Cerebral vasculatures other than perforators and its ...conplus.co.kr/~kcr2015/down/abstract_book/Scientific Program/SP... · anterior medial surface of the brain, from the frontal

The arterial supply to the cerebral hemispheres is de-rived from the anterior circulation provided by the bilateral-ly paired internal carotid arteries, as well as by the posteri-or circulation provided by the bilateral vertebral arteries.Anterior and posterior circulations meet in an anastomoticring called the circle of Willis, from which all major cerebralvessels arise. The circle of Willis provides abundant op-portunities for collateral flow; however, a complete ring ispresent in only approximately 25% of individuals.

The three main cerebral arteries (ACA, MCA, PCA) giverise to numerous branches that travel in the subarachnoidspaces over the surface of the brain and into the sulci.Small penetrating branches arise from these vessels tosupply the superficial portions of the brain, including thecortex and underlying white matter. The anterior cerebralartery passes forward to travel in the interhemispheric fis-sure as it sweeps back and over the corpus callosum. Theanterior cerebral artery supplies most of the cortex on theanterior medial surface of the brain, from the frontal to theanterior parietal lobes, usually including the medial senso-rimotor cortex. The middle cerebral artery turns laterally toenter the depths of the Sylvian fissure. Within the Sylvianfissure it usually bifurcates into the superior division andinferior division. The superior division supplies the cortexabove the Sylvian fissure, including the lateral frontal lobeand usually including the peri-Rolandic cortex. The inferiordivision supplies the cortex blow the Sylvian fissure, in-cluding the lateral temporal lobe and a variable portion ofthe parietal lobe. The posterior cerebral artery curves backafter arising from the top of the basilar artery and sendsbranches over the inferior and medial temporal lobes andover the medial occipital cortex.

Recognition of the classic syndromes produced by in-farcts of the MCA, ACA, and PCA territories remains a cor-nerstone of neurologic assessment and continues to playan important role in evaluating patients with acute stroke.

Middle cerebral artery

Infarcts and ischemic events are more common in themiddle cerebral artery than in the anterior or posteriorcerebral arteries, at least in part, because of the relativelylarge territory supplied by the middle cerebral artery. MCAinfarcts occur in three general regions: 1. Superior divi-sion; 2. Inferior division; 3. Deep territory. Proximal MCAocclusions affecting all three of these regions are calledMCA stem infarcts. Neurologic deficits according to vascu-

lar territories are presented as follows.

1. Left MCA superior division: Right face and arm weak-ness of the upper motor neuron type, and a non-fluentor Broca’s aphasia. In some cases, there may also besome right face and arm cortical-type sensory loss.

2. Left MCA inferior division: Fluent, or Wernicke’saphasia and a right visual field deficit. There may alsobe some right face and arm cortical-type sensoryloss. Motor findings are usually absent, and patientsmay initially seem confused or crazy, but otherwiseintact, unless carefully examined. Some mild right-sided weakness may be present, especially at the on-set of symptoms.

3. Left MCA stem: Combination of the above, with righthemiplegia, right hemianesthesia, right homonymoushemianopia, and global aphasia. There is often a leftgaze preference, especially at the onset, caused bydamage to left hemisphere cortical areas importantdriving the eyes to the right.

4. Right MCA superior division: Left face and arm weak-ness of the upper motor neuron type. Left hemine-glect is present to a variable extent. In some casesthere may be some left face and arm cortical-typesensory loss.

5. Right MCA inferior division: Profound left hemine-glect. Left visual field and somatosensory deficits areoften present. Motor neglect with decreased volun-tary or spontaneous initiation of movements on theleft side can also occur. Some mild left-sided weak-ness may be present, especially at the onset of symp-toms. There is often a right gaze preference, espe-cially at the onset.

6. Right MCA stem: Combination of the above, with lefthemiplegia, left hemianesthesia, left homonymoushemianopia, and profound left hemineglect. There isusually a right gaze preference, especially at the on-set, caused by damage to right hemisphere corticalareas important driving the eyes to the right.

Anterior cerebral artery

ACA infarcts typically produce contralateral lower ex-tremity cortical-type sensory loss and weakness of the up-per motor neuron type. There may also be a variable de-gree of frontal lobe dysfunction depending on the size ofthe infarct. Such dysfunction may include a grasp reflex,

Neuroradiology(NI) 323Neuroradiology(NI) Sep 10, Thu

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RC 01 NR(NI)-01 Neurovascular imaging

Chairperson(s) : Chul Ho Sohn Seoul National University Hospital, KoreaDong Joon Kim Yonsei University College of Medicine, Korea

Cerebral vasculatures other than perforators and its clinical implication

Woong Yoon Chonnam National University Hospital, Korea. [email protected]

impaired judgment, flat affect, apraxia, abulia, and inconti-nence.

1. Left ACA: Right leg weakness of the upper motorneuron type and right leg cortical-type sensory loss.Grasp reflex, frontal lobe behavioral abnormalities,and transcortical aphasia can also be seen. Larger in-farcts may cause right hemiplegia.

2. Right ACA: Left leg weakness of the upper motorneuron type and left leg cortical-type sensory loss.Grasp reflex, frontal lobe behavioral abnormalities,and left hemineglect can also be seen. Larger infarctsmay cause left hemiplegia.

Posterior cerebral artery

PCA infarcts typically cause a contralateral homony-mous hemianopia. PCA infarcts that involve the left occipi-tal cortex and the splenium of the corpus callosum canproduce alexia without agraphia.

1. Left PCA: Right homonymous hemianopia. Extensionto the splenium of the corpus callosum can causealexia without agraphia. Larger infarcts including thethalamus and internal capsule may cause aphasia,right hemisensory loss, and right hemiparesis.

2. Right PCA: Left homonymous hemianopia. Larger in-

farcts including the thalamus and internal capsulemay cause aphasia, left hemisensory loss, and lefthemiparesis.

Borderzone infarcts

When the blood supply to two adjacent cerebral arteriesis compromised, the regions between the two vessels aremost susceptible to ischemia and infarctions. These re-gions between cerebral arterial territories are called water-shed zones. Watershed infarcts can produce proximal armand leg weakness because the regions of homunculus in-volved often include the trunk and proximal limbs. In thedominant hemisphere, watershed infarcts can causetranscortical aphasia syndromes. MCA-PCA watershedinfarcts can cause disturbances of higher-order visual pro-cessing. In addition to watershed infarcts between the su-perficial territories of different cerebral vessels, watershedinfarcts can also occasionally occur between the superfi-cial and deep territories of the MCA.

Reference

1. Blumenfel H. Neuroanatomy through clinical cases.Sinauer Associates, Inc.

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Neuroradiology(NI) Sep 10, Thu

1. Basal ganglia

1) Functional anatomyBasal ganglia (BG) include the caudate nucleus, the

lentiform nucleus, the subthalamic nucleus and the sub-statia nigra. The inferior part of the caudate head is con-nected with the putamen at the ventral part, at the nucleusaccumbens. The globus pallidus (GP) has two parts, me-dial and lateral. The medial medullary lamina separatesthe medial from the lateral GP. The lateral medullar lami-nar separates the lateral GP from the putamen. The sub-thalamic nucleus is a small lentiform nucleus located at theborder between the midbrain and the diencephalon (thala-mus), i.e., ventral to the thalamus, dorsal to the substantianigra and medial to the internal capsule. The substantia ni-gra lies in the ventral tegmentum of the midbrain. The parscompacta is the largest part; it is dorsocaudal to the parsreticulata.

BG help the cortical areas involved in movement controlin order to smoothly orchestrate motor behaviors, forminga major center in the complex extrapyramidal motor sys-tem. Its motor actions are mediated through the pyramidalsystem, as the BG do not make direct output connectionsto the spinal cord. The caudate and putamen receive in-puts from associative areas of the neocortex and the sen-sorimotor cortex (dorsal BG circuit). The nucleus accum-bens receives input from the orbitofrontal cortex and otherlimbic cortical areas, the hippocampus and amygdale(ventral BG circuit). The efferent neurons of the straitum,all GABAergic, are divided into a dual projection. Someneurons project to the internal GP (striatal direct pathway)and the substantia nigra pars reticulate and others to theexternal GP (striatal indirect pathway). The direct pathwayis the striatum to the internal GP to VA/VL to motor cortex,and this pathway is for increase excitatory inputs to themotor cortex. The indirect pathway is the striatum to theexternal GP to the subthalamic nucleus to the internal GPto VA/VL to motor cortex, and this pathway is for inhibitoryinput to the motor cortex.

Ansa lenticularis, located under the posterior limb of theinternal capsule, conveys information from the globus pal-lidus (GP) to motor thalamus (centromedian nucleus).Lenticular fasciculus conveys information from the caudalpart of globus pallidus to another motor thalamus(ventroanterior nucleus; VA, ventrolateral nucleus; VL)through the posterior limb of the internal capsule. The

ansa lenticularis, lenticular fasciculus and cerebellothala-mic fibers join together to head for VA/VL, forming the thal-amic fasculus. All cortical areas involved in the planningand execution of movements project to the striatum (thecaudate nucleus and putamen). Striatal neurons receivingthese cortical inputs then project to the GP, which in turnprojects to the VA, VL. The cells of VA, VL in turn projectsto motor cortex.

Striatal neurons are modulated by two important neuro-modullatory systems (dopaminergic and cholinergic sys-tems). Nigrostriatal axon terminals release dopamine intothe striatum. Dopamine has an excitatory effect on cells inthe striatum via the direct pathway. Also dopamine has aninhibitory effect upon striatal cells associated with the indi-rect pathway. In other words, the direct pathway (whichturns up motor activity) is excited by dopamine while theindirect pathway (which turns down motor activity) is inhib-ited. Both of these effects lead to increased motor activity.Cholinergic neurons in the striatum synapse on theGABAergic striatal neurons that project to the internal andexternal GP. The cholinergic actions inhibit striatal cells ofthe direct pathway and excite striatal cells of the indirectpathway. Thus the effect of cholinergic neurons is to de-crease motor activity.

BG are also involved in many neuronal pathways hav-ing emotional, motivational, associative and cognitivefunctions as well. This is because that neuronal outputsfrom BG (and cerebellum, CBLL), throughout the thala-mus, project to the premotor, oculomotor, prefrontal andinferotemporal areas of cortex. These circuits: (i) have animportant regulatory influence on cortex, proving informa-tion for both automatic and voluntary motor responses tothe pyramidal system; (ii) play a role in predicting futureevents, reinforcing wanted behavior and suppressing un-wanted behavior, and (iii) are involved in shifting attention-al sets and in both high-order processes of movement initi-ation and spatial working memory (1).

2) Blood supplyThe medial striate artery (MSA) from the anterior cere-

bral artery (ACA) and the lateral striate artery (LSA) fromthe middle cerebral artery (MCA) are distributed within thecorpus striatum after entering the anterior perforated sub-stance and forming similar fan-shaped configurations.Variations in the distribution of the striate arteries dependupon the degree to which the ACA has taken over the terri-tory of the MCA and how much is still supplied by the





Basal ganglia and thalamus: functional anatomy and blood supply

Hak-Jin Kim Pusan National University Hospital, Korea. [email protected]

MCA. There is a state of balance between the distributionof the MSA and LSA. A dominant branch of the MSA, re-ferred to as the recurrent artery of Heubner (RAH), usuallyoriginated from the ACA at the level of the anterior com-municating artery supplies the anterior portion of the cau-date nucleus, the anterior third of the putamen, the inter-posed anterior limb of the internal capsule, the tip of theouter segment of the GP, and the anterior hypothalamus.Minute vessels of the MSA arising from the proximal por-tion of the ACA perfuse the area of the anterior hypothala-mus and the medial third of the anterior commissure andonly occasionally supply the caudate nucleus and GP.Several branches of the LSA arise from the sphenoidalportion of the MCA and enter the brain through the lateraltwo third of the anterior perforated substance, supply thebody of the caudate nucleus as well as the superior aspectof its head, the putamen, the lateral GP, the substantia in-nominata, and the lateral half of the anterior commissure.The inferior portion of the anterior limb of the internal cap-sule is supplied by the MSA, while most of the inferior por-tion of the posterior limb is supplied by the anteriorchoroidal artery and the superior segments of both limbsare supplied by the LSA. The genu and the most anteriorportion of the posterior limb are also supplied by the thala-motuberal artery of the posterior communicating artery.

2. Thalamus

1) Functional anatomyThe thalamus is a relay center subserving both sensory

and motor functions, often referred to as the gateway tocortex. A single thalamus nucleus gives efferent fibers tomultiple cortical areas and receives back information fromthose cortices. The corticofugal projection provides posi-tive and negative feedback. Multiple ascending pathwaysof sensory and motor functions headed to the thalamustraverse the brainstem. The most common subdivision us-es the internal medullary lamina to divide the thalamus ontopographical grounds. The internal medullary lamina is athin sheet of white matter running longitudinally throughthe thalamus, separating the thalamus into medial and lat-

eral nuclear masses. The lateral mass contains the medialnuclear group. The lateral nuclear group consists the later-al nuclear group and the ventral nuclear group. In the ros-tral part of the thalamus the internal medullary laminasplits to form a partial capsule around the anterior nucleargroup. A fifth nuclear group, termed the intralaminar nu-clear group, is within the internal medullary lamina.Nucleus perithalamicus (reticular nucleus), which sur-rounds much of the thalamus like an eggshell, especiallyon its lateral side. It contains inhibitory GABAergic neu-rons. The reticular nucleus controls the activity of thalamo-cortical channels. The intralaminar nuclei have been in-cluded in the non-specific ascending reticular activatingsystem projecting to extensive areas of the cerebral cortexthe inputs received from the brainstem reticular formation.These nuclei have been functionally associated with atten-tion, arousal and consciousness. The anterior nucleus re-ceives projections from the mamillary body (mamillothala-mic tract) and projects to the cingulated gyrus belonging tothe Papez circuit, the neural circuit for emotion and memo-ry. Lesions involving the anterior nucleus resulted in apha-sia, memory impairments. Medial nucleus receives a largeprojections from the rhinal and prefrontal cortices, amyg-dale, ventral GP and nigral projections, and projects to theorbital and prefrontal cortex, has been implicated in cogni-tion, recognition memory, habituation, olfaction, the wake-sleep cycle, respiration and in endocrine circadian activi-ties. The pulvinar-lateral posterior nucleus complex, whichhas reciprocal connections with the associated parieto-oc-cipito-temporal corticies, is involved in visual and languagefunctions. The pulvinar has a role in selective visual atten-tion. The ventral posteromedial nucleus (VPM) is the relayfor pain and temperature sensation including visceral infor-mation. The medial geniculate body (MGB) receives so-matosensory, vestibular and auditory afferents and visualinputs. The lateral GB receives visual afferents and givesefferents to the optic radiation. The lateral dorsal (LD) andlateral posterior nucleus (LP) are the relay for gustatorysensation. The motor thalamus (LA, VL) inputs from thesubstatia nigra, the GP, the cerebellum and gives effer-ents to the prefrontal, supplementary, premotor, motor and

326 KCR 2015


Fig. 1. Squema of nuclei of the thalamus

Group Nuclei Receives input from Gives input to Function

Anterior Anterior Limbic system Cingulated gyrus

Medial DM Olfactory cortex & Insular, orbitofrontal cortex Smell PainSpinothalamic tract Prefrontal cortex

Lateral LD Limbic system Cingulated gyrus

Pulvinar, LP Many different sites Parietal, temporal, occipital Sensory

Ventral VA, VL CBLL, GP, SN Motor cortices Motor

VP Medial lemniscus, anterolateral Somatic sensory cortex, Pain, temperature, system, trigeminothalamic tract, Insular cortex Touch, Positionspinothalamic tract, Taste (insular)

MGB Inferior colliculus Auditory cortex Hearing

LGB Retina Occipital lobe Vision

Intralaminar CM Globus pallidus, substantia nigra Motor cortex Motorgroup

Table 1. Summary of important points of thalamic circuits

somatosensory cortices.There are lots of literatures concerning the BG and the

thalamus, the function remains controversial. Further-more, both nuclei are closely located and have intimateand highly specific afferent/efferent fibers with cerebralcortex, they should not be considered as nuclei with arole independent of both structures.

2) Blood supplyThe thalamus is supplied by several groups of perforat-

ing and choroidal arteries, to which many names havebeen applied. The thalamotuberal (TTA), which originatefrom the posterior communicating artery (PCoA), enter thebrain at the tuber cinereum and are distributed within thehypothalamus and anterior thalamus. The thalamoperfo-rate arteries (TPA), which originate from the interpeduncu-lar segment of the posterior cerebral artery (PCA), pene-trate the posterior perforated substance and are distrib-uted within the anteromedial thalamus along the lateralwall of the third ventricle. The thalaogeniculate arteries(TGA), which arise from the ambient segment of the PCA,enter the brain in and between the MGB and LGB, are dis-tributed within the anterolateral thalamus. The medial pos-terior choroidal arteries (MPChA) is distributed in the pos-teromedial and dorsomedial portions of the thalamus. Thechoroidal vessels of the lateral ventricle (ChVLV), whicharise from the lateral posterior (LPChA) and anteriorchoroidal arteries (AChA). LPChA seems to distribute themost lateral region of the pulvinar and also in the dorsolat-eral thalamus. Although these vessels are well estab-lished, there is still some disagreement as to the role of theAChA n the supply of the thalamus and that of the TGA inthe supply of the posterior limb of the internal capsule. Inaddition, opinions differ as to the vascularization of thethalamic nuclei, specially the centromedian nucleus.

References

1. Middleton FA, Strick PL. Basal ganglia and cerebellarloops: motor and cognitive circuits. Brain Res Rev2000;31(2-3):236-250

2. Anne RL, Young AB, Penny JB. The functional anatomyof basal ganglia disorders. Trends Neurosci1989;12(10):366-375

3. Herrero MT, Barcia C, Navarro JM. Functional anatomyof thalamus and basal ganglia. Childs Nerv Syst2002;18(8):386-404

4. Temel Y, Blokland A, Steinbusch HW, et al. The function-al role of the subthalamic nucleus in cognitive and limbiccircuits. Prog Neurobiol 2005;76(6):393-413

5. Parent A, Hazrati LN. Functional anatomy of the basalganglia. I. The cortico-basal ganglia-thalamo-corticalloop. Brain Res Brain Res Rev 1995;20(1):91-127

6. Parent A, Hazrati LN. Functional anatomy of the basalganglia. II. The place of subthalamic nucleus and externalpallidum in basal ganglia circuitry. Brain Res Brain ResRev 1995;20(1):128-154

7. Smith Y, Raju DV, Pare JF, et al. The thalamostriatal sys-tem: a highly specific network of the basal ganglia circuit-ry. Trends Neurosci 2004;27(9):520-527

8. Nakano K, Kayahara T, Tsutsumi T et al. Neural circuitsand functional organization of the striatum. J Neurol2000;247 Suppl 5:V1-V15

9. Takahashi S, Goto K, Fukusawa H, et al. Computed to-mography of cerebral infarction along the distribution ofbasal perforating arteries. Part I. Striate arterial group.Radiology 1985;155(1):107-118

10. Takahashi S, Goto K, Fukusawa H et al. Computed to-mography of cerebral infarction along the distribution ofbasal perforating arteries. Part II. Thalamic arterial group.Radiology 1985;155(1):119-130


The anatomy of the infratentorial arteries that supply thecerebellum and critical parts of the brainstem may be com-plex and different from well-known normal anatomy. In themanagement of patients with a vascular pathology of theinfratentorial artery who are candidates for interventionalor surgical treatment, unawareness or unfamiliarity of thedetailed arterial anatomy and variations may lead a misin-terpretation and poor clinical results.

Surgical management of the infratentorial vascular le-sions poses a greater risk than that of supratentorial le-

sions due to deep or destructive surgical exposure, manyimportant perforating arteries and complex neural struc-tures such as cranial nerves. Therefore, endovascular ap-proach has become the current mainstay of the manage-ment the infratentorial vascular lesions. For neuroradiolo-gists and interventional neuroradiologists, knowledge ofanatomy and variations of the infratentorial arteries will im-prove the diagnostic reliability and safety of the endovas-cular treatment.

328 KCR 2015





Infratentorial arteries (vertebral artery to basilar trunk) and clinicalimplication

Hong Gee Roh Konkuk University Medical Center, Korea. [email protected]

Spinal vasculatures develop from the metamerism thatis a series of body segments. However, most of the radicu-lar arterial sources regress and only few of them remain toprovide blood flow of spinal cord. The spinal arteries havetypical course along the nerve roots. The anterior spinalartery (radiculomedullary artery) runs longitudinally in theventral median fissure and supplies centromedullary por-tion of spinal cord. The posterior spinal artery (radiculopialartery) feeds the dorso-peripheral portion of spinal cord.Pial networks from posterior spinal arteries are inter-con-nected and give rise to perforators anastomosing with per-forators from the anterior spinal artery, which is called in-trinsic intramedullary network.

Spinal vascular diseases consist of spinal vascular mal-formations, spinal aneurysms, and spinal cord arterial is-chemia. They are relatively rare, but should be kept in thedifferential diagnosis for tumors, demyelinations, or com-pressive myelopathies.

Spinal dural AVFs refer to a shunting lesion betweendural branches of the segmental artery and a radicularvein. They are the most common form of spinal vascularmalformations. They are presumed to be acquired lesionsand most frequently found in the thoracolumbar region ofelderly men presenting with progressive myelopathies andadditional autonomic symptoms. AV shunts induce spinalvenous pressure elevation, spinal cord congestion, re-duced tissue perfusion, and cord ischemia. Spinal cordswelling and dilated perimedullary veins may be noted onMRI. Selective spinal catheter angiography is the goldstandard. Both embolization and surgery are available fortreatment. The most distal part of the feeding artery andthe proximal draining vein should be obliterated.

Spinal cord AVMs are intradural shunting diseases,comprising about 20%~30% of all spinal vascular malfor-mations. They can be subdivided into perimedullary or in-tramedullary, nerve root, and filum terminale lesions ac-cording to their anatomical location and resultant feedingartery. The gross angioarchitecture at their transition fromartery into vein can be either of a nidus or fistulous type.Spinal cord AVMs are fed by radiculomedullary arteries orradiculopial arteries, and drained by spinal veins, per-imedullary veins, and/or radicular veins. PerimedullaryAVFs are direct AV shunts without intervening nidus. Theycan clinically present with either acute hemorrhage or pro-gressive myelopathy. Intramedullary AVMs refer to nidus-type AVMs and may be considered as the counterpart ofpial brain AVMs. The nidus is usually located in the spinal

cord, however, a superficial compartment can also be ex-posed to the subarachnoid space. The clinical presenta-tions are either due to acute hemorrhage or progressivemyelopathy. Radicular AVFs refer to the shunt betweenthe radicular artery and radicular vein at the level of the in-tradural nerve roots. Filum terminale AVFs refer to a raretype of shunt between the artery of the filum terminale andthe spinal vein. The shunts are located at lumbosacral re-gion. They usually are clinically presented with progres-sive myelopathy or conus medullaris syndrome.

Paravertebral AVFs (= epidural AVFs) are relatively rarelesions and occurs outside the dura mater between radic-ular artery and epidural venous plexus. They typically pre-sent with benign clinical symptom such as radiculopathyfrom a compressive mass effect on nerve roots.

Metameric AVMs refer to multiple vascular malforma-tions that affect more than one tissue derived from thesame spinal metameric segment.

Spinal cord cavernomas are non-shunting vascular mal-formations that are analogous to the ones in the brain.Intramedullary hematoma with repeated episodes cancause acute, recurrent, and progressive myelopathy, con-tinued oozing of blood from the cavernoma can presentwith intramedullary edema.

Spinal aneurysms arising within the spinal canal arevery rare. Most of them are thought to be associated withspinal AVMs, coarctation of the aorta, or renal transplanta-tion. Solitary spinal aneurysms are even rarer and postu-lated pathogenesis includes inflammatory processes, dis-section, and intimal defects. They usually present with he-morrhage, but can sometimes manifest as a compressivelesion by mass effect.

Spinal cord arterial infarct is mostly a single event andthe main etiologies are interventions and pathologies af-fecting the aorta. It needs to be differentiated from othercauses of acute noncompressive myelopathies such asacute transverse myelitis or multiple sclerosis. The infarctsare most commonly found as an isolated pencil-like areaof T2 hyperintensity at the centromedullary territory of theanterior spinal artery in the thoracolumbar region, oftenencompassing more than 2 vertebral segments. Diffusion-weighted imaging is useful for earlier detection of spinalcord arterial infarct, though there are several technical diffi-culties such as motion artifacts, susceptibility artifacts, andlow signal-to-noise ratio.





Spinal vascular anatomy and imaging of spinal vascular lesions

Young-Jun Lee Hanyang University College of Medicine, Korea. [email protected]

References

1. Berenstein A LP, Terbrugge K. Classification of spinalcord arteriovenous malformations, in surgical neuroan-giography, ed 2. New York: Springer, 2004:767-774

2. Krings T, Geibprasert S. Spinal dural arteriovenous fistu-las. AJNR Am J Neuroradiol 2009;30(4):639-648

3. Jellema K, Tijssen CC, van Gijn J. Spinal dural arteriove-nous fistulas: a congestive myelopathy that initially mim-ics a peripheral nerve disorder. Brain 2006;129(Pt12):3150-3164

4. Kataoka H, Miyamoto S, Nagata I, et al. Venous conges-tion is a major cause of neurological deterioration inspinal arteriovenous malformations. Neurosurgery2001;48(6):1224-1229; discussion 1229-1230

5. da Costa L, Dehdashti AR, terBrugge KG. Spinal cordvascular shunts: spinal cord vascular malformations anddural arteriovenous fistulas. Neurosurg Focus2009;26(1):E6

6. Yamamoto S, Kim P. Spinal arteriovenous fistulas and ar-teriovenous malformations - Complicated vasculatureand surgical imaging. http://dx.doi.org/10.5772/56367.Accessed on July 24, 2015

7. Jin YJ, Kim KJ, Kwon OK, et al. Perimedullary arteriove-nous fistula of the filum terminale: case report.

Neurosurgery 2010;66(1):E219-220; discussion E2208. Lim SM, Choi IS, David CA. Spinal arteriovenous fistulas

of the filum terminale. AJNR Am J Neuroradiol2011;32(10):1846-1850

9. Nishio A, Ohata K, Takami T, et al. Spinal arteriovenousmalformation associated with a radicular arteriovenousfistula suggested a metameric disease. A case report.Interv Neuroradiol 2003;9(1):75-78

10. Kiyosue H, Tanoue S, Okahara M, et al. Spinal ventralepidural arteriovenous fistulas of the lumbar spine: an-gioarchitecture and endovascular treatment.Neuroradiology 2013;55(3):327-336

11. Niimi Y, Uchiyama N, Elijovich L, et al. Spinal arteriove-nous metameric syndrome: clinical manifestations andendovascular management. AJNR Am J Neuroradiol2013;34(2):457-463

12. Zevgaridis D, Medele RJ, Hamburger C, et al. Cavernoushemangiomas of the spinal cord. A review of 117 cases.Acta Neurochir (Wien) 1999;141(3):237-245

13. Berlis A, Scheufler KM, Schmahl C, et al. Solitary spinalartery aneurysms as a rare source of spinal subarachnoidhemorrhage: potential etiology and treatment strategy.AJNR Am J Neuroradiol 2005;26(2):405-410

14. Masson C, Pruvo JP, Meder JF, et al. Spinal cord infarc-tion: clinical and magnetic resonance imaging findingsand short term outcome. J Neurol Neurosurg Psychiatry2004;75(10):1431-1435

330 KCR 2015


1. Introduction

Stroke is the second leading cause of death (1) and themajor cause of adult disability in Korea. According to thereports analyzing insurance claim database of the KoreanHealth Insurance Review Agency, ischemic stroke ac-counted for 76.1% and hemorrhagic stroke 23.9% in 2009(2). Atherosclerotic occlusive disease of the extracranialcarotid artery (carotid stenosis) is thought to be responsi-ble for approximately 15% to 25% of such ischemicstrokes (3), with a prevalence that varies from approxi-mately 0.5% at 60 years of age to approximately 10% at80 years of age (4). And, vertebral artery atherosclerosismay be the causative basis for approximately 20% of pos-terior circulation strokes (5). These statistics make ex-tracranial carotid and vertebral artery revascularization animportant surgical tool in the prevention of new ischemicstrokes.

2. Carotid endarterectomy (CEA)

Carotid endarterectomy (CEA) was first introduced inthe 1950s (6). Through the several landmark trials in the1990s, it was established as the gold standard treatmentof stroke prevention in patients with carotid stenosis (7-10).

In these landmark trials (NASCET, ECST, ACAS, andACST), highly experienced surgeons treated carefully se-lected, low-surgical-risk patients only. To achieve the ben-efit described in these trials, the perioperative complicationrate must be 6% or less for symptomatic patients and 3%or less for asymptomatic patients.

However, in the general population, studies havedemonstrated perioperative stroke and death rates as highas 11.1% for symptomatic patients and 5.5% for asympto-matic patients (11). Moreover, there are several clinicaland anatomic features that are considered high risk forsurgery and have a profound negative impact on the finalsurgical outcome (12) (Table 1).

As a result of these limitations of open surgery, a mini-mally invasive endovascular approach alternative to CEA,carotid artery angioplasty and stenting (CAS), has evolvedin the last 2 decades and has now become an acceptedalternative for carotid revascularization, especially in highsurgical-risk patients.

3. Carotid artery stenting (CAS)

Percutaneous transluminal angioplasty (PTA) of thesupraaortic arteries has been established in the last 35years as an alternative procedure to surgical repair. Afteranimal experiments in 1976, Mathias and colleagues treat-ed the first carotid artery stenosis in 1979. Balloon angio-plasty had some limitations in atherosclerotic disease. Theplacement of self-expandable stent resulted in less resid-ual stenosis, no plaque dissections and no elastic recoil ofthe vessel wall (13).

In 1984, Theron et al. (14) independently developed dis-tal cerebral protection with balloons, which led to commer-cially available balloon protection devices. In 1998, devel-opment of PercuSurge GuardWire system make it possi-ble to use distal protection balloon with smaller profile andto perform protected balloon angioplasty and stenting (15).After that period, protected carotid stenting has been per-

Neuroradiology(NI) 331N

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SF 10 NR(NI)-01 Endovascular therapy

Chairperson(s) : Sang-Hoon Cha Chungbuk National University Hospital, KoreaByung Moon Kim Yonsei University School of Medicine, Severance Hospital, Korea

Decision-making for candidate for CAS and VA orifice stenting

Hae Woong Jeong Inje University Busan Paik Hospital, Korea. [email protected]

Table 1. Anatomic and clinical high-risk features for CEA

Anatomic Clinical

Recurrent carotid stenosis Recent or evolving myocardial infarctionPrevious cervical surgery Preoperative coronary artery bypass graftContralateral laryngeal palsy Presence of congestive heart failurePresence of tracheostomy Renal failureFollowing cervical radiation therapy Angina pectorisCarotid lesion above C2 vertebra Recurrent cerebrovascular attackContralateral carotid occlusion Crescendo transient ischemic attacksPresence of tandem carotid stenosis Fluctuating neurologic deficitPresence of intraluminal thrombus Stroke in evolutionCarotid lesion below clavicle

formed with various type of distal filter and proximal bal-loon protection such as MO.MA.

4. Selection criteria

Patients can be selected according to multiple factorssuch as degree of stenosis, presence of symptoms, pa-tient age, and presence of factors related with high risk ofcomplications from CAS (16).

5. Symptomatic patients

Symptomatic patients has been defined as those withsymptoms of acute ischemic stroke or transient ischemicstroke within 90 to 180 days of trial entry.

Data from the NASCET, ECST, Veterans Affairs trialshowed carotid endarterectomy was highly beneficial inthose with 70% stenosis or greater without near occlusionand was of marginal benefit in those with 50-69% stenosis(in this document, all reporting of the degree of stenosisfollows the NASCET criteria, Fig. 1).

Fig. 1. Diagram shows the NASCET, ECST, and com-mon CC to calculated stenosis.A. narrowest diameter of the internal carotid artery;B. expect diameter of the carotid bulb;C. normal diameter of the internal carotid artery;D. normal diameter of the common carotid artery (19).

In 2008, the Health Insurance Review & AssessmentService (HIRA) in Korea announced the indication of insur-ance coverage for CAS as more than 70% narrowing and50% narrowing with surgically high risk or unsuitable pa-tients (17).

The Korean HIRA also allowed the insurance coverageas more than 50% narrowing in the special cases of ulcer-ative plaque, restenosis after CEA, tandem lesion, dissec-tion, fibromuscular dysplasia, Takayasu’s arteritis, andstenosis after radiotherapy. In the cases of flow distur-bance due to dissection, arterio-venous fistula, andpseudoaneurysm, CAS is included in the insurance cover-

age by HIRA regardless of stenosis degree (18).ACC and AHA reported in their guidelines that CAS is

indicated as an alternative to CEA for a patient with symp-tomatic carotid stenosis of more than 50% as documentedby catheter angiography (19). The “2013 Clinical PracticeGuideline for Stroke” in Korea recommended the sameguideline as ACC/AHA in terms of stenosis degree (20).Therefore, the indication for CAS in Korea needs to bebroadened to the patients with more than 50% narrowingand standard surgical risk.

6. Asymptomatic patients

In the asymptomatic carotid stenosis, the evidence doesnot show either CEA or CAS having a clear benefit com-pared with treatment by medication alone.

The only large, well-constructed, randomized, controlledtrial published to date comparing surgical endarterectomywith medical therapy in asymptomatic carotid stenosis isthe Asymptomatic Carotid Atherosclerosis Study (ACAS)(9). ACAS reported that the patients with more than 60%stenosis have absolute risk reduction of 5.9% for CEA ascompared to medical therapy over a 5-year period.

ACC/AHA reported that CAS might be considered forhighly selected patients with asymptomatic stenosis ofmore than 60% by angiography (19). HIRA allowed the in-surance coverage for patients with more than 80% nar-rowing for CAS (17).

7. CEA versus CAS

The first clinical trial comparing surgical and endovascu-lar treatments for carotid stenosis was the Carotid andVertebral Transluminal Angioplasty Study (CAVATAS),published in 2001 (21). In this trial, there was no significantdifference in the risk of stroke or death between surgicaland endovascular treatment arms.

The Stenting and Angioplasty with Protection in Patientsat High Risk for Endarterectomy (SAPPHIRE) study, pub-lished in 2004 (22). The 1-year rates of major adverseevents (composite of death, stroke, or MI within 30 days ofintervention or death or ipsilateral stroke between day 31and 1 year) were 20.1% in the CEA group and 12.0% inthe CAS group. Because of these results, CAS performedwith the use of an embolic protection device was consid-ered noninferior to CEA and was granted FDA approval foruse in high-surgical-risk patients in 2004.

Several European studies (EVA-3S [23), SPACE [24],ICSS [25]) attempted to compare CAS with CEA in stan-dard-surgical-risk patients. These trials failed to demon-strate the noninferiority of CAS when compared with CEA.However, they all suffered from serious limitations in de-sign, including lack of embolic protection requirement, lackof experience by endovascular operators, and lack of sta-tistical power.

The largest study comparing CAS versus CEA amongstandard-risk surgical patients was the CarotidRevascularization Endarterectomy versus Stenting Trial(CREST), carried out at 117 sites in the United States andCanada and published in 2010 (26).

There was no statistically significant difference betweenCAS and CEA for the primary end point of death, stroke, orMI, either periprocedurally or during the 4-year follow-upperiod (CAS 7.2%; CEA 6.8%). When examined separate-

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ly, minor strokes were more frequent after CAS than CEA(4.1% vs. 2.3%), whereas MI was more frequent after CEAthan CAS (2.3% vs. 1.1%). This trial definitively showedthat CAS and CEA are equivalent procedures for stan-dard-risk surgical patients.

8. Vertebral Artery Orifice Stenting

Symptomatic obstructive disease of the vertebral arter-ies is encountered less commonly in clinical practice thancarotid stenosis. Vertebral artery atherosclerosis may bethe causative basis for approximately 20% of posterior cir-culation strokes (5). There is insufficient evidence fromrandomized trials to demonstrate that endovascular man-agement is superior to best medical management (19).

HIRA allowed the insurance coverage for symptomaticpatients with more than 70% narrowing and flow distur-bance due to dissection or risk of hemorrhage for extracra-nial vertebral artery stenting (17).

9. Summary

Percutaneous transluminal angioplasty and stenting inextracranial carotid artery and vertebral artery orifice is anactive treatment method for arterial stenosis and it hasmany advantages as compared to surgical intervention.For symptomatic patients with high surgical risk, the bene-fit of CAS is well established and unquestionable. Forsymptomatic patients with standard surgical risk, CAS andCEA are currently equally effective. For asymptomatic pa-tients with carotid stenosis, there still remains the questionof whether revascularization adds any benefit to aggres-sive modern medical management. And, for vertebralartery orifice stenosis, there is insufficient evidence fromrandomized trials to demonstrate that endovascular man-agement is superior to best medical management.

References

1. Statistics Korea. Progress of mortality rate due to majorcause of death 2013. Accessed July 24, 2015

2. Clinical research center for stroke. Clinical practice guide-lines for stroke. Seoul: Korea. 2013

3. Kolominsky-Rabas PL, Weber M, Gefeller O, et al.Epidermiology of ischemic stroke subtypes according toTOAST criteria: incidence, recurrence, and long-term sur-vival in ischemic stroke subtypes: a population-basedstudy. Stroke 2001;32(12):2735-2740

4. Prati P, Vanuzzo D, Casaroli M, et al. Prevalence and de-terminants of carotid atherosclerosis in a general popula-tion. Stroke 1992;23(12):1705-1711

5. Wehman JC, Hanel RA, Guidot CA, et al. Atheroscleroticocclusive extracranial vertebral artery disease: indica-tions for intervention, endovascular techniques, short-term and long-term results. J Interv Cardiol2004;17(4):219-232

6. DeBakey ME. Successful carotid endarterectomy forcerebrovascular insufficiency. Nineteen-year follow-up.JAMA 1975;233(10):1083-1085

7. North American Symptomatic Carotid EndarterectomyTrial Collaborators. Beneficial effect of carotid en-darterectomy in symptomatic patients with highgradecarotid stenosis. N Engl J Med 1991;325(7):445-453

8. Randomised trial of endarterectomy for recently sympto-

matic carotid stenosis: final results of the MRC EuropeanCarotid Surgery Trial (ECST). Lancet1998;351(9113):1379-1387

9. Endarterectomy for asymptomatic carotid artery stenosis.Executive Committee for the Asymptomatic CarotidAtherosclerosis Study. JAMA 1995;273(18):1421-1428

10. Halliday A, Mansfield A, Marro J, et al. Prevention of dis-abling and fatal strokes by successful carotid endarterec-tomy in patients without recent neurological symptoms:randomised controlled trial. Lancet2004;363(9420):1491-1502

11. Hartmann A, Hupp T, Koch HC, et al. Prospective studyon the complication rate of carotid surgery. CerebrovascDis 1999;9(3):152-156

12. Eller JL, Snyder KV, Siddique AH, et al. Endovasculartreatment of carotid stenosis. Neurosurg Clin N Am2014;25(3):565-582

13. Mathias K. Historical background: 25 years of endovas-cular therapy for obstructive carotid artery disease. In: Al-Mubarak N, Roubin GS, Iyer SS, eds. Carotid arterystenting: current practice and techniques. LippincottWilliams & Wilkins, 2004:18-22

14. Theron JG, Payelle GG, Coskun O, et al. Carotid arterystenosis: treatment with protected balloon angioplastyand stent placement. Radiology 1996;201(3):627-636

15. Henry M, Amor M, Henry I, et al. Carotid stenting withcerebral protection: first clinical experience using thePercuSurge GuardWire system. J Endovasc Surg1999;6(4):321-331

16. Higashida RT, Meyers PM, Phatouros CC, et al.Reporting standards for carotid artery angioplasty andstent placement. J Vasc Interv Radiol 2009;20(7Suppl):S349-S373

17. Indication of insurance coverage for percutaneous ex-tracranial carotid artery stenting and vertebral artery ori-fice stenting. The Health Insurance Review &Assessment Service (HIRA) in Korea, 2008 (2008-169,treatment device)

18. Chang HW, Shin SH, Suh SI, et al. Recommendations forcarotid stenting in Korea. Neurointervention2015;10(1):7-13

19. Brott TG, Halperin JL, Abbara S, et al. 2011ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the manage-ment of patients with extracranial carotid and vertebralartery disease. Stroke 2011;42(8):e464-e540

20. Stetler W, Gemmete JJ, Pandey AS, et al. Endovasculartreatment of carotid occlusive disease. Neuroimag Clin NAm 2013;23(4):637-652

21. Endovascular versus surgical treatment in patients withcarotid stenosis in the Carotid and Vertebral ArteryTransluminal Angioplasty Study (CAVATAS): a ran-domised trial. Lancet 2001;357(9270):1729-1737

22. Yadav JS, Wholey MH, Kuntz RE, et al. Protectedcarotid-artery stenting versus endarterectomy in high-riskpatients. N Engl J Med 2004;351(15):1493-1501

23. Mas JL, Chatellier G, Beyssen B, et al. Endarterectomyversus stenting in patients with symptomatic severecarotid stenosis. N Engl J Med 2006;355(16):1660-1671

24. SPACE Collaborative Group, Ringleb PA, Allenberg J, etal. 30 day results from the SPACE trial of stent-protectedangioplasty versus carotid endarterectomy in sympto-matic patients: a randomised non-inferiority trial. Lancet2006;368(9543):1239-1247



25. International Carotid Stenting Study investigators, EderleJ, Dobson J, et al. Carotid artery stenting compared withendarterectomy in patients with symptomatic carotidstenosis (International Carotid Stenting Study): an interimanalysis of a randomised controlled trial. Lancet

2010;375(9719):985-99726. Brott TG, Hobson RW 2nd, Howard G, et al. Stenting ver-

sus endarterectomy for treatment of carotid artery steno-sis. N Engl J Med 2010;363(1):11-23

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Non-enhanced computed tomography (NECT) is cur-rently the imaging modality of choice for evaluation of pa-tients with acute stroke. In the pivotal National Institute ofNeurological Disorders and Stroke (NINDS) RecombinantTissue Plasminogen Activator (rt-PA) Stroke Study, NECTwas used as a screening tool to exclude intracranial hem-orrhage (ICH) before rt-PA administration. The EuropeanCooperative Acute Stroke Study (ECASS) first identifiedthe importance of assessing early ischemic changes(EICs, < 3 hours from symptom onset) on NECT to predictthe benefit from intravenous thrombolysis. The authorssuggested that involvement of greater than one-third of themiddle cerebral artery territory on early NECT scan was asignificant risk factor for hemorrhage and that patients withthese findings did not appear to benefit from treatment.However, in the absence of a standardized methods ofsuch an estimation, the 1/3 rule has poor inter-observer re-liability (1). To address this issue, NINDS rt-PA StrokeStudy scans adopted definitions of early ischemic changesin NECT as followings: 1) loss of gray/white matter distinc-tion, 2) hypodensity or hypoattenuation, and 3) compres-sion of CSF spaces. In addition, the Alberta stroke pro-gram early CT score (ASPECTS) was developed to offerthe reliability and utility of a standard CT examination witha reproducible grading system to assess EICs on pretreat-ment CT studies in patients with acute ischemic stroke ofthe anterior circulation. ASPECTS is a topographic scoringsystem, and divides the MCA territory into 10 regions of in-terest. The baseline ASPECTS value correlated inverselywith the severity of the stroke on the National Institute ofHealth Stroke Scale (NIHSS) (p < 0.001) and predictedfunctional outcome and symptomatic intracerebral hemor-rhage (p < 0.001 and p = 0.012, respectively). A sharp in-crease in dependent or fatal outcomes occurred with AS-PECTS of 7 of less. The inter- and intraobserver reliabilityof ASPECTS was good to excellent (k = 0.71-0.89) andconsistently superior to the 1/3 rule between observerpairs from the same specialty (2).

Rapid and reliable distinction of irreversibly damaged is-chemic tissue from tissue that can be salvaged with reper-fusion therapy in patients with ischemic stroke would be ofgreat clinical value. First-pass CT perfusion (CTP) cancharacterize cerebral perfusion with quantitative parame-ters such as cerebral blood volume (CBV), cerebral bloodflow (CBF), mean transit time (MTT), and time-to-peak(TTP). Previous studies have demonstrated that regionswith low CBV correlate very well with initial diffusion MR

imaging abnormality and with final infarct size, even insuccessfully recanalized patients. Consequently, the CBVabnormality is considered a core of tissue highly likely toinfarct. Penumbral regions were characterized by a mis-match between CBF and CBV. In the penumbra, CBF wasreduced, and CBV was maintained or elevated above con-tralateral values. Increased CBV in the penumbra is a re-sult of direct autoregulatory responses by the brain tomaintain CBF by dilating the precapillary vessels in re-sponse to decreased perfusion pressure (3). Systematicreview of all CTP parameters proposed a combined ap-proach using 2 distinct parameters to define both the in-farct core and the penumbra. The absolute CBV, with athreshold at 2.0 ml x 100 g-1, is the parameter allowing themost accurate delineation of the acute infarct core. Themismatch between the absolute CBV, with a threshold at2.0 ml x 100 g-1, and the relative MTT, with a threshold at145%, affords the most accurate delineation of the tissueat risk of infarction in the absence of recanalization (4).Defining the penumbra and infarct using CBV, CBF, andMTT values from CTP could help in selecting patients forthrombolytic therapy within and possibly outside the cur-rent 3- to 6-hour treatment window, where it has beenshown that penumbra may persist for > 12 hours.

Recently, CT angiography (CTA) has emerged as an ef-ficient and accurate noninvasive modality in evaluation ofthe etiology of acute stroke. A systemic review concludedthat combination of cerebral CTA and CTP is needed toachieve the most accurate assessment of the site of occlu-sion, infarct core, salvageable brain tissue, and collateralcirculation in patients suspected of acute stroke. CTA hasseveral advantages: it is 1) minimally invasive; 2) per-formed quickly; 3) less susceptible to motion artifacts thanMRA; 4) less dependent on hemodynamic effects com-pared to MRA; and 5) more widely available in the generalcommunity than MRA and DSA. Recent published multi-center randomized controlled trials have utilized multi-phase CTA that reduces uncertainty in clinical decisionmaking and may be slightly better in the prediction of clini-cal outcome than currently used techniques (5).

Despite advances in various imaging modalities, CT-based imaging techniques such as NECT, multiphaseCTA, and CTP remain the most used imaging modality inacute stroke. CT imaging is readily available around theclock in most hospitals, is relatively inexpensive comparedwith other imaging techniques, is more rapidly accessibleto stroke patients than MRI, and can be used to exclude






CT-based protocol for selection of patient for endovascular therapy: pros and cons

Byungjun KimKorea University Anam Hospital, Korea. [email protected]

intracranial hemorrhage, identify occlusion site, and possi-bly differentiate infarct from penumbra.

References

1. Barber PA, Demchuk AM, Zhang J, et al. Validity and reli-ability of a quantitative computed tomography score inpredicting outcome of hyperacute stroke before throm-bolytic therapy. Lancet 2000;355(9216):1670-1674

2. Pexman JH, Barber PA, Hill MD, et al. Use of the AlbertaStroke Program Early CT Score (ASPECTS) for assess-ing CT scans in patients with acute stroke. AJNR Am JNeuroradiol 2001;22(8):1534-1542

3. Murphy BD, Fox AJ, Lee DH, et al. Identification of

penumbra and infarct in acute ischemic stroke usingcomputed tomography perfusion-derived blood flow andblood volume measurements. Stroke 2006;37(7):1771-1777

4. Wintermark M, Flanders AE, Velthuis B, et al. Perfusion-CT assessment of infarct core and penumbra: receiveroperating characteristic curve analysis in 130 patientssuspected of acute hemispheric stroke. Stroke2006;37(4):979-985

5. Menon BK, d’Esterre CD, Qazi EM, et al. Multiphase CTAngiography: a new tool for the imaging triage of patientswith acute ischemic stroke. Radiology 2015;275(2):510-520

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When a stroke is suspected in any patient in an emer-gency room, the neuroimaging plays a very important rolein diagnosis and triage of the treatment. The primary aimof neuroimaging in acute stroke is to rule out hemorrhagicstroke, and in accordance with its results, IV thrombolysiswould be performed. And, then CT or MR to triage of en-dovascular therapy is conducted to determine whether toimplement intra-arterial revascularization therapy. Thecurrent lecture will deal with pros and cons of MR-basedprotocol for triage of patient for endovascular therapy in or-der to help you understand the recent evidences.

It is obvious that MR has the advantage in terms of diag-nostic accuracy, compared with CT. According to theprospective study on the diagnosis of acute stroke, MR indiagnosing acute stroke showed a sensitivity of 83% andCT had a sensitivity of 26%. Along with no ionization radia-tion, MR also has the advantage in diagnosing lacunar in-farct as well as the acute infarct in posterior circulation.

However, the protocol for the triage of the treatment hasnot been standardized. One of the obstacles against stan-dardization of MR-based protocol is that perfusion imagingin clinical trials and case series has been used with the dif-ferent definition of the penumbra. The automated softwareprogram used to classify patients into a favorable penum-bral pattern or nonpenumbral pattern for the stratified ran-domization in MR RESCUE failed, in real-time, to classify42% of cases. The definition of the penumbral pattern dif-fered from the more typical mismatch approaches used inother penumbral imaging trials. In a study, the size of thepenumbra may appear different to an extent of 40% ac-cording to the definition of penumbra.

Onset to reperfusion time has a profound impact on pa-tient’s prognosis in hyperacute stroke with large arterialocclusion. Any type of protocols should assess the size ofinfarct core and level of occlusion without delaying therevascularization therapy. Furthermore, multi-society con-sensus quality improvement guideline that was released in2013, recommended that image should be achieved within25 minutes and interpreted within 45 minutes from admis-sion into hospital.

Because the acquisition time of MR is long, and in theacute setting, accessibility is lower than CT for each hospi-tal, CT has also been recommended as the triage protocolof acute ischemic stroke as well as MR. Recent clinical tri-als such as MR-CLEAN, EXTEND-IA, SWIFT-PRIME,and REVASCAT, employed MR or CT for inclusion or ex-clusion criteria for eligibility of endovascular therapy, ex-

cept ESCAPE trial. As a result, the AHA / ASA guidelinehas been recently published after success of major clinicaltrials on endovascular therapy. It included the recommen-dations on intra-arterial therapy, neuroimaging and systemorganization. The main points of the recommendationsabout the neuroimaging were that noninvasive vascularimaging such as CTA or MRA should be performed, andCT or MR perfusion imaging has not been proven to helpin patient’s selections for endovascular therapy. This wasalso highlighted that delay of treatment should not be al-lowed by acquisition and interpretation of neuroimaging.Then, on the basis of clinical evidence to date, what is im-portant to improve the MR-based protocol seems to re-duce the acquisition and interpretation time without signifi-cant loss of diagnostic power. For example, Nael et al pro-posed a protocol to obtain a DWI, EPI-FLAIR, EPI-GRE,CE-MRA, MR perfusion (DSC) 6 minutes that was feasiblein terms of diagnostic performance.

In summary, while MR imaging is the best modality inthe diagnosis of acute stroke, it has the weakness in termsof the phrase that “Time is brain”, and then that the demeritseemed to preclude the MR to be accepted as a standardprotocol for hyperacute ischemic stroke. Therefore, in or-der to take full advantage of the MR image, time-savingMR protocol without loss of an accuracy of diagnosisshould be focused in the future clinical trial as well as stan-dardization of the assessment of penumbra.

References

1. Chalela JA, Kidwell CS, Nentwich LM, et al. Magnetic res-onance imaging and computed tomography in emergencyassessment of patients with suspected acute stroke: aprospective comparison. Lancet 2007;369(9558):293-298

2. Powers WJ, Derdeyn CP, Biller J, et al. 2015 AHA/ASAfocused update of the 2013 guidelines for the early man-agement of patients with acute ischemic stroke regardingendovascular treatment: a guideline for healthcare pro-fessionals from the American Heart Association/American Stroke Association. Stroke 2015 [Epub aheadof print]

3. Wintermark M, Sanelli PC, Albers GW, et al. Imaging rec-ommendations for acute stroke and transient ischemic at-tack patients: a joint statement by the American Societyof Neuroradiology, the American College of Radiology,and the Society of NeuroInterventional Surgery. AJNRAm J Neuroradiol 2013;34(11):E117-E127






MR-based protocol for selection of patient for endovascular therapy: pros and cons

Cheolkyu Jung Seoul National University Bundang Hospital, Korea. [email protected]

4. Parsons MW, Albers GW. MR RESCUE: is the glass half-full or half-empty? Stroke 2013;44(7):2055-2057

5. Leigh R, Urrutia VC, Llinas RH, et al. A comparison of twomethods for MRI classification of at-risk tissue and coreinfarction. Front Neurol 2014;5:155

6. Nael K, Khan R, Choudhary G, et al. Six-Minute MagneticResonance Imaging Protocol for Evaluation of AcuteIschemic Stroke: Pushing the Boundaries. Stroke 2014;45(7):1985-1991

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Introduction

Brain arteriovenous malformations (AVMs) are complexstructures composed of a network of abnormal arteriesand veins that lack a normal capillary bed, resulting in thehigh-flow arteriovenous shunting of blood. Treatment ofbrain AVMs includes different modalities (embolization,surgery, radiosurgery) either alone or in combination.

Recent reports (ARUVA) (1) suggested that medicalmanagement may be superior to interventional therapy forunruptured AVMs, at least in the short term, and now, risk-benefit analysis become all the more critical. When weplan to treatment of unruptured AVM, the natural history ofthe AVM is considered against the risks of embolization.

Rates of brain AVMs detection determined by popula-tion-based studies range from 0.89 to 1.34 cases per100,000 person-years. Symptomatic brain AVM patientshave a 4% annual risk of hemorrhage, a 1.7% annual riskof morbidity, and an annual mortality risk of 1%. From theirreview of the literature, Bendok et al. assessed the risk ofdeath after an AVM-associated hemorrhage to be from10% to 15% while overall morbidity and mortality was esti-mated to be 15% per episode of hemorrhage.

Overall AVM embolization complication rates of approx-imately 5% to 15% have been reported. A recent meta-analysis by van Beijnum et al. (2) found that complicationsleading to permanent neurological deficits or death oc-curred in 6.6% (range, 0-18%) of patients after AVM em-bolization.

Candidate of AVM endovascularembolization

1. Curative embolizationCurative embolization is now offered as an alternative to

radiosurgery or surgery in selected patients with smallsized AVMs. To achieve an endovascular cure, all nidalfilling and early venous drainage must be eliminated. vanRooij et al. (3) reported 100% of complete angiographicobliteration of the AVM with Onyx in a single session wasachieved in 24 patients. In their series curative emboliza-tion was considered in patients with small sized (< 3 cm)superficially located AVMs with feeding arteries accessiblefor microcatheters and allowing for reflux of Onyx for 2-3cm, with a well-delineated nidus and recognizable proxi-mal parts of the draining veins emerging from the nidus.

Curative embolization was generally not considered inlarge AVMs with feeders from different territories; in AVMslocated in basal ganglia, thalamus, or brain stem with per-forating arteries as feeding vessels; in AVMs with a diffusenidus; and “en passage”, leptomeningeal, or tiny and elon-gated feeders.

Saatci et al. (4) published their large series of AVMstreated with Onyx (51% cure rate). Their candidate forAVM embolization are follows:

In small AVMs ( 3 cm), endovascular therapy was of-fered as a first-line treatment unless,

1) the AVM was so small that the pedicle could hardlybe recognized (that is, the catheterization of the feed-ing pedicle was anticipated to be risky);

2) the AVM was in the brainstem or in a deep locationwhere it was fed by the anterior choroidal artery, sothat the reflux might result in neurological deficit;

3) the feeding vessels of the AVM were originating as“en-passage” vessels, and there was not a sufficientsegment for Onyx reflux. In such cases radiosurgerywas considered as the first-line treatment unless thepatient presented with hemorrhage.

In patients with unruptured small AVMs, the natural his-tory of the AVM is considered against the risks of em-bolization.

2. Premicrosurgical embolizationThe general strategy for premicrosurgical embolization

includes eliminating deep arterial pedicles that are en-countered only during the latter stages of surgical resec-tion and securing AVM-related aneurysms. In patientswho require embolization of multiple pedicles, a stagedapproach with each session separated by a week or moreis safest.

3. Preradiosurgical embolizationThe goals of preradiosurgical embolization are as fol-

lows: 1. to eliminate high-risk angiographic features (flow-related or intranidal aneurysms) that predispose to hemor-rhage during the latency period after radiosurgical treat-ment 2. to achieve AVM volume reduction to a sizeamenable to radiosurgical treatment (to 10 cc or less (< 3cm)).It is noteworthy, however, that a number of reports in-dicate a negative association between successful AVM ra-diosurgical obliteration and previous embolization. For thisreason, employing a strategy of preradiosurgical em-bolization for the purpose of AVM volume reduction is con-






Decision-making for candidate for vascular malformation

Jun Soo Byun Chung-Ang University Medical Center, Korea. [email protected]

troversial at best.

4. Targeted and palliative embolizationTargeted embolization of an AVM consists of oblitera-

tion of high-risk features of an AVM in which complete cureis not considered possible. These high-risk features mayinclude high flow fistulas, or intranidal or flow-relatedaneurysms. Palliative embolization relies on the idea thathigh-flow AVMs may become symptomatic by stealingblood flow from normal brain.

References

1. Mohr JP, Parides MK, Stapf C, et al. Medical manage-ment with or without interventional therapy for unrupturedbrain arteriovenous malformations (ARUBA): a multicen-

tre, non-blinded, randomised trial. Lancet 2014;383(9917):614-621

2. van Beijnum J, van der Worp HB, Buis DR. Treatment ofbrain arteriovenous malformations: a systematic reviewand meta-analysis. JAMA 2011;306(18):2011-2019

3. van Rooij WJ, Jacobs S, Sluzewski M, et al. Curative em-bolization of brain arteriovenous malformations with onyx:patient selection, embolization technique, and results.AJNR Am J Neuroradiol 2012;33(7):1299-1304

4. Saatci I, GeyikS, YavuzK, et al. Endovascular treatmentof brain arteriovenous malformations with prolonged in-tranidal Onyx injection technique: long-term results in 350consecutive patients with completed endovascular treat-ment course. J Neurosurg 2011;115(1):78-88

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Introduction

Intracranial aneurysms occur in around 3% of the popu-lation (1). Owing to the rising availability of brain imaging,the number of incidentally discovered aneurysms is in-creasing (2). Despite improvements in the management ofaneurysmal subarachnoid hemorrhage (SAH), overallcase fatality is still high (≈ 40%) (3, 4). For this reason, un-ruptured intracranial aneurysms (UIA) have been operatedon since the 1970s even at quite low-risk levels, to elimi-nate any conceivable aneurysm rupture (4).

But, decision-making for treatment of saccular UIA iscomplex and controversial because of incomplete andconflicting data about the natural history of these lesionsand the risks associated with their repair (5). And most un-ruptured aneurysms (65% to 85%) are small, < 5 to 7 mmin diameter, 3-7 and carry quite a low-rupture risk ( 1%per year) (1, 5-9).

The risks of treatment have to be balanced carefullyagainst the risk of rupture. However, prediction of the riskof rupture is difficult (10). Many prognostic factors foraneurysm rupture have been proposed. Risk factors forSAH include aneurysm size and site, with higher risks forlarger aneurysms and aneurysms in the posterior circula-tion. Multiple aneurysms, female sex, young age, historyof SAH, and cigarette smoking have been suggested asrisk factors in some studies, but not in others (1, 5, 7, 8-11), Moreover, estimation of absolute risk of aneurysmrupture in a patient based on combination of risk factors iscomplex and a clinical risk score for aneurysm rupturedoes not exist. With literatures review of prospective co-

hort studies, this topic aim is provide a brief summary onrupture risk factors and decision-making for candidate forUIAs.

Prospective Cohort Studies for UIAs

The International Study of Unruptured IntracranialAneurysms (ISUIA) (5) is the first multicenter, prospectivecohort study done in 60 centers in the USA, Canada, andEurope. 4060 patients were assessed and 2368 of them(58.3%) were treated before aneurysmal rupture. The co-hort without aneurysm treatment included 1692 patientswho were included between 1991 and 1998. 5-year cumu-lative rupture rates for patients who did not have a historyof SAH with aneurysms located in internal carotid artery(ICA), anterior communicating (Acom) or anterior cerebralartery (ACA), or middle cerebral artery (MCA) were 0%,2.6%, 14.5%, and 40% for aneurysms less than 7 mm, 7-12 mm, 13-24 mm, and 25 mm or greater, respectively,compared with rates of 2.5%, 14.5%, 18.4%, and 50%, re-spectively, for the same size categories involving posteriorcirculation and posterior communicating artery aneurysms(Pcom) (Table 1). These rupture rates were somewhatlower than previous estimates. Patients’ age was a strongpredictor of surgical outcome, and the size and location ofan aneurysm predict both surgical and endovascular out-comes. This study suggested that the rupture risk of UIAsincluded aneurysmal size ( 7 mm) and location (posteri-or circulation), history of SAH, and age (< 50 years).

In the Netherlands, a short-term clinical and radiologicalfollow-up study was done by two centers in patients with ahistory of SAH or familial intracranial aneurysms (FIA) in






Decision-making for candidate for unruptured intracranial aneurysm

Tae Hong Lee Pusan National University Hospital, Korea. [email protected]

whom an aneurysm of 5 mm or smaller was detected atscreening but not treated (12). The baseline examination(between 2002 and 2004) included 93 patients. Follow-upCT or MR angiography was done after 1 or 2 years.Patients did not undergo surgical clipping or endovasculartreatment. This study concluded that the only statisticallysignificant risk factor for growth and rupture of UIA was ahistory of both SAH and FIA.

In Japan, 419 patients with 529 saccular UIAs in singlecenter were observed without treatment between 2003and 2006 (7). CT angiography follow-up was obtainedevery 6 months. The mean follow-up duration was 905.3days. The annual rupture rate was 1.4%. This study con-cluded that Size ( 10 mm), history of SAH, and posteriorcirculation aneurysms were significant risk factors for pre-diction of rupture of UIAs, however, one should note thatsize of the UIA alone should not be applied for the final de-cision of the treatment of UIAs.

The Small Unruptured Aneurysm Verification Study(SUAVe study) is a multicenter (12 centers in Japan)prospective study to assess the annual risk of rupture ofUIAs less than 5 mm in size (9). The baseline examination(between 2000 and 2004) included 374 patients with 448UIAs. All incidentally found saccular UIAs less than 5 mmin size were registered and followed up at 6, 12, 18, 24, 30,and 36 months and yearly thereafter. The most commonaneurysm size was 3.0 to 3.9 mm (n = 193, 43.1%) andAcom aneurysms were considerably lower than those ofICA and MCA aneurysms. Patients could undergo surgicalclipping or endovascular intervention at the investigator’sdiscretion, if aneurysms enlarged by 2 mm or more in di-ameter or developed a bleb during the course of observa-tion. The average annual risks of rupture associated withsmall aneurysms were 0.54% overall, 0.34% for singleaneurysm, and 0.95% for multiple aneurysms. Althoughthe annual rupture rate associated with small UIAs wasquite low, this study concluded that if the patient is < 50years of age, has hypertension, multiple aneurysms, andsize of 4 mm, treatment should be considered to pre-vent future aneurysmal rupture. In addition, during follow-up, 30 aneurysms (25 cases) enlarged. The significant in-dependent risk factors for aneurysm enlargement were re-vealed to be women, 4.0 mm size, multiple aneurysms,and current smoking. In the 10 cases with aneurysmsgrowing by 2 mm or aneurysms with blebs, rupture wasconsidered to be more likely. Therefore, these aneurysmswere surgically clipped or embolized by an endovascularprocedure at the center where the patient was followed.

The Unruptured Cerebral Aneurysm Study of Japan(UCAS Japan) is a large, multicenter, prospective cohortstudy (8). The baseline examination (between 2001 and2004) included 5720 patients with newly identified, unrup-tured saccular aneurysms 3 mm or larger in diameter.Patients could undergo surgical clipping or endovascularintervention at the investigator’s discretion. The annualrupture rate was 0.95%. The risk of rupture increased withincreasing size of the aneurysm. With aneurysms thatwere 3 to 4 mm in size as the reference, the hazard ratiosfor size categories were as follows: 5 to 6 mm, 1.13; 7 to 9mm, 3.35; 10 to 24 mm, 9.09; and 25 mm or larger, 76.26.In this study, the rupture risk factors were size ( 7.0mm), location (Acom & Pcom), and shape with a daughtersac.

In Finland, 142 patients with 181 unruptured intracranial

aneurysms were diagnosed between 1956 and 1978 andfollowed up thereafter (11). The median follow-up timewas 21.0 (range, 0.8-52.3) years. In this long-term, single-institution cohort study, most (92%) patients harbored ad-ditional aneurysms discovered in the diagnostic work-up ofanother ruptured aneurysm. Patients did not undergo sur-gical clipping or endovascular treatment during the first 25years of follow-up and were followed up until death orSAH, or until 2011 to 2012. The average annual rupturerate was 1.1%. The cumulative rate of bleeding was10.5% at 10 years, 23.0% at 20 years, and 30.1% at 30years. None of the index aneurysms bled after a follow-upof 25 years. Finnish people had 3.6-times increased rup-ture risk in Finland than other western countries becauseUIAs were not treated before rupture and incidence ofSAH is higher in Finland than in other western countries(10). This study concluded that Cigarette smoking, patientage inversely, and the size and location of the unrupturedintracranial aneurysm seem to be risk factors foraneurysm rupture. The risk of bleeding decreases with avery long-term follow-up.

In 2013, Greving et al. (10) presented the PHASESscore for prediction of risk of rupture of UIAs. The scoringsystem was developed from a pooled analysis of individ-ual patient data from 8382 participants in six prospectivecohort studies. Predictors included age, hypertension, his-tory of SAH, aneurysm size, aneurysm location, and geo-graphical region, and were independently associated with

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the rupture risk of an intracranial aneurysm. According tothe PHASES score, a high PHASES score corresponds toa great 5-year risk of aneurysm rupture (Table 2). It is notyet complete, but this study is the first proposal to reliablypredict the long-term risk of aneurysm rupture and a riskprediction chart could serve as a valuable aid for treatmentof an UIA (13).

After extensive literature search and review by KoreanSociety of Interventional Neuroradiology (KSIN), Jeong etal. (13) recommended that treatment of UIAs might beconsidered for patients who have a life expectancy ofmore than 10-15 years and have one or more of followingconditions.

1) Size of 5 mm or more2) Size under 5 mm at high risk of rupture3) Symptomatic intracranial aneurysm4) Aneurysm located in the posterior circulation, Acom,

or Pcom5) History of previous SAH6) Aneurysm undergoing increase in size or change in

morphology during follow-up7) Patients with age less than 50 years, hypertension

and multiple aneurysms8) Aneurysm with high aspect ratio (the ratio of

aneurysm height to neck width) or high size ratio (theratio of aneurysm size to the parent artery size), oraneurysm with multilobule or bleb

9) Patients who have anxiety or depression because ofthe diagnosis of an aneurysm

The treatment decision for an UIA should be determinedafter taking into account the patient-specific factors of age,comorbidity, and health condition and aneurysm-specificfactors of size, location, and morphology. In the decision-making process, the PHASES score may be consideredfor predicting a patient’s risk of aneurysm rupture.

Fig. 1. PNUH guideline for treatment of UIAs.

Conclusion

Decision-making for treatment of UIA is complex andcontroversial, but all important issue. The several prospec-tive studies suggested various rupture risk factors of UIAs,but optimal management remains still unclear. Physiciansneed to compare the aneurysm’s natural history to the riskof treatment while considering the aneurysm location,size, shape, age, clinical presentation, and medical co-morbidities.

References

1. Vlak MH, Algra A, Brandenburg R, et al. Prevalence ofunruptured intracranial aneurysms, with emphasis onsex, age, comorbidity, country, and time period: a sys-tematic review and meta-analysis. Lancet Neurol2011;10(7):626-636

2. Gabriel RA, Kim H, Sidney S, et al. Ten-year detectionrate of brain arteriovenous malformations in a large, mul-tiethnic, defined population. Stroke 2010;41(1):21-26

3. Nieuwkamp DJ, Setz LE, Algra A, Linn FH, et al.Changes in case fatality of aneurysmal subarachnoidhaemorrhage over time, according to age, sex, and re-gion: a meta-analysis. Lancet Neurol 2009;8(7):635-642

4. Steiner T, Juvela S, Unterberg A, et al. European strokeorganization guidelines for the management of intracra-nial aneurysms and subarachnoid haemorrhage.Cerebrovasc Dis 2013;35(2):93-112

5. Wiebers DO, Whisnant JP, Huston J 3rd, et al.Unruptured intracranial aneurysms: natural history, clini-cal outcome, and risks of surgical and endovascular treat-ment. Lancet 2003;362(9378):103-110

6. Juvela S, Porras M, Poussa K. Natural history of unrup-tured intracranial aneurysms: probability of and risk fac-tors for aneurysm rupture. J Neurosurg 2000;93(3):379-387

7. Ishibashi T, Murayama Y, Urashima M, et al. Unrupturedintracranial aneurysms: incidence of rupture and risk fac-tors. Stroke 2009;40(1):313-316

8. UCAS Japan Investigators, Morita A, Kirino T, et al. Thenatural course of unruptured cerebral aneurysms in aJapanese cohort. N Engl J Med 2012;366(26):2474-2482

9. Sonobe M, Yamazaki T, Yonekura M, Kikuchi H. Smallunruptured intracranial aneurysm verification study:SUAVe study, Japan. Stroke 2010;41(9):1969-1977

10. Greving JP, Wermer MJ, Brown RD Jr, et al.Development of the PHASES score for prediction of riskof rupture of intracranial aneurysms: a pooled analysis ofsix prospective cohort studies. Lancet Neurol2014;13(1):59-66

11. Juvela S, Poussa K, Lehto H, et al. Natural history of un-ruptured intracranial aneurysms: a long-term follow-upstudy. Stroke 2013;44(9):2414-2421

12. Wermer MJ, van der Schaaf IC, Velthuis BK, et al. Yieldof short-term follow-up CT/MR angiography for smallaneurysms detected at screening. Stroke 2006;37:414-418

13. Jeong HW, Seo JH, Kim ST, et al. Clinical practice guide-line for the management of intracranial aneurysms.Neurointervention 2014;9(2):63-71



Neuroradiology(NI)16:00-18:00 Grand Ballroom 104Endovascular therapy in cerebrovascular diseases

Chairperson(s)Sang-il Suh Korea University Guro Hospital, KoreaDeok Hee Lee University of Ulsan College of Medicine,

Asan Medical Center, Korea

SS 37 NR(NI)-01 16:00 The impacts of color-coded DSA in managementof DAVF and sinus stenotic disorders in thebrainWan-Yuo Guo, Chung-Jung Lin, Sheng-Che Hung,Feng-Chi Chang, Chao-Bao Luo, Wen-Yuh Chung Taipei Veterans General Hospital and School ofMedicine, National Yang-Ming University, Taiwan. [email protected]

PURPOSE: Color-coded DSA provides quantitative mea-surement of blood circulation time with high reliability. It isa useful tool for quantification of circulation time for diag-nosis, treatment-strategy making and peri-therapeuticmonitoring. The current study is aimed to present theapplication of color-coded DSA in venous componentsand to define its impacts in the management of dural arte-riovenous fistulae (DAVF) in the brain.MATERIALS AND METHODS: Since 2011, color-codedDSA (iFlowⓇ, Siemens Healthcare) becomes an in-angio-suite routine post-processing in out institute till now. Thecurrent study includes 40 patients with DAVF of trans-verse-sigmoid and superior sagittal sinuses with/withoutsinus stenotic disorders. Among them, 32 are treated withradiosurgery alone; the other eight patients are treatedwith combined radiosurgery and either sinusplasty by bal-loon dilatation or stents placement for associated sinusstenosis. iFlowⓇ is used for these patients focusing onboth circulation time measurement (defined by the select-ed region-of-interest (ROI) of arteries and sinus) andwaveforms analysis of the sinus flows.RESULTS: Among the 32 DAVF, 20 (63%) present multi-ple-phasic waveforms of sinus flows. The multiple-phasicwaveforms indicate that the sinuses drain both arteriove-nous (AV) shunting flows and physiologically returningflows. Although the flows in sinuses have been “partly”arterialized due to the AV shunting, the sinuses still workphysiologically to drain the returning flows from theirvenous territories. Of the other eight DAVF, circulationtime differences between proximal and distal to thestenotic sinuses are found. The differences indicate pres-sure gradients across the sinus stenosis and cause corti-cal venous reflux and engorgement proximally to thestenosis. The time differences and pressure gradients arevanished after sinusplasty or stent-placement. Favorableclinical outcome are achieved in the eight patients after acombined radiosurgery following or preceding the sinus-plasty or stent-placement.CONCLUSION: The application of iFlowⓇ in the venouscomponents of cerebral vascular disorders has neverbeen reported previously. The current study quantitativelydemonstrates the pathophysiology of DAVF from hemo-

dynamic perspectives. It enhances the importance ofquantitative measurement of venous blood flows in onehand and supports the taking of treatment strategy forcerebral DAVF in the other.

SS 37 NR(NI)-02 16:10 In vitro evaluation of radio-density dynamicsduring injection of Onyx focusing on thedifference between continuous injection andintermittent injectionYuan Yuan Jiang1, Ye-eun Jo2, Jung Min Woo2, Ok Kyun Lim2, Deok Hee Lee2

1Dongguk University, 2Asan Medical Center, Korea. [email protected]

PURPOSE: Poor radiopacity of the precipitates duringplug formation has been one of the technical difficulties inusing Onyx. The purpose of this in vitro experiment is toevaluate the X-ray radio-density dynamics during Onyxinjection.MATERIALS AND METHODS: On a radiolucent plate,we placed a microcatheter (Apollo) simulating a realmicrocatheter positioning during brain AVM embolization.The Onyx was injected at a rate of 0.05 mL/min through-out the experiment and the Onyx droplets were collectedfor radio-density measurement. Forty droplets were col-lected during continuous injection (injection period) andthen 5 droplets were collected during intermittent injection(1 min. pause and 2 sec. injection) (pause period). Threebottles of Onyx was injected while serial radiographswere obtained. Using ImageJ, time to radio-densitycurves were obtained for both injection and pause peri-ods and their difference was analyzed. The radiodensitydifference between the two periods and the relationshipbetween the ROI area and radiodensity value were ana-lyzed.RESULTS: There were 9 phases of both injection andpause periods. Serial radiographs of the microcathetershowed intermittent sedimentation of the dense materialat the concave parts of the microcatheter curvatures.Repeated measures ANOVA showed that the radio-den-sities of the pause period were significantly lower thanthose of injection period (p < 0.05). There was a tendencyof gradual decrease of the radiodensity during pause peri-od (Fig. 1). There was a significant inverse relationshipbetween the droplet ROI area and radio-density (p <0.001) (Fig. 2).

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CONCLUSION: We could observe intermittent sedimen-tation of radiodense materials at the concave parts of themicrocatheter curvatures and poor radiopacity problemduring pause period. This may explain heterogeneity ofthe Onyx radiopacity and why the precipitates were diffi-cult to see during plug formation.

SS 37 NR(NI)-03 16:20 Associations between cerebral embolism andcarotid intraplaque hemorrhage during protectedcarotid artery stentingJae-yeong Jeong, Shin Ae Choi, Hyo-Sung Kwak,Gyung-Ho Chung, Seung-Bae Hwang Chonbuk National University Hospital, Korea. [email protected]

PURPOSE: The aim of this study was to determine if IPHis a significant risk factor for cerebral embolism duringCAS.MATERIALS AND METHODS: This prospective studyassessed 94 consecutive patients with severe carotidstenosis. These patients underwent preprocedural carotidmagnetic resonance imaging and postprocedural diffu-sion-weighted imaging (DWI) after CAS. IPH was definedas the presence of high signal intensity within the carotidplaque that was greater than 200% of the signal from theadjacent muscle on magnetization-prepared rapid acqui-sition with gradient echo (MPRAGE).RESULTS: Forty-three patients (45.7%) had IPH on anMPRAGE image. Maximal wall thickness was more com-monly seen in the IPH group than in the non-IPH group(6.2 ± 1.4 mm vs. 5.0 ± 1.4 mm; p = 0.000). There wasno significant difference in the incidence of postprocedur-al ipsilateral ischemic events and primary outcomesbetween the IPH and non-IPH group. However, postpro-cedural ipsilateral ischemic events were more frequentlyobserved in the symptomatic group (17/41; 41.5%) than

in the asymptomatic group (8/53; 15.1%; p = 0.005).CONCLUSION: IPH is not a significant risk factor forcerebral embolism during CAS in patients with severecarotid stenosis. Symptomatic patients should receivemore careful treatment during CAS because of the higherrisk of postprocedural ipsilateral ischemic events.

SS 37 NR(NI)-04 16:30 Single center experience of proximal cerebralprotection device for carotid artery stentingfocusing on device failure and occlusionintoleranceWonhyong Park1, Yudhi Adrianto2, Ku Hyun Yang1,Hae Won Goo1, Deok Hee Lee1

1Asan Medical Center, Korea, 2Soetomo GeneralHospital/Airlangga University Hospital, AirlanggaUniversity Medical Faculty, Indonesia. [email protected]

PURPOSE: The Mo.MaⓇ Ultra device (MoMa) is one ofthe proximal anti-embolic devices for carotid artery stent-ing (CAS) by cessation of blood flow through temporaryocclusion of the external and common carotid arteries(ECA, CCA). We are reporting our single center experi-ence with the device for last three years focusing on thecauses of the device failure and occlusion intolerance.MATERIALS AND METHODS: Between April 2012 andMarch 2015, 125 patients (107 men; median age 70)underwent elective CAS. MoMa was used for protect in90 patients (72%). We analyzed the device success(MoMa could be used as the protection device) rate, thecauses of failure, and occlusion intolerance rate and itsinfluence on the procedure. And then procedural success(CAS was done with less than 30% of residual stenosis)rate and 30-day clinical outcome was analyzed.RESULTS: The device success rate was 92.2% (83/90).Both lesions were treated in 11 patients. The causes offailure was patient’s incooperation (n = 1), marked tortu-osity of the aortic arch or supraaortic arteries (n = 3), intol-erance to occlusion (n = 1), lesion cross failure (n = 1),and aspiration failure after stenting (n = 1). The procedurewas switched to CEA in 2, done with distal protectiondevice in 4, and aborted in 1. Patient became sympto-matic during occlusion in 8.1% (7/86), however procedur-al switch to distal protection device was required in only 1.Procedural success rate was 96.7% (87/90). Significantamount of debris was noted in 7 (8.1%) (Figure). Therewas no mortality with any adverse event rate of 7.8%(7/90). On 30-day symptomatic rate was 3.8%.CONCLUSION: For the successful application of proxi-mal protection device, we should consider its technicallimitations. Occlusion intolerance occurs not infrequently,however, device switch is required rarely.



SS 37 NR(NI)-05 16:40 Comparison of embolization protection deviceswith proximal balloon device and filter device:procedural complication and embolic infarctionson DWIMyung Ho Rho, Eun Chul Chung, Hun Pyo Hong Kangbuk Samsung Hospital, Korea. [email protected]

PURPOSE: Embolic protection devices (EPDs) consist-ing of an internal carotid artery (ICA) filter or balloonocclusion are typically used during carotid artery stenting(CAS). This study compares the related complication andthromboembolic infarction on diffusion weighted image(DWI) encountered using these two types of EPD.MATERIALS AND METHODS: A retrospective reviewwas conducted of patients undergoing CAS using a bal-loon occlusion EPD (MOMA) or filter EPD (Spider FX).Symptomatic stenosis, degree of stenosis, site of steno-sis, and ulceration were evaluated. Complications weredefined as minor stroke, National Institutes of Health(NIH) stroke scale < 3; major stroke, NIH stroke scale ≥3; transient ischemic attack (TIA), reversible focal neuro-logic impairment; technical, reversible neurologic compro-mise during EPD deployment, inability to cross lesion,ICA spasm requiring treatment. Procedure time, newinfarctions on DWI after CAS (tiny: < 3 mm, small: < 10mm, medium: < 20 mm, large: > 20 mm), and 30 daysclinical result after CAS also were evaluated.RESULTS: CAS (n = 108) was performed in 106 patients(75.9% men) with a mean age of 70.6 of years.Demographic data between two groups was similar statis-tically except for age and stenosis percentage in statisti-cal significance (p < 0.05). Symptomatic and asympto-matic complication rate was slightly higher in MOMAgroup (26.3%) than Spider group (20%) and new tinyinfarctions on DWI was higher in Spider group thanMOMA group (p < 0.05). The 30-day event rate was 1.9%major stroke, 3.7% minor stoke, no myocardial infarction,and no death. The overall combined 30-day stroke,death, and myocardial infarction rate was 5.6%. The 30-day stroke rate was 5.2% in the balloon group (n = 38)and 5.7% in the filter group (n = 70, p < 0.05). Technicaldifficulties included a 10% incidence of reversible neuro-logic compromise during balloon deployment comparedwith 0% in the filter group (p = 0.002).CONCLUSION: During CAS, both balloon occlusion andfilter devices provide acceptable results with similar com-plication rate and clinical results. Although Filter has high-er new tiny infarctions than balloon occlusion, Filters havecan be used preferentially to avoid a 10% incidence ofreversible neurologic compromise associated with balloonocclusion, especially poor anterior communicating collat-erals and bilateral severe stenosis.

SS 37 NR(NI)-06 16:50 Onyx embolization for aggressive-type isolateddural arteriovenous fistula using the double-lumen balloon catheterJin Woo Kim, Byung Moon Kim, Dong Joon Kim,Keun Young Park, Jang Hyun Baek, Hong Joon Jeon Severance Hospital, Korea. [email protected]

PURPOSE: This study aimed to compare the results oftransarterial Onyx embolization using a dual-lumen bal-loon catheter with those using non-balloon catheter foraggressive-type (Borden type, 2 or 3) isolated dural arteri-ovenous fistula (ai-DAVF).MATERIALS AND METHODS: A total of 29 patients(mean age, 52 years; M:F = 20:9) underwent transarterialOnyx embolization for ai-DAVF using a dual-lumen bal-loon or non-balloon catheters between November 2007and November 2014. Since introduction of the dual lumenballoon catheter, it has been exclusively used for Onyxembolization of ai-DAVF. We compared balloon cathetergroup (n = 15) with historical non-balloon catheter group(n = 14) in treatment-related complication, angiographicoutcome, total procedural and Onyx injection times, andthe number of feeders embolized.RESULTS: The balloon group showed complete occlu-sion of ai-DAVF in 13 and near complete in 2 patients,while the non-balloon group showed complete occlusionin 5, near complete in 5, and incomplete in 4 patients (p <0.05). Treatment-related complications occurred in 2patients; cranial nerve palsy in 1 patient (6.7%) of the bal-loon group and Onyx migration to middle cerebral arteryin 1 patient (7.1%) of the non-balloon group, respectively.The median number of feeders needed to be embolizedwas 1 (range, 1-3) in the balloon and 2 (range, 1-4) inthe non-balloon group, respectively (p < 0.05). The meantotal procedural time was 62 minutes ± 32 minutes in theballoon and 171 minutes ± 88 minutes in the non-balloongroup (p < 0.05). The mean Onyx injection time was 10minutes ± 6 minutes in the balloon and 49 minutes ± 32minutes in the non-balloon group (p < 0.05).CONCLUSION: The utilization of the dual-lumen ballooncatheter for Onyx embolization of ai-DAVF seemed to sig-nificantly increase immediate complete occlusion rate andto significantly decrease both total procedural and Onyxinjection times and the number of feeders needed to beembolized.

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SS 37 NR(NI)-07 17:00 Impact of pretreatment DWI-ASPECTS onfunctional outcome after Stent-retrieverthrombectomy for acute anterior circulationstroke Seul Kee Kim, Woong Yoon, Tae Wook Heo, Byung Hyun Baek, Heoung Keun Kang Chonnam National University Hospital, Korea. [email protected]

PURPOSE: It is unclear whether pretreatment diffusion-weighted imaging (DWI) predicts outcomes after stent-retriever thrombectomy in patients with acute ischemicstroke. This study aimed to investigate the impact ofAcute Stroke Prognosis Early CT score (ASPECTS)applied to DWI images (DWI-ASPECTS) on functionaloutcome in acute stroke patients receiving stent-retrieverthrombectomy.MATERIALS AND METHODS: We retrospectively ana-lyzed the clinical and imaging data from 177 consecutivepatients with acute anterior circulation stroke who weretreated with stent-retriever thrombectomy within 6 hoursof symptom onset. Pretreatment DWI-ASPECTS scoreswere assessed by two readers. DWI-ASPECTS scoreswere categorized into 0-3 (n = 6), 4-7 (n = 89), or 8-10 (n= 82) for analysis of prognostic impact on outcome. Goodoutcome was defined as an mRS score of 0-2 at 3-month.RESULTS: Overall, successful revascularization (definedas modified TICI grades 2b or 3) occurred in 83.1%(147/177), symptomatic hemorrhage in 3.4% (6/177), andgood outcome in 45.8% (81/177) of patients. Mortalitywas 9% (16/177) at 3 months. No patient with DWI-ASPECTS scores 0-3 showed a good outcome. Goodoutcome was achieved in 43.8% (39/89) of patients withDWI-ASPECTS 4-7 and 51.2% (42/82) of those with highDWI-ASPECTS 8-10; this difference was not statisticallysignificant (p = 0.360). There were also no significant dif-ferences in the rates of successful revascularization,symptomatic hemorrhage, and mortality between patientswith DWI-ASPECTS 4-7 and those with DWI-ASPECTS8-10.CONCLUSION: Outcomes after stent-retriever thrombec-tomy in acute anterior circulation stroke were not differentbetween patients with intermediate DWI-ASPECTSscores and those with high scores. Our study suggeststhat acute stroke patients with intermediate DWI-ASPECTS scores can benefit from stent-retrieverthrombectomy.

SS 37 NR(NI)-08 17:10 Intra-arterial therapy for basilar artery occlusion;the past and present status in real practiceSeunguk Jung, Cheolkyu Jung, Byung Se Choi, Jae Hyoung Kim, Beom Joon Kim, Moon-Ku Han,Hee-Joon Bae, Yun Jung Bae Seoul National University Bundang Hospital, Korea. [email protected]

PURPOSE: Endovascular devices that allow for mechan-ical thrombectomy have been developed and are widelyused in patients with acute large arterial occlusion.Recently published reports showed that mechanical

thrombectomy leads to better procedural and clinical out-comes in patients with acute large arterial occlusion ofanterior circulation. However, those beneficial effects onthe outcomes in patient with acute BAO are uncertain.The aim of this study was to evaluate the procedural andclinical outcomes in patients with acute BAO treated withintra-arterial therapy (IAT) using the different methods.MATERIALS AND METHODS: After retrospectivelyreviewed our registry of consecutive patients with acuteischemic stroke who underwent IAT from September2003 to January 2015, patients with acute BAO admittedto our hospital within 12 hours from stroke onset or firstabnormal time were enrolled. And then they were catego-rized as thrombolytic-based IAT group (TLG) andthrombectomy-based IAT group (TEG) according to theprimary technical option. We compared the proceduraland clinical outcomes between the groups.RESULTS: Fifty-seven patients (mean age, 69.2 years;SD, 9.3) with an acute BAO were included in this study.Twenty-four patients were assigned to TLG and remain33 patients were assigned to TEG. The time from groinpuncture to reperfusion was significantly shorter in TEGthan in TLG (median [interquartile range], 48.5 [25.3 to87.8] vs. 92 [44 to 179], min; p = 0.02) And the rate ofreperfusion with modified TICI ≥ 2b was significantlyhigher in TEG than in TLG (87.9% vs. 41.7%; p < 0.01).The favorable outcome of mRS ≤ 2 at 3 months weremore frequent in TEG than in TLG (39.4% vs. 16.7%; p =0.06) However, it was not significantly associated withfavorable outcome in multivariable analysis (adjusted OR,2.77; 95% CI, 0.57-13.41). The 3-month mortality ratewas not significantly different between the groups (15.2%vs. 20.8%; p = 0.58).CONCLUSION: Although thrombectomy based IAT inpatients with acute BAO seems to be superior to throm-bolytic based IAT in terms of the reduction of time fromgroin puncture to reperfusion and the improvement of therate of complete reperfusion, we failed to show its benefi-cial effect on the clinical outcome of these patients.

SS 37 NR(NI)-09 17:20 Factors affecting the clinical outcome aftersuccessful recanalization via mechanicalthrombectomy in patients with acute ischemicstroke due to basilar artery occlusionDae Seob Choi, Seungnam Son Gyeongsang National University Hospital, Korea. [email protected]

PURPOSE: Mechanical thrombectomy for patients withacute ischemic stroke has been reported improved reper-fusion and functional outcome compared with intravenousthrombolysis. However, successful recanalization still didnot always lead to a good outcome. We collected data on34 patients with acute ischemic stroke (AIS) due to basi-lar artery occlusion (BAO) who were achieved successfulrecanalization via mechanical thrombectomy. To deter-mine which factor could affect the clinical outcome, weanalyzed the differences between the good and poor clin-ical outcome groups based on score of 3 months modi-fied Rankin Scale.MATERIALS AND METHODS: 46 patients with AIS dueto BAO received mechanical thrombectomy within 8 h of



stroke symptom onset, or with unclear-onset stroke within12 h from ‘last normal time’ using Solitaire stent and/orPenumbra reperfusion catheter. Among them, 38 patientsachieved successful recanalization defined as TICIscores of 2b or 3 (82.6%). Three were excluded becausethey were not performed MRI. We divided 35 includedpatients as a good outcome group (n = 19), defined as amRS score of 0-2 at 3 months, and a poor outcomegroup (n = 15), defined as a score of 3-6. We collecteddata on baseline characteristics, stroke risk factors, initialneurological status, thrombectomy results, clinical out-comes at discharge and at 3 months. In addition, we cal-culated posterior circulation Acute Stroke Prognosis EarlyCT Score (pcASPECTS) by using the initial MR-DWI andthe contrast staining on the post-thrombectomy CT.RESULTS: Initial NIHSS score was significantly lower ingood clinical outcome group (17.9 ± 8.9 vs. 27.6 ± 8.5,p = 0.003). But the other factors including age, presenta-tion time, stroke risk factor, stroke subtype, intravenousthrombolysis, treatment time and procedure time were notdifferent between two groups. Patients in good clinicaloutcome group had a higher pcASPECTS measured byinitial MR-DWI and post-thrombectomy CT (MR-DWI; 7.8± 1.6 vs. 5.4 ± 1.8, p = 0.001, post-thrombectomy CT;9.2 ± 1.5 vs. 6.3 ± 2.2, p < 0.000). And the contraststaining in the brainstem on the post-thrombectomy CTwas more frequent in patients with poor clinical outcome(81.6% vs. 15.8%, p < 0.000)CONCLUSION: Initial NIHSS score, pcASPECTS mea-sured by initial MR-DWI and post-thrombectomy CT andcontrast staining in the brainstem on the post-thrombecto-my CT could affect the clinical outcome after successfulrecanalization via mechanical thrombectomy in patientswith AIS due to BAO.

SS 37 NR(NI)-10 17:30 Preliminary experience of tirofiban infusion incoil embolization of ruptured intracranialaneurysmsChang Hyo Yoon, Young Soo Kim, Seung Kug Baik Pusan National University Yangsan Hospital, Korea. [email protected]

PURPOSE: Thromboembolic complications are the mostcommonly reported complications during endovasculartreatment of intracranial aneurysms with coils. There havebeen some reports on the use of intraarterial tirofiban inruptured aneurysms. We represent our experience withintravenous tirofiban infusion in patients who havereceived coil embolization for intracranial aneurysms.MATERIALS AND METHODS: Between December2008 and November 2014, we retrospectively reviewed249 ruptured intracranial aneurysms that treated with coil-ing at our institutions. 28 patients harboring 31 rupturedintracranial aneurysms underwent intravenous tirofibaninfusion during and after coil embolization procedure.Intraarterial tirofiban infusion through a microcatheter wasalso performed to resolve thrombus formation in 26patients during the procedure.RESULTS: 26 aneurysms (83.9%) were located in theanterior circulation. The mean size of aneurysms was 6.0mm. 26 aneurysms were saccular and 13 aneurysmstreated with stent-assisted coiling. Antiplatelet premedica-

tion was administered in only three cases before proce-dure and thrombus formation during procedure wasdetected in 24 cases. Two intracranial hemorrhagic com-plication (increase in the amount of hematoma) occurredduring a follow up period. In addition, two systemic hem-orrhagic complications were also found.CONCLUSION: Intravenous tirofiban as a monotherapyor in addition to intraarterial tirofiban seem to be safe dur-ing and after coil embolization in patients with rupturedintracranial aneurysms.

348 KCR 2015

Neuroradiology(N

I) Sep 12, Sat

SS 37 NR(NI)-11 17:40 Central retinal artery occlusion: the value aswarning sign of carotid artery atherosclerosisSe Jeong Jeon, See-Sung Choi, Dea-Won Kim,Yun-Sik Yang Wonkwang University College of Medicine, Korea. [email protected]

PURPOSE: Central retinal artery occlusion (CRAO) is arare disease with poor visual prognosis. Atherosclerosisis implicated as the inciting event in most cases and thepathophysiology of CRAO is similar that cerebral infarc-tion. Unfortunately there is no proved treatment forCRAO. So, we reviewed the patients with CRAO andevaluated clinical effectiveness of local intra-arterial (IA)thrombolysis and the rate of accompanying carotid ather-osclerosis as a cause of CRAO.MATERIALS AND METHODS: A total 34 patients withCRAO were enrolled in this retrospective study between2009 and 2014. Thirty patients underwent local IA throm-bolysis, 4 were excluded due to time window and inac-cessible carotid lesion. The patients were divided into twogroups as follow: Group 1 (treated within 24 hours),Group 2 (treated after 24 hours). Thrombolysis was per-formed with Urokinase with/without nimodipine. We eval-uated carotid lesion by CTA or DSA, visual acuity (VA)before and after treatment, and VA improvement evaluat-ed by ophthalmologist.RESULTS: In group 1 (18/34 patients), 3 patients(16.7%) had full recovery, 5 (27.8%) had partial recoveryand 6 (55.8) were not recovered. All patients of group 2were not recovered. There was 1 (3.3%) periproceduralcomplication. Among 34 patients, 11 patients (32.3) hadcarotid lesion which was same side of ophthalmologicsymptom.CONCLUSION: Although, the efficacy of intra-arterialthrombolysis for the treatment of CRAO needs to be fur-ther evaluated in a controlled trial, we suggest that oph-thalmic artery thrombolysis may improve visual acuity ofpatients who are treated within 24 hours after the onset ofsymptoms. Also, CRAOs are related to carotid lesionmore than we are expected. Therefore, CRAO should bemanaged like ischemic stroke.

SS 37 NR(NI)-12 17:50 Low dose angiographic protocol: effect onpatient radiation dose reduction in diagnosticand interventional procedures for intracranialaneurysmJoonsung Choi1, Bum-soo Kim1, Jihye Song1, Yong-Sam Shin1, Yon-Kwon Ihn2

1The Catholic University of Korea, Seoul St. Mary’sHospital, 2The Catholic University of Korea, St.Vincent’s Hospital, Korea. [email protected]

PURPOSE: To describe effect of low dose angiographyprotocol on reduction of patient radiation dose in diagnos-tic and interventional procedures for intracranialaneurysms.MATERIALS AND METHODS: Retrospective analysis ofradiation dose area product (DAP) in Gy-cm2 and airkerma (AK) in Gy for 1046 diagnostic and 317 therapeutic

procedures for intracranial aneurysms in 1137 patients(M:F = 338:799; median age, 56 years; range, 13-88years) between January 2012 and June 2014 was per-formed. Since April 2013, low dose angiographic protocolwas applied (from 3.6 μGy/f to 1.8 μGy/f). DAP and AKwere statistically compared in groups before (group 1)and after (group 2) application of low dose protocol.RESULTS: For diagnostic procedure, mean DAP and AKwere 140.8 ± 48.1 Gy-cm2 and 1.02 ± 0.42 Gy in group1 and 82.0 ± 30.0 Gy-cm2 and 0.6 ± 0.3 in group 2(41.8% and 40% reduction for DAP and AK respectively).For therapeutic procedure, mean DAP and AK were246.0 ± 148.3 Gy-cm2 and 3.67 ± 2.66 Gy in Group 1and 169.8 ± 111.6 Gy-cm2 and 3.31 ± 3.21 Gy in group2 (39.7% and 10% reduction for DAP and AK respective-ly).CONCLUSION: Application of low dose angiography pro-tocol has significantly decreased DAP and AK in bothdiagnostic and therapeutic procedures in patients withintracranial aneurysm.

Neuroradiology(TH)08:00-09:30 Grand Ballroom 104

Thyroid imaging and intervention 1

Chairperson(s)Jeong-Ah Kim Gangnam Severance Hospital, KoreaYoonjung Choi Kangbuk Samsung Hospital,

Sungkyunkwan University School ofMedicine, Korea

SS 02 NR(TH)-01 08:00 Comparison of computed tomography featuresbetween follicular neoplasm and nodularhyperplasiaKwanghwi Lee1, Dong Wook Kim2, Ji Hwa Ryu1, Hye Jin Baek1

1Inje University Haeundae Paik Hospital, 2InjeUniversity Busan Paik Hospital, Korea. [email protected]

PURPOSE: No previous studies have compared thecomputed tomography (CT) characteristics of the thyroidnodules which were diagnosed as Bethesda IV on cytol-ogy. This study aimed to compare CT features of follicularneoplasm (FN) and nodular hyperplasia (NH) and to findspecific CT features that distinguish FN from NH.MATERIALS AND METHODS: In 122 patients whounderwent preoperative neck CT and thyroid surgery, 59FNs and 65 NHs were included. In each case, non-enhanced and contrast-enhanced CT images wereobtained, and a single radiologist retrospectively analyzedCT images, including degree and pattern of attenuation,nodular configuration, margin, shape, pattern of calcifica-tion, degree and pattern of nodular enhancement, and CThalo sign.RESULTS: In univariate analysis, iso-attenuation,intraglandular configuration, smooth margin, ovoid shape,decreased enhancement, and absence of CT halo signwere more frequently revealed in NH (p < 0.05), whereas

Neuroradiology(TH) 349Neuroradiology(TH) Sep 10, Thu

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Cerebral vasculatures other than perforators and its ...conplus.co.kr/~kcr2015/down/abstract_book/Scientific Program/SP... · anterior medial surface of the brain, from the frontal