Arteries to the Brain and Meninges
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Comprehensive knowledge of anatomy forms the basis for understanding and treatment of neurological disease. Intracranial arteries are involved in many neurologic disorders. Knowledge of arterial anatomy, variants, and areas involved in disease is essential to define the location of neurovascular lesions, delineate the extent and involvement of branching perforators, and assess the effects on downstream perfusion.
Arterial anatomy adds to the complexity of neurologic localization, providing a unique classification of neurovascular disorders. Arterial anatomy is also intertwined with pathophysiology, as vessel morphology influences hemodynamic variables. Only marginal advances regarding pathology of these arterial segments has been made since autopsy series performed hundreds of years ago.
Angiography and numerous noninvasive imaging methods have been developed to image intracranial arterial anatomy, [1, 2] yet these modern vascular imaging techniques including transcranial Doppler (TCD) ultrasonography, computed tomographic angiography (CTA), and magnetic resonance angiography (MRA) are not as accurate as the gold standard of conventional or digital subtraction angiography (DSA) (see the image below).
The internal carotid artery (ICA) embryologically develops from the third primitive aortic arch. This artery arises from the common carotid artery in the neck, entering the head at skull base via the carotid canal, and terminates at the bifurcation into the anterior cerebral artery (ACA) and middle cerebral artery (MCA). This bifurcation is often referred to as the “carotid T” (because of its shape) or the “top-of-the carotid” (because of its location).
Extracranial and intracranial segments of the ICA
The extracranial segment of the ICA is from the origin of the ICA to the skull base. There are no branches rising from extracranial ICA.
The intracranial segment of the ICA is divided into petrous, cavernous, supraclinoid portions.
The petrous portion of the intracranial ICA segment extends for about 25-35 mm from the skull base to the cavernous sinus, [3] bends anterior to the tympanic cavity near the apex of the petrous bone, and traverses the posterior aspect of the foramen lacerum. This portion gives rise to the caroticotympanic artery, supplying the tympanic cavity, and the pterygoid or vidian branch passing through the pterygoid canal. [3] The vidian artery anastomoses with the internal maxillary artery. On occasion, the persistent stapedial branch of the petrous segment traverses a bony canal and continues as the middle meningeal artery. [3]
The cavernous portion of the intracranial ICA segment crosses the membranes of the cavernous sinus, winding anteriorly and superomedially, then ascends vertically in a groove along the sphenoid bone, and then passing along the medial aspect of the anterior clinoid process. The cavernous segment averages 39 mm in length and gives rise to far more branches, including the meningohypophyseal trunk, the anterior meningeal artery, the artery to the inferior portion of the cavernous sinus, and the ophthalmic artery.
Upon exiting the cavernous sinus, the ICA extends through the meninges to become the supraclinoid segment. The supraclinoid or cerebral ICA bends posteriorly and laterally between the oculomotor (III) and optic (II) nerves. This gives rise to the superior hypophyseal perforators to the anterior pituitary and stalk, posterior communicating artery (PCoA), and anterior choroidal artery (AChA) before bifurcating into the ACA and MCA (see the image below). [4]
The 2 ACAs connect through the anterior communicating artery (ACoA), thus joining the left and right carotid circulations.
The PCoA extends posteriorly to connect with the primary segment of the posterior cerebral artery (PCA), allowing collateral flow to pass between the anterior and posterior circulations. At its origin, the PCoA often has a widened segment, referred to as the infundibulum. The PCoA passes ventral to the optic tract, with perforators that supply the optic tract, posterior aspect of the chiasm, posterior hypothalamus, and anterior and ventral nuclei of the thalamus.
This vascular network, referred to as the circle of Willis (see the following image), plays a critical role in shunting blood flow between adjacent territories in the brain.
The AChA arises from the posterior aspect of the ICA, about 2-4 mm distal to the origin of the PCoA and about 5 mm proximal to the carotid terminus. [5] The AChA is relatively small, yet it serves as an important landmark in delineating important structures at angiography. [6] The AChA anastomoses with lateral branches of the posterior choroidal artery, PCoA, PCA, and MCA. [6, 7]
There are 2 segments of the AChA, including the cisternal and plexal segments.
Cisternal segment
The cisternal segment passes posteriorly from the lateral to medial aspect of the optic tract in close proximity to the PCA, extending for about 12 mm (to a total length of about 26 mm). This segment gives off penetrating braches to the optic tract, globus pallidus, and genu and posterior limb of the internal capsule.
Subsequent branches extend laterally to supply the medial temporal lobe cortex, hippocampal and dentate gyri, caudate, and amygdala. Medial branches supply the cerebral peduncle, substantia nigra, red nucleus, subthalamus and ventral anterior and lateral nuclei of the thalamus. More distally, the AChA extends through the choroidal fissure to become the plexal segment.
The AChA is the only branch of the ICA that supplies a portion of both the anterior and posterior circulation, although the midbrain and thalamic supply is very variable.
Plexal segment
The juncture of the AChA at the choroidal fissure is often referred to as the plexal point. The plexal segment then enters the choroid plexus near the posterior aspect of the temporal horn. Arterial supply of this segment includes the lateral geniculate body, optic radiations, and posterior limb of the internal capsule.
After diverging from the terminal ICA below the anterior perforated substance, the MCA courses horizontally and slightly anteriorly to reach the Sylvian fissure where branches perfuse the frontal, parietal, and some extent of the temporal and occipital cortices.
The MCA provides arterial blood flow to the largest extent of the intracranial circulation and is typically 75% of the caliber of the parent ICA. [8]
Proximal MCA segment
The proximal portion of the MCA refers to the horizontal or M1 segment of the artery, averaging around 15 mm in length (yet may be as long as 30 mm) and around 2.5 in internal diameter. [8] Overall, this portion gives rise to 5-17 lenticulostriate arteries that feed the globus pallidus, putamen, internal capsule, corona radiata, and caudate nucleus. [8]
The lateral lenticulostriate arteries ascend for 2-5 mm posteromedially from the M1 segment and then course laterally and superiorly for an additional 9-30 mm to penetrate the internal capsule. They supply the lateral portion of the anterior commissure, the putamen, the lateral segment of the globus pallidus, the superior half of the internal capsule, the adjacent corona radiate, and the body and head of the caudate nucleus.
The medial lenticulostriate arteries arise in perpendicular fashion to the parent MCA or ACA yet bend in mesial fashion. The areas supplied by the medial lenticulostriate arteries, including the prominent recurrent artery of Heubner, and the AChA are adjacent to the territories of the lateral lenticulostriate arteries.
The largest branch of the proximal MCA is the anterior temporal artery, which extends from the middle of the proximal MCA and winds anteriorly and inferiorly.
Distal MCA segment
The configuration of the distal MCA often varies, although the vessel most often splits into 2 or more principal divisions (M2 segment) near the Sylvian fissure. A study including 62 patients with normal MRA and 54 patients with MCA aneurysm showed the M2 branches were more symmetric in healthy patients compared with aneurismal patients (eg, the width of the M2, the lateral angle between the M1 and M2). [9] The anterior and posterior divisions of the MCA extend into the Sylvian fissure and spread out over the hemisphere. These cortical branches include the temporopolar, frontobasal, operculofrontal, precentral, postcentral, posterior parietal, angular, anterior temporal, middle temporal, and posterior temporal arteries.
As the MCA branches loop over the insula in the Sylvian fissure, they form the Sylvian triangle, a landmark classically used to identify mass lesions on angiography. Terminal branches of the MCA form collateral anastomoses with the ACA and PCA. [10]
The ACA develops from residual elements of the primitive olfactory artery at the terminus of the ICA. The paired primitive olfactory arteries from each side form a plexus in the midline that gives rise to the ACoA.
The ACA is typically 50% of the caliber of the parent ICA; the internal diameter of the A1 segment is usually 0.9-4 mm, with hypoplasia defined as a diameter less than 1 mm. [11]
The ACA extends anteromedially between the optic chiasm (70% of individuals) or optic nerve (30% of individuals) and the anterior perforated substance to join the contralateral ACA through an anastomosis via the ACoA.
Anterior communicating artery
The anterior communicating artery (ACoA) forms the anterior aspect of the circle of Willis, a critical route for collateral flow between the cerebral hemispheres. This artery is the shortest cerebral artery, measuring only 0.1-3 mm in length. [11] The anatomy of the ACAs-ACoAs is variable with hypoplasia of different segments, including absence of the ACoA. Accessory routes, fenestrations, and other complex azygous connections between the proximal ACAs are also described.
A1 segment
Measures 7-18 mm, with an average span of 12.7 mm. [11] Refers to the proximal segment before the rising of the ACoA. The proximal ACA or A1 segment gives off numerous perforating arteries that supply the adjacent optic nerves and chiasm inferiorly, and the hypothalamus, septum pellucidum, anterior commissure, fornix, and corpus striatum. These mesial lenticulostriate vessels often include a prominent recurrent artery of Heubner that supplies the caudate head, putamen, and anterior limb of the internal capsule. [12]
A2 segment
The A2 segment begins at the juncture of the ACA with the ACoA and extends to the genu of the corpus callosum. The ACAs course over the cerebral hemispheres in the interhemispheric fissure as paired vessels, with their distal extent typically determined by the corresponding anatomy of the PCAs. Subsequent divisions include the pericallosal and callosomarginal arteries that divide to provide arterial supply to the corpus callosum and anteromesial cortices.
Cortical branches of the ACA include the orbitofrontal, frontopolar, callosomarginal, and pericallosal arteries. As the terminal portion of the ACA travels along the corpus callosum, its anterior pericallosal branches form anastomoses with the posterior pericallosal branches of the PCA. [13]
The recurrent artery of Heubner (or distal medial striate artery) arises from the A2 segment in 49-78% of individuals, [11] usually less than 5 mm downstream from the ACA to ACoA junction. It terminates in 1-3 stems, which enter the medial part of the anterior perforated substance. It supplies the anteromedial part of the caudate nucleus, the anterior limb of the internal capsule, the anterior third of the putamen, and the globus pallidus. [14]
The vertebral arteries originate from subclavian arteries, entering the skull at the level of C1 through the foramen magnum.
Intracranial/intradural segment
The intracranial or intradural (V4) segment of the vertebral artery ascends anteriorly to the medulla, approaching midline at the pontomedullary junction where it meets the contralateral vertebral artery to form the basilar artery. The paired longitudinal arteries that form the arterial supply to the posterior circulation during early fetal development retain their proximal course as the vertebral arteries. The terminal vertebral artery yields several branches that supply the rostral end of the spinal cord and posterior inferior aspect of the cerebellum.
Anterior and posterior spinal arteries extend from the intracranial/intradural segment. Each anterior spinal artery fuses with its counterpart, supplying the ventral medulla and rostral spinal cord. The posterior spinal arteries do not pair in the midline but descend the spinal cord at the level of the dorsal roots.
The posterior inferior cerebellar artery (PICA) branches from the vertebral to supply the inferior aspect of the cerebellum.
The PICA is the largest tributary of the vertebral artery, arising 10-20 mm before the vertebrobasilar junction. [15] In 20% of individuals, the PICA arises from below the foramen magnum. [16]
PICA course
There are 4 segments of the PICA, including the anterior, lateral, posterior medullary, and supratonsillar PICAs, or 5 segments, including the anterior medullary, lateral medullary, tonsillomedullary, telovelotonsillar, and cortical segments. [17] Numerous perforating arteries extend from the first 3 segments of the PICA to supply the anterior, lateral, and posterior aspects of the medulla.
The anterior medullary segment travels laterally near the inferior aspect of the olive of the medulla oblongata, continuing in a loop that courses between the cerebellum and medulla. The PICA then extends posteriorly in the tonsillomedullary fissure adjacent to the glossopharyngeal (IX) and vagus (X) nerves. Then, the PICA curves over the cerebellar tonsil to become the supratonsillar segment, extending further across the cerebellum as the medial and lateral terminal PICA branches. At the juncture of the posterior medullary and supratonsillar segments of the PICA, perforating vessels arise to feed the choroid plexus of the fourth ventricle. This choroidal point is used as a landmark to identify masses within the posterior fossa.
During embryologic development, paired vessels on the ventral surface of the hindbrain fuse to form the basilar artery, which extends from the confluence of the vertebral arteries near the pontomedullary junction to the terminal bifurcation as the PCAs at the level of the midbrain (see the image below).
The basilar artery is often tortuous or serpentine, with a straight course noted in about 25% of the time. The length of the basilar artery is consistently 25-35 mm, irrespective of body size. [18] The diameter is about 2.7 to 4.3 mm at the proximal portion. The luminal diameter of the basilar artery tends to taper toward the distal end.
Numerous smaller perforators embrace the brainstem, coursing from the midline ventral aspect around the surface to the lateral dorsal surface and diving deep into the substance of the brainstem between fiber tracts. These pontine perforators are grouped into medial and lateral subdivisions, often referred to as paramedian and circumferential arteries. Lateral pontine perforators extend to also supply the ventrolateral surface of the cerebellum, whereas the medial perforators perfuse midline structures of the midbrain.
The largest branches of the basilar artery include the anterior inferior cerebellar artery (AICA) and superior cerebellar artery (SCA). Owing to the paired structure of posterior circulation arteries, asymmetries or relative dominance of one artery such as the PICA, AICA, or SCA may occur. Contralateral cerebellar infarction may therefore result from occlusion or disease of one cerebellar artery.
The AICA extends off of the basilar artery approximately one third to halfway through its course, [19] then goes laterally and inferiorly, in close proximity to the abducens (VI) nerve, crosses the anteroinferior aspect of the cerebellum to supply the middle cerebellar peduncle, flocculus, and adjacent cerebellum. It can be divided in to 4 segments: anterior pontine, lateral pontine, flocculopeduncular, and cortical. [17] The AICA supplies a rather small, variable portion of the anterior inferior cerebellum. [20]
Numerous pontine perforators may arise from the proximal segment of the AICA. The lateral branch runs across the cerebellum in the horizontal fissure. The medial branch of the AICA courses inferiorly to supply the biventral lobule.
The SCA extends from the basilar artery in symmetric fashion, just proximal to the terminal bifurcation of the basilar into the proximal PCA. This artery courses laterally below the oculomotor (III) nerve, passing around the cerebral peduncles and below the trochlear (IV) nerve. [21] . It can be divided into 4 segments: anterior pontomesencephalic, lateral pontomesencephalic, cerebellomesencephalic, and cortical. [17]
Numerous perforators extend from the proximal or ambient SCA to supply the adjacent pons and midbrain, whereas distal segments split into the lateral marginal and superior vermian branches. These divisions may also arise independently from the basilar artery or even the PCA.
The SCA variably divides into medial SCA and lateral SCA branches. The lateral marginal SCA supplies the anterosuperior cerebellum, superior cerebellar peduncle, middle cerebral peduncle, and dentate nuclei. The superior vermian SCA supplies the superior cerebellar peduncle, tentorium, inferior colliculi, cerebellar hemispheres and dentate nuclei.
The PCA embryologically develops from the terminal aspect of the PCoA at the distal end of the carotid circulation. Most often, it then extends posteriorly to spread over the ipsilateral cortex, whereas the proximal connection with the PCoA regresses. In this common scenario, the primary arterial supply shifts to a source from the terminal basilar artery. [22]
The PCA originates from the terminal portion of the basilar artery in the interpeduncular cistern, then passes above the oculomotor (III) nerve to circle the midbrain above the tentorium. The PCA passes along the free edge of the tentorium to eventually reach the medial aspect of the occipital lobe.
Proximal PCA segment
As the PCA passes through the peduncular, ambient, and quadrigeminal cisterns, numerous perforators supply adjacent structures. [23] This pattern of arterial limbs includes paramedian perforators, short circumferential and long circumferential branches that typify the general structure of the major arterial territories in the posterior circulation.
The artery of Davidoff and Schechter extends from the P1 segment to supply part of the inferior surface of the tentorium. The midbrain receives arterial blood from the peduncular or P1 segment before posterior thalamoperforatoring arteries arise. In the successive ambient segment, the thalamogeniculate arteries diverge to supply the lateral geniculate and pulvinar nuclei. Medial and lateral branches of the posterior choroidal arteries extend from this portion of the PCA to supply the pineal gland, third ventricle, dorsomedial thalamus, pulvinar, lateral geniculate body and choroid plexus. [24]
Distal PCA segment
The PCA passes along the free edge of the tentorium to eventually reach the medial aspect of the occipital lobe. Further branching within the hippocampal fissure produces cortical divisions that course over the inferior and mesial aspects of the hemisphere. The cortical territories of the PCA are supplied via the anterior and posterior divisions, fanning out to follow the architecture of the cortical surface in these regions.
Cortical branches of the PCA include the hippocampal, anterior temporal, middle temporal, posterior temporal, parietooccipital, calcarine, and posterior pericallosal or perisplenial arteries. [25] Anastomoses of the PCA allow for collateral flow into the MCA via the anterior and posterior temporal arteries and into the ACA via pericallosal divisions that arise from the quadrigeminal PCA. [10]
Blood supply of thalamus
The P1 or proximal PCA serves as an important blood supply of thalamus with variable contributions from the basilar artery, PCoA and AChA.
The anterior thalamoperforating arteries consist of about 7-10 branches that arise from the superior and lateral surfaces of the PCoA. [26] A larger branch, the premamillary artery, is often noted. [27] This vessel courses from the posterior aspect of the PCoA, penetrates the hypothalamus, and subsequently terminates in branches that supply the anterior and ventroanterior nuclei of the thalamus.
Posteriorly, the thalamus is supplied by a combination of vessels arising from the posterior circulation. The most posterior reaches of the thalamus are supplied via the posterior choroidal arteries, arising from more distal aspects of the subcortical PCA. The posterior choroidal arteries adjoin and overlap to some extent with distal reaches of the AChA, extending from the ICA to supply lateral and posterior regions of the thalamus.
The interpeduncular branches from the basilar artery and P1 segment ascend superiorly to perfuse mesial aspects of the thalamus. More lateral aspects of the thalamus, including the ventroposteromedial and ventroposterolateral nuclei are supplied by the thalamogeniculate arteries. [28]
Several features distinguish intracranial arteries from arteries of similar caliber elsewhere in the body. Intracranial arteries have a well-developed internal elastic lamina with only a minimal degree of elastic fibers scattered in the media, [29] and they do not have an external elastic lamina. As the internal carotid artery (ICA) courses distally, there is progressive disappearance of the external elastic lamina. The middle cerebral artery (MCA) is a terminal continuation of the ICA with a gradual change in blood vessel wall characteristics or histopathology.
In general, the cerebral arteries have a smaller wall-to-lumen ratio than arteries elsewhere in the body. [30] Overall, the intimal layer accounts for about 17% of total vessel wall thickness, with the media comprising 52% and adventitia only 31%. [31, 32] Other distinctive features include the presence of tight endothelial junctions with a relative paucity of pinocytic vesicles, and differing distribution of enzymes within the vessel wall.
Cerebral endothelial cells with tight junctions form a critical element of the blood-brain barrier. [33] These endothelial cells are not fenestrated, and the tight junctions bestow only selective permeability to this boundary, preventing exchange of numerous substances. Cerebral endothelial cells have a high concentration of mitochondria, denoting their active metabolic role and possibly, their vulnerability to ischemia. [34] Endothelial cells in cerebral arteries and arterioles play an active role in regulation of hemodynamics by expression of a wide array of vasoactive substances, including endothelin and nitric oxide. [34]
Beyond the endothelial layer, the cerebral arteries have protuberances at distal branching sites that also modulate flow, which have been variably defined as intimal cushions, bifurcation pads, or subendothelial protuberances. Underneath the luminal surface, these structures contain groups of smooth muscle cells arranged in irregular fashion, with intertwined collagenous fibrils, and are encompassed by the split internal elastic membrane. [35] It appears that these structures help alter flow via fluid shear stress mechanisms.
Smooth muscle cells compose 72% of the media, whereas this composition is radically altered under pathophysiologic conditions such as intracranial atherosclerosis or chronic hypertension. [29] Age-related changes are found in the composition of the media.
Autonomic nerves located in the tunica adventitia have connections with these subendothelial structures via intercellular smooth muscle cell contacts.
Within the media, smooth muscle cells are generally oriented in a pattern circumferential to the lumen, except at bifurcations. [31] Adjacent collagen and elastin fibers run perpendicular to the smooth muscle layer or in parallel with the long axis of the vessel.
Relative to systemic vessels, the thin, medial layer of intracranial arteries is thought to be related to compliance differences associated with the surrounding cerebrospinal fluid (CSF).
Autonomic nerves located in the tunica adventitia have connections with these subendothelial structures via intercellular smooth muscle cell contacts. Within the adventitia, loose connective tissue surrounds autonomic nerve fibers, and all vessel wall structures are enclosed by spindle-shaped fibrocytes. Once beyond the dura mater, the intracranial arteries have no vasa vasorum. The external surface of the intracranial arteries in these regions is in direct contact with the surrounding CSF. A rete vasorum in the adventitia is permeable to large proteins, allowing ingress or exchange with the CSF in the subarachnoid space. [36]
Numerous variant configurations of the internal carotid artery (ICA) exist, including its rare absence or hypoplasia. The amount of blood volume supplied to distal structures can vary depending on the caliber of the terminal ICA.
The course of the ICA sometimes varies, coursing through the middle ear or bending toward the midline in a configuration termed “kissing ICAs” at the cavernous segments. Anomalous origins of the posterior fossa arteries from the ICA, including the superior cerebellar artery (SCA), anterior inferior cerebellar artery (AICA), or posterior inferior cerebellar artery (PICA), may also occur.
Persistent fetal connections to the posterior circulation may involve the posterior communicating artery (PCoA); trigeminal, otic or acoustic, hypoglossal artery; and proatlantal intersegmental arteries. The persistent trigeminal artery is the most common persistent embryonic connection (85%), arising from the cavernous ICA and joining the upper basilar artery (see the image below). [37]
The persistent otic artery is very rare, connecting the petrous ICA with the basilar artery inferior to AICA.
The persistent hypoglossal connects the distal cervical ICA with the distal vertebral artery.
The anterior choroidal artery (AChA) may have a single origin or may consist of several smaller vessels (4% of individuals). [5, 21] The AChA arises from the MCA or PCoA in 2-11% of individuals. [21] Complete absence of the AChA has also been reported. [6]
In 15% of individuals, the PCoA continues distally as the posterior cerebral artery (PCA). [38, 39] Great variability may be noted in the caliber of PCoA, ranging from less than 1 mm to greater than 2 mm.
The anatomy of the PCoA differs in various populations and in clinical conditions associated with ischemia. [39, 40] Hypoplasia or absence of the PCoA is found in a minority of cases at autopsy, with bilateral hypoplasia in only 0.25% of individuals. [38] The configuration and size of the PCoA also differs between rates from autopsy studies and angiography series.
Variation in MCA anatomy is less common than variants in other intracranial arteries. Fenestration of the M1 segment occurs, and duplicated M1 segments may also arise from the ICA. [41] The M1-M2 junction is characterized by a bifurcation in 64-90% of individuals, trifurcation in 12-29%, and complex branching in isolated individuals. [8] The accessory middle cerebral artery usually originates between the A1 and proximal A2 segments of the ACA, reaches the sylvian fissure, and supplies the territory of the MCA. This anomaly has been associated with cerebral aneurysms and Moyamoya disease. [42]
Variant anatomy of the ACA most commonly includes hypoplasia or absence of the A1 segment (10% of individuals). [11] Other variations may include anomalous origin of the ACA from the ICA, agenesis or accessory branches, direct connection of bilateral A1 segments, or other combinations that involve azygous orientation of distal ACA segments.
The left vertebral artery is larger than the right 42% of the time, whereas the right is larger than the left 32% of the time. In the remainder of individuals, the vertebral arteries are equivalent in caliber. Vertebral artery hypoplasia is fairly common, often involving the right side.
Differentiation of hypoplasia from a diseased arterial segment may be difficult to define on the basis of luminal dimensions alone. The configuration or compensatory enlargement of neighboring segments may provide clues to this distinction.
The vertebral artery may also terminate in the PICA rather than extend to the junction with the artery. In such cases, the vertebral artery is generally smaller than the contralateral vertebral artery.
Fenestration of the vertebrobasilar system is a rare anatomical variation with a prevalence rate of 1-2.77%, [43, 44, 45] specifically 0.54% at the intracranial vertebral artery, 0.18% at vertebrobasilar junction, 2.07% at basilar artery, and 17% of 92 patients with fenestration have cerebral aneurysm but not at the fenestration site. [45]
Variations in PICA anatomy include hypoplasia or absence of this branch (10-20% of individuals), typically accompanied by a prominent ipsilateral AICA. Absence of the PICA is also accompanied by numerous medullary perforators that arise directly from the vertebral artery. Duplication of the PICA may occur and PICA-AICA connections are quite common. On occasion, both inferior cerebellar territories may be supplied by a bihemispheric PICA originating from one vertebral artery. [46]
Similar to absence of the PICA, the AICA may be absent or hypoplastic and is typically accompanied by a prominent PICA.
Duplication of the SCA is noted in 28% of individuals, with bilateral duplication in 10%. [9]
In some individuals, the PCA supply continues from what has been termed a fetal PCoA. Variants of PCoA anatomy include a diverse range of caliber in this segment, complete agenesis, and anomalous origins of other vessels from this arterial segment. [22]
Numerous variations of normal arterial anatomy occur in the presence of disease, as collateral vessels are often recruited (see the image below).
Collateral circuits may have innumerable variations that alter the normal appearance of arterial anatomy.
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Qing Hao, MD, PhD Resident Physician, Department of Neurology, State University of New York Downstate Medical Center
Qing Hao, MD, PhD is a member of the following medical societies: American Society of Neuroimaging
Disclosure: Nothing to disclose.
David S Liebeskind, MD, FAAN, FAHA, FANA Professor of Neurology and Director, Neurovascular Imaging Research Core, Director, Vascular Neurology Residency Program, Department of Neurology, University of California, Los Angeles, David Geffen School of Medicine; Director, UCLA Outpatient Stroke and Neurovascular Programs; Director, UCLA Cerebral Blood Flow Laboratory; Associate Neurology Director, UCLA Stroke Center
David S Liebeskind, MD, FAAN, FAHA, FANA is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, American Society of Neuroimaging, American Society of Neuroradiology, National Stroke Association, Stroke Council of the American Heart Association
Disclosure: Nothing to disclose.
Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Association
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Acorda, Livanova, Eisai, Greenwich, Lundbeck, Neuropace, Sunovion, Upsher-Smith.<br/>Serve(d) as a speaker or a member of a speakers bureau for: Livanova, Eisai, Greenwich, Lundbeck, Neuropace, Sunovion.<br/>Received research grant from: Acorda, Livanova, Greenwich, Lundbeck, Sepracor, Sunovion, UCB, Upsher-Smith.
Arteries to the Brain and Meninges
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