 Q: Where is this aneurysm located? A: left MCA bifurcation

Slide 59 Q: Who is at increased risk for developing aneurysms? A: Several heritable conditions associated with intracranial aneurysm formation, including autosomal dominant polycystic kidney disease, neurofibromatosis type I, Marfan syndrome, multiple endocrine neoplasia type I, pseudoxanthoma elasticum, hereditary hemorrhagic telangiectasia, and Ehlers-Danlos syndrome type II and IV. Smoking, excessive alcohol consumption and hypertension have been associated with higher rates of aneurysm

Slide 60 Q: Who should we screen? A: Incidence of intracranial aneurysm in the general population is reported to be 1-6% in general population. Most of these DO NOT rupture and we do not screen the general population. Screening is very controversial because of morbidity and mortality associated with treatment of aneurysms. In populations with two or more first degree relative with intracranial aneurysm, screening programs have demonstrated an increased incidence of intracranial aneurysms, but cost effectiveness of screening in these populations has not been evaluated. Screening in these individuals should be considered on case by case basis (do they have other risk factors? if aneurysm detected, affect life insurance etc.)

Slide 61 Q: What is the preferred modality for aneurysm screening? A: When screening is indicated, the usual practice is to screen with MRA on yearly basis for 3 years and if no aneurysm detected, expand screening interval to every 5 years. MRA has excellent sensitivity for aneurysms 5 mm and > and no XRT or contrast needed. When conservative management is chosen, it is important that blood pressure and cholesterol are monitored closely.

Slide 62 These are sagittal (left) and coronal (right) images from CT angiography reformats. Given the small size of the aneurysm and the patient does not have symptoms related to the aneurysm, conservative management will be considered. Imaging surveillance is typically performed on an annual basis. Universal treatment protocols for patients with unruptured intracranial aneurysms (UIAs) have yet to be established. However, in patient who are asx, most advocate observation of aneurysms that are < 5 mm.Q: Should this be followed with CT angiography, MR angiography or conventional angiography? A: CT angiography and MR angiography both good for surveillance and high sensitive and specificity for aneurysms >= 3-4 mm. MRA is better choice in this patient because no XRT. Imaging surveillance should be performed on an annual basis.

Slide 63 Q: Is this a primary headache or a secondary headache? A: Primary headache. While this does sound like a classic migraine headache, this patient did end up having an MRI. This leads us to the question on the next slide.

Slide 64 . Q: What are indications to order an MRI in the clinical setting of headache? A: 1. new headache and abnormal neurologic exam 2. progressively worsening h/a 3. h/a with signs of increased intracranial pressure 4. new onset headache w/ know underlying brain lesions or systemic illness (e.g. HIV, TB, CA)

Slide 65 Q: So then why did she get an MRI? A: We could postulate that perhaps the h/a was progressively worsening but that history was not provided at the time of exam. However, the point to make here is that It is not always easy for clinicians to rule out a secondary headache caused by an underlying lesion and physicians often err on the side of caution, ordering neuroimaging for many patients with headache. As a result, there is a high referral rate for neuroimaging, most of which results in either normal scans or show incidental abnormalities.Q: This was a normal study but for practice, what sequences do we have here? A: (left to right) FLAIR, T1 T2. These images represent superior to inferior sections of the brain.

Slide 66 Q: is a primary or secondary h/a? A: This is a secondary headache. We are concerned that this is a secondary headache which is due to mass effect.

Slide 67 Q: What is is diff dx? A: stroke (tends to be more abrupt onset but still must consider), septic emboli, neoplasm (primary [glioma] or secondary [metastasis/lymphoma]), demyelinating d/e, abscess.

Slide 68 Q: What type of imaging study would you order? A: This patient has both headache and neurologic deficits which is one of the clinical indications to obtain an MRI in the setting of headache. Just for review, the clinical indication for MRI in the setting of headache are: 1. new headache and abnormal neurologic exam 2. progressively worsening h/a 3. h/a with signs of increased intracranial pressure 4. new onset headache w/ know underlying brain lesions or systemic illness (e.g. HIV, TB, CA)

Slide 69 Q: What sequences do we have here. A: T1 (top left), T1 post gadolinium (top right), T2 (bottom left), DWI (bottom right). Advance to next slide so can work with labeled images.

Slide 70 Q: How would one describe this lesion? A: ring enhancing lesion/peripherally enhancing lesions with surrounding edema; the lesion demonstrates restricted diffusion. Q: What type of ring enhancing lesions do we think about in the immunocompetent population? A: metastasis, primary glioma, abscess, (these are the answers I would expect to hear); more advanced learners may answer demyelinating disease, resolving hematoma

Slide 71 Q: How does restricted diffusion shape your differential? A: Restricted diffusion can be seen in acute infarcts, abscesses, blood products, and hypercellular tumor (e.g. lymphoma)

Slide 72 Q: This lesion has restricted diffusion, why do we not think this is an infarct? A: 1. Arterial infarcts tend to be wedge shaped, unless very small. 2. The have abrupt onset of sx; If this infarct occurred 2 weeks ago (onset of sx was 2 weeks ago), the restricted diffusion would have reversed by now. Abscesses demonstrate restricted diffusion because of complex proteinaceous molecules e.g. fibrinogen, which bind water.

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