Ct brain by prof. Wael samir
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Ct brain by prof. Wael samir
- 2. Intending Learning Objectives (ILOs) Discuss the radiation hazards of CT Demonstrate the usage of different contrast agents safely Identify normal anatomical landmarks on CT brain Interpretation of CT perfusion in cerebral ischemia Interpretation of CT angiogram of cranial and cervical vasculature.
- 4. Radiation Dose Considerations Single Radiographs Effective Dose, mrem (mSv) Skull (PA or AP)1 3 (0.03) Skull (lateral)1 1 (0.01) Chest (PA)1 2 (0.02) Chest (lateral)1 4 (0.04) Chest (PA and lateral)5 6 (0.06) Thoracic spine (AP)1 40 (0.4) Thoracic spine (lateral)1 30 (0.3) Lumbar spine (AP)1 70 (0.7) Lumbar spine (lateral)1 30 (0.3) CT study Effective Dose, mrem (mSv) CT head1 200 (2.0) Lumbar spine series6 180 (1.8) Thoracic spine series6 140 (1.4) Cervical spine series6 27 (0.27)
- 5. Contrast Facts Serum Creatinine Levels (in mg/dL) Indicating an Estimated Glomerular Filtration Types: Rate of less than 60 mL/min/1.73 m2 Ionic: Age (years) 20 30 40 50 60 70 80 Nonionic: Dimer or monomer Men (not African American) 1.57 1.47 1.39 1.34 1.30 1.26 1.23 Dose: Contrast African Name Molecula Iodine Osmolalit Viscosity 0.97 0.95 Women (notissues:American) safety Trade Medium 1.21 1.13 1.08 1.03 1.00 Viscosity r Weight Conc y at 20 C at 37 C Men Idiosyncratic (nondose dependent), allergylike reactions: (African American) 1.86 1.73 1.65 1.58 1.53 1.49 (cP) (Dalton) (mgI/mL) (mOsm/kg (cP) 1.46 Acute water) Late: Ionic CM, monomer (High osmolar CM) Women (African American) 1.44 1.34 1.27 1.22 1.18 1.15 1.12 Iothalamate3 Dose-dependent 809 Conray 60% 282 1,400 6.02 (nonidiosyncratic) Reactions: 4.0 CVS: Nonionic CM, monomer (Low osmolar CM) Iohexol CIN: Omnipaqu 821 300-&350 672 11.8 6.3 Thyroid function e 844 20.4 10.4 Drug interactions: Iopromide Ultravist 791 300& 370 607 9.2 4.9 774 22.0 10.0
- 6. Preventive Measures for CMEN
- 8. Superior frontal sulcus Superior frontal gyrus Precentral sulcus Precentral gyrus Postcentral Central sulcus gyrus
- 9. Corpus callosum (genu) Lateral ventricle (anterior horn) Caudate nucleus (head) Foramen of Monro Lentiform Third ventricle nucleus Internal Pineal gland capsule Lateral ventricle Thalamus (trigone with choroid plexus)
- 10. External capsule insular cistern Quadrigeminal plate (colliculus) Insula Quadrigeminal and ambient cisterns
- 11. Interhemispheric cistern Sylvian fissure insular cistern Hypothalamus 3rd ventricle Cerebral peduncle Interpeduncular Aqueduct cistern Ambient cistern Midbrain Quadrigeminal cistern Vermis of cerebellum
- 12. Sphenoid ridge Optic chiasm Lateral ventricle (temporal horn) Pons Fourth ventricle Petrous ridge
- 13. Frontal air sinus Frontal lobe Orbital roof Pituitary fossa Greater wing of sphenoid Cavernous carotid Ant. clinoid Basilar artery Dorsum sella Pons Prepontine cistern 4th ventricle Cerebello pontine Cerebellar cistern hemisphere
- 14. Straight gyrus and olfactory bulb Ethmoid sinus Optic nerve Orbit Sphenoid sinus Temporal lobe SOF Mastoid air cells EAC VII / VIII complex Vermis
- 15. Crista galle Optic foramen SOF Auditory canal Cerebello medullary fissure Medulla
- 16. SOF Optic foramen
- 17. Orbit Paranasal sinuses Petrous bone
- 18. Skull Base
- 20. Principles of CT perfusion (CTP) CBF 50-80 ml/100 gm/min normal 15-20 ” Neurological dysfunction <10 ” infarction
- 21. CT Brain with Stroke window
- 22. Infarct signs on NCCT B C
- 23. CTP 1) Mean Transition Time (MTT) or time to peak (TTP) 2) Cerebral Blood flow (CBF) , 3) Cerebral Blood Volume (CBV), A B C
- 25. Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke Cutoff morphology:
- 26. Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke Tram track (nonocclusive or recanalized clot):
- 27. Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke The tandem morphology:
- 28. Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke Tapered morphology :
- 29. Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke meniscus or flattened shape to clot (recent) versus reverse meniscus (older) :
- 30. Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke Delayed (antegrade) flow :
- 31. Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke Retrograde collateral flow :
- 32. Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke Aneurysms: CTA:sagittal MPR CTA:3D color VR
- 33. References
- 34. Sits (Information adapted from www.radiologyinfo.org
Notas do Editor
- 1) Wall BF, Hart D. Revised radiation doses for typical x-ray examinations. The British Journal of Radiology 70:437-439; 1997. (5,000 patient dose measurements from 375 hospitals) 5) National Council on Radiation Protection and Measurements. Sources and magnitude of occupational and public exposures from nuclear medicine procedures. Bethesda, MD: National Council on Radiation Protection and Measurements; NCRP Report 124; 1996. 6) United Nations Scientific Committee on the Effects of Atomic Radiation. Sources and effects of ionizing radiation, Vol. 1: Sources. New York, NY: United Nations Publishing; 2000.
- Contrast Materials types (1): The diagnostic use of x-ray contrast media is exclusively based on the physical ability of iodine to absorb x-rays. They are either negatively charged ionic (ionic CM) or nonionic (nonionic CM) monomers or dimers (Dimers are the largest molecules and are generally more viscous than monomers). In addition to ionicity and chemical structure (monomer vs. dimer), CM are also differ in the iodin concentration, osmolarity ((high-osmolar, low-osmolar, and iso-osmolar). , viscosity (it increased with increased iodine concentration, and low temperature). nonionic CM are generally safer than ionic contrast media, with less idiosyncratic (nondose-dependent, e.g., allergylike) adverse reactions (5,6,7,8). Ionic CM also have a greater potential to cause acute nausea and vomiting, and—as a result—motion, when injection rates greater than 2.0 to 2.5 mL/s are used. Furthermore, extravasation of ionic CM is less well tolerated than nonionic CM. Adverse effects to nonionic CM occur in approximately 3.13%. They are generally categorized into idiosyncratic (nondose dependent), allergylike reactions and nonidiosyncratic (dose dependent) reactions.Contrast dose and rate of infusion:1) adult: 150 ml of 240 mg/dl non-ionic contrast @ 0.6 ml/sec (4.2 minutes). injection flow rates for CT angiography (CTA) is up to 5 or 6 mL/s 2) pediatric: 2 ml/kg of 240 non-ionic contrast @ 0.6 ml/sec 3) Dose of gadolinium-based (Gd) contrast media in the setting of MRI is up to 0.3 mmol/kgContrast materials (CM) safety issues (1):Idiosyncratic (nondose dependent), allergylike reactions:Acute allergylike reaction: Risk factors include: 1) History of prior moderate or severe CM adverse reaction 2) History of significant allergy (requiring medical treatment) 3) Asthma 4) History of drugs intake whichincrease risk of allergy as Beta-blockers because it decreases effect of adrenaline. Patient must be NPO for 6 hours prior to the exam.Delayed cutaneous reactions to contrast agents, presumably immune mediated, may occur 1 to 7 days after administration especially in patients taking Interleukin-2 or HydralazineDose-dependent (nonidiosyncratic) Reactions:Cardiovascular effects: It is not excluded that high injection flow rates and volumes can cause cardiopulmonary decompensation in patients with cardiocirculatory compromise.Interaction with Endocrine Function: CM are contradindicated in patients with manifest hyperthyroidism. Risk of thyrotoxicosis in patients with Graves disease and multinodular goiter with autonomous thyroid tissue, notably in areas of iodine deficiency. CM compromises thyroid scintigraphy and radioiodine treatment of thyroid malignancies for 2 months. Contrast medium–induced nephrotoxicity (CIN): Porter [1] defined CIN as a serum creatinine increase of: (a) greater than 25% if baseline serum creatinine is less than 1.5 mg/dl, or (b) greater than 1.0 mg/dl if baseline serum creatinine is greater than 1.5 mg/dl, when either occurs within 72 hours after the contrast administration in the absence of alternative etiology (29). CIN due to nonionic contrast agents is rare in the general population (less than 2%), but the incidence may be greater than 25% in patients with risk factors (32). Risk factors include 1) History of renal disease 2) Previous kidney surgery (including transplantation) 3) Diabetes 4) Proteinuria 5) Hypertension 6) Gout (hyperuricaemia) 7) Multiple myeloma (needs hydration) 8) Documented decrease of renal function (estimated glomeruler filtration rate “eGFR” <60 mL/min/1.73 m2). While CIN is reversible in the vast majority of cases, it may cause considerable morbidity and mortality. There are two practical consequences in the setting of CTA. It is necessary to screen for patients at risk, and once a patient at risk is identified, it is necessary to take measures to reduce the likelihood of CIN. Screening for Patients at Risk: 1) For all patients: Questionnaire for all risk factors mentioned before 2) For patients older than 70 years or younger patients with positive questionnaire: routine measurement of serum creatinine and calculate the estimated glomerular filtration rate from it according to the table. Serum creatinine is an imperfect marker of renal dysfunction, and in the setting of CIN, its primary limitation is that a fixed threshold of “normal” creatinine (e.g., 1.3 mg/dL) may not detect even a more than 50% reduction of the glomerular filtration rate and thus miss a significant proportion of patients at risk. It has been suggested that a patient's glomerular filtration rate should be estimated instead of using serum creatinine. This can be done most easily using the 4-variables abbreviated version of the original 6-variable MDRD (modification of diet in renal disease) formula (37,38,39), which calculates a patient's glomerular filtration rate per body surface area (thus correcting for body size already), based on patient age, sex, race, and serum creatinine. When an estimated glomerular filtration rate equal to or less than 60 mL/min/1.73 m2 is used as a threshold to identify patients at risk, one can again simplify the matter and tabulate the creatinine thresholds above which a patient would be considered to have renal insufficiency and thus be at risk for CIN 3) For those patients with documented high risk take preventive measures Prevention in Patients at Risk: 1) Other imaging modalities such as magnetic resonance imaging (MRI) 2) The lowest possible dose of a low osmolar or iso-osmolar dose should be used 3) Nephrotoxic drugs, such as nonsteroidal anti-inflammatory drugs (NSAID), should be stopped at least 24 hours before CM administration. 4) Volume expansion with IV fluid is known to reduce the risk of CIN. It is not entirely clear if oral hydration would be adequate as well; it certainly does no harm. Studies have shown that it is important to start fluid injection (e.g., 100 mL per hour of normal 0.9% saline) several hours before CM injection and to continue for several hours thereafter (40). 5) There are numerous studies, meta-analysis, and reviews published regarding the pharmacological prevention of CIN using vasodilators (e.g., fenoldopam), receptor antagonists of endogenous vasoactive mediators (e.g., theophyllin), or cytoprotective drugs (e.g., acetylcysteine), all of which do not seem to offer consistent protection against CIN (40). 6) Retest serum creatinine 3 days after the exam and if it increased more than 25% over the base line then it is CINCM Extravasation Injury (1): Increased risk in noncommunicative patients, notably in unconscious such as infants and children, the elderly, or unconscious patients. Severe extravasation injuries such as skin necrosis and ulceration, or compartment syndrome, have occasionally been reported even with nonionic agents (21). Drug Interactions (1):the folowing drugs may have interaction with the contrast material:Nephrotoxic drugs (Aminoglycoside antibiotics, NSAIDs,Chemotherapy (cyclosporine, cisplatin) Interleukin-2 (CM precipitates IL-2 toxicity; IL-2 increases risk of CM-induced acute urticarial reaction Beta-blockers (see acute reactions) Hydralazine (may predispose to acute cutaneous vasculitis) Metformin: For contrast exams, patients on metformin (glucophage) must not take medications the day of the test. Additionally, the patient must stay off these medications for 48 hours after the CT if renal impairment is suspected. The patient must return to their referring physician in 48 hours and have a creatinine drawn. Based on those results, the patient may resume medication per their physician instructions.Pregnancy and contrast materials:Intravenous Contrast Material (Iodine and Gadolinium) and Breast-feeding: Manufacturers of intravenous contrast indicate mothers should not breast-feed their babies for 24 to 48 hours after contrast medium is given. However, both the American College of Radiology (ACR) and the European Society of Urogenital Radiology note that the available data suggest that it is safe to continue breast-feeding after receiving intravenous contrast. 1) Dominik Fleischmann: Contrast Medium Administration in Computed Tomographic Angiography in CT and MR Angiography: Comprehensive Vascular Assessment. Rubin, Geoffrey D.; Rofsky, Neil M (eds). 1st Edition. Lippincott Williams & Wilkins. 2009 5) Katayama H, Yamaguchi K, Kozuka T, et al. Adverse reactions to ionic and nonionic contrast media. A report from the Japanese Committee on the Safety of Contrast Media. Radiology 1990;175:621–628.6) Palmer FJ. The RACR survey of intravenous contrast media reactions. Final report. AustralasRadiol. 1988;32:426–428.7) Wolf GL, Arenson RL, Cross AP. A prospective trial of ionic vs nonionic contrast agents in routine clinical practice: comparison of adverse effects. AJR Am J Roentgenol. 1989;152:939–944.8) Hill JA, Winniford M, Cohen MB, et al. Multicenter trial of ionic versus nonionic contrast media for cardiac angiography. The Iohexol Cooperative Study. Am J Cardiol 1993; 72:770-775.21) Bellin MF, Jakobsen JA, Tomassin I, et al. Contrast medium extravasation injury: guidelines for prevention and management. EurRadiol. 2002;12:2807–2812.29) Porter GA. Contrast medium-associated nephropathy. Recognition and management. Invest Radiol 1993; 28 Suppl4:S11–18.37) Levey AS, Bosch JP, Lewis JB, et al. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group. Ann Intern Med. 1999;130:461–470.38) Levey AS, Greene T, Kusek JW, et al. A simplified equation to predict glomerular filtration rate from serum creatinine. J Am Soc Nephrol. 2000;11:155A.39) Lamb EJ, Webb MC, Simpson DE, et al. Estimation of glomerular filtration rate in older patients with chronic renal insufficiency: is the modification of diet in renal disease formula an improvement? J Am Geriatr Soc. 2003;51:1012–1017.
- Normal values for CBF are between 50 and 80 ml of blood per 100 g of brain tissue per minute. Areas of the brain with high energy requirements such as the cortical surface or the basal ganglia exhibit CBF values which are some 2-3 times higher than those for white matter. Below a CBF of 20 ml/100 g/min, the synaptic function of the nerve cells is retarded due to the lack of energy, i.e. there is neurological failure. This loss may, however, be completely reversible if blood flow is normalised again. Below a CBF of 10-15 ml/100 g/min the metabolism of the nerve cells can no longer be maintained. If CBF remains below this so called ischaemia threshold for 2-10 minutes, the result is irreversible cell damage. The primary goal of CTP and PWI is to determine potential brain (territory) at risk of infarction, which is thought to represent an ischemic penumbra that is salvageable if treated appropriately Then using the cerebral blood flow and the mean transit time generate a brain map showing:1) The infarct core2) The ischemic penumbra Therapeutic window (1): Diagnosis in the first 3 hours postictus provides the opportunity for intravenous or intraarterialthrombolysis and intra-arterial clot mechanical treatment (attempts at removing the clot or breaking it into smaller pieces), which has been shown to improve outcome [12,15,16,21]. Diagnosis in the time period between 3 and 6 hours provides an opportunity for intra-arterial thrombolysis and mechanical treatment (no intravenous thrombolysis). Diagnosis in the first 12 hours provides the opportunity for administration of neuroprotective agents, which may improve outcome. Involvement of the posterior circulation, especially the basilar artery, is treated by some physicians regardless of time of onset or up until 12 to 24 hours in some practices. New studies are being performed to evaluate the possibility of basing treatment on imaging rather than a time window related to ictal onset 1) Mark E. Mullins (2006): Modern Emergent Stroke Imaging: Pearls, Protocols, and Pitfalls. RadiolClin N Am 44 (2006) 41–62
- Use of stroke window and level settings has been shown to improve infarct detection on NCCT A 49-year-old woman with transient ischemic attack and headache and visual field loss. (A) Right MCA territorial infarct is illustrated with a right insular ribbon sign on noncontrast head CT with brain windows (arrow) and (B) infarct extent better visualized using stroke windows (arrows, border infarct extent). (1) 1) Mark E. Mullins (2006): Modern Emergent Stroke Imaging: Pearls, Protocols, and Pitfalls. RadiolClin N Am 44 (2006) 41–62
- Infarct signs of MCA on NCCT [51] include the following : 1) Obscuration of the lentiform nucleus (figure A); 2) loss of gray-white interface of the insular cortex (insular ribbon sign). (figure B); 3) hyperdense artery(figure C); and the MCA dot (en face) and dash sign (in profile) [52]. The author’s data [52] suggest that not all dense arteries correspond to clot on CTA.Last figure: Right ICA territory stroke in evolution. Non-contrasted CT scan demonstrates a hyperdense distal ICA/proximal MCA sign (arrowheads) signifying acute thrombus involving these arteries (A). The following three images show the progressively demarcated infarction in the right ACA and MCA territories, on admission, with loss of sulcal markings consistent with early edema (B), 1 day later (C), and 2 days later (D). (53) [51] Lev MH. CT versus MR for acute stroke imaging: is the ‘‘obvious’’ choice necessarily the correct one? AJNR Am J Neuroradiol 2003;24:1930–1.[52] Mullins ME, Schwamm L, Maqsood M, et al. Assessment of the dense vessel sign on noncontrast head CT I: evaluation of the hyperdense middle cerebral artery sign by CTA. In: Proceedings of the American Society of Neuroradiology (ASNR) annual meeting. Oak Brook (IL): ASNR; 2004. p. 153–4.[53] Isaac E Silverman, Marilyn M Rymer: An Atlas of Investigation and Treatment (2009): ISCHEMIC STROKE Atlas Medical Publishing Ltd Oxford OX2 0JX, UK. Chapter 3 Page 31-55
- Fig. 1: Typical time/density curves after injection of a contrast medium bolus in perfusion CT. The density sequences are imaged (idealised view) in an arterial vessel (middle branch of the cerebral artery: blue), a venous vessel (confluence of sinuses: yellow) and in the cerebral parenchyma (thalamus: red). Note the typical staggered time between the arterial and venous time/density curves and the flattened and slightly delayed density sequence in the parenchyma compared with the arterial curve (Fig. modified according to [3]).To obtain functional information about cerebral blood flow, in CTP a short intravenous contrast medium bolus is given during which one slice, or with MSCT, several CT slices, can be acquired repeatedly at fixed time intervals. Usually, for instance, 40 ml of contrast medium are administered with a scanning period of 45 seconds and an imaging frequency of 1 image/secondThe examination is based on the indicator dilution theory: following administration of an intravenous contrast medium bolus the X-ray density of the brain temporarily increases. Conclusions about cerebral blood flow can be drawn from the extent and course over time of this increase in density. Using various mathematical algorithms parameters denoting cerebral perfusion are calculated and represented in the form of colour-coded parameter images. The routine perfusion maps that the author uses are (1) 1) Mean transit time (MTT) (similar to time to peak “TTP”), 2) cerebral blood flow (CBF), and 3) Cerebral Blood Volume (CBV). Mean transit time (MTT) (similar to time to peak “TTP”) map (1) : Interpretation usually starts with the mean transit time map, because it yields typically the largest potentially abnormal area. On this map, increased signal is bad, indicative of delayed blood supply to this brain parenchyma.Cerebral blood flow (CBF) map (1) : On the cerebral blood flow map, decreased signal is bad and is usually contained within the mean transit time abnormal region, representing delayed or decreased blood flow to the brain parenchyma through the normal antegrade arterial pathways. Cerebral blood flow is the most important parameter. It indicates how much blood is flowing through the brain tissues in a specific period, and it is measured in ml blood/100 g brain tissue/min. Cerebral blood volume (CBV) map (1) : CBV maps are likely the best estimate of collateral flow. Here, decreased signal is bad, indicative of delayed or decreased blood volume or flux into the brain parenchyma. CBV is likely the best predictor of final infarct volume but most patients end up with a final infarct volume somewhere between the size of the cerebral blood flow abnormality and the CBV abnormality (which is usually smaller than and contained within the cerebral blood flow abnormality). Increased signal may be obtained with luxury perfusion and reperfusion. Cerebral blood volume (CBV) is defined as the percentage of blood vessels in a specific volume of tissue. Highly vascularised areas of the brain such as the basal ganglia or the cortical surface therefore have a higher CBV than the less vascularised cerebral white matter. The CBV, however, is also a functional parameter and alters if vessel size changes in the context of vascular auto-regulation. Unlike CBF, which in ischaemia is reduced both in the infarct core and in the penumbra, the CBV in the penumbra usually increases. This is caused by cerebral auto-regulation: the fall in CBF has to be compensated for by dilation of the vessels concerned. In contrast, in the irreversibly damaged infarct core, auto-regulation usually no longer functions, so that the CBV is decreased. This is very helpful in diagnosing strokes: areas showing reduced CBV in the acute stage of ischaemia are as a rule irreversibly damaged. If the abnormal regions on CBV and cerebral blood flow are matched, this scenario likely represents completed infarct without good collaterals. If the abnormal regions on cerebral blood flow are greater than CBV, this is suggestive of some normalization and indicative of likely good collaterals; this situation is unlikely to extend to complete infarct if treated appropriately and aggressively. This patient is likely the best candidate for therapy If the abnormal regions on mean transit time are greater than cerebral blood flow or CBV, no one has shown for certain what the area abnormal on mean transit time mean transit time only represents, but some clinicians treat this as potential territory at risk for infarction. If there is a perfusion deficit of any kind and the patient has hypotension or hypoxia, these regions may become ischemic or infarcted. First pictures set(1): A- (arrow) : CTP illustrates a large area of prolonged mean transit time within the left MCA distribution, B- (arrow): matched decreased cerebral blood flow, C-: nearly normalized cerebral blood volume. Second pictures set (2): CTP of the brain in a patient with acute stroke. Note the reduced mean transit time (MTT) (A) and cerebral blood flow (CBF) (B) in the medial cerebral artery territory. The cerebral blood volume (CBV) is reduced only in the region of the infarct core (arrow) (C). By visually displaying those areas with CBF <10mL/s in green and areas with CBV <2 mL/100g tissue in red, one can more easily distinguish areas of penumbra (potentially salvageable tissue) and the (nonsalvageable) infarct core (D). However, one has to be careful not to overinterpret such fixed thresholds because of substantial interindividual variations. 1) Mark E. Mullins (2006): Modern Emergent Stroke Imaging: Pearls, Protocols, and Pitfalls. RadiolClin N Am 44 (2006) 41–62 2) Mathias Prokop: Principles of Computed Tomographic Angiography: in CT and MR Angiography: Comprehensive Vascular Assessment. Rubin, Geoffrey D.; Rofsky, Neil M (eds). 1st Edition. Lippincott Williams & Wilkins. 2009
- CTA is an excellent first-line examination for evaluation of the head and neck arteries When proctoring a CTA, account for patency of the bilateral internal carotid and vertebral arteries. If there is lack of apparent contrast material filling on the initial images, the author immediately performs delayed images to see if there is delayed filling as a manifestation of hairline lumen (which usually is treated surgically) as opposed to occlusion (which likely does not undergo surgery) [45]. Moreover, CTA illustrates not only arterial stenosis or occlusion, but also the vessel wall. This factor is most important for evaluation of intramural dissection. five different Signs that are evaluated in CTA include (1): [For each morphology, the portion of the vessel with normal blood flow and luminal caliber is depicted as black, whereas areas devoid of flow are depicted as white.]1) Vessel occlusion or cutoff related to thromboemboli 2) Tram track (nonocclusive or recanalized clot) 3) The tandem morphology consists of proximal partially obstructive and distal occlusive lesions resulting from two serial intraluminal thrombi; the proximal lesion is depicted as a tram-track lesion and the distal lesion is depicted as a gray intraluminal region surrounding a central white focus. The central white focus represents intraluminal thrombus, and the peripheral gray region represents possible areas of intraluminal flow depending on whether the distal lesion is cutoff, meniscoid, tram-track, or tapered (2) . 3) Tapered Arterial dissection (smooth narrowing of lumen at young age especially if post traumatic) 4) meniscus or flattened shape to clot (recent) versus reverse meniscus (older) 5) delayed (antegrade) flow (manifest as decreased whole-brain perfusion on CTA); and 6) (retrograde) collateral flow [55]. 7) aneurysms; 1) Mark E. Mullins (2006): Modern Emergent Stroke Imaging: Pearls, Protocols, and Pitfalls. RadiolClin N Am 44 (2006) 41–62[45] Lev MH, Romero JM, Goodman DN, et al. Total occlusion versus hairline residual lumen of the internal carotid arteries: accuracy of single section helical CT angiography. AJNR Am J Neuroradiol 2003;24:1123–9. [55] Coutts SB, Lev MH, Eliasziw M, et al. ASPECTS on CTA source images versus unenhanced CT: added value in predicting final infarct extent and clinical outcome. Stroke 2004;35:2472–6. 2) Jay J. Pillai, Charles F. Lanzieri, Salvador B. Trinidad, Robert W. Tarr, Jeffrey L. Sunshine, Jonathan S. Lewin (2001): Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke as a Predictor of Outcome of Thrombolysis: Initial Experience. Radiology 2001; 218:733–738
- [For each morphology, the portion of the vessel with normal blood flow and luminal caliber is depicted as black, whereas areas devoid of flow are depicted as white.]2) Tram track (nonocclusive or recanalized clot) Posteroanterior projection from a superselectivemicrocatheter injection into the basilar artery via a right vertebral base catheter demonstrates a tram-track occlusive lesion involving the distal basilar arteryJay J. Pillai, Charles F. Lanzieri, Salvador B. Trinidad, Robert W. Tarr, Jeffrey L. Sunshine, Jonathan S. Lewin (2001): Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke as a Predictor of Outcome of Thrombolysis: Initial Experience. Radiology 2001; 218:733–738
- [For each morphology, the portion of the vessel with normal blood flow and luminal caliber is depicted as black, whereas areas devoid of flow are depicted as white.] 3) The tandem morphology consists of proximal partially obstructive and distal occlusive lesions resulting from two serial intraluminal thrombi; the proximal lesion is depicted as a tram-track lesion and the distal lesion is depicted as a gray intraluminal region surrounding a central white focus. The central white focus represents intraluminal thrombus, and the peripheral gray region represents possible areas of intraluminal flow depending on whether the distal lesion is cutoff, meniscoid, tram-track, or tapered. Left anterior oblique projection from a superselectivemicrocatheter injection into the left middle cerebral artery via an indwelling base catheter within the left internal carotid artery demonstrates a tandem occlusive lesion in the M3 segment of the middle cerebral arteryJay J. Pillai, Charles F. Lanzieri, Salvador B. Trinidad, Robert W. Tarr, Jeffrey L. Sunshine, Jonathan S. Lewin (2001): Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke as a Predictor of Outcome of Thrombolysis: Initial Experience. Radiology 2001; 218:733–738
- [For each morphology, the portion of the vessel with normal blood flow and luminal caliber is depicted as black, whereas areas devoid of flow are depicted as white.] 4) Tapered morphology as in srterial dissection (smooth narrowing of lumen at young age especially if post traumatic) Left anterior oblique projection from a selective left vertebral artery injection demonstrates a tapered occlusive lesion involving the proximal basilar artery just distal to the vertebrobasilar junction. Jay J. Pillai, Charles F. Lanzieri, Salvador B. Trinidad, Robert W. Tarr, Jeffrey L. Sunshine, Jonathan S. Lewin (2001): Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke as a Predictor of Outcome of Thrombolysis: Initial Experience. Radiology 2001; 218:733–738
- [For each morphology, the portion of the vessel with normal blood flow and luminal caliber is depicted as black, whereas areas devoid of flow are depicted as white.] 5) meniscus or flattened shape to clot (recent) versus reverse meniscus (older); Posteroanterior projection from a selective right internal carotid artery injection demonstrates a meniscoid occlusion of the carotid terminus.Jay J. Pillai, Charles F. Lanzieri, Salvador B. Trinidad, Robert W. Tarr, Jeffrey L. Sunshine, Jonathan S. Lewin (2001): Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke as a Predictor of Outcome of Thrombolysis: Initial Experience. Radiology 2001; 218:733–738
- 6) delayed (antegrade) flow (manifest as decreased whole-brain perfusion on CTA); and
- 7) retrograde collateral flow [55]. [55] Coutts SB, Lev MH, Eliasziw M, et al. ASPECTS on CTA source images versus unenhanced CT: added value in predicting final infarct extent and clinical outcome. Stroke 2004;35:2472–6.
- 8) aneurysms;(A) MPR image in view and (B) 3D color VR image in superior view show a medium- sized saccular aneurysm (arrow) at the right MCA bifurcation with fundus pointing superolaterally.
- Jerry V. Glowniak, Anthony L. Alcantara, Todd Getzen,AnujDhawan:Navigating the Skull Base: An interactive program for learning skull base anatomy . In Wayne state University, school of medicine site http://www.med.wayne.edu/diagradiology/anatomy_modules/axialpages/Home_Page.html. Reviewedin 08/29/2011