Persistent fetal origin of posterior cerebral artery

Fig. 4.1

Large posterior communicating artery supplying the posterior cerebral artery; associated with hypoplasia or absence of connection between the basilar artery and the ipsilateral posterior cerebral artery.

Represents persistence of embryonic configuration; common vascular variant seen in ~20% of arterio-grams.

Hypoplasia of the A1 segment of the anterior cerebral artery

Hypoplasia or absent A1 segment associated with a patent anterior communicating artery supplying blood to the ipsilateral A2 segment.

Anatomical variant seen in ~10% of arteriograms.

Persistent trigeminal artery

Fig. 4.2a, b

Anomalous anastomosis connecting the internal carotid artery in the cavernous sinus to the basilar artery at the level of the trigeminal nerve; basilar artery below anastomosis and vertebral arteries are usually small.

Most common type of anomalous carotid/basilar anastomosis (0.5% of cerebral arteriograms); failure of involution of persistent embryonic circulatory configuration. Associated with increased incidence of aneurysms and vascular malformations. Other less common types of anomalous carotid/basilar anastomoses include persistent hypoglossal artery (adjacent to cranial nerve XII), persistent otic artery, and proatlantal intersegment artery.

Duplications of cerebral, carotid, vertebral, or basilar arteries

Fig. 4.3

Duplication of arteries usually occurs as two parallel arteries from two separate origins, as seen on CTA, MRA, and conventional angiography.

Duplicated arteries have two origins and variable courses with or without eventual fusion. Duplication of intracranial or cervical arteries is an infrequent type of vascular variant compared with anomalies involving other intracranial arteries. Other less common types of variants include fenestrations and accessory arteries.

Arterial fenestration

Fig. 4.4a–c

Duplication of a portion of an artery whose main trunk is derived from a single origin, as seen on CTA, MRA, and conventional angiography.

Developmental variation when there are double segments involving portions of the vertebral, basilar, or carotid arteries. With arterial fenestration, a vessel with a single origin divides into two parallel segments along its course.

Vein of Galen aneurysm

Fig. 4.5a–c

Multiple tortuous contrast-enhancing vessels involving choroidal and thalamoperforate arteries, internal cerebral veins, vein of Galen (aneurysmal formation), straight and transverse venous sinuses, and other adjacent veins and arteries. The venous portions often show contrast enhancement. CTA shows contrast enhancement in patent portions of the vascular malformation.

Heterogeneous group of vascular malformations with arteriovenous shunts and dilated deep venous structures draining into and from an enlarged vein of Galen, with or without hydrocephalus, with or without hemorrhage, with or without macrocephaly, with or without parenchymal vascular malformation components, with or without seizures, high-output congestive heart failure in neonates.

Venous angioma (developmental venous anomaly)

Fig. 4.6

No abnormality or small, slightly hyperdense zone prior to contrast administration. Contrast enhancement seen in a slightly prominent vein draining a collection of small veins.

Considered an anomalous venous formation typically not associated with hemorrhage; usually an incidental finding except when associated with cavernous hemangioma.

Sturge-Weber syndrome

Fig. 4.7a, b

Prominent localized unilateral leptomeningeal enhancement usually in parietal and/or occipital regions in children, with or without gyral enhancement; mild localized atrophic changes in brain adjacent to the pial angioma, with or without prominent medullary and/or subependymal veins, with or without ipsilateral prominence of choroid plexus. Gyral calcifications > 2 y, progressive cerebral atrophy in region of pial angioma.

Also known as encephalotrigeminal angiomatosis, neurocutaneous syndrome associated with ipsilateral “port wine” cutaneous lesion and seizures; results from persistence of primitive leptomeningeal venous drainage (pial angioma) and developmental lack of normal cortical veins, producing chronic venous congestion and ischemia.

Moyamoya

Fig. 4.8a, b

Multiple tortuous, small, enhancing vessels may be seen in the basal ganglia and thalami secondary to dilated collateral arteries, with enhancement of these arteries related to slow flow within these collateral arteries versus normal-sized arteries. Contrast enhancement of the leptomeninges related to pial collateral vessels; decreased or absent contrast enhancement in the supraclinoid portions of the internal carotid arteries and proximal middle and anterior cerebral arteries. CTA shows stenosis and occlusion of the distal internal carotid arteries with collateral arteries (lenticulostriate, thalamoperforate, and leptomeningeal); best seen after contrast administration enabling detection of slow blood flow.

Progressive occlusive disease of the intracranial portions of the internal carotid arteries with resultant numerous dilated collateral arteries arising from the lenticulostriate and thalamoperforate arteries, as well as other parenchymal, leptomeningeal, and transdural arterial anastomoses; term translated as “puffof smoke,” referring to the angiographic appearance of the collateral arteries (lenticulostriate, thalamoperforate); usually nonspecific etiology, but can be associated with neurofibromatosis, radiation angiopathy, atherosclerosis, and sickle cell disease; usually children > adults in Asia.

Thoracic outlet syndrome (TOS)

Fig. 4.9a–c

Cervical ribs or fibrous bands located adjacent to the subclavian artery, subclavian vein, and/or brachial plexus.

Signs and symptoms of TOS occur from compression of the brachial plexus (neurogenic TOS), subclavian artery (arterial TOS), and/or subclavian vein (venous TOS). Neurogenic TOS accounts for ~90% of TOS cases. Compression of the thoracic outlet structures can be static or positional. Causes of the compression include cervical ribs, fibrous bands, hypertrophy, and anomalies involving the scalene muscles.

Stenosis/occlusive vascular disease

Arterial stenosis/occlusion

Fig. 4.10

Fig. 4.11

Fig. 4.12

Fig. 4.13

Fig. 4.14a, b

Focal narrowing (stenosis) or absence (occlusion) of luminal contrast enhancement on CTA in artery, with or without narrowing of flow signal distal to site of stenosis.

Arterial stenosis or occlusion may result from atherosclerosis, emboli, fibromuscular disease/dysplasia, collagen vascular disease, coagulopathy, encasement by neoplasm, surgery, or radiation injury.

Subclavian steal syndrome

Fig. 4.15a–c

CTA shows occlusion of the proximal subclavian artery with reconstitution beyond the occlusion via reversed blood flow from the ipsilateral vertebral artery.

Stenosis or occlusion of the proximal subclavian artery can cause reversal of blood flow of the ipsilateral vertebral artery to supply the subclavian artery distal to the stenosis. The reversed blood flow can result in signs of vertebrobasilar insufficiency (syncope, nausea, ataxia, vertigo, diplopia, headaches, etc.) elicited with exercise of the upper extremity on the same side where the stenosis/occlusion of the subclavian artery occurs.

Arterial dissection

Fig. 4.16a–d

The involved arterial wall is thickened in a circumferential or semilunar configuration and has intermediate attenuation. Lumen may be narrowed or occluded.

Arterial dissections can be related to trauma, collagen, vascular disease (e.g., Marfan and EhlersDanlos syndromes), or idiopathic. Hemorrhage occurs in the arterial wall and can cause stenosis, occlusion, and stroke.

Vasculitis

Fig. 4.17a–f

Zones of arterial occlusion, and/or foci of stenosis and post-stenotic dilation. May involve large, medium, or small intracranial and extracranial arteries. with or without cerebral and/or cerebellar infarcts.

Uncommon mixed group of inflammatory diseases/disorders involving the walls of cerebral blood vessels. Can result from noninfectious etiology (polyarteritis nodosa, Wegener granulomatosis, giant cell arteritis, Takayasu arteritis, sarcoid, drug-induced, etc.) or be related to infectious causes (bacteria, fungi, TB, syphilis, viral).

Intracranial venous sinus thrombosis

Fig. 4.18a-d

CTA shows patent veins and venous sinuses to have high attenuation compared with zones of thrombus with lower attenuation.

Venous sinus occlusion may result from coagulopathies, encasement or invasion by neoplasm, dehydration, and adjacent infectious/inflammatory processes.

Aneurysms

Arterial aneurysm

Fig. 4.19a, b

Fig. 4.20a, b

Fig. 4.21a–c

Saccular aneurysm: Focal, well-circumscribed zone of contrast enhancement.

Fusiform aneurysm: Tubular dilation of involved artery.

Dissecting aneurysms (intramural hematoma): Initially, the involved arterial wall is thickened in a circumferential or semilunar configuration and has intermediate attenuation with luminal narrowing. Evolution of the intramural hematoma can lead to focal dilation of the arterial wall hematoma.

Abnormal fusiform or focal saccular dilation of artery secondary to acquired/degenerative etiology, polycystic disease, connective tissue disease, atherosclerosis, trauma, infection (mycotic, oncotic), AVM, vasculitis, and drugs. Focal aneurysms are also referred to as saccular aneurysms, which typically occur at arterial bifurcations and are multiple in 20%. The chance of rupture of a saccular aneurysm causing subarachnoid hemorrhage is related to the size of the aneurysm. Saccular aneurysms > 2.5 cm in diameter are referred to as giant aneurysms. Fusiform aneurysms are often related to atherosclerosis or collagen vascular disease (e.g., Marfan and Ehlers-Danlos syndromes). Dissecting aneurysms: hemorrhage occurs in the arterial wall from incidental or significant trauma.

Vascular malformations

AVM

Fig. 4.22a, b

Fig. 4.23a–c

Lesions with irregular margins that can be located in the brain parenchyma (pia, dura, or both locations). AVMs contain multiple tortuous enhancing blood vessels secondary to patent arteries with high blood flow, as well as thrombosed vessels with variable attenuation, areas of hemorrhage in various phases, calcifications, and gliosis. The venous portions often show contrast enhancement. CTA can provide additional detailed information about the nidus, feeding arteries, and draining veins, as well as the presence of associated aneurysms. Usually not associated with mass effect unless there is recent hemorrhage or venous occlusion.

Supratentorial AVMs occur more frequently (80%–90%) than infratentorial AVMs (10%–20%). Annual risk of hemorrhage. AVMs can be sporadic, congenital, or associated with a history of trauma. Multiple AVMs can be seen in syndromes: Rendu-Osler-Weber (AVMs in brain and lungs and mucosal capillary telangiectasias) and Wyburn-Mason (AVMs in brain and retina, with cutaneous nevi).

Vein of Galen aneurysm

Fig. 4.24a, b

Multiple tortuous blood vessels involving choroidal and thalamoperforate arteries, internal cerebral veins, vein of Galen (aneurysmal formation), straight and transverse venous sinuses, and other adjacent veins and arteries. The venous portions often show contrast enhancement. CTA can show patent portions of the vascular malformation.

Heterogeneous group of vascular malformations with arteriovenous shunts and dilated deep venous structures draining into and from an enlarged vein of Galen; with or without hydrocephalus, with or without hemorrhage, with or without macrocephaly, with or without parenchymal vascular malformation components, with or without seizures, high-output congestive heart failure in neonates.

Dural AVM

Dural AVMs contain multiple tortuous tubular blood vessels. The venous portions often show contrast enhancement. CTA can show patent portions of the vascular malformation and areas of venous sinus occlusion or recanalization. Usually not associated with mass effect unless there is recent hemorrhage or venous occlusion. With or without venous brain infarction.

Dural AVMs are usually acquired lesions resulting from thrombosis or occlusion of an intracranial venous sinus with subsequent recanalization resulting in direct arterial to venous sinus communications. Transverse, sigmoid venous sinuses > cavernous sinus > straight, superior sagittal sinuses.

Carotid cavernous fistula

Fig. 4.25a–d

CTA shows marked dilation of the cavernous sinuses, as well as the superior and inferior ophthalmic veins and facial veins.

Carotid artery to cavernous sinus fistulas usually occur as a result of blunt trauma causing dissection or laceration of the cavernous portion of the internal carotid artery. Patients can present with pulsating exophthalmos.

Cavernous hemangioma

Single or multiple multilobulated intra-axial lesions that have intermediate to slightly increased attenuation, minimal or no contrast enhancement, with or without calcifications.

Supratentorial cavernous angiomas occur more frequently than infratentorial lesions. Can be located in many different locations, multiple lesions > 50%. Association with venous angiomas and risk of hemorrhage.

Venous angioma

Fig. 4.26

On postcontrast images, venous angiomas are seen as a contrast-enhancing transcortical vein draining a collection of small medullary veins (caput medusae).

Considered an anomalous venous formation typically not associated with hemorrhage; usually an incidental finding except when associated with cavernous hemangioma.

Capillary telangiectasia

No apparent findings on noncontrast enhanced CT; may be seen as small poorly defined zones of contrast enhancement, no abnormal mass effect.

Small venous malformations consisting of collections of dilated capillaries lacking smooth muscle and elastic fibers in walls; located in pons > other portions of brainstem, brain; typically show no enlargement over time.