Internal carotid artery (ICA) is the main artery for feeding the supra-tentorial brain structure. There are several systems for identifying the anatomical segments of ICA such as traditional numbering and Fischer system.
The different parts and segments of ICA
1. Cervical Part: It begins from the carotid bifurcation and extends into the
carotid canal of petrous bone
2. Petrous Part: Still accompanied by PGSN extends into the foramen lacerum
to Gasserian ganglion
3. Cavernous Part: Surrounded by vascular sinuses, still lies in PGSN and gives out the following branches:
Proximal branch meningo-hypophyseal trunk
Anterior meningeal artery
Lateral Posterior Choroidal Artery: arise from PCA and supplies atrium, temporal horn and body of lateral ventricle.
Circle of Willis is a symmetrical communicating arterial pathway formed by an arterial polygon as the internal carotid and vertebral systems anastomose around the optic chiasm and infundibulum of the pituitary stalk. This communicating pathway allows equalization of blood-flow between two sides of the brain through the connection between the middle cerebral artery with the posterior cerebral artery and basilar system.
A complete circle of Willis, in which no component is absent or hypoplastic is only seen in 20-25% of anatomical specimens, whereas posterior circle anomalies are seen in nearly 50% of individuals.
according to Fischer 5 segments of ACA
A1 extends from the bifurcation of ICA to anterior communicating artery.
A2 extends from anterior communicating artery to the junction of rostrum and genu of corpus callosum.
A3 extends from genu to the point where the artery turns back to rostral.
A2 & A3 branches called ascending segment.
A4 & A5 extend from genu to splenium. Both segments together are called horizontal segment.
The four segments of middle cerebral artery (MCA) are:
M1 or sphenoidal segment originates from the bifurcation and extends to the limen insula. The bifurcation occurs before the limen insula.
M2 insular segment extends from limen insula to the circular sulcus.
M3 opercular segment extends to the opercular compartment.
M4 cortical segment runs from the Sylvain fissure to the lateral surface of brain.
Vertebral arteries and basilar artery are the main feeding arteries of posterior fossa. The basilar artery is built from the joining of 2 vertebral arteries.
The vertebral arteries arise from subclavian arteries and extend to the junction of vertebrobasilar.
Vertebral arteries and basilar artery are the main feeding arteries of posterior fossa. The basilar artery is built from the joining of 2 vertebral arteries.The vertebral arteries arise from subclavian arteries and extend to the junction of vertebrobasilar.
Basilar artery is built from joining of two vertebral arteries and located at the anterior surface of pons. It gives several perforating branches usually in three groups such as caudal, middle, and the rostral. The caudal perforators vary in number from 2-5, and occasionally branched off in ponto-medullary, pyramidal and the hypoglossal branches.
It arises from basilar artery and supplies the upper brainstem colliculi and deep cerebellar nuclei.
It divides itself into four main segments shown in below table.
The main segment of SCA
Anterio-lateral ponto-mesencephalic segment
AICA originates from the caudal third of the basilar artery at the level of the junction between the medulla oblongata and the pons in the brainstem. It sweeps backward to anastomosing with the PICA. It is principal vessel of the cerebellopontine angle. It divides into two branches; rostro-lateral and caudomedial arteries and supplies the ponto-medullar junction laterally, the anterior inferior quarter of the cerebellar cortex. It also proceeds to the inner ear through the labyrinthine artery. However, the labyrinthine artery can arise as a branch of the basilar artery in others investigations too.
The vertebral artery gives off the branch PICA for supplying the medulla, inferior part of cerebellar hemisphere as well as vermis and IV ventricle. It divides into two main lateral and medial branches and additionally into 5 segments .
Generally there are two superficial and deep venous systems of brain.
Deep Venous System divided into ventricular- and cisternal group and also medial and surface of brain.
* The Ventricular Group: drains the ventricle system and Thalamus and is named according to its location and course. These consist of all veins located in the temporal horn and drain into the vein of Rosenthal.
* The cisternal Group: drains the basal surface of the brain via its 3 main veins as following:
a) Inferior frontal veins that drain the frontal lobe to the inferior sagittal sinus
b) Inferior temporal veins drain the temporal lobe via lateral and medial groups into the sinuses of tentorium and basal vein (Rosenthal).
This is a truly the deep vein belongs to the deep venous system and is located right above the third ventricle. It collects a very large amount of bunches including basal ganglia, thalamus, and lots of deep white matter. Its tributaries are divided into smaller medial group that drains septum pellucidum and fornices and a much more impressive lateral group. Its lateral caudate vein followed by thalamostriate vein is in itself an important collector.
The vein of Galen (AKA the great cerebral vein), is named for its discoverer, the Greek physician “Galen”. It is one of the largest vein of brain draining the cerebral blood.
It is a deep/internal vein and formed by the union of the two internal cerebral veins, thalamostriate vein and choroid vein at the interventricular foramen. It ends at the confluence of the inferior sagittal sinus and anteriorly at the straight sinus. Most of the blood in the deep venous system collects into the Vein of Galen.
Veins of the medulla oblongata drain into the veins of the spinal cord, the adjacent dural venous sinuses, or into variable radicular veins which accompany.
the last four cranial nerves to either the inferior petrosal or occipital sinuses, or to the superior bulb of the jugular vein.
Anterior and posterior median medullary veins may run along the anterior median fissure and posterior median sulcus, to become continuous with the spinal veins in corresponding positions.
Pontine veins, which may include a median vein and a lateral vein on each side.
Acute occlusion of cerebral arteries results in a stroke with sequel neurological deficits, depending on the location of the lesion. This basically occurs in two forms such as ischemic (Brain infarction) in about 80% of patients and hemorrhagic infarct in 20% of cases. An ischemic stroke occurs when a region of cerebral blood flow is suddenly stopped or limited. This may occur by vessel occlusion or by low blood flow.
Acute cerebral artery occlusion by an embolus or thrombosis is the most common causes. Due to the interruption of blood flow to a brain area, neuron metabolism is disturbed caused by lock of oxygen and glucose delivering through the involved artery. Cell death may occur after approximately 6 minutes of halted blood circulation.
These may vary from lethargic to comatose, but some patients may present agitation associated with sensory Motor dysfunction. Occasionally, the cranial nerves also are involved with resultant in CN paresis.The immediate thrombolytic therapy after onset is the best intervention of choice to reopen and to reestablish the blood flow to brain parenchyma.
Hemorrhagic transformation (reperfusion injury of blant stroke) represents the conversion of an ischemic stroke (bland infarction) into a hemorrhagic infarct. This may occur as a petechial hemorrhage (Extravasation of red cells from weakened capillaries) or as a real intra-parenchymal hematoma.
In hemorrhagic stroke, bleeding occurs directly into the brain parenchyma. The usual mechanism is thought to be leakage from small intracerebral arteries damaged by chronic hypertension (Atherosclerosis).
Symptoms in Patients with hemorrhagic infarct are worse than those with ischemic stroke. These are such as headache, nausea and vomiting, and/or marked hypertension signs of elevated ICP, as well as seizures and focal neurologic deficits. None of these deficits and symptoms reliably distinguishes between hemorrhagic and ischemic stroke ).
It is a Japanese word and means “Puff of smoke” called for the first time by Suzuki and Takaku. This is an angiopathetic disease with vascular changes associated with poor intracranial perfusion. Etiology and pathogenesis of the disease has still not been clearly understood, however it usually occurs in patients with known disease such as arteriosclerosis. That may cause the ischemic strokes or spontaneous intracerebral hemorrhages.
Approximately, 100 new cases occur worldwide each year. It tends to be higher in females than males. Familial version has been identified.
Basic pathological mechanism of the disease is a disposition of smooth muscles of cerebral vessels associated with a chronic inflammatory response. This phenomenon may lead slowly and long-term to the proliferation of smooth muscles and progressive occlusion of vessels. However, the precise mechanism
still seems to be unclear. Some studies, particularly genetic studies, have suggested a multifactorial mechanism.
The disease may lead to cerebral ischemic events such as TIAs or stroke with various clinical symptoms. The most common symptoms in children younger than 10 years are seizure, headache, visual disturbances, and also retardation.
The most common manifestation of the disease in adults is cerebral hemorrhage, particularly in basal ganglia and thalamus, but also intra-ventricle and SAB have been reported.
Cerebral venous thrombosis (CVT) is usually a rare pathological process, which may involve the cortical and deep cerebral veins and also dural sinus with nontypical signs.
The first report of a superior sinus thrombosis was at the beginning of the 19th century by Ribs at an autopsy.
It is very rare and an exact incidence is not known. CVT occurs in all ages and sexes, but it is more common in women between 20-40 years, maybe due to contraceptives. Cerebellar vein thrombosis is extremely rare and fatal.
There are numerous factors that may play a significant role in the development of venous thrombosis such as alterations in the chemical and hemodynamic properties of blood flow and also physical and anatomical changes of the vasculature. Vascular trauma, vascular compression through the mass lesions, arteriovenous fistula, but also factors involved in hypercoagulability including protein C & S anti-thrombin III may contribute to CVT. Some inflammatory bowel diseases and infections may contribute to CVT, particularly cavernous
and lateral sinus thrombosis are more common in patients with craniofacial infections such as sinusitis or/and mastoiditis. Despite the several possible causes for CVT, nevertheless about 40% of cases are idiopathic as reported by some authors.
SAH is a pathologic condition and is based on the existence of blood in the subarachnoid space. The most common cause of SAH is head injury in about 33% to 39 % of patients with GCSS of 8 to 14.The most common spontaneous SAH is aneurysm rupture. Cocaine use and sickle cell anemia may be associated
with aneurysmal SAH.
This accounts for about 6% to 8% of all stroke cases, approximately 11 cases in 100,000 populations per year. SAH usually occurs in 43% of cases during stressful time, in 34% during non-stressful time, in 12% during rest and sleeping time, and in 11% of cases with unknown circumstances.
The SAH may occur traumatically or non-traumatically such as rupture of an aneurysm or even no known cause (idiopathically). However the clinical signs and symptoms will be depended upon the volume and location of bleeding. This varies from a negligible amount to massive bleeding which may even be fatal.
There is a general correlation between the volume of SAB and risk of mortality or complications such as vasospasm and clinical grade according to the GCSS. It may cause further complications such as increase of ICP, reducing the CBF and metabolism, Hydrocephalus and systematic disorders.
This is a cerebral arterial narrowing after SHA demonstrated on angiography.This may lead to the cerebral ischemia with corresponding symptoms. It is a prolonged and even severe complication of SAH, that commonly occurs one day after SAH, but it is certainly a reversible process.
The first angiographic report was in 1951 by Ecker and Schneider. The first clinical report about the usefulness of hypertension in association with vasospasm was in 1976 by Kosnik & Hunt and Giannotta & colleagues. Miller Fisher and colleagues described in 1980 the relationship between SAH clots and
the increased risk of vasospasm. The first publication of administration of calcium antagonist (Nimodipine) after SAH was in 1983 by Allen and colleagues. And also the first use of transluminal balloon angiography for
dilating the narrowing arteries was in 1984 by Zubkov and co-workers. In the meantime it is a standard part of vasospasm treatment. Time Course and Incidence of Vasospasm Generally, the development of vasospasm may occur during the first week of initial SAH and last about 3 to 4 weeks. The peaks of severity can be in the 2ndweek.
Incidence of angiographic vasospasm depends on the timing of angiography and has been reported in literature variously from 20% to 100%, but it accounts for roughly 50% of cases with SAH.
There are several causes for developing vasospasm, but the most common causes for vasospasm are the local or diffuse thick layers of blood clots. However there are also some non-aneurysmal causes and risk factors such as Trauma, AVM, incomplete circle of Villis, pre-existing hypertension, poor clinical condition, age younger than 35 years, and excessive smoking for developing of vasospasm.
Cavernous segment is one of the four segments of ICA such as Cervical, Petrous, Cavernous and Supra-clinoid segment. It begins from the carotid canal (CC) of the petrous bone at the foramen lacerum and runs through the cavernous sinus to the carotid-oculomotor membrane (COM). The cavernous segment is about 2 cm long and composed of 4 divisions as following:
‐ Posterior vertical segment
‐ Posterior genu
‐ Horizontal segment
‐ Anterior genu1
The oculomotor nerve (III. CN) is located within the cavernous sinus (CS) and runs into the orbit through supraorbital fissure (SOF). Trochlear nerve (IV. CN) is also located within the lateral wall of CS and runs just beneath and parallel to the oculomotor nerve. Abducens nerve (V1.CN) nerve courses below the oculomotor and trochlear nerves. There are two arteries arising from CavSeg:
Meningo-hypophyseal and infero-lateral trunk, which supply the pituitary gland and Dura in the middle fossa floor (4, 5). McConnell’s capsular artery is a rare branch and arises in 80% from the anterior genu and distal horizontal segment of Cav. Segment and supplies the capsule of pituitary gland.
Approximately up to 15% of all angiographic identified intracranial aneurysms arising from ICA. Cavernous Segment aneurysms account for about 3% to 5% of all IC-aneurysms. These mostly originate from horizontal segment followed by anterior and posterior genu. It is much more common in females with a female – to-male ratio of 9:1. High peak of age is V. and VI. decadeof life.Approximately, 1/3 of CavSeg. aneurysms harbor more than one aneurysm.
The clinoidal segment of ICA is the anterior vertical segment after anterior genu of cavernous segment. It is located neither within venous canal nor within SAS, but it is an intradural segment. The ClinSeg has no arterial perforators. There are two types of ClinSeg aneurysms based on the site of origin and the direction of Vascular Disease of CNS ‐ 54 projection of the aneurysms as follows:
It arises from anterolateral surface of the ClinSeg underneath the anterior clinoidal process (ACP) and may expand laterally and anteriorly to the ascending ICA.
Small aneurysms may erode the under-surface of ACP and cause compression on ipsilateral optic nerve within the canal, whereas large aneurysms may compress optic system (chiasm) within the SAS.
It arises from the medial surface of the CliSeg and extends beneath the diaphragma sella into the pituitary fossa.
Its enlargement and eventually rupture may cause hypopituitarism or pituitary apoplexy. Both above
types are located interadurally below the dural ring and SAS. SAH in small aneurysms (<1 cm) usually is very rare.
Ophthalmic segment is the sub-division of supra-clinoidal segment of ICA and extends from COM to the origin of posterior communicated artery (PCA). It lies entirely within the SAS. There are some arterial branches arising from the OphSeg as follow:
– Ophthalmic artery: It is the most significant branch and arises from posteromedial surface of ICA below the optic nerve. It accompanies the optic nerve through the optic canal and supplies the retina and orbit.
– Sup. Hypophyseal Artery aneurysms: It arises from the inferior and inferomedial surface of the ICA and project towards and below diaphragma sella
These are aneurysms mostly arising from ICA trunk, intracranial carotid artery bifurcation, anterior cerebral artery (ACA), MCA, ACoA, PCoA, and also form anterior choroidal artery. They are mostly saccular form aneurysms.
They account for about 30% to 50% of all intracranial aneurysms.
They usually arise from the ventral wall of ICA and are very rare. These may project anteromedially, displacing the pituitary stalk or anterior perforators. They are mostly seen in patients with pre-existing arthero-sclerotic changes. Therefore, clipping of these aneurysms should be performed very carefully
under proximal control of ICA preventing the intraoperative hemorrhage.
This is the dividing point of ICA to the ACA and MCA. It gives lenticulo-striate perforators. These usually supply the basal ganglia and hypothalamus, mesial temporal lobe and optic apparatus. Aneurysms of ICA bifurcation usually project towards the anterior perforated substance.
They account for about 5% to 15% of all intracranial aneurysms.
These are based on the behavior of aneurysms to enlarge the size and cause compression on the optic apparatus. They also present symptoms due to the SAH or ntracerebral hemorrhage, particularly into the basal ganglia.
PCoA is one of the two arteries, which arises from communicating segment of ICA and builds left and right sides of Circle of Vilisi. PCoA arises from posteromedial surface of the ICA, distal to the takeoff of the artery and extends through the membrane of liliquest medial to the occulumotor nerve. It joins the posterior cerebral artery at the junction of P1 and P2 to the MCA of ICA. The mass effect of PCoA aneurysm may cause an acute III. nerve palsy.
In the case of a hypoplastic PCoA, it can be very risky to clip the aneurysm with PCoA together. It may be treated in another way to guarantee the potency of thePCoA.These account for about 50% of ICA aneurysms and are common in females.
This artery arises from the posterior communicating segment according to the new classification system. It usually follows the optic tract and supplies a branch to the mesial temporal structures. Its duplication occurs in about 30% of cases, detected mostly in autopsy specimens.
Because of the high location of aneurysms above the tentorium, cranial nerve deficits are very rare. SAH usually occurs in the ambient cistern and supra-sellar region. In the case of intra-ventricular hemorrhage that usually involves the temporal lobe, particularly the uncus.
CT-Scans are usually the first modality of choice. It can be completed by MRA and other radiological studies such as Pan-angiography.
Proximal ACA and ACoA are the most common sites for intracranial aneurysms. The ACA is divided into 5 segments by Perlmutte and Rhoton as follows:
starts at the division of ICA into ACA and MCA and ends at the ACoA. Its average diameter is about 2.6 mm (0.9 to 4.0 mm). Hypoplasia of the A1 segment occurs in about 10% of cases. Paired A1 Segments have an equal diameter in about 50% of cases. There are several perforator arteries called
medial lenticulo-striate arteries, which should be distinguished from lateral lenticulo-striate, which arise from M1 segment. Both groups terminate in the anterior perforated substance.
starts at the ACoA junction and ends at the junction of rosterum and genu of corpus callosum. There is an important perforator artery called medial striate artery or recurrent artery of Heubner. It arises in 78% of cases from A2-segment and 14% of cases from A1-Segement. Its length is about 23.4 mm (range 12 to 38 mm), whereas the length of A1 is about 12.7 mm. Recurrent artery of Heubner supplies the anterior striatum
(caudate nucleus and putamen), and a portion of Globus Pallidus and internal capsule. It can be confused with the orbitofrontal artery during the operation which also originates from A2-segment.
extends over the curve of the genu and ends where the ACA turns above the genu.
Extend over the body of corpus callosum. Transition from A4 to A5 occurs at the level of coronal suture.
ACoA: It has a diameter about half that of the A1 segment of about 2.6 mm. The average diameter of the ACoA is about 1.5 mm. There is a constant relationship between the diameters of both arteries. Double ACoA have been seen in about 30%, and three ACoA in 10% of cases. Absence of the ACoA is extremely rare.
In this chapter we will discuss the aneurysms of proximal ACA (A1& A2), and ACoA.
Aneurysms that arise beyond the ACoA junction are called distal ACA aneurysms. These include the A2-segment to A5-segment of the ACA, and arise from ACA as well as from its branches distal to the ACoA. These are frequently associated with other IC-aneurysms and usually cause intra-parenchymal hemorrhage.
They are rare and account for about 2.8% to 5% of all intracranial aneurysms. Approximately 41% of them have one or more additional IC-aneurysms. The most common site of them is the MCA aneurysms in 43% of cases. Distal ACA is after MCA the most common site for aneurysms caused by trauma or infections. Traumatic aneurysms of distal ACA are common in children and infants (called shaken baby syndrome). It accounts for about 36.7% of all traumatic intracranial aneurysms. Distal ACA also is a common site for
infectious aneurysms, particularly in patients with bacterial endocarditis.
MCA starts from the ICA bifurcation and is divided into 4 segments :
M1 segment is the MCA trunk arises from ICA bifurcation and ends in the MCA bifurcation (70%-80% of cases), in the trifurcation (in 20%) and in the quadrifurcation (1%).
M2 segment is about 11 mm long and begins from the bifurcation and ends in the M3 segment.
M3 Segment that extends over fronto-parietal and temporal opercula.
M4 segment courses over the cortical surface.
It accounts for about 20% of all intracranial aneurysms. However it varies among genetically different populations. According to several studies, incidence of a single MCA and also mirror aneurysm of the contralateral MCA is about 11%. An association with other multiple IC- aneurysms has been reported in Yasargil’s series of 184 patients with MCA aneurysms in about 32% of cases . Approximately, 10-15% of all MCA aneurysms arise from the M1 segment. And 80%-85% of them are located at the division of the main M1 trunk. Aneurysms between M1 to M4 are rare and account for about 5% of all MCA aneurysms. Giant MCA aneurysms are relatively rare, only 3 cases in Yasargil’s series of 184 patients harbored giant aneurysms, but in the series of Sundt and Piepgras (Mayo Clinic) 12% of cases were giant aneurysms.
Approximately, 90% of MCA aneurysms present with rupture and SAH. IChematoma is also the most common clinical presentation in 40%-50% of patients with ruptured MCA aneurysms. Mass effect of the un-ruptured giant aneurysms may cause focal neurological deficits such as hemiparesis as well as seizure. Further symptoms are cortical stroke caused by distal thrombus or embolization.
It is appropriate for un-ruptured and uncomplicated aneurysms located at the MCA bifurcation. It is not recommended in patients with ruptured aneurysm and SAH, because this approach leads to the dome of aneurysm before the exposure of the M1-segment.
It is appropriate for aneurysms that arise from a short M1 trunk. It is also an approach for complicated aneurysms with a high risk of re-rupture at the time of exposure. The Sylvain fissure is opened medially to laterally by dissecting arachnoid bands between the mesial anterior temporal and frontal lobe. This may reduce the frontal lobe retraction.
It is useful for patients with intracerebral hematomas, because the evacuation of hematoma may lead to brain relaxation and better access to the ICA bifurcation, therefore it is the preferred approach for patients with MCA bifurcation aneurysms. The anterior aspect of superior temporal gyrus should be split about 2-3 cm parallel to the Sylvain fissure to identify the bifurcation. A transpial extension into the Sylvain fissure makes it possible to identify the MCA branch aneurysms. This approach has been described and advocated by Heros and coworkers.
Generally, there are four important issues which should be considered as preoperative management in the aneurysmal surgery. These are: Managing and Preventing the vasospasm, hydrocephalus, electrolyte abnormalities, as well as the risk of re-bleeding. Serum electrolyte abnormalities and hydrocephalus may occur earlier, within a few hours after the SAH. Re-bleeding is a devastated onset and may occur in first 48 hours after SAH. The vasospasm peaks may be reached at the 3. to14. day after the initial onset. (see also chapter of vasospasm). All these above issues must be managed before planning a surgical intervention. Calcium channel blockers (nimodipine 60 mg every 4 hours), avoiding the hypotension and hypo-volume and eventually Balloon angiography will be necessary to prevent the vasospasm. Anticonvulsants can be used in the case of developing seizures following SAH. And also broad-spectrum antibiotics should be given 1 hour before the scalp incision, intravenous steroids as well as the intraoperative monitoring are routinely performed. Achieving the intraoperative brain relaxation related with minimal brain retraction during the operation using of 20% mannitol (0.5 g / kg body weight) 20 minutes before dural opening is advocated. Timing of Aneurysmal Surgery This either occurs on an early surgery, or a delayed surgery.
The early surgical intervention usually occurs on an urgent basis after admitting the patient to the ICU. After completing the radiographic examination and placing the patient as a candidate for surgery. Timing of surgery usually depends on clinical grade at the time of surgery. Patients with Hunt & Hess grade 1 and 2 have the best outcome of early surgery. They are usually operated earlier, within 24-72 hours. Disadvantage and distinct risk of this early surgical timing is intraoperative rerupture of the aneurysm, which can be minimized with meticulous microsurgical technique
has been the rule in patients with poor clinical grade 3-4, unless there is a life-threatening lesion requir-ing prompt evacuation of intracerebral hematomas. Patients with poor clinical grade may be treated by the endovascular technique, which likely plays an increasingly significant role in the management of these aneurysms
Posterior circulation aneurysms are anatomically and surgically much more complicated than anterior circulation. These are very close to the lower cranial nerves and brain stem, therefore their surgical intervention may carry much higher morbidity and mortality. In other words, these lesions can’t be left untreated, because of their propensity for fatal re-bleeding. In the below chapters we will discuss the vertebral trunks, PICA, vertebrabasilar junction, basilar trunk and Apex, as well as PCA aneurysms.
Posterior circulation aneurysms are relatively uncommon and account for about 8%-9% of all intracranial aneurysms. 25% of these arise from vertebral artery, PICA and vertebra-basilar junction and account for about 2% of all intracranial aneurysms. Fusiform non-sacular aneurysms at the vertebra-basilar location due to dissection of vertebral artery are much more common than anterior circulation. These account for about 28% of all posterior circulation aneurysms.
Vertebral arteries arise from subclavian arteries and ascend through the transverse processes of the upper six vertebrae. They pass posteriorly to the lateral mass of the atlas and anteriorly to the atlanto-occipital membrane into subdural space. They pass across the pyramid to join together near the pontomedullary sulcus to build the vertebra-basilar junction. The vertebral trunk begins from the dural ring to the vertebra-basilar junction. The first extradural branch of vertebral arteries is the posterior meningeal artery for dural and the first intradural branch is the posterior apical artery. The second most significant and largest intradural branch is posterior inferior cerebellar artery (PICA). PICA has about 4 segments such as anterior, lateral, tonsillo- medullary, and telovelo-tonsillary for supplying the medulla, and posterior surface of cerebellar hemispheres. The last branches of vertebral arteries are the anterior spinal arteries (ASA) which join together to form the midline anterior spinal artery. This supplies the pyramids, lemniscus, hypoglossal nuclei and cranial nerves.
Aneurysms of the basilar trunk are rare, but they are the most difficult challenges in neurovascular surgery. Aneurysms of basilar trunk are those arising between the vertebra-basilar junction and superior cerebellar arteries (SCA). Most of them are located at the origin of AICA and usually projected laterally in association with AICA. The aneurysms from the other perforators, particularly from lateral pontine arteries, usually project posteriorly or anteriorly against the clivus and have close relationship to the VI cranial nerve. Anatomy The basilar trunk artery begins from the vertebra-basilar junction at the level of ponto-medullary sulcus and extends superiorly in the basilar sulcus of the pons and ends at the origin of superior cerebellar artery (SCA). This gives several branches such as AICA, which supplies the inferior surface of cerebellar hemisphere. The second important branch is SCA, which travels through the pontomesencephalic sulcus and supplies superior cerebellar hemisphere. It finally ends in its basilar apex in the inter-peduncular fossa and gives its largest branch posterior cerebral artery (PCA). Additionally, it gives several intermediate most vital perforator arteries such as ponto-medullary, and lateral pontine arteries for supplying the pontine and medullary surface. These are divided into three groups: cuadal, middle and rosteral perforators.
These are the aneurysms arising from the top of the basilar bifurcation. Deep midline location of the basilar apex and bony enclosure of the clivus, posterior clinoid process and also the anatomic complexity of the inter-peduncular cistern make basilar apex aneurysm surgery one of the technically challenging procedures for neurosurgeons.
PCAs arise at the basilar bifurcation supplying the deep structures of the midbrain such as thalamus, plexus choroid of third and lateral ventricles as well as some portions of the brain hemispheres. Microsurgical Anatomy: PCA is divided into three important segments of PCAs.
P1-Seg. : It runs from basilar bifurcation to the PCoA
P2-Seg. (Ambient segment): This begins at the PCA – PCoA and extends to the midbrain. It is divided into two P2a and P2b and gives brainstem and ventricular branches.
P3-Seg. It courses over the tentorium from pulvinar into the quadrigiminal cistern and supplies posterior temporal lobes.
PCAs give the second group of perforator arteries which supply the geniculate nuclei, mammillary bodies, cerebral peduncles and posterior mesencephalon. The third group of perforator arteries arises from PCoA. SCAs arise just below the PCAs and supply brainstem and cerebral peduncle through its perforating arteries. Incidence The incidence of PCA aneurysms range from (0.7% to 2.2%), is published in literature. In a series of 115 PCA aneurysms identified in literature by Zeal and Rhoton, 15% arose from P1, 16% from P1-P2 junction, 20% from proximal P2A, 36% from P2B, and 13% from distal of the artery. The giant aneurysm of PCA is very common. In a series of 14 PCA aneurysm reported by Yasargil, 50% were giant and in series of Drake it was 42%.
Cerebral aneurysms with a dimension of 25 mm or more are considered as giant aneurysms. They are sometimes mistaken for brain tumors. Their anatomic complexity and poor natural history make these aneurysms to the most challenging lesion for neurosurgeons. History The first description of a giant aneurysm was in 1875 by Hutchinson. At the beginning of the 20th century the only treatment procedure of aneurysms was hunterian ligation of ICA. Dandy was the first, who exposed a cerebral aneurysm and clipped its neck.
Approximately 2% -5% of all IC aneurysms are giant aneurysms. There is an equal distribution related with gender and age (fourth through sixth). According to different studies, about 34% – 67% of giant aneurysms are associated with ICA, 11% – 40% with anterior circulation and 13% to 56% with posterior circulation.
These can be sporadic as well as congenital malformation.
These are vascular malformations composed of enlarged capillaries with normal capillary structures and without increasing the number of capillaries.
There is not much information about the incidence of Capillary Telangiectasia (Cap. T.). It accounts for about 0.06-0.4%, of all CNS vascular lesions based on large autopsy series. They are the second most identified lesions in the autopsy series.These are mostly located in pons. These occur in each age, but commonly in adults in their 30s to 60s
(Cavernoma (CMs) = Cavernous Angioma = or Cavernous Hemangioma)
CMs are comprised of a large proportion of vascular components which may occur sporadic (non-hereditary) or congenital and familiarly.
These account for about 0.5% of all IC- vascular lesions based on clinical series. They usually occur at any age and equally in men and women, however they are diagnosed more in adults in their 20s to 30s.
Etiology of CMs is still uncertain, but some authors have advocated the same pathogenetic process for CMs as for capillary telangiectasia, or developmental venous anomalies (DVA). They are usually small and the average size tends to be between 1-2 cm, but lesions measuring 8 cm have also been reported. There are several theories regarding the mechanism of growth of the CMs, but one of the most accepted theories is process of bleeding and thrombosis within the lesions.
(Venous Malformations = Venous Angiomas) Introduction They are congenital cerebral anomalies that occur in any age and sex. However there is no evidence of a familiar role in developing the venous anomalies. According to the retrospective imaging study, they account for about 0.5- 0.7% of all intracranial malformations, which rises to 2.6% in autopsy series.
The etiology of VAs is still not clear, but it is usually formed in the late stage of fetal maturation probably due to an intrauterine accident resulting from an ischemia. This is anatomically an abnormal lesion with thickened and hyalinized veins, with physiologically normal low venous outflow. They mostly occur in frontal lobes and posterior fossa within brain parenchyma and are not likely presented with hemorrhage.
These are an abnormal intracranial connection between the arterial and venous system without the normal intervening capillary bed. These are congenital and may be caused by some genetical and familial disorders. Approximately, 0.1% of population may harbor an AVM, about 2% of these are multiple lesions
They are lesions with congenital origin. Pathogenesis of AVMs is very complex and based on several predisposing factors such as angiogenic humoral immune factors, abnormal venous drainage, as well as hormonal influence. The familial and genetic factors also may play a role as predisposing factors. They occur mostly in Asian populations. AVMs normally exist of directly fistulous connections of arteries and veins and are usually attached to the base towards the meninges. Microscopically; there is evidence of recanalization, prior thrombosis, hemosiderin-laden and marked surrounding gliosis. The latter may occur due to the high-blood-flow, and low resistance of the AVM shunt known “stealing phenomenon”.
Malformations It is not usual to see the lesions composed of the true AVMs and other vascular abnormalities. But there are some reports in literature describing such mixed lesions, particularly the coexistence of AVMs and DVAs.Awad and colleagues reported 3 cases of AVMs in association with DVA.
There are several studies that attempt to classify the relationship between both lesions based on distance and flow relationship of aneurysms to the AVMs.
There is evidence in literature about a genetic predisposition for developing vascular malformations in association with the two following syndromes
It is presented by collection of extra-and intracranial features based on autosomal dominant disorders. Microscopically, lesions consist of dilatation venules into telangiectasia without elastic fibers. The accompanied AVMs are rarely identified.
In this chapter we discuss the sporadic (non-hereditary) as well as congenital vascular malformations.
The most common types of Arteriovenous Fistulas are:
Dural Arteriovenous Fistulas (DAVFs)
Sinus Dural Arteriovenous Fistulas (SDAVFs)
Cavernous Carotid Fistulas (CCFs)
It is a direct shunt between dural arterial supply and dural draining venous system. Occipital and meningeal arteries are the most involved feeding arteries. Venous drainage occurs through the dural sinus or other leptomeningeal venous channels. They are usually acquired lesions, but they can also be an idiopatic lesion.
The exact prevalence of DAVFs, is not well known, because of the number of the asymptomatic DAVFs, that have not been reported. However, they account for about 10% to 15% of all intracranial vascular malformations.
The most common location is the transvers sinus with a prevalence of 50% of all DAVFs. It usually occurs solitary, but multiplicity has also been seen in about 7% of cases. The peak age is between 40 and 60 years.
It is a simple manual self-compression therapy that may be useful, if the DAVF is supplied only by the occipital meningeal artery. Patients may be advised by the physician to compress the pulsatile occipital artery 3 times a day for about 30 minutes. Approximately, 25% of such cases can be thrombosed completely. A control angiogram should be induced to rule out any pathologic change in venous drainage patterns.
The management of the superior sagittal DAVM is always almost the same as the transverse/sigmoid described previously.
A simple fistula may be occluded by accessing the feeding arteries through the fistulous site into the venous recipient vein. If the fistula is fed solely by the superficial temporal artery, arterial compression may be effective to occlude the fistula within several weeks. But the feeding arteries usually are multiple and
deep which often requires an open invasive surgery. Reed more
The CCF is either a direct shunt between the ICA and cavernous sinus or an indirect shunt via DAVMs.
The original name of pulsatile exophthalmos drives from the orbital symptoms caused by these lesions.
It causes an elevated pressure within the cavernous sinus which is transmitted anteriorly to the orbital vein producing exophthalmos and orbital bruit.
The most common signs of carotid cavernous fistulas are orbital findings such as exophthalmos, chemosis, proptosis in about 90% of patients, but also bruit, diplopia and double vision due to the abdusence palsy.
One of the most important consequences of carotid cavernous fistulas is the visual loss in about 50% to 89% of patients.The different mechanisms of visual losing based on retina’s perfusion in case of a CCF are:
Elevation of the intra-orbital venous pressure
Elevation of the intra-orbital pressure generally
The blood supplying of vertebral column are variable. It is depended on 3 vessels of the segmental arteries that arise from aorta. Segmental Arteries of the vertebral column supply radicular arteries which arise from posterior aspect of aorta and are known as intercostal and lumbar arteries in thoracic and lumbar regions. These segmental arteries proceed to intervertebral foramina appropriate to their level, where they divide into terminal branches. The largest radicular artery in thorasic spine is arteria radicularis magna (ARM) or Artery of Adamkiewicz. It is one of the largest segmental arteries and mostly arises at T10 on left side, however, position may vary from T7 to L4 and it usually enters a single intervetebral foramen between the levels of T9-T11.
Spinal cord blood supply occurs through two longitudinal pathways include the anterior spinal artery (ASA) and posterolateral arteries (PSA). Medullary perforating arteries from the ASA supply the anterior 2/3 of spinal cord as well as the central portions of SC (grey matter score) consisting the corticospinal and
The pial circumferential arteries (pial netork) from the (PSA) supply posterior 1/3 of spinal cord as well as entire dorsal column and a portion of the corticospinal tracts. Circumferential, pial network of the spinal cord is mainly supplied by dorsal feeding arteries called radiculo-pial arteries. There are about 10–20 dorsal radiculo-pial vessels persist. The anterior spinal artery anastomoses around the conus medullaris with the posterior spinal arteries in the arterial ‘basket’ Both of the above systems are supplied by medullary arteries.
Drainage System of Spinal Column and Spinal Cord (SC) Basically, the spinal venous system is complex and variable. Generally, the venous drainage system of the spine and spinal cord is accomplished through a
complex network of venous structures including the intrinsic, extrinsic, and intra-osseous systems. It is divided into three systems; intradural (intra- and extra-medullary veins), extradural (epidural veins plexus) and intra-osseous of para-spinal veins.
The intramedullary veins are known as radial veins. However there are two anterior and posterior longitudinal spinal veins named “anterior and posterior coronal veins” that run along the SC in an interconnecting fashion with the radial veins and collected blood from radial- and other veins to build the intradural plexus.
The intrathecal veins have no valves, but the penetration sites of the medullary veins at the dural level present as the functional valve the retrograde venous flow from Batson’s plexus to the intradural space.
The communication site between the spinal cord venous- and brainstem system is the cervico-medullary
The extrinsic network consists of anterior epidural plexus and a generally smaller posterior epidural plexus. The medullary veins drain into a venous network within and around the nerve sheath which is called “emissary veins”. These dorsal and ventral emissary veins connect the dorsal and ventral epidural
plexuses (Batson’s Plexus) which run cranial and caudal along the vertebral body.
They are a heterogeneous group of abnormal vascular lesions that occur as congenital or acquired malformations. Therefore their nature, treatment and outcome usually depend on the type of lesion.
The modern classification system of spinal cord vascular lesions is based more on radiographic features of the nidus concept, obtained by selectiveangiography. This and the following chapters discuss the spinal cord vascular lesions according to a probably widely accepted modified classification proposed recently by R. F. Spetzler & colleagues.
These are divided into two main groups such as
1) Spinal Cord Arteriovenous Malformations (SC-AVMs)
2) Dural Arteriovenous Fistulas (DAVFs)
These are a direct or an indirect connection between spinal feeding arteries and spinal venous system with the presence of a nidus like the cerebral AVMs. These can be located extradural or intra-dural as well extra-medullary or intramedullary.
They are uncommon spinal lesions and are known as juvenile, metameric, or Type III AVMs in the older nomenclature. They respect no tissue boundaries and involve the skin, vertebrae and the spinal cord with both extra- and intradural components.
They are either intramedullary (within spinal cord) or partially intra- and extramedullary. They are usually more uniformly distributed than cerebral AVFs and are mostly associated with other vascular abnormalities. This suggests that they may be congenital lesions. These are supplied by one or more medullary arteries as the feeding arteries. There are some different types of intradural AVMs such as Juvenile, and Glomus types.
These have a voluminous arteriovenous nidus fed by several enlarged medullary arteries. They may involve the vertebral body and paraspinal soft tissue.
These usually have a compact nidus confined to a segment of spinal cord. They are usually located anteriorly to the SC, and are fed by one or two medullary arteries.
Dural AVFs are a direct connection between dural feeding arteries and venous system (mostly a solely medullary vein). These have mostly no marked nidus and are distributed more diffused than AVMs. They are divided into two main types such as extradural arteriovenous fistulas and intra-dural DAVFs.
– Extradural DAVFs
– Intradural DAVFs: Dorsal or Ventral Intra-dural AVFs
They are represented by a direct connection between an extradural artery and vein which leads to developing of a high flow fistula and enlargement of the epidural venous complex. The epidural venous engorgement is the result of an exclusive drainage to the extradural venous system, but drainage into both extradural and intradural veins has also been reported in some cases.
They are the most controversial lesions regarding to their origin, pathophysiology and also therapy. These are subdivided into two types as following:
1) Intradural dorsal DAVFs (Type I, according to the Spetzler’s classification of AVMs)
Type I (Intradural Dorsal AVFs) is the most common type of spinal dural AVFs, and mostly occurs in males in
about 85% of cases.
2) Intradural Ventral DAVFs (Type IV of SC-AVMs,- see also chapter of SCAVMs)
Type IV is for ventral DAVFs was termed in 1986 by Gueguen and colleagues.Recently, Spetzler and colleagues subdivided Type IV into three subtypes such as (IVa), (IVb), and (IVc).These usually harbor large shunts with a high-flow rate and are associated with large aneurysms. These lesions are mostly associated with several vascular syndromes such as Rendu-Oslar-Weber syndrome, and neurofibromatosis.
Their location and angiographic features composing of AVFs (multiple direct shunts) and AVMs make these lesions as a distinguished malformation. These may be comprised of both extra- and intramedullary AVMs. They usually have multiple feeding arteries, more than one nidus and also have a complex venous drainage system (Spetzler & colleague).
These are usually pain and progressive radiculo-myelopathey and also hemorrhage.
MRI is the best first study of choice followed by spinal angiography. This may demonstrate location, feeding arteries, and complex venous patterns of lesions. Reed more
They are usually associated with spinal cord AVMs. Pathogenesis of the lesion is based on high flow rate and dissection of the arteries. These may involve Adamkiewicz, anterior spinal artery and further radicular arteries.These are sudden-onset of pain and also SAH.
This consists of treatment of both lesions AVM and aneurysm. The strategy is the same as described previously for spinal AVMs. This is the endovascular embolization of the feeding arteries combined with surgical procedure.
Significant advances of the modern MRI technique (rapid- sequence imaging) and selective intraoperative arteriography permit a defined diagnosis of various subtypes as well as details of anatomy and patho-physiology of the lesions.
When selective angiography has established the diagnosis of an AVM or AVF, all therapy options should be considered. These can be solely endovascular intervention with interval screening, or microsurgery alone based on limited risk, or a combination of both.
In general, microsurgery follows the endovascular embolization, but in the case of assessment of an intraoperative unacceptable risks associated with complete excision, embolization should be performed after the surgery.
These occur either sporadically in a familial pattern or spontaneously. The mostcommon lesions of this group are cavernous angiomas or hemangiomas.
They are comprised of sinusoidal vascular channels surrounded by a hemosiderin-stained gliotic rim of tissue. They are angiographically an occult lesion and may be seen in any location of the neuro-axis from cerebrum to the spine. They usually occur intramedullary, but they may be presented as an epidural lesion and involve more than one level of the spine.
They occur sporadically as well as spontaneously in association with familial multiple cavernous angiomas related to an autosomal-dominant trial mapped to the chromosome 7q. They usually are low-flow lesions and pathogenesis of myelopathy mostly is hematomyelia.
Myelopathy is the most common symptom, particularly in young patients through to middle age. Progressive neuropathy is usually associated with repeated small hemorrhages. Small lesions may remain asymptomatic throughout the life.
These are usually associated as a familial lesion with von Hippel-Lidau disease. Hemangioblastomas usually occur in cerebellum, but they have also been seen in spinal cord mostly intramedullary, or along the nerve root. Despite the various locations of the lesions histopathology of the intra-spinal and intra-cranial
tumors are similar.