Circle of Willis Anatomy
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The circle of Willis encircles the stalk of the pituitary gland and provides important communications between the blood supply of the forebrain and hindbrain (ie, between the internal carotid and vertebro-basilar systems following obliteration of primitive embryonic connections). [1] Although a complete circle of Willis is present in some individuals, it is rarely seen radiographically in its entirety; anatomical variations are very common and a well-developed communication between each of its parts is identified in less than half of the population. [1]
The circle of Willis begins to form when the right and left internal carotid artery (ICA) enters the cranial cavity and each one divides into two main branches: the anterior cerebral artery (ACA) and middle cerebral artery (MCA). [2] The anterior cerebral arteries are then united and blood can cross flow by the anterior communicating (ACOM) artery. The ACAs supply most midline portions of the frontal lobes and superior medial parietal lobes. The MCAs supply most of the lateral surface of the hemisphere, except the superior portion of the parietal lobe (via ACA) and the inferior portion of the temporal lobe and occipital lobe. The ACAs, ACOM, and MCAs form the anterior half, better known as the anterior cerebral circulation. Posteriorly, the basilar artery (BA), formed by the left and right vertebral arteries, branches into a left and right posterior cerebral artery (PCA), forming the posterior circulation. [3] The PCAs mostly supply blood to the occipital lobe and inferior portion of the temporal lobe.
The PCAs complete the circle of Willis by joining the anterior circulation formed by the ICAs via the posterior communicating (PCOM) arteries. See the images below.
A1 segment and anterior communicating artery
The A1 segment of the anterior cerebral artery (ACA) extends from the internal carotid artery (ICA) bifurcation in a medial and superior direction to the ACA’s junction with the anterior communicating artery (ACOM) within the inter-hemispheric fissure. Branches include the medial lenticulostriate arteries (A1) that supply the anterior hypothalamus, anterior commissure, fornix, striatum, optic chiasm, and optic nerves. [4] ACOM branches include perforators that supply the hypothalamus, optic chiasm, corpus callosum, and fornix.
See the image below. [5]
A2 segment
This portion of the ACA extends from the ACOM artery to the ACA’s division into the pericallosal and callosomarginal arteries, at the genu of the corpus callosum. Branches include perforators to the frontal lobe, as well as the recurrent artery of Heubner, which is a large, lenticulostriate vessel. This latter vessel supplies the caudate nucleus, internal capsule, and putamen. Other branches of A2 include the orbitofrontal and frontopolar arteries.
A3 segment
This segment includes all branches of the ACA distal to the origin of the pericallosal and callosomarginal arteries, but other subdivisions have been used. Many anastomoses occur with distal branches of the middle cerebral artery (MCA) and posterior cerebral artery (PCA). [2] The pericallosal artery travels posteriorly over the corpus callosum and anastomoses with the splenial artery from the parieto-occipital branch of the PCA. The callosomarginal artery courses over the cingulate gyrus. A paracentral artery arises from the pericallosal or callosomarginal arteries and supplies the paracentral lobule. The A3 segment terminates by providing parietal arteries to the corpus callosum and precuneus.
Middle cerebral artery
Most classification schemes divide the MCA into 4 segments, including M1 (from the ICA to the bifurcation [or trifurcation]), M2 (from the MCA bifurcation to the circular sulcus of the insula), M3 (from the circular sulcus to the superficial aspect of the Sylvian fissure), and M4, which is made up of cortical branches.
M1 segment
Most anatomic studies define the M1 segment as ending where the MCA branches take a right angled turn within the Sylvian fissure; however, the division point of the MCA trunk is considered by most clinicians to be the M1/M2 junction. [6] The MCA most commonly bifurcates but may also trifurcate or quadfurcate. [3] Branches include lenticulostriate arteries, which supply the anterior commissure, internal capsule, caudate nucleus, putamen, and globus pallidus, and an anterior temporal artery, which supplies the anterior temporal lobe. [4]
M2 segment
The M2 segment extends from the main division point of the M1 segment, over the insula within the Sylvian fissure, and terminates at the margin of the insula. The M2 commonly divides into two divisions: the superior and inferior division. Broadly speaking, the superior division is responsible for the frontal convexity and the inferior division is responsible for the temporal lobe. [7]
M3 segment
The M3 segment begins at the circular sulcus of the insula and ends at the surface of the Sylvian fissure. This part travels over the surface of the frontal and temporal opercula to reach the external surface of the Sylvian fissure. The M3 and M2 segments give rise to stem arteries from which cortical branches are derived.
M4 segment
The M4 segment begins at the surface of the Sylvian fissure and extends over the surface of the cerebral hemisphere. Its cortical branches, which supply the frontal, parietal, temporal, and occipital lobes, include the following:
The MCA branches that form the so-called “candelabra” are the prefrontal, precentral, and central arteries. [8]
Posterior cerebral artery
A commonly used subdivision for this vessel includes dividing it into a P1 segment from the basilar artery bifurcation to the junction with the posterior communicating (PCOM) artery, a P2 segment from the PCOM artery to the posterior aspect of the midbrain, a P3 segment from the posterior aspect of the midbrain to the calcarine fissure, and a P4 segment that describes terminal branches of the PCA distal to the anterior aspect of the calcarine fissure.
P1 segment and posterior communicating arteries
The P1 segment supplies perforating branches to the brainstem. These are termed the posterior thalamoperforators to distinguish them from the anterior thalamoperforators, which arise from the PCOM artery. The direct perforators supply the thalamus, brainstem, and internal capsule. Short and long circumflex arteries supply the thalamus and midbrain. A meningeal branch may supply the inferior surface of the tentorium cerebelli. [6] The P1 segment lies within the interpeduncular cistern.
P2 segment
The P2 segment begins at the PCOM artery junction and travels around the lateral aspect of the midbrain. Direct perforators supply the thalamus, internal capsule, and optic tract. Branches include the posteromedial choroidal artery, which supplies the midbrain, pineal gland, thalamus, and medial geniculate body, and the posterolateral choroidal artery, which supplies the choroid plexus, thalamus, geniculate bodies, fornix, cerebral peduncle, pineal body, corpus callosum, tegmentum, and temporal occipital cortex. A hippocampal artery may be present.
The inferior temporal arteries anastomose with anterior temporal branches of the MCA. The parieto-occipital artery arises as a single trunk from the P2 segment more commonly than from the P3 segment. This artery supplies the posterior parasagittal region, cuneus, precuneus, and lateral occipital gyrus. The P2 segment lies within the ambient cistern.
P3 segment
The P3 segment extends from the tectum to the anterior aspect of the calcarine fissure. The PCA often divides into 2 terminal branches, the calcarine artery and the aforementioned parieto-occipital artery. The P3 segment lies within the quadrigeminal cistern.
P4 segment
The P4 segment begins at the anterior limit of the calcarine fissure and often includes one of the 2 main terminal branches of the PCA, the calcarine artery. The other main terminal branch of the PCA, the parieto-occipital artery, frequently arises from the P2 or P3 segment. The splenial artery arises from the parieto-occipital artery in most individuals and usually anastomoses with the pericallosal artery. [9] The P4 segment lies and terminates within the calcarine fissure. [10]
Basilar artery
The basilar artery originates at the junction between the left and right vertebral arteries and travels anterior to the brainstem. Branches include the superior cerebellar artery (SCA) and the anterior inferior cerebellar artery (AICA). [11] The SCA arises from the basilar artery immediately prior to the basilar bifurcation. The SCA often comes into contact with the trigeminal nerve and is usually the target of surgical microvascular decompression for trigeminal neuralgia. [4, 8] AICA, arising at the junction between the pons and medulla, often comes into contact with the facial nerve and causes hemifacial spasm. [12] It can also come in contact with the glossopharyngeal nerve and vestibular nerve causing glossopharyngeal neuralgia and vestibular paroxysmia, respectively. [13]
The artery sends branches to the tectum, the vermis, and the medial aspect of the cerebellar hemisphere. The AICA travels toward the cerebellopontine angle. The posterior inferior cerebellar artery (PICA) is the largest of the cerebellar arteries and arises from the vertebral artery. It supplies the medulla, cerebellar tonsils and vermis, and inferolateral cerebellar hemisphere. PICA can come in contact with the glossopharyngeal nerve, and is associated more with glossopharyngeal neuralgia than AICA. [14] Of note, the anterior spinal artery also arises from the vertebral arteries prior to PICA.
The anterior cerebral arteries may be united in a single trunk, which runs in the longitudinal fissure, giving branches to both hemispheres. The left and right A1 segments are asymmetrical in size in most individuals and may be absent or fenestrated; rarely, this segment may travel inferior to or through the optic nerve. [15]
An accessory anterior cerebral artery (ACA) may be present, and the A1 segment may arise from the cavernous or contralateral internal carotid artery (ICA).
The right and left ACAs may run as 1 vessel (azygos), to divide distally, or one may be a branch of the contralateral artery. Other variations of the anterior communicating (ACOM) artery include aplasia, fenestration, and duplication. [16] This vessel may be curved, kinked, or tortuous. The artery is rarely absent.
One A2 segment may be hypoplastic; thus, the contralateral A2 supplies both hemispheres. A2 may be duplicated. In an azygos ACA, both A1 segments join to form a single A2 segment. Branches to the contralateral hemisphere may be found.
Beginning with the vertebral artery, asymmetry due to hypoplasia, absence, or termination into PICA of one of the vertebral arteries can also be seen. The left vertebral is dominant about 45% of the time, right vertebral artery is dominant about 30% of the time, and the two arteries are co-dominant about 25% of the time. [17]
When a fetal posterior communicating (PCOM) artery is present, the ipsilateral P1 is typically hypoplastic, and the PCOM is larger in caliber. [10] Variations of the P1 segment include duplication, fenestration, and a bilateral shared origin of the posterior cerebral artery (PCA) and superior cerebellar artery (SCA). [15] A prominent perforating branch may supply portions of the ipsilateral and contralateral thalamus and, potentially, the midbrain. The posterior cerebral may course below, rather than over, the oculomotor nerve, or it may be absent and replaced by an accessory contralateral vessel. The PCA may arise from the internal carotid.
The PCOM artery may be absent, or the branch representing it may fail to join the posterior cerebral. Fenestration of the basilar artery is found in less than 1% of cases. [18]
The basilar artery may exist as 2 longitudinal trunks united across the midline. The SCA may be duplicated or absent. The internal auditory artery, commonly known as the labyrinthine artery, is most often a branch of the anterior inferior cerebellar artery (AICA), but it may arise from the SCA or the basilar artery. [5]
Asymmetry of the circle of Willis results in significant asymmetry of flow and is one important factor in the development of intracranial aneurysms and ischemic stroke. [8] Patients with aneurysms are more likely to have asymmetry or an anomaly of the circle. Eighty-five percent of saccular aneurysms arise from arteries of the circle of Willis, with 35% from the anterior communicating artery, 30% from the internal carotid artery, 22% from the middle cerebral artery, and the rest from the posterior circulation. [14]
Furthermore, the presence of a nonfunctional anterior collateral pathway in the circle of Willis in patients with ICA occlusive disease is strongly associated with ischemic stroke. [19] Furthermore, vertebral artery dominance may also contribute to basilar artery curvature and posterior circulation infarctions. [20]
Uncommonly, persistence of fetal anastomoses involving the circle of Willis is found, including persistent trigeminal, otic, hypoglossal, and proatlantal arteries. These arteries more or less unite the internal carotid and vertebrobasilar systems. The persistent primitive trigeminal artery (TA) is the most common of the persistent fetal anastomoses (83%), and connects the cavernous sinus to the basilar artery. The persistent otic artery (OA) is the least common to persist and connects the petrous carotid to the basilar artery. The persistent hypoglossal artery (HA) connects the petrous or distal cervical ICA to the vertebral artery. The persistent proatlantal intersegmental artery (ProA) connects the cervical ICA to the vertebral artery. [21]
Asymmetry of the circle of Willis results in significant asymmetry of flow and is one important factor in the development of intracranial aneurysms and ischemic stroke. [8] Patients with aneurysms are more likely to have asymmetry or an anomaly of the circle. Eighty-five percent of saccular aneurysms arise from arteries of the circle of Willis, with 35% from the anterior communicating artery, 30% from the internal carotid artery, 22% from the middle cerebral artery, and the rest from the posterior circulation.
Furthermore, the presence of a nonfunctional anterior collateral pathway in the circle of Willis in patients with internal carotid artery (ICA) occlusive disease is strongly associated with ischemic stroke. [19] Furthermore, vertebral artery dominance may also contribute to basilar artery curvature and posterior circulation infarctions. [20]
Uncommonly, persistence of fetal anastomoses involving the circle of Willis is found, including persistent trigeminal, otic, hypoglossal, and proatlantal arteries. These arteries more or less unite the internal carotid and vertebrobasilar systems. The persistent primitive trigeminal artery (TA) is the most common of the persistent fetal anastomoses (83%), and connects the cavernous sinus to the basilar artery. The persistent otic artery (OA) is the least common to persist and connects the petrous carotid to the basilar artery. The persistent hypoglossal artery (HA) connects the petrous or distal cervical ICA to the vertebral artery. The persistent proatlantal intersegmental artery (ProA) connects the cervical ICA to the vertebral artery. [21]
The internal carotid arteries begin forming at day 24 of embryological development from a combination of the third branchial arch and the distal segments of the paired dorsal aortae. [22] At day 28, the internal carotid artery (ICA) will then branch into the anterior and posterior division. Later on in development, the anterior division becomes the anterior cerebral arteries (ACAs), middle cerebral arteries (MCAs), and anterior choroidal; the posterior division becoming the fetal PCAs (and posterior choroidal). [23, 24, 25, 26] The ACAs begin to fully form on day 51, growing medially and eventually forming the anterior communicating artery (ACOM). [23, 24] The MCAs begin to fully form on day 35, and pierce the cerebral hemispheres. [27] This all forms the anterior circulation of the circle of Willis. The posterior circulation of the circle of Willis forms when the fetal posterior cerebral artery (PCA) becomes the PCOM, the adult PCA connects with the basilar artery (BA), and the posterior choroidal artery incorporates into the BA. [23, 24]
On days 31 to 35, the basilar artery, which supplies the hindbrain and brainstem (more details below) begins to form from two parallel neural arteries (or channels). These channels receive blood from the carotid-vertebrobasilar anastomoses given by the trigeminal artery (TA), the otic artery (OA), the hypoglossal artery (HA), and the proatlantal artery (ProA). [21]
On days 35 to 38, the vertebral artery begins to form transverse anastomoses between cervical intersegmental arteries, and downward to the 6th intersegmental artery. [27]
The circle of Willis (circulus arteriosus cerebri) is an anastomotic system of arteries that sits at the base of the brain. The “circle” was first described in a book written by Dr. Thomas Willis in 1664, Cerebri Anatome. [28] Although the text went on to have tremendous impact on neurological sciences and anatomy, Willis initially published the text pursuant to his understanding of the philosophical soul. During his time at Oxford, Willis believed that understanding cerebral anatomy was a paramount tool to help investigate the human concept. [29] Through autopsy, dissection and rudimentary experimentation, Willis captured many findings, including a vascular “circle” to be included in Cerebri Anatome. Interestingly, the term “circle of Willis” was aptly named by one of Willis’ students, Richard Lower, and later cited by prominent physiologist, Albrecht von Haller, roughly a century later. [30] The term “circle of Willis” was not eponymously propagated until the 1774 text of Bibliotheca Anatomica. [29] See the image below.
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Gaurav Gupta, MD Assistant Professor, Section Head, Endovascular and Cerebrovascular Neurosurgery, Fellowship Director, Endovascular Neurosurgery Fellowship (Site), Department of Surgery, Division of Neurosurgery, Rutgers Robert Wood Johnson Medical School
Gaurav Gupta, MD is a member of the following medical societies: American Academy of Neurology, American Association for the Advancement of Science, American Association of Neurological Surgeons, American College of Surgeons, American Heart Association, American Medical Association, Congress of Neurological Surgeons, Facial Pain Association, Society for Neuroscience, Society of NeuroInterventional Surgery
Disclosure: Nothing to disclose.
Aria Mahtabfar Rutgers Robert Wood Johnson Medical School
Aria Mahtabfar is a member of the following medical societies: American Association of Neurological Surgeons, American Medical Association, American Medical Student Association/Foundation, Society for Neuro-Oncology
Disclosure: Nothing to disclose.
Ahmed Meleis, MD Resident Physician, Department of Neurosurgery, Rutgers New Jersey Medical School
Disclosure: Nothing to disclose.
Brian H Kopell, MD Associate Professor, Department of Neurosurgery, Icahn School of Medicine at Mount Sinai
Brian H Kopell, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, American Society for Stereotactic and Functional Neurosurgery, Congress of Neurological Surgeons, International Parkinson and Movement Disorder Society, North American Neuromodulation Society
Disclosure: Received consulting fee from Medtronic for consulting; Received consulting fee from Abbott Neuromodulation for consulting.
Todd C Hankinson, MD, MBA Associate Professor of Neurosurgery, Children’s Hospital Colorado, University of Colorado School of Medicine
Todd C Hankinson, MD, MBA is a member of the following medical societies: American Association of Neurological Surgeons, American Society of Pediatric Neurosurgeons, Congress of Neurological Surgeons, International Society of Pediatric Neurosurgery
Disclosure: Nothing to disclose.
R Shane Tubbs, MS, PA-C, PhD Director, Research Section of Pediatric Neurosurgery, Department of Surgery, Division of Neurosurgery, Children’s Hospital of Alabama
R Shane Tubbs, MS, PA-C, PhD is a member of the following medical societies: American Association of Anatomists, American Association of Neurological Surgeons, American Academy of Physician Assistants, American Association of Clinical Anatomists, Congress of Neurological Surgeons
Disclosure: Nothing to disclose.
The authors wish to thank Drs. George Salter, Aaron Cohen-Gadol, and W Jerry Oakes for their suggestions and comments.
Circle of Willis Anatomy
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