CEREBRAL ANEURYSM Dr. Crystal K C 2 nd Year Resident MD, R adiodiagnosis NAMS, Bir hospital
Vessels Supplying Brain
Cerebral Arteries A1-segment Anterior cerebral artery from carotid bifurcation to anterior communicating artery gives rise to the medial lenticulostriate arteries. A2-segment Part of anterior cerebral artery distal to the anterior communicating artery. P1-segment Part of the posterior cerebral artery proximal to the posterior communicating artery. The posterior communicating artery is between the carotid bifurcation and the posterior cerebral artery) P2-segment Part of the posterior cerebral artery distal to the posterior communicating artery
Middle Cerebral Artery Horizontal M1-segment gives rise to the lateral lenticulostriate arteries which supply part of head and body of caudate, globus pallidus , putamen and the posterior limb of the internal capsule. Notice that the medial lenticulostriate arteries arise from the A1-segment of the anterior cerebral artery. Sylvian M2-segment Branches supply the temporal lobe and insular cortex (sensory language area of Wernicke ), parietal lobe (sensory cortical areas) and inferolateral frontal lobe Cortical M3-segment Branches supply the lateral cerebral cortex
Vertebral Artery V1 ( preforaminal ): origin to transverse foramen of C6 V2 ( foraminal ): from the transverse foramen of C6 to the transverse foramen of C2 V3 ( atlantic , extradural or extraspinal ): from C2 to the dura V4 ( intradural or intracranial): from the dura to their confluence to form the basilar artery
V1: segmental cervical muscular and spinal branches V2: anterior meningeal artery, muscular and spinal branches V3: posterior meningeal artery V4: anterior and posterior spinal arteries (ASA and PSA), perforating branches to medulla, posterior inferior cerebellar artery
Basilar Artery Branches Before terminating at the upper pontine border where it divides into the two posterior cerebral arteries , it provides several paired branches: anterior inferior cerebellar artery (AICA) labyrinthine artery (variable origin; more commonly a branch of AICA ) pontine arteries superior cerebellar artery (SCA)
Aneurysms They result from focal degeneration of the arterial wall. They are the most common cause of SAH. They are of 3 types : Saccular ( outpouching from arterial bifurcation) - Lacks internal elastic lamina Fusiform (arterial dilatation) Dissecting (pseudo-aneurysm)
SACCULAR ANEURYSM Berry like vesel outpouching arising from the bifurcation of the arteries. 80% of Intracranial aneurysms 85% - anterior circulations 15%- Posterior circulations.
FUSIFORM ANEURYSM No definitive neck. Long course of circumferential thickness. Dolichoectasia . Vertebrobasilar system commonly affected.
DISSECTING ANEURYSM May be intracranial or extra-cranial. Intracranial vertebral or posterior inferior cerebellar arteries – SAH Extra-cranial carotid and vertebral arteries – Stroke (in young)
Presentation Aneurysm may present clinically in three different ways. S ubarachnoid hemorrhage (90%). Cranial nerve palsy {CN III} Headache Seizure Neurological dysfunction.
INCIDENCE General population is 0.5-5 % Women >> Men Increases with advancing age. Genetic Predisposition. Overall risk of rupture = 0.5-2 % per annum,
Risk Factor of Rupture Daughter sac Multi- lobulations Irregular surface Bottle-neck shape Interval growth Increase ratio of maximum aneurysm diameter to parent vessel diameter.
Location Most cerebral aneurysms arise from the circle of Willis and middle cerebral artery bifurcations. Ninety percent involve the anterior circulation, and 10% the posterior circulation.
Multiple aneurysm Multiple aneurysms are found in 15% to 30% of patients, Women: Men= 5:1 ratio, Most frequently involve the middle cerebral artery. Of the patients with multiple cerebral aneurysms, 75% have two, 15% have three 10% have four or more.
Bilateral symmetrical aneurysms are called Mirror Aneurysms , and most often involve the ICA or the MCA bifurcations . When one of multiple aneurysms ruptures and causes subarachnoid hemorrhage, it is most often the largest, although this is not always the case. For instance, Nehls and colleagues have reported the propensity for anterior communicating aneurysms to rupture when several are present simultaneously.
Etiology Primary Causes Atherosclerosis Hypertension Smoking Abuse of cocaine, methamphetamine, ephedrine, heroin, and other drugs that produce arteritis or hypertension Vascular malformations - fibromuscular dysplasia, spontaneous cervical carotid or vertebral artery dissection, Takayasu's arteritis , neurofibromatosis I C onnective tissue disorders , such as Marfan's syndrome and Ehlers- Danlos syndrome
Secondary Causes Penetrating and nonpenetrating trauma Dissection (posttraumatic or otherwise ) Inflammation or mycosis due to septic Neoplasm infundibulum represents the residua of a developmental vessel that has undergone incomplete regression. It most commonly involves the junction of the internal carotid artery and posterior communicating artery and less commonly involves the origin of the anterior choroidal artery from the internal carotid artery. Infundibula are usually 3 mm or less in diameter.
CTA :a distal posterior cerebral artery territory mycotic pseudoaneurysm with adjacent parenchymal hematoma in a patient with mitral valve vegetations.
Pathology Pathologically, a number of patients with cerebral aneurysms demonstrate collagen type III abnormalities. The walls of saccular cerebral aneurysms contain intima and adventitia, but the media and internal elastic membrane are thinned or absent . Neoplasm : Pitutary adenoma – Growth hormone Mycotic - spread of infection to vasa vasorum .
Features Need To Be Assessed size: ideally 3 axis maximum size measurements neck: maximal width of the neck of an aneurysm the shape and lobulation orientation: the direction in which the aneurysm points is often important in both endovascular and surgical planning
Cont…. any smaller branches in the vicinity of an aneurysm any branch taking off from the aneurysm the presence of other aneurysms relevant arterial variant anatomy (that may complicate or exclude endovascular treatment
Imaging Evaluation Imaging objectives for the identification of a cerebral aneurysm are Visualization of subarachnoid hemorrhage, Confirmation of the size, location, and morphology of the cerebral aneurysm, Evaluation of the adjacent cerebral vasculature, including evidence of spasm, atherosclerosis, displacement, and incorporation into the aneurysm's wall , and Demonstration of any accompanying adjacent brain pathology.
The typical patient with a ruptured cerebral aneurysm is a woman between 40 and 60 years of age who presents with “the worst headache of life,” with or without a neurologic deficit. Clinical assessment of the patient classifies into Hunt and Hess grades I through V or World Federation of Neurological Surgeons grades 1 through 5
Imaging modalities Computed tomography and CTA MRI and MRA DSA Transcranial ultrasound Earlier Lumbar Puncture
Lumbar Puncture Before CT, it was the only method to confirm the diagnosis of SAH but presently it is only indicated when CT is normal in patients with sudden, severe headache. CSF is bloody not clearing with sequential tubes, Xanthrochromia is present after 1-2 days of SAH.
Computed Tomography Acute Subarachnoid Hemorrhage The most important role for CT in the patient with a cerebral aneurysm is in the identification of ASAH, Increased density within a cisternal space .
ACOM Septum pellucidum , interhemispheric fissure and intraventricular PCOM Sylvian fissure MCA Temporal lobe, Sylvian fissure and intraventricular Basilar Prepontine cistern ICA Sylvian fissure and intra-ventricular Pericallosal artery Corpus callosum PICA Foramen magnum , Fourth Ventricle
CT is also excellent for identifying Hydrocephalus, Intraventricular hemorrhage (seen in 13% to 28% of cases ), Parenchymal hematoma (20% to 30 %), and The occasional subdural hematoma
SAH with Hydrocephalus CT scan showing SAH , intraventricular HHG and hydrocephaus
Plain CT Head Blood in the CSF space has feathery, curvilinear or serpentine appearance as it fills the sulci and cistern H yperdense appearance of basal cistern (50-60HU) Acute blood hyperdense Days to weeks later density reduces to iso dense Decreased visualisation of hypoattenuating CSF space Negative CT cannot exclude SAH Acute diagnostic workup should include noncontrast head CT, which, if nondiagnostic , should be followed by lumbar puncture
Plain CT Pitfalls Sensitivity – 93-100% within 24 hrs 85% at day 5 50% at 1 wk False Positive- Diffuse brain edema with venous congestion in SA space - pseudo SAH - HU <43 False Negative Small amount of blood Old SAH days to weeks later
Cerebral Aneurysm CT examination is secondarily important to identify cerebral aneurysms, typically 5 mm or larger in diameter. The rate of identification of cerebral aneurysms - at least 67% for aneurysms 3 to 5 mm in diameter and to approach 100% for larger aneurysms. Giant aneurysms are most commonly identified in middle-age women; are typically located in the extradural carotid artery, the middle cerebral artery bifurcation, or the basilar summit ; and usually manifest with mass effect
NECT – Patent aneurysm : Well-delineated round/lobulated extra-axial mass Slightly hyperdense to brain (may have mural Ca ++) Partially/completely thrombosed aneurysm - Moderately hyperdense ( Ca ++ common) CECT - Lumen of patent SA enhances strongly, uniformly Completely thrombosed SA may have reactive rim enhancement
Nonenhanced CT scan of a middle-aged man with headaches, the patient had a giant aneurysm of the LT ICA in its intracavernous segment, this aneurysm is densely calcified and is easily depicted NCCT
Magnetic Resonance Imaging Acute Subarachnoid Hemorrhage Conventional MRI (T1WI and T2WI) are not very sensitive in detecting SAH in acute stage (first 24-48 hours ) # in which stage CT is the preferred modality. FLAIR sequences has been found to be quite sensitive in detecting acute SAH. However , with elapsing time, in subacute and chronic SAH, MRI is the best modality (after 48 hours to over 1 month) and can even detect haemorrhage when CSF examination and CT becomes normal. # Normal Po2 (partial pressure of oxygen) in cerebrospinal fluid (CSF) inhibits the development of deoxyhemoglobin .
Standard spin echo ( SE: T1, PD, T2) and gradient echo (GE) and susceptibility sequences are used. MRI also depicts complications of SAH i.e. Hydrocephalus, mass effects, infarcts etc.
MR Findings • T1WI: "Dirty" CSF ( isointense to brain) • T2WI: Hyperintense CSF • FLAIR: Hyperintense (not pathognomonic for SAH!) • T2* GRE: Hypointense hemosiderin deposition in 70-75% of patients with prior SAH • DWI: May show multifocal restrictions FLAIR AXIAL
Cerebral Aneurysm MRI is superior to CT for the localization of cerebral aneurysms , their relationship with adjacent structures, and associated changes in neighboring brain tissue.
MR Findings • T1WI Patent aneurysm (signal varies) • 50% have "flow void" on T1WI • 50% iso /heterogeneous signal Partially/completely thrombosed aneurysm • Signal depends on age(s) of clot • Common = mixed signal, laminated thrombus
• T2WI o Typically hypointense on T2WI o May be laminated with very hypointense rim • DWI : +/- Foci of restricted diffusion secondary to vasospasm , ischemia • T1 C+ o Slow flow in patent lumen may enhance o Increases phase artifact in patent SAs
MR angiography It is possibly the best non invasive modality to evaluate the etiology of SAH. The two principle techniques of data acqusition are time of flight (TOF) and phase contrast (PC) in both 2D and 3D planes. Multiple overlapping thin slab acqusitions (MOTSA) with or without magnetisation transfer has special value in evaluation of circle of Willis. MRA is also useful as a noninvasive tool for the follow up imaging of coiled aneurysms.
No radiation exposure With or with out the use of contrast Sensitivity > 5 mm- 94%. < 3mm low Limited spatial resolution Intraparenchymal clot can obscure aneurysm Giant aneurysm not completely visualised due to slow flow at fundus
CT Angiogram Standard parameters for CT angiographic acquisitions are 1.00 mm section thickness, 0.5 mm section interval, pitch of 3 and 80-120 kvp , 150-400mAs, 14 cm FOV. Scanning time – approx. 14-16 sec for 16 slice scanner. The scanning volume includes from 1 st cervical vertebrae to a point 1 cm above the level of the lateral ventricles as determined on non enhanced study. Scanning time is approximately 7-8 seconds for a 128 slice scanner.
80-100 ml of non-ionic low osmolar iodinated contrast At the rate of 4 ml/sec via a 18 gauge catheter Fixed delay of 16 seconds or a bolus chase technique is used The source images are reconstructed directly into 3D formats and recorded in Maximum intensity projection (MIP), Shaded surface delay (SSD), Volume rendering (VR) Ray sum projection.
CTA may be considered in the workup of SAH. If an aneurysm is detected by CTA, this study may help guide the decision for type of aneurysm repair, but if CTA is inconclusive, DSA is still recommended (except possibly in the instance of classic perimesencephalic SAH )
CTA also has the ability to characterise the relevant preoperative surgical anatomy such as A neurysmal neck morphology, Calcifications , Thrombosis , Parent and feeding vessels, D iagnosing additional small aneurysms and collateral circulation at the circle of W illis .
Pitfalls of CTA includes: Lack of visibility of small arteries Difficulty differentiating the infundibular dilatation at the origin of an artery from an aneurysm The kissing vessel artifact Inability to identify thrombosis and calcification on 3D images Beam hardening artifact produced by aneurysmal clips . Radiation exposure Potential contrast complication.
Conventional Angiogram Gold standard Cerebral angiography can provide the following important surgical information in the setting of SAH: Cerebrovascular anatomy Aneurysm location and source of bleeding Aneurysm size and shape, as well as orientation of the aneurysm dome and neck Relation of the aneurysm to the parent artery and perforating arteries Presence of multiple or mirror aneurysms
4 vessel angiogram Angiography should be performed as soon as possible following SAH because: the rebleed rate of aneurysm is greatest during the first 48 hrs vasospasm can adversely affect the quality of angiograms performed several days after the haemorrhage . If a negative angiogram is due to vasospasm, a repeat study after a few weeks is indicated.
Transfemoral catheterization of both internal carotid and one vertebral artery is generally done. Contralateral vertebral artery catheterization is required if the visualisation of the PICA is not seen through reflux. Cross compression study should routinely be done in all cases of anterior or posterior communicating artery aneurysms and ICA aneurysm to delineate cross circulation.
Transcranial Doppler Ultrasound It is used to study the changes in cerebral artery flow velocity after SAH to correlate the onset of clinical vasospasm. Doppler flow velocity is proportional to the flow through the artery and inversely proportional to the cross sectional diameter of the artery. Proximal MCA is normally studied. Mean MCA flow velocity (normal value- 60 cm/sec) of over 120 cm/sec is 100% specific and 59% sensitive whereas 200 cm/sec is 100% sensitive for detecting vasospasm on angiography.
Management of intracranial aneurysms The goal of preoperative management is to stablize the patient for aneurysm obliteration and prevent the development of systemic complications or secondary cerebral insults such as hypotension or hypoxia. Ideally successful management of acutely ruptured aneurysm begins with adequate ventilation and oxygenation, normovolemia , hemodynamic stability, normoglycemia and ICP control.
After initial stabilisation , a thorough radiographic evaluation is undertaken . Surgical Methods : Current surgical options include direct aneurysmal clipping and endovascular exclusion -- Surgical Clipping or Coil Embolization for the specific indications for treating an aneurysm surgically, endovascularly , or both).
Endovascular methods GDC COILS - Of the various endovascular options currently available, Guglielmi detachable coils (GDCs) have had the largest influence with respect to treatment of subarachnoid hemorrhage ; GDCs are first-line therapy nowdays . These coils are soft, flexible, and can be contoured to the configuration of the aneurysm. Sizes range from 2 to 20 mm in diameter and 2 to 30 cm in length. Balloon embolization is efficacious in selected patients, but it has a higher incidence of complications than coil embolization.
Better Outcome Neck diameter < 5mm Neck to widest portion ratio <0.5 Poor Outcome MCA aneurysm Giant aneurysm >25mm Very small aneurysm <3 mm
Indications for endovascular treatment Posterior circulation aneurysms, especially basilar apex. Patients with poor clinical grade ( ie , Hunt and Hess grades 4-5). Patients who are medically unstable. Symptomatic cavernous aneurysms. Small-neck aneurysms in the posterior fossa. Patients with vasospasm. Cases in which the aneurysm lacks a defined surgical neck (although these are also difficult to "coil") Patients with multiple aneurysms in different arterial territories if the surgical risk is high
Stent placed in case of larger neck for the stabilization of the coil.
Step 5: Check the coils Step : Remove the catether
Evaluation after open /endovascular surgery MRI – MRI compatible clips Fatal cerebral hemorrhage if incompatible CTA superior to MRI DSA Catheter Angiography superior
References CT & MRI of Whole body – Haaga Diagnostic imaging Brain - Osborn Textbook of Radiology and imaging – David Sutton