Anatomy and intervention in cerebral vasculature


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  • ICALarger branch of CCAAt C3 level
  • Not truly a circle but an arterial polygonBest potential collateral flow in occlusive vascular disease
  • A1 in lamina terminalis , A2 starts in lamina terminalis and then in interhemispheric fissure
  • The cortical branches of the A4 and the A5 usually supply the posterior third of the superior frontal gyrus, part of the cingulate gyrus, a portion of the premotor, motor, and somatic sensory areas.
  • Branches :Anterior inferior cerebellar ASuperior cerebellar arteriesPerforating branchesPosterior cerebral arteries
  • Knowledge of the presence and clinical relevance of normal variants such as fenestrations, duplications,and persistent fetal arteries plays a crucial role in the diagnosisand management of acute stroke and subarachnoid hemorrhage and may aid in surgical planning.
  • A duplication is defined as two distinct arteries with separate origins and no distal arterial convergence (3) (Fig 1). Fenestration, by contrast, is defined as a division of the arterial lumen into distinctly separate channels, each with its own endothelial and muscularis layers, while the adventitia may be shared (
  • It may be difficult to differentiate an accessory middle cerebral artery from a duplicated middle cerebral artery. A smaller middle cerebralartery branch arising from the anterior cerebral artery is designated as an accessory middle cerebral artery, whereas a smaller middle cerebral artery branch arising from the distalcarotid artery is called a duplicated middle cerebral artery
  • The persistent trigeminal artery is the most common and most cephalic of the persistent carotid vertebrobasilar anastomoses Two types of persistent trigeminal artery havebeen described—lateral and medial. A persistent trigeminal artery also is classified according to the configuration of the ipsilateral posterior cerebral artery: In the presence a Saltzmantype 1 persistent trigeminal artery,the posterior communicating artery is absent and the persistent trigeminal artery supplies the entire vertebrobasilar system distal to the site of anastomosis. In the presence of a Saltzmantype 2 persistent trigeminal artery there is a fetalposterior cerebral artery, and the ipsilateral P1segment is absent (
  • Normal arterial variants that may be identified within the skull base include persistent stapedialartery, aberrant internal carotid artery, and hypoplasia or agenesis of the internal carotid artery.
  • Basal v of Rosenthal -form in sylvianfiss—amb cist—v of GalenGreat v of Galen=short(1-2cm) single midline origin under splenium of corpus callosum—curve posteriorly & towards straight sinusMajor anastomotic veins According to DiChiro, the vein of Labbé predominates in the dominant hemisphere nearly twice as often as it predominates in the non dominanthemisphere, andthe vein of Trolard predominates in the non dominanthemisphere with approximately the same frequencyThe deep veins are divided into a ventricular group, composed of the veins draining the walls of the lateral ventricles, andacisternal group, which includes the veins draining the walls of the basal cisterns.
  • Latex balloons are more distensible and compliant than silastic balloons, and therefore more readily conform to the shape of a vessel reducing the risk of vessel rupture. Latex also has afar greater coefficient of surface friction than silastic balloons. large high flow vessels as in trapping procedures and in the treatment of carotid-cavernous sinus fistulae.
  • Risks associated with the use of ethanol include peritumoral swelling, pain and necrosis of normal peritumoral tissue via normal microscopic anastomotic branches.
  • Discussion in later slides
  • Streptokinase allergy
  • Snare is cork screww like intraarterial device ( flexiblkenetinol , nickel and titaniumThe device consists of the Merci retriever, the Merci balloon guide catheter,and the Mercimicrocatheter (Concentric Medical). . Can be useed 8 hr …recent Merci retriever system Concentric Medical) and the Catch system (a tiny wire basket that retrieves thethrombus. Both devices work at the distal end of the clot. Two mechanical recanalization devices evolvedduring the last year. …now a days These are the Phenox Clot Retriever (Phenox, Bochum, Germany) and the Penumbra System(Penumbra)fda 2008.
  • the Phenox Clot Retriever was able to filter micro- and macrofragments that wereformed during penetration and retrieval.
  • Carotid stenting with and without embolic protection devices continues to improve with newer designs.
  • Carotid endarterectomy in greater than 70%stenosis.
  • Principle ECA feeders are :1-Int. maxillary artery –distal branches2-MMA –meningealbranch3-Accessory meningealartery –meningealbranch4-Ascending pharyngeal artery-meningealbranch􀂾ICA feeders –Duralbranches from cavernous segment-C5 branches and the inferolateraltrunk
  • Spetzler Martin Grading system (Drawbacks)Definition of eloquenceNidus compactness (Needs consideration)Posterior fossa AVM: not usefulDifficulty in comparing modality other than surgery(Only applicable for surgical outcome)No homogeneity in Grade III AVM
  • Progressive headache visual disturbance personality change( female) Modified Dandy criteriaFriedman and Jacobso1. Symptoms of raised intracranial pressure (headache,nausea, vomiting, transient visual obscurations, orpapilledema)2. No localizing signs with the exception of abducens(sixth) nerve palsy3. The patient is awake and alert4. Normal CT/MRI findings without evidence ofthrombosis5. LP opening pressure of >25 cmH2O and normalbiochemical and cytological composition of CSF6. No other explanation for the raised intracranialpressure
  • Drug RelatedCauses of Increased ICP• Tetracycline. Minocycline, Doxycycline• Nitrofurantoin• Isotretinoin• Tamoxifen• Nalidixic acid• Lithiu• Steroid withdrawal• Anabolic steroids•Growth hormone• Vitamin A. Systemic Causes of Increased ICPAnemia (severe) Malignant hypertension Cushings and AddisonsHypoparathyridism Sleep Apnea Chronic renal failure
  • 36 yr female complaint of headache , visuladisturbacne, bilaterL PAPILLOEDEMA, MILD NEUROLOGICAL DISTR.{ BILateral lateral sinus narrowing. Typical MRI Findings Partially empty sella: 70%• Small ventricles• Flattened posterior sclera: 80%• Enlarged perioptic nerve sheath: 45%
  • For cushing syndrome….imptn question
  • Anatomy and intervention in cerebral vasculature

    1. 1. ANATOMY AND INTERVENTION OFCEREBRAL VASCULATURE Presenter: Charusmita Chaudhary Moderator: Dr. R.K.Gogoi Deptt. of Radio Diagnosis
    2. 2. NORMAL ANATOMY• ARTERIAL SUPPLY • 2 Internal Carotid Artery • 2 Vertebral Arteries• VENOUS DRAINAGE • Outer/superficial segment : Scalp vein • Intermediate segment : diploe, emissary , meningeal and dural sinus • Inner segment :Cerebral Veins (Superficial & Deep)
    3. 3. STA In Max A Occ. A Facial A Fac. A Ling.A Lingual A Sup thy ABranches of Left External Carotid artery
    4. 4. INTERNAL CAROTID ARTERY5 ARBITRARY SEGMENTS EXTRACRANIAL • carotid bulb • cervical segment INTRACRANIAL • petrous segment • cavernous C1 segment C4 • supraclinoid C2 C5 segment C3 A P
    5. 5. Internal carotid arteryAP VIEW Lateral view
    7. 7. CIRCLE OF WILLIS• Grand Vascular Station of the Brain• Classical –18% to 20% COMPONENTS• Internal carotid arteries• Horizontal segments of Anterior cerebrals(A1)• Anterior communicating artery• Proximal segments of posterior cerebrals(P1)• Posterior communicating arteries• Basilar artery
    8. 8. Anterior cerebral artery (ACA)The ACA is divided into five segments A1 segment is located between the ICA bifurcation and the ACoA. A2 segment extends from the ACoA to the region between the rostrum and the genu of the corpus callosum (GCC) A3 segment curves around the GCCand ends at the rostral part of the body of the corpus callosum. A4 and A5 segments follow the superior surface of the corpuscallosum with a virtual plane of division at the level of the coronary suture.
    9. 9. Branches of ACA• A1- medial lenticulostriate artery• ACoA- Perforating branches• A2- Recurrent artery of Heubner (RAH) Orbitofrontal artery Frontopolar artery• A3- Pericallosal and Callosomarginal a.• A4 & A5- Cortical branches
    10. 10. ACA
    11. 11. MIDDLE CEREBRAL ARTERY• Larger terminal branch of ICA• Run laterally in stem of lateral sulcus• Curves on superolateral surface &• Runs backwards in depth of posterior ramus of lateral sulcus • M1 segment =horizontal segment from origin to its bifurcation (it is in sylvian fissure) • M2 segment =lacunar segment -in the insula loops over insula—laterally to exit from sylvian fissure • M3 segment = opercular branch-from sylvian fissure & ramify over cerebral cortex • Anomalies of MCA are uncommon
    12. 12. MCA
    13. 13. POSTERIOR CEREBRAL ARTERY• P1-Peduncular/Precommunicating• P2-Ambient segment• P3-Quadrigeminal segment• P4-Cortical branches 2 major terminal br of PCA—parieto occipital art & calcarine art
    14. 14. PCA
    15. 15. POSTERIOR FOSSA• Vertebral arteries• Basilar artery
    16. 16. Vertebral arteries• Originate from the subclavian arteries.• Left VA is dominant in 60% cases
    17. 17. Branches• Extracranial -numerous branches to the meninges,spinal cord & muscles -Posterior meningeal artery• Intracranial -Anterior spinal artery -Posterior inferior cerebellar A Anterior medullary Lateral medullary Tonsillomedullary Telovelotonsillar Cortical branches
    18. 18. BASILAR ARTERY• Right and left VA unite to form basilar artery• Courses infront of pons (Prepontine cistern) & terminates in the interpeduncular cistern• 3cm in length,1.5 to 4mm in width• >4.5mm width-abnormal
    19. 19. Normal VARIANTS1. Fenestrations and duplications,2. Variants of the circle of Willis,3. Persistent carotid-basilar anastomoses4. Anomalies identified in the skull base. 19
    20. 20. Fenestration of the anterior communicatingDuplication of the anterior communicatingArtery each vessel originating separately arteryfrom an anterior cerebral artery. Fenestrations of the anterior cerebral artery 20
    21. 21. Normal Variants of the Circle of WillisAzygos anterior cerebral artery Trifurcation of the anterior cerebral artery Hypoplasia of an A1 segment of the anterior cerebral arteryBihemispheric anterior cerebral artery Absence of an A1 segment of the anterior cerebral 21 artery
    22. 22. Accessory middle cerebral arteryAbsence of the anterior communicating artery Bilateral fetal posterior cerebral arteries Early bifurcation of the middle cerebral artery. CT angiogram shows a posterior communicatingartery (arrowhead) that arises from the apex of a funnel-shaped infundibulum (arrow) 22
    23. 23. Persistent Carotid-Basilar Artery AnastomosesPersistent Trigeminal CT angiogram depicts a hypoglossal artery (arrowhead) that arises from the proximalArtery internal carotid artery (arrow) 23
    24. 24. Normal Variant Arteries in the Skull Base 1. Persistent stapedial artery, 2. Aberrant internal carotid artery 3. Hypoplasia or agenesis of the internal carotid artery. 24
    25. 25. VENOUS ANATOMY• Dural sinuses• Cerebral veins
    26. 26. DURAL SINUSES• Superior sagittal sinus• Inferior sagittal sinus• Straight sinus• Transverse sinuses• Occipital sinus• Tentorial sinuses• Sigmoid sinuses• Cavernous sinuses
    27. 27. VENOUS SINUSES
    28. 28. CAVERNOUS SINUS• Hexadron--shaped space• Either side of sella turcica• Along convergence of the sphenoid bone & petrous bone.
    29. 29. Cerebral veins• Superficial cortical veins• Near vertex they cross Subdural Space to enter SSS• Most are unnamed Superficial Middle cerebral vein( along sylvian fissure) Vein of Trolard Vein of Labbe• Deep cerebral veins Vein of Galen Basal veins of Rosenthal Subependymal / Medullary veins
    30. 30. BLOOD SUPPLY TO RELEVENT PARTS OF BRAIN• In general-cortical branches of 3 cerebral art• Motor area-frontal cortical branch of MCA; Precentral area and paracentral lobule-anterior cerebral artery• Auditory area-temporal cortical branch. Of MCA• VISUAL AREA-occipital cortical branches of PCA• Speech area –cortical branches of MCA 33
    31. 31. IMAGING TECHNIQUES• Conventional Angiography• Digital Subtraction Angiography• Ultrasonography• CT Angiography• MR Angiography 34
    32. 32. Conventional angiography• It is gold standard because of the outstanding resolution and anatomical nature of the information• Main disadvantage is it is a invasive procedure and is associated with complications 35
    33. 33. Sites :• Femoral artery• Popliteal• Axillary• Brachial• Radial 36
    34. 34. Contraindications• Pregnancy• Anticoagulant therapy and bleeding diathesis• Hepatic and renal failure• Systemic hypertension, cushing syndrome• Connective tissue disorders 37
    35. 35. Digital subtraction angiography• DSA have arisen as a result of digital data acquisition, storage and processing.• The technique uses lower doses of contrast medium because of superior contrast resolution.• Fluoroscopy technique used in interventional radiology to clearly visualize blood vessels in bony or dense soft tissue environment 38
    36. 36. Digital Subtraction Angiography(DSA)• Images produced using contrast medium by subtracting pre-contrast image from later images with contrast• Vessels are subtracted ―live‖ – instantly see non-bony superimposed images• The major disadvantage of DSA is reduced spatial resolution. 39
    37. 37. 40
    38. 38. ULTRASONOGRAPHY• EQUIPMENT : • High resolution linear array transducer• Used in cases of infants for evaluation of the brain parenchyma• Windows : • Anterior fontanelle • Posterior fontanelle • Mastoid 41
    39. 39. 42
    40. 40. CT ANGIOGRAPHY CT Angiography provides a comprehensive analysis of the vascular anatomy including the location, size, and length of the arteries and veins. CT Angiography is used to detect; • Dissections • Aneurysms • Plaque • Stenosis Optimal image quality depends on two factors: • Morphological layout and CT angiography technique (scan aberrations protocol, contrast• Pre and Post surgical assessments material injection protocol, image reconstruction methods) and data visualization technique(image postprocessing). 43
    41. 41. ADVANTAGES ARTEFACTS• The more slices that can be • Motion artifacts reduced by acquired per rotation faster scanning • The longer the volume that can be scanned • The higher the resolution • Stair-step artifacts in 3D possible reconstructions reduced by • The better the reproduction of using thinner slices 2D and 3D reconstructions • The greater the detail available • Partial volume artifacts in all 3 axis (x,y and z) reduced by using thinner slices• Patient comfort• Non invasive investigation• Easily available to all levels of socioeconomic status
    42. 42. POST PROCESSING• Coronal and Sagittal MPR (multi planar reconstructions) • Shaded surface display, or surfacerendering, is an algorithm that provides a good 3D impression ofthe surface of an object. 3D volumetric images with rotationalimages comprising of bone and non bone backgrounds. • MIP (Maximum intensity projections) • Measurements 45
    43. 43. MR ANGIOGRAPHYconstitutes group of MR imaging techniques that can be used to directly imageflow in arteries, veins, and cerebrospinal fluid.Time-of-flight imaging is susceptible to saturation effects, and short Tisubstances may simulate flow.•Two-dimensional time-of-flight imaging is useful in cranial venography inassessing the patency of the dural sinuses or venous drainage from anarteriovenous malformation.•Three-dimensional time-of-flight images depict small and medium-sizedaneurysms.Phase-contrast imaging has excellent background suppression, allowsvariable velocity encoding, and provides directional flow information.•Two-dimensional phase-contrast imaging is useful in the assessment of thepatency of major vascular structures.•Three-dimensional phase contrast imaging (with 30-cm/sec velocityencoding) is also useful in depicting small and medium-sized aneurysms•Cine Phase contrast imaging – hemodynamic flow information. Allow imagingof csf, venous and arterial flow. 46
    44. 44. 47
    45. 45. Vascular Interventional procedures ofbrain Part II
    46. 46. INTRODUCTION:• Interventional and Endovascular Neurology is the Neurological subspecialty focused on endovascular and other minimally invasive approaches to the diagnosis and management of vascular and non- vascular neurological diseases.• The section is committed to advancing all diagnostic and therapeutic interventional procedures that involve the neurological patient community and to support education and research initiatives that will expand this field.• Endovascular therapies include1. Embolotherapy2. Cerebral revascularization Non vascular aspects of interventional neuroradiology include pain management, percutaneous biopsies and vertebroplasty.
    47. 47. • Cath lab.-known as ―operating room‖ or ―special procedures room‖.• Radiographic Imaging Equipments• Biplane angiography with digital subtraction ability, high resolution image intensifier is recommended. Digital Road map fluoroscopy capability is mandatory, preferably with simultaneous live unsubtracted imaging . Now a days 3D CT is used too.• Critical care of patients undergoing endovascular and interventional procedures.
    48. 48. VASCULAR INTERVENTION:• Embolotherapy continues to evolve in its active consideration in the preoperative management of aneurysms, vascular malformations and vascular tumors.• This progressive increase in demand has been principally as a result of development of newer microcatheter delivery systems and of safer and more varied embolic agents.• more target specific embolization with a greater degree of preservation of adjacent normal vascular anatomy.• These include particulate emboli, coils, balloons, tissue adhesives, non adhesive agents, sclerosing agents and chemotherapeutic agents.
    49. 49. Classification: Embolic agentsI. Particulate embolic agents( agent of choice). Absorbable Non AbsorbableII. Mechanical embolic agentsIII. Liquid embolic agents.Absorbable agent:Gelfoam( Powder /sheet), AviteneUse: topical thrombotic agent in conventional surgery. to "protect" normal vessels.Non absorbable: PVA(150 to 1000 microns), particles (Ivalon, Biodyne, Contour Emboli).• PVA: small( embolization of vascular tumors) and large size( occlusion of larger, high flow vascular malformations).MOA—Adhere to vessel wall(lumen occluded),necrotising vaculitis. Temporary effect—Weeks to Month
    50. 50. • Recently, a newer class of microembolic agent has been introduced• Soft, smooth surfaced, deformable particles ( Embospheres (Microsphere) and Bead Block (Terumo))• tend to ovalize when confined, a trait that makes these agents more effective in more distal embolotherapy.• ADV: do not adhere to vessel walls as do crystalline PVA particles, particles are more likely to reach the capillary bed of the tumor. Bead Block
    51. 51. COILS :Guglielmi detachable micro coil. (GDC)• Platinum micro coils soldered on stainless steel micro wires. once in desired position detached by passing Direct current which causes electrolysis at the soldered site.• can be positioned, withdrawn and repositioned repeatedly until the desired position is obtained. Advantage: Coil can be withdrawn before final placement.The Hydrocoil (Microvention) is unique in that it is coated with a hydrogel that expands after deployment.
    52. 52. BALLOONS• Latex and silastic balloons• Advantages: 1) the ability to occlude a vessel at a precise location 2) the ability to flow navigate attached, partially inflated balloons to distal locations along a tortuous course3) the ability to rapidly occlude vessels larger than the caliber of the catheter4) the ability to inflate, deflate and reposition repeatedly until the desired position is achieved.
    53. 53. LIQUID EMBOLIC AGENTS• n-butyl cyanoacrylate (NBCA)• Histoacryl• This agent will rapidly polymerize on contact with any ionic substance such as blood, saline, ionic contrast media and vessel epithelium.• ADV:rapidly occlude high flow arteriovenous malformations with a more permanent result• DISADV:The catheter must be rapidly withdrawn after each injection of NBCA, resulting in frequent, time consuming catheter exchanges• Onyx: non adhesive liquid embolic agent safer and effective than NBCA
    54. 54. SCLEROSING AGENTS• Absolute ethanol• Sotradecol (sodium tetradecyl sulfate) behaves similarly to alcohol, but with less associated pain.• Hypertonic saline and glucose solutions are also effective sclerosing agents that work rapidly in both the arterial and venous systems.• The results of embolotherapy with ethanol when compared to the particulate agents and NBCA have shown a more permanent occlusion of abnormal vessels without the inherent risks associated with tissue adhesives.
    55. 55. CEREBRAL REVASCULARIZATION…..• Intra-arterial cerebral revascularization incorporates several new technologies and newer applications of techniques that have been well established in peripheral revascularization. The focus on acute stroke reversal offers an exciting new aspect to interventional neuroradiology.
    56. 56. Vascular Interventional procedure of brain Endovascular procedures. Direct percutaneous procedures. Endovascular procedures:1. Endovascular technique for lumen restoration.2. Endovascular technique for lumen obliteration.3. Endovascular treatment of A V shunts.4. Endovascular treatment for vein of galen aneurysal malformation.5. Endovascular treatment of dural arteriovenous shunts.6. Brain tumour embolisation and chemotherapy.7. epistaxis endovascular therapy: Embolization of refractory head and neck bleeds.8. WADA and functional testing.9. petrosal venous sinus sampling for Cushing disease10. pseudotumor cerebri endovascular therapy with venous sinus stenting11. endovascular repair of traumatic head and neck vascular injuries
    57. 57. Direct percutaneus procedures:(1) Image guided Embolisation of tumour.(2) Image guided embolisation of AVM.(3) Image guided photodynamic therapy.
    58. 58. Hyperacute ischemic stroke 1)Intra-arterial thrombolysis : It involves the direct infusion of thrombolytic agents into the occluding thrombus . Higher local concentration of drug.• Lower systemic concentration.• Fewer extracranial haemorrhagic complications.• Faster and more complete recanalisation .• This allows a longer time window of 3–6 hours or longer if perfusion studies are favourable.
    59. 59. Thrombolytic agents: 1) Recombinant tissue plasminogen activator (rTPA). 2)Streptokinase. 3)Urokinase. 4)Pro-urokinase. 5) Ancord .
    60. 60. 2) Mechanical procedures1)Microguidewire applied to disrupt the clot facilitate the action of the thrombolytic agent.2) Clot retrieval devices or Snare which may actually extract the thrombus from the occluded artery, achieving reperfusion much more readily.
    61. 61. Recent mechanical thromolitics The BONnet consists of a self-expanding nitinol braiding with polyamide filaments passing through the interior to enlarge the surface area and enable better fixation of the thrombus mass. The system can be either put distal to the thrombus or released into the thrombus. B, The CRC is based on a fiber work of polyamide filaments whose lengths fromproximal to distal end increase. The CRC has an additional nitinol thread cage at the proximal end of its fiber brush. This nitinol cage gives it a higher radial range. C, ThePhenox pCR is based on perpendicularly oriented polyamide microfilaments that create an attenuated palisade. The Penumbra System is based on an aspiration platform that includes reperfusion microcatheters connected to an aspiration pump. A teardrop-shaped separator is advanced and retracted within the lumen of the reperfusion catheter to debulk the clot for ease of aspiration.
    62. 62. . 3) Balloon Angioplasty or stent placement If thrombus is superimposed upon a stenosis. (Atherosclerotic plaque).Solitaire FR stent (ev3). A self-expanding stent that can be fullydeployed and then completely retrieved
    63. 63. Disadvantages Additional time delays. Risks of procedure Arterial embolisation. Arterial perforation. Haemorrhagic infarction. Retroperitoneal haematoma. Groin haematoma. Terminal basilar artery occlusion Collectively risk estimated -- 5%
    64. 64. • A. Left Vertebral Artery Injection demonstrating extensive clot in the basilar artery .• B. Following Urokinase via a microcatheter there is complete resumption of normal flow.
    65. 65. TREATMENT OF CEREBRAL VASOSPASMCerebral vasospasm represents a significant cause ofmorbidity and mortality in patient with subarachnoidhaemorrhage leading to ischemic deficits.Medical treatment(Triple H ) Hypertension Hypervolemia Haemodilution Endovascular treatment:(1)Pharmacological relaxation of spastic vessel by Selectiveintra-arterial papavarine infusion. (2) Mechanical dilatation of spastic segment (balloondilatation).
    66. 66. • Cerebral vasospasm (MCA)• Treatment----Balloon dilatation
    67. 67. Angioplasty and stenting of extracranial and intracranial vessels. Indications• Carotid stenosis(>70%)• Vertebro basilar artery stenosis.• MCA stenosis(>50%) Purpose: Reduce incidence of recurrent stroke (TIA).
    68. 68. Percutaneous transluminal angioplasty(PTA) Pre treated with antiplatelet agents. Under LA via femoral artery. The patient is systemically heparinised and the carotid artery catheterised, a guide wire crosses the stenosis, a protection device is deployed . Balloon inflation (8 atmospheric pressure for 10 sec) deflated if significant stenosis persists repeat procedure for 2 to 3 times. Clopidogrel and aspirin are maintained for three months.
    69. 69. Stenting• Method of choice• Under LA• Pre operative antiplatelet therapy(Aspirin and clopidogrel)• Following pre operative angiography ,a guiding catheter(6Fr) is placed to common carotid artery  the stenosis is crossed with a soft tip guidewire,a protection device is deployed .The stenosis is predilated using an angioplasty balloon, and a stent is deployed across the stenosis and redilated.
    70. 70. pathophysiological process ofcarotid artery dissectionproceeding from the acutestage to either spontaneoushealing (1), formation of falselumen (2), residual stenosisof varying degree or completeocclusion (3), and formation ofa pseudoaneurysm (4). A stentis used in cases notresponding to medical therapyeither to relieve ahemodynamically significantstenosis, to occlude a falselumen, or to serve as ascaffold to enable coilembolization of a wide-neckedpseudoaneurysm.
    71. 71. Carotid Cavernous sinus fistulaCarotid cavernous fistulas (CCFs) result from spontaneous or acquired , abnormal connection(s) between the cavernous ICA and venous channels of the cavernous sinus, and are either high or low flow. Barrow’’s Classification (1985) trauma Treatment modalities: Type A—High flow type Detachable balloons is the treatment of choice for most type A CCFs .The currently available latex balloon is deployed up the ICA, through the defect and inflated within the cavernous sinus, occluding the fistula and preserving the ICA.
    72. 72. Carotidcavernous fistula
    73. 73. Transcatheter coil embolisation- Routes –Trans venous (Preferred)—Femoral vein—inferior petrosal sinus cavernous sinus-Platinum micro coils with attached dacron fibres is used. Trans arterial route---GDC coils are used to reduce the risk of recoiling in the ICA.
    74. 74. Liquid embolic agents Onyx can be deployed through the micro catheter via venous route into the cavernous sinus, with balloon protection (non-detachable) in the ICA .Type B—Low flow Carotid cavernous sinus fistula Polyvinyl alcohal (PVA)---150—250 micron Size . selective embolisation of external carotid artery feeders is done. If Recanalisation,, occur, transvenous coil occlusion of the cavernous sinus either through the jugular vein and inferior petrosal sinus or through the superior ophthalmic vein achieves cure in most patients.Carotid compression maneuver Facilated thrombus formation.
    75. 75. Endovascular treatment of intracranial aneurysmsAn aneurysm is a sac filled with blood which is in direct communication with the lumen of an artery. True AneurysmLocal dilatation of the artery. False aneurysm Sac with walls formed of condensed perivascular connective tissue which communicate with the Common site of intracranial Aneurysm artery through an aperture in its wall.
    76. 76. • Clip vs CoilWhat to choose ?• • This decision needs to be made withknowledge of:‐‐‐ the safety and efficacy data‐‐‐the patient’s expected longevity‐‐‐aneurysm factors – size‐‐ configuration‐‐ location• ‐‐‐the operator’s experience.• Equally important to consider whether the aneurysm• ‐‐‐unruptured• ‐‐‐ruptured• This complex decision requires entertaining all the variables, ensuring that patients receive the most appropriate care .
    77. 77. Coil embolisation:Through trans-arterial route a micro catheter is placed in the lumen of the aneurysm- through the micro catheter ,soft platinium coils are packed in the aneurysm.
    78. 78. Large ruptured aneurysm, pre embolization (A), and post embolization with GDC coils ( B&C).Assisted aneurysm coiling techniques, including balloon assist (A) (Hyperform balloon catheter, MTI) and 84 Neuroform stent assisted technique (B,C) ( Target Therapeutics Corp / Boston Scientific )
    79. 79. Newer technique to reduce coil compaction and recanalisation• Coils with more complex shapes.• Bioactive coils (coated with polyglycolic polylactic acid).• Hydrogel coils.• Radioactive coils (incorporated with P32 emitting ß radiation).
    80. 80. • When patency of the parent vessel cannot be assured (Fusiform or serpentine ,wide- necked aneurysm,false aneurysm)-Vessel may be permanently occluded by balloon or coil embolisation with prior test occlusion..
    81. 81. Giant Aneurysm Size more than 2.5cm.• Giant aneurysms are often sub-optimally treated using coils alone.• The accepted treatment ----parent vessel occlusion.• Trial balloon occlusion (TBO) .• When parent vessel occlusion cannot be tolerated. Surgical bypass procedures. Embolisation (high density onyx). stent .
    82. 82. Parent vessel (left ICA) occlusion in the management of a giant cavernous carotid aneurysm.
    83. 83. Endovascular treatment of cerebral AVMArteriovenous malformation (AVMs) are a complexconglomerate of abnormal arteries and veins. They lackan intervening capillary bed and there is resultant highflow arteriovenous shunting through one or morefistulae. Therapeutic options 1) Neurosurgery 2) Embolisation 3) Stereotactic radiosurgery. Aim of treatment 1)Obliterate the AVM completely . 2)Eliminate the risk of haemorrhage. 3)Reduce the effects of steal or venouscongestion .
    84. 84. Spetzler Martin grading system (Grade 1 to 5) Reflects the degree of surgical difficulty and risk of surgical morbidity and mortality, and the scale is based upon AVM size, venous drainage, and location .AVM Size--- Small ---- 0 to 3 cm - 1 point. Medium --3 to 6 cm - 2 points. Large ----- > 6 cm - 3 points. AVM location--- Non-eloquent region -- 0 point. Eloquent region --------1 point. Pattern of venous drainage--- Superficial ----------0 point. Deep -----------------1 point.
    85. 85. Treatment rationale: Grades 1 and 2 and some grade 3 ---surgery recommended. Grade 3 AVMs with deep inaccessible feeders, surgery with embolisation or stereotactic radiosurgery is considered . Grade 4 and 5 AVMs is usually multidisciplinary Embolisation under general anaesthesia. Superselective catheterisation of the feeding arteries using a microcatheter with or without the aid of a micro guidewire. Liquid embolic agents are generally used, either onyx or n-butyl Cyano acrylate (NBCA). other embolic agents like balloon,Liquid coil can be used.
    86. 86. Onyx embolisation of a right perisylvian AVM
    87. 87. Onyx embolisation of a right perisylvian AVM
    88. 88. A middle aged patientpresenting with an AVMnear the visual area of theleft hemisphere whichhemorrhaged once.Presurgical embolisation Before Treatmentwas conducted to reducethe size of the AVM. Pre-embolisation image Aversus post embolisation Bshows the substantialreduction in size. She hadan excellent outcome fromsurgery. Following Embolisation in preparation for surgery
    89. 89. Dural AV fistula Dural arteriovenous fistulas (DAVFs) abnormal arteriovenous connections within the dura, usually within the walls of a dural sinus .• They are acquired lesions idiopathic most common venous sinus thrombosis and/or venous hypertension.• Thrombosis triggers the stimulation of angiogenesis and engorgement of microscopic arteriovenous channels that normally exist in the dura.• The cavernous sinus, transverse and sigmoid sinuses are most often implicated, but any sinus may be involved ..• Premature visualization of intracranial veins orvenous sinuses during arterial phase-Characteristic
    90. 90. Cognard’s classification• Type I includes DAVFs which drain into a sinus with normal antegrade flow.• Type II DAVFs --insufficient antegrade flow with reflux into either venous sinuses (IIa), cortical veins (IIb), or both (IIa+b).• Type III fistulas drain into cortical veins without venous distension.• Type IV drain into cortical veins with venous ectasia.• Type V drain into spinal perimedullary veins.
    91. 91. Management• Type I fistulas --carotid or occipital artery compression , arterial embolisation using PVA particles Type IIa treatment of choice is arterial embolisation of ECA feeders using PVA particles• types IIb and IIa+b --Transvenous coil occlusion of the involved dural sinus.• Types III and IV---endovascular occlusion of the draining cortical vein itself using coils may occlude the fistula preserving dural sinuses.
    92. 92. Transvenous coil occlusion duralarteriovenous fistula
    93. 93. Vein of galen Aneurysmal malformationtypes—1)Direct AVM--Choroidal arteries/Thalomoperfora te actually communicate with the vein of galen.2)Indirect ---AVM in the thalamus or mid brain veins drain into the vein of galen.
    94. 94. Intervention If possible intervention deferred to allow growth of the child, as intervention in neonate is difficult and hazardous .Criteria for neonatal or infantile intervention: Cardiac failure unresponsive to medical therapy. Progressive macrocephaly. Seizures. Developmental delay. Reversible neurological deficit.• AIM— TO REDUCE THE AMOUNT OF AV SHUNT.• Arterial approach ---Permanent embolic agent--- NBCA glue, Onyx.• Transvenous route tried.
    95. 95. xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxNBCA glue embolisation of vein of galen Aneurysmal Malformation
    96. 96. CEREBRAL VENOUS SINUS THROMBOSIS Intravenous anticoagulation — most cases are successful Local thrombolysis INDICATIONS: Presentation in coma. Clinical deterioration despite full anticoagulation. Treatment modalities 1) Pharmacological thrombolysis of the cerebral venous sinuses is usually performed via the Transvenous femoral route in an anaesthetised patient.
    97. 97. 2)Pharmaco-mechanical thrombolysis may also beachieved using a microcatheter,microwire ormicrosnare. Local pharmacomechanical thrombolysis in superior sagittal sinus (SSS) thrombosis.
    98. 98. . 3)Mechanical— Saline jet vacuum device -- It consists of a double lumen 5 French catheter tapering to 3.5 French, high velocity saline jets, exiting the catheter at a pressure of 2500 psi, are directed through one lumen, connected to a bag of heparinised saline. A venturi effect breaks up the thrombus and the Saline jet vacuum device debris is directed down the other lumen and collected in a bag.
    99. 99. Examples of mechanical measures to remove clot. A, low pressure angioplasty, B clot disruption with the Neurojet (Possis) and c. clot retrieval with the Merci device. 105
    100. 100. AngioJet catheter treatment -dural sinus thrombosis
    101. 101. IDIOPATHIC INTRACRANIAL HYPERTENSION• remains a diagnosis of exclusion( Friedman D., Jacobson D.: Neurology 59, 2002)• To clarify the relation of IIH to associate narrowing of lateral dural sinuses• The neuro interventional community is still debating and strives to justify neurovascular strategies for treatment.--Causes• Focal narrowing in the transverse sinuses unilateral or bilaterally.• Secondary to raised central venous pressure .
    102. 102. IDIOPATHIC INTRACRANIAL HYPERTENSION• Investigation :MRI, MRV• Catheter angiography with retrograde venography• Pull-back manometry• Focus of interest of venous manometry: a) gradients across the irregularities of lateral sinus b) gradients at confluence of sinuses/jugular bulbIntervention---Stenting• General anaesthesia is required for stent deployment because the dura and sinuses are sensitive to pain. Stenting is achieved directly through a percutaneous jugular venous puncture. A guide catheter is manipulated into the transverse sinus and a self expanding stent deployed across the stenosis .
    103. 103. Optic papilla protrusion Endovasal manometry: lft Compliant balloon angioplasty of lateral sinus Follow up 6 we Gd MRIInitial Gd MRI
    105. 105. SKULL BASE TUMOURS Common tumours requiring preopreative embolisation are• Meningiomas.• Angiofibromas.• Glomus tumours . Objective selective obliteration of arterial feeder before surgical resection.• Delivered under sedation by trans femoral route by selective catheterisation of the vascular pedicle.• Aim to occlude the pre capillary arteriole.
    106. 106. • Embolic agent —PVA(150-250 microns). If intra tumoural shunts are present -- Particle size increase. Slurry of PVA and AVitene. Small coil or silk sutures. Liquid coils.Embolisation should be performed 24–72 hours before surgery to allow progressive thrombosis.• If very small size particle are used then skin necrosis and cranial nerve palsy occur.
    107. 107. Polyvinyl alcohol (PVA) embolisation of a glomusjugulare tumour.
    108. 108. Glomus jugulare tumour
    109. 109. Meningioma
    110. 110. Inferior Petrosal sinus sampling To obtain blood sample in pituitary microadenoma
    111. 111. Brain tumour chemotherapyPrinciple→Intra arterial infusion of chemotherapeutic agents ↓ 1)increased concentration of c.t.agents locally ↓ 2)increase cytotoxicity, Decreased side effects.Procedure: Selective catheterization of the artery supplying the tumour done under systemic heparinisationc.t. agents infused.
    112. 112. ChemoembolizationChemoembolization works to attack the tumour in two ways. 1) Delivers a very high concentration of chemotherapy directly into the tumor, without exposing the entire body to the effects of those drugs. 2) The procedure cuts off blood supply to the tumor, depriving it of oxygen and nutrients, and trapping the drugs at the tumor site to enable them to be more effective.• Super selective catherisation of the vascular pedicle is done.• Chemotherapeutic agents mixed with particulate embolic agents infused through the micro catheter.
    113. 113. Image guided percutaneoustreatment
    114. 114. Direct percutaneous embolisation in vascular malformation of head and neck Low flow malformation like haemangio-lymphangioma or venous malformation. Under image guidance needle is placedpercutaneously in the lesion ↓Contrast injected through the needle to delineate the vascular compartment and venous drainage ↓ Concentrated alcohol injected to the lesion.
    115. 115. Image guided photodynamic therapyPhotodynamic therapy is a minimally invasive palliative treatment for malignancy . Intra venous injection of photosensitizing drugs. Image guided needles placed in the tumour Fibre optic cables are placed through the needles,providing a foccused delivery of laser light. Laser light + Photosensitising drugs Activates the drugSinglet oxygen(highly cytotoxic) Interacts with Oxygen
    116. 116. CONCLUSION• Proper knowledge of vascular anatomy is very important . Proper pre surgical ,clinical and radiological assessment helps in surgical planning and avoid catastrophy.• There has been enormous growth and development in neuro endovascular expertise and technology in recent years, and this expansion continues allowing increasingly safe and more effective ways to treat many intracranial and extra cranial vascular lesions .• It is necessary to provide the patient with all treatment options. Considering cost-effectiveness and that endovascular treatment has lower morbidity and mortality rates than does neurosurgery. It is crucial for the group to take a leading role in the future of neurointervention.
    117. 117. OLD NEWER Recent principle In medical science Minimum Access - Maximum Result