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The brain and meninges are supplied by branches that originate from the aorta. The brachiocephalic trunk (or innominate artery ) divides behind the right sternoclavicular joint into a right common carotid artery (CCA) and a right subclavian artery that supplies the arm. The next aortic branches are the left common carotid artery and the left subclavian artery, arising directly from the aortic arch. The vertebral arteries are early branches of the subclavian arteries of each side. The common carotid arteries bifurcate in the neck, usually opposite the upper border of the thyroid cartilage, most often at the level of the body of the fourth cervical vertebra, into the internal carotid arteries, which are direct (nearly 180-degree extensions of the common carotid artery) and the external carotid arteries (ECAs), which course more anteriorly and laterally and supply branches to the face and its structures.
The internal carotid arteries (ICAs) ascend vertically in the neck, posterior and slightly medial to the external carotid artery. These arteries are positioned medial to the sternocleidomastoid muscle and travel behind the faucial pillars of the pharynx until they reach the carotid canal at the skull base. They have no branches within the neck. At the skull base, the carotid arteries lie adjacent to the 9th to 12th cranial nerves, which exit the skull from the jugular and hypoglossal foramina. The arteries then enter the skull through the carotid canal within the petrous bone and form an S -shaped curve. The portion of the internal carotid arteries within this curve is referred to as the carotid siphon . There are three divisions of the internal carotid arteries within the siphon: an intrapetrous portion, an intracavernous portion within the cavernous sinus, and a supraclinoidal portion.
Branches . Two branches arise from the petrous segment : the caroticotympanic artery supplying the tympanic cavity and the artery of the pterygoid canal (vidian artery) supplying the pharynx and the tympanic cavity. The cavernous segment gives off the meningohypophyseal trunk supplying branches to the pituitary gland and meninges and the anterior meningeal artery. Within the cavernous sinus, the internal carotid artery lies in close relationship to the nerves that control eye movement (III, IV, and VI) and the ophthalmic and maxillary divisions of V. Soon after leaving the cavernous sinus, medial to the anterior clinoid process, the internal carotid artery gives off the ophthalmic artery . The ophthalmic artery passes through the optic canal into the orbit just below and lateral to the optic nerve.
The internal carotid arteries penetrate the dura mater, forming the supraclinoid segment . They ascend slightly posteriorly and laterally, passing between the oculomotor and optic nerves. The branches of the proximal supraclinoid region are the anterior choroidal, superior hypophyseal, and posterior communicating arteries, which arise and course posteriorly. The termination of the intracranial internal carotid arteries (the so-called T portion because of its shape) is the bifurcation into the anterior cerebral arteries, which course medially, and the middle cerebral arteries, which course laterally.
Segments. The first branch of each subclavian artery is the vertebral artery (VA). The thyrocervical and costocervical trunks originate from the subclavian arteries just after the vertebral artery and can serve as collateral channels when the vertebral artery becomes occluded. The vertebral arteries course upward and backward during their first segment (V 1 ) until they enter the transverse foramina of the sixth or fifth cervical vertebra. Then the artery ascends as the second segment (V 2 ), which courses within the intravertebral foramina, exiting from the transverse process of the atlas. The third segment (V 3 ) passes posteriorly behind the articular process of the atlas; it lies in a groove on the upper surface of the posterior arch of the atlas, behind the atlas, before piercing the dura mater to enter the foramen magnum. The intracranial portion (V 4 ) ends at the medullopontine junction, where the two VAs join to form the basilar artery.
Branches . The cervical portion of the vertebral arteries gives rise to many muscular and spinal radicular branches. The spinal branches pass through the intervertebral foramina and enter the spinal canal to supply the cervical portion of the spinal cord and the periosteum and bodies of the cervical vertebra. A small anterior and larger posterior meningeal artery originate from the distal extracranial segments (V 2 , V 3 ). The intracranial vertebral arteries give off posterior and anterior spinal artery branches, penetrating arteries to the medulla , and the large posterior inferior cerebellar arteries.
The external carotid arteries give off many branches that supply structures within the face and neck. They extend from the upper border of the thyroid cartilage to the neck of the mandible, where they divide into temporal and maxillary arteries. There are eight major branches. The superior thyroid, lingual, and facial arteries arise from the anterior aspect of the ECAs and course medially. The occipital and posterior auricular arteries arise from the posterior aspect of the artery. The temporal and mandibular artery branches arise behind the neck of the mandible. There are the deep and superficial temporal branches of the temporal artery.
The ECAs have two branches that supply the face and can provide collateral blood flow to the ICA system: the facial arteries, which course along the cheek toward the nasal bridge, where they are termed the angular arteries, and the preauricular arteries, which terminate as the superficial temporal arteries. The internal maxillary artery and ascending pharyngeal branches of the ECAs also can contribute to collateral circulation when an ICA occludes. The internal maxillary arteries give off the middle meningeal artery branches, which penetrate into the skull through the foramen spinosum. Another important arterial supply of the face involves the frontal and supratrochlear branches that originate from the ophthalmic arteries that supply the medial forehead above the brow. When an ICA occludes, these ECA branches can be important sources of collateral blood.
The right common carotid artery and right subclavian arteries may arise as separate branches directly from the aortic arch. The right vertebral artery may arise directly from the brachiocephalic trunk instead of the right subclavian artery. The left vertebral artery may also arise from the brachiocephalic trunk. The right subclavian artery can arise from the aortic arch distal to the left subclavian artery, in which case it then crosses to the right side. Sometimes the left common carotid and the left subclavian arteries arise from a common (left brachiocephalic) trunk. Rarely, a VA can arise from a common carotid artery.
The internal carotid (anterior) circulation supplies the anterior and most of the lateral portions of the cerebral hemispheres, while the vertebrobasilar (posterior) circulation supplies the brainstem, cerebellum, and the posterior portion of the cerebral hemispheres. About 40% of the brain's blood flow comes through each internal carotid artery, while 20% flows through the vertebrobasilar arterial system.
This anastomosis at the base of the brain (more a hexagon than a circle) serves to connect the major arteries of the anterior and posterior circulations, and the arteries from both sides. The horizontal portions of the anterior cerebral artery branches of the internal carotid arteries are connected to the anterior communicating artery, forming the anterior portion of the circle. The posterior communicating artery branches of the internal carotid arteries on each side connect to the posterior cerebral artery branches of the basilar artery, forming the lateral sides and posterior portion of the “circle.”
The superior hypophyseal arteries arise as the first branches of the supraclinoid portion of the internal carotid arteries, giving off branches to the optic chiasm and participating in an anastomosis that supplies the pituitary gland, which is composed of arterial branches from each side and branches of the right and left meningohypophyseal trunk.
The posterior communicating artery (about 1.5 cm in length) proceeds posteriorly and medially to join the posterior cerebral arteries on each side about 1 cm from their origins from the basilar artery. Small branches feed the optic tract and the posterior portion of the optic chiasm, the posterior hypothalamus, and the walls of the third ventricle. The tuberothalamic (polar) artery most often arises from the middle third of the posterior communicating artery but may also arise from the proximal segment of the posterior cerebral artery. The polar artery supplies the anteromedial and anterolateral portions of the thalamus.
The basilar artery is formed by the union of the two intracranial vertebral arteries at the medullo-pontine junction. It courses rostrally in a groove closely applied to the anterior surface of the pons, where it is located within the prepontine cistern behind the clivus. The distal segment enters the interpeduncular cistern, where it is often separated from the basal surface of the brainstem. The distal portion of the artery lies between the cerebral peduncles and ends at the pontomesencephalic junction, just after passing between the two oculomotor nerves, by dividing into the two posterior cerebral arteries. The basilar artery is often curved and tortuous and may deviate from the midline. The basilar artery averages about 33 cm in length, and the diameter usually is between 4 and 4.5 mm. The main branches of the artery are the anterior inferior and superior cerebellar arteries, paramedian arteries that penetrate directly into the pons, and short circumferential arteries that course around the pons and give off lateral basal and lateral tegmental penetrating arteries.
The posterior cerebral arteries originate from the terminal bifurcation of the basilar artery rostral to the third cranial nerves and then encircle the midbrain above the level of the tentorium cerebelli. As the posterior cerebral arteries course the dorsal surface of the midbrain, they divide into cortical branches. The arteries are divided into peduncular, ambient, and quadrigeminal segments, named after the cisterns through which they pass. The proximal portion of the arteries, before the posterior communicating artery branch, is referred to as the precommunal, P1 segment, or the mesencephalic artery.
Branches that supply the midbrain and thalamus arise from the proximal peduncular and ambient segments. Paramedian mesencephalic arteries arise from the first 3 to 7 mm of the arteries. The thalamic-subthalamic arteries (also called thalamoperforating ) also arise proximally to supply the paramedian portions of the posteromedial thalamus. The medial posterior choroidal arteries also arise proximally from the peduncular segments and supply the quadrigeminal plate in the midbrain and the choroid plexus of the third ventricle. More distally, the peduncular perforating and thalamogeniculate arteries originate from the ambient segments. These supply the basolateral midbrain and the anterolateral thalamus, respectively. Each consists of a fan of parallel arteries.
Further in their course, after the posterior cerebral arteries have circled the midbrain, the lateral posterior choroidal artery branches arise, which will supply the pulvinar, dorsal thalamus, and the lateral geniculate bodies as well as the choroid plexus of the temporal horns of the lateral ventricles. There are four main cortical branches of the posterior cerebral arteries: the anterior temporal, posterior temporal, parieto-occipital, and calcarine arteries. The anterior temporal arteries arise first from the ambient segments, usually as single arterial trunks or as multiple branches to supply the inferior portion of the temporal lobe. The posterior temporal arteries course posteriorly on the inferior parietal and occipital lobes. The parieto-occipital and calcarine arteries are more variable, usually arising independently from the ambient segments and supplying the occipital and medial inferior parietal lobes. The posterior pericallosal arteries that circle the posterior portion of the corpus callosum to anastomose with the anterior pericallosal artery branches of the anterior cerebral arteries usually arise from the parieto-occipital arteries within the quadrigeminal cisterns.
The anterior choroidal arteries are relatively small arteries that originate from the internal carotid arteries after the origins of the ophthalmic and posterior communicating arteries. The ophthalmic artery projects anteriorly into the back of the orbit, whereas the anterior choroidal and posterior communicating arteries project posteriorly from the internal carotid artery. The anterior choroidal arteries course posteriorly and laterally, running along the optic tract. They first give off penetrating artery branches to the globus pallidus and posterior limb of the internal capsule and then supply branches that course laterally to the medial temporal lobe, and branches that course medially to supply a portion of the midbrain and the thalamus. The anterior choroidal arteries end in the lateral geniculate body, where they join with lateral posterior choroidal artery branches of the posterior cerebral arteries and in the choroid plexus of the lateral ventricles near the temporal horns.
The anterior cerebral arteries are the smaller of the two terminal branches of the internal carotid arteries. They course medially until they reach the longitudinal fissures and then run posteriorly over the corpus callosum. The first portion of the ACA is sometimes hypoplastic on one side, in which case the ACA from the other side supplies both medial frontal lobes. The anterior communicating artery connects the right and left anterior cerebral arteries and provides potential collateral circulation from the anterior circulation of the opposite side.
The horizontal segment of the anterior cerebral artery gives rise to multiple branches. Some course inferiorly to supply the upper surface of the optic nerves and the optic chiasm. Dorsally directed branches penetrate the orbital brain surface to supply the anterior hypothalamus, the septum pellucidum, the medial part of the anterior commissure, the columns of the fornix, and the basal frontal lobe structures (called the anterior perforated substance or substantia innominata). The largest horizontal segment branch is called the recurrent artery of Heubner . It most often arises from the anterior cerebral artery near its junction with the anterior communicating artery. Most often “Heubner's artery” is a group of parallel small arteries rather than a single vessel. They supply the anteromedial portion of the caudate nucleus and the anterior inferior portion of the anterior limb of the internal capsule.
The proximal interhemispheric portions of the anterior cerebral arteries have medial orbitofrontal branches that travel anteriorly along the gyrus rectus to supply the medial part of the orbital gyri and the olfactory bulbs and tracts, and frontopolar artery branches to the superior frontal gyri. The anterior cerebral artery then passes around the genu of the corpus callosum and, in that general location, divides into callosomarginal and pericallosal branches. The callosomarginal artery passes over the cingulate gyrus to course posteriorly within the cingulate sulcus. It supplies anterior, middle, and posterior branches to the medial frontal lobes. The pericallosal artery courses posteriorly, below and parallel to the callosomarginal artery, in a sulcus between the corpus callosum and the cingulate gyrus. It supplies branches to the precuneus and medial superior parietal lobes. The pericallosal artery anastomoses with the pericallosal branch of the posterior cerebral artery variably, usually near the splenium of the corpus callosum.
The middle cerebral arteries arise from the internal carotid artery bifurcation just lateral to the optic chiasm. The “mainstem” (M1) portion of the arteries courses horizontally in a lateral direction to enter the sylvian fissure. Three to six medial and lateral lenticulostriate arteries arise from the mainstem middle cerebral artery and penetrate the anterior perforated substance to supply the basal ganglia and deep portions of the cerebral hemispheres. The medial lenticulostriate arteries supply the outer portion of the globus pallidus and the medial parts of the caudate nucleus and putamen. The lateral lenticulostriate arteries supply the lateral portion of the caudate nucleus, the putamen, the anterior portion and genu of the internal capsule, and the adjacent corona radiata. Anterior temporal and frontopolar branches arise from the mainstem middle cerebral artery after the lenticulostriate origins.
As they near the sylvian fissures, the middle cerebral arteries divide into large superior and inferior divisions (referred to as M2 portions). The superior division supplies the lateral portions of the cerebral hemispheres above the sylvian fissures, and the inferior division supplies the temporal and inferior parietal lobes below the sylvian fissures. These main divisions turn upward around the inferior portion of the insula of Reil to continue upward and backward in the deepest part of the sylvian fissure between the outer surface of the insula and the medial surface of the temporal lobe. The superior division of the middle cerebral artery has lateral orbitofrontal, ascending frontal, rolandic, and anterior and posterior parietal branches. When the mainstem of the middle cerebral artery is short, the lenticulostriate branches may arise from the proximal portion of the superior division. The inferior division provides posterior temporal and angular branches to supply the lateral portions of the cerebral hemispheres below the sylvian fissures.
The meningeal arteries and veins are located along the outer portion of the dura, grooving the inner table of the skull. They supply the dura, the adjacent bony structures, and form anastomoses across both sides of the skull and with cerebral arteries. Their major clinical importance is (1) injuries to the skull, especially fractures, can cut across meningeal arteries, leading to epidural hemorrhages that require urgent drainage, and (2) meningiomas are often fed by meningeal arteries. Contrast opacification of meningeal arteries is often diagnostic in confirming that lesions are meningiomas, and interventional blockage of these feeding arteries can lead to shrinkage of a meningioma.
The middle meningeal artery, originating from the external carotid system via the external maxillary artery, is the largest of the meningeal arteries. It supplies the major blood supply to the dura mater and arises from the maxillary artery and ascends just lateral to the external pterygoid muscle to enter the calvarium through the foramen spinosum. The middle meningeal artery then passes forward and laterally across the floor of the middle cranial fossa and divides into two branches below the pterion. The frontal (anterior) branch climbs across the greater wing of the sphenoid and parietal bone, forming a groove on the inner table of the calvaria and then dividing into two branches that supply the outer surface of the dura from the frontoparietal convexity to the vertex and as far posteriorly as the occiput. The smaller parietal (posterior) branch curves backward over the temporal region to supply the posterior part of the dura mater.
The accessory meningeal artery may also arise from the maxillary artery or from the middle meningeal artery. It ascends through the foramen ovale to supply the trigeminal ganglion and the adjacent dura within the middle cranial fossa.
The bone and dura of the posterior fossa are supplied by (1) the meningeal branches of the ascending pharyngeal artery, which pass through the jugular foramen, foramen lacerum, and the hypoglossal canal; (2) the meningeal branches of the occipital artery, which pass through the jugular foramen and the condylar canal; and (3) the small mastoid branch of the occipital artery, which passes through the mastoid foramen.
Branches of the Internal Carotid System. The meningohypophyseal trunk has three major branches. The tentorial branch enters the tentorium cerebelli at the apex of the petrous bone, supplying the anterolateral free margin of the tentorial incisura and the base of the tentorium near the attachment to the petrous bone. A dorsal branch supplies the dura mater of the dorsum sella and clivus, sending small twigs to supply the dura around the internal auditory canal. The artery to the inferior portion of the cavernous sinus originates from the lateral aspect of the cavernous segment of the internal carotid artery.
An anterior meningeal artery arises from the anterior aspect of the cavernous carotid artery and passes over the top of the lesser wing of the sphenoid to supply the dura of the floor of the anterior fossa.
As the ophthalmic artery passes medially and then above the optic nerve, it gives off a lacrimal branch . The recurrent meningeal artery arises from this branch and passes through the superior orbital fissure to supply the dura of the anterior wall of the middle cranial fossa.
The ophthalmic artery also provides several ethmoidal branches. The posterior ethmoidal artery leaves the orbit to supply the posterior ethmoid air cells and the dura of the planum sphenoidale and the posterior half of the cribriform plate. The anterior ethmoidal artery passes through the anterior ethmoidal canal to supply the mucosa of the anterior and middle ethmoidal air cells and the frontal sinus. It then enters the cranial cavity, where it gives off an anterior meningeal branch ( anterior falx artery ) to the dura mater and the anterior portion of the falx cerebri.
Branches of the Vertebral Artery . The meningeal branches enter the skull through the foramen magnum. The anterior meningeal branch originates from the distal part of the second segment of the vertebral artery just before its lateral bend at the level of the atlas. It ascends and passes anteromedially to supply the dura of the anterior margin of the foramen magnum. The posterior meningeal branch arises from the third segment of the vertebral artery between the atlas and the foramen magnum. It passes between the dura and the calvaria, supplying the posterior rim of the foramen magnum, the falx cerebelli, and the posteromedial portion of the dura of the posterior fossa.
Strokes are divided into two broad categories: hemorrhage and ischemia. Hemorrhage refers to bleeding inside the skull into the brain or cerebrospinal fluid or membranes surrounding the brain. Brain ischemia refers to insufficient blood flow. Hemorrhage and ischemia are polar opposites. Hemorrhage is characterized by too much blood inside the skull, and in ischemia, there is not enough blood supply to allow continued normal functioning of the effected brain tissue. Brain ischemia is much more common than hemorrhage. About four fifths of strokes are ischemic.
The four designations of hemorrhage are named for their locations. Hemorrhages within brain substance (inside the pia mater) are called intracerebral hemorrhages ; those between the pia mater and arachnoid are labeled subarachnoid hemorrhages . Hemorrhages outside the arachnoid but inside the dura mater are called subdural hemorrhages , and hemorrhages outside the dura mater but inside the skull are called epidural hemorrhages . The different sites of bleeding have different causes.
Intracerebral hemorrhages develop gradually and are located between normal brain tissues. The bleeding is due to rupture of small blood vessels, arterioles, and capillaries within the brain substance. The bleeding is most often due to uncontrolled hypertension. Bleeding disorders, vascular malformations, and fragility of blood vessels, for example, due to infiltration with amyloid in cerebral amyloid angiopathy, are other common causes. The blood usually oozes into the brain under pressure and forms a localized hematoma . The hematoma separates normal brain structures and interrupts brain pathways. Hematomas also exert pressure on brain regions adjacent to the collection of blood and can injure these tissues. Large hemorrhages are often fatal because they increase pressure within the skull compressing the brainstem.
Subarachnoid hemorrhages are usually caused by rupture of an aneurysm that breaks, spilling blood instantly into the spinal fluid. The sudden release of blood under arterial pressure increases intracranial pressure, causing severe sudden-onset headache, often with vomiting and often a lapse in brain function so that the patients may stare, drop to their knees, or become confused and unable to remember. The symptoms in patients with subarachnoid hemorrhage relate to diffuse abnormalities of brain function because usually there is no bleeding into one part of the brain. In contrast, in patients with intracerebral hemorrhages, the hematoma is localized and causes loss of function related to the area damaged by the local blood collection.
Subdural and epidural hemorrhages are most often caused by head injuries that tear blood vessels. In subdural hemorrhages, the bleeding is usually from veins located between the arachnoid and the dura mater. In epidural hemorrhages, the bleeding most often results in tearing of meningeal arteries. The tear is often caused by a skull fracture. Arterial bleeding develops faster than venous bleeding so that symptoms develop sooner after head injury in patients with epidural hemorrhages. In subdural hemorrhages, the bleeding can be slow so that symptoms may be delayed for weeks after head injury.
Insufficient blood supply to the brain is called ischemia. When ischemia is prolonged, it leads to death of tissue— infarction.
There are three different major categories of brain ischemia— thrombosis, embolism, and systemic hypoperfusion; each indicates a different mechanism of blood vessel injury or reason for decreased blood flow. The difference between these mechanisms is easiest to understand by using an analogy to house plumbing. Suppose, turning on the faucet in the second floor bathroom results in no flow, or instead, water dribbles out. The malfunctioning could be due to a local problem, such as rust buildup in the pipe supplying that sink. This is analogous to thrombosis, a term used to describe a local problem that involves an artery supplying the brain. Atherosclerosis or another condition often narrows the arterial lumen. When the lumen becomes very narrow, blood flow is severely reduced, causing localized stagnation of the blood column. This change in flow causes blood to clot, resulting in total arterial occlusion. This is a local problem in one pipe; a plumber would try to fix the damaged blocked pipe. Similarly, treating physicians could try to open or bypass a stenotic or occluded artery.
Alternatively, blockage of that second floor sink pipe could be due to debris in the water system that came to rest in that pipe rather than a local problem that began within the pipe. A neck or cranial artery supplying the brain can become blocked by thrombi or other particulate matter that breaks loose from a downstream site. The source could be from the heart, the aorta, or from a major artery in the neck or head located before the blocked artery along the same circulatory pathway. The process of particles breaking loose and blocking a distant artery is known as embolism . The source of the material is called the donor site, and the receiving vessel is called the recipient site. The material is called an embolus , and the process is called embolism . Treatment of embolism could involve unblocking the recipient artery but also trying to prevent further embolization.
Another reason for poor flow in the second floor sink might be a general problem with the water tank, water pump, or water pressure. In that case, flow through all pipes in the house should be affected. Turning on the faucets elsewhere in the house will reveal the nature of the problem. In the body, this type of problem is called systemic hypoperfusion . Abnormal cardiac performance could lead to low pressure in the system. Abnormally slow or fast heart rhythms, cardiac arrest, and failure of the heart to pump blood adequately can all lead to diminished brain perfusion. Hypotension and hypoperfusion due to an inadequate amount of fluid in the vascular compartment of the body are other causes. Bleeding, dehydration, and shock all lead to inadequate brain perfusion. This would be akin to having a very low water tank.
In patients with brain embolism and thrombosis, one artery is usually blocked, leading to dysfunction of the part of the brain supplied by that blocked artery. This causes focal abnormalities of brain function, such as aphasia or hemiparesis. These abnormalities are similar to those found in patients with local brain hematomas. In contrast, systemic hypoperfusion leads to more diffuse abnormalities, such as light-headedness, dizziness, confusion, dimming of vision and hearing, and so forth. Patients appear pale and generally weak. These symptoms are attributable to a generalized reduction in blood flow and not to loss of function in one local brain region.
In intracerebral hemorrhage patients, symptoms and signs gradually develop over minutes or hours. Improvements and fluctuations do not occur during this time. In aneurysmal subarachnoid hemorrhage, symptoms begin instantaneously. In ischemia, the severity of the decreased perfusion, the ability of collateral circulation to accommodate for blockages, and the vulnerability of various brain structures vary greatly. Arteries bring oxygen, sugar, and other nutrients necessary for survival of the brain. The underperfusion can be temporary, resulting in a focal deficit that lasts only a few minutes; these episodes are referred to as transient ischemic attacks (TIAs) . At times the ischemia is sufficient to cause more persistent symptoms and signs but not sufficient to cause brain infarction. Brain tissue is stunned but can recover if the supply of nutrients is restored soon enough. In ischemic patients, the time course varies and can fluctuate with periods of improvement, worsening, and stabilization.
Transient ischemic attacks are very important to recognize. Many studies show that patients with TIAs have a high risk of having a stroke during the succeeding hours and days. TIAs demand urgent diagnosis and management of the cause. TIAs provide a window of opportunity for clinicians to intervene before a stroke happens, and strokes do happen often in patients who have had TIAs. Most TIAs are very brief, lasting minutes and usually less than an hour. Recent magnetic resonance imaging (MRI) studies of patients with clinical TIAs who have no residual symptoms or signs shows that many actually have had brain infarcts—strokes. The distinction between TIAs and strokes is blurred and has been overemphasized in the past. Many clinicians now prefer the term acute ischemic cerebrovascular syndrome, which includes both TIAs and acute strokes. Management depends on the nature, location, and severity of the causative cardiocerebrovascular-hematologic cause of the brain ischemia. Finding the cause and treating it is much more important than characterizing the time course.
Therapeutic strategies relate to four different time epochs. Prevention involves strategies of identifying and controlling potential risk factors before a stroke occurs. Strategies during acute ischemia involve reperfusion of the ischemic area and neuroprotection (rendering the ischemic area more resistant to infarction). After a stroke, recovery and rehabilitation are facilitated.
The most important diagnostic information is gained from a thorough history from the patient and sometimes a loved one or a colleague, with subsequent thoughtful vascular and neurologic examinations. The history is directed to answering what (the cause of the condition—the pathology and pathophysiology) and where (brain and vascular location) queries. The neurologic symptoms and signs and vascular examinations yield information about the where question. The differential diagnosis of the what question depends on information from the history about (1) the time and activity at and before the onset of symptoms; (2) the course of the symptoms—transient, gradually progressive, remitting, fluctuating, and so forth; (3) the past and present known medical and surgical conditions, especially hypertension, diabetes, heart disease, smoking, excess alcohol intake, drug use, peripheral vascular disease, and obesity; (4) past strokes; (5) the presence, nature, and timing of any transient ischemic attacks; (6) headache before, at, or after stroke onset; and (7) the occurrence of a seizure, vomiting, or change in level of consciousness.
All stroke suspects require blood tests with brain and vascular imaging. A complete blood count (CBC), including platelet count, blood sugar, blood urea nitrogen or creatinine with a glomerular filtration rate, and a prothrombin time or international normalized ratio (INR) are obtained. The brain and the arteries that supply it and the veins that drain it can be imaged using either computed tomography (CT) or MRI. The questions to be answered by brain and vascular imaging are (1) Is/are the brain lesion(s) caused by ischemia or hemorrhage, or is it related to a nonvascular stroke mimic? (2) Where is/are the brain lesion(s), and what is/are its/their size, shape, and extent? (3) What are the nature, site, and severity of the vascular lesion(s), and how does/do the vascular lesion(s) and brain perfusion abnormality(ies) relate to the brain lesion(s)?
CT is readily available in most hospitals and reliably demonstrates the presence or absence of intracerebral hemorrhage. Immediately after the onset of bleeding, intracerebral hematomas (ICHs) are seen on CT as well-circumscribed areas of high density with smooth borders. Edema develops within the first days and is seen as a dark rim around the white hematoma. Subarachnoid bleeding is demonstrated by a high-density signal within the cerebrospinal fluid and brain cisterns. Early signs of brain infarction include obscuring of the basal ganglia density, blurring of the distinction between the grey matter of the cerebral cortex and the underlying white matter, and loss of definition of the insular cortex. Later, infarction appears as a low-density lesion. Specific vascular abnormalities include hyperdense arteries, indicating thrombosis or slow flow and calcific emboli within arteries. The signs of infarction on CT scans are often subtle when images are taken within several hours of the onset of symptoms. Viewing images on a computer with the ability to vary the contrast helps identify subtle abnormalities and asymmetries.
Diffusion-weighted MRI images (DWI) and fluid-attenuated inversion recovery (FLAIR) images are particularly useful and sensitive for detection of acute brain infarcts. Infarcted areas appear bright on DWI and dark on apparent diffusion coefficient (ADC) images. The location, pattern, and multiplicity of DWI ischemic lesions help to suggest the most likely causative stroke mechanism. DWI positivity wanes during the first 7 to 10 days after stroke onset. Lesions seen on DWI images (and confirmed by ADC) usually, but not always, correspond to areas of infarction. T2-weighted scans show established infarcts as bright. MRI can also accurately show ICH, especially when echo-planar gradient-echo susceptibility-weighted images (T2*) are performed. These T2*-weighted (susceptibility) images can also show thrombi within intracranial arteries and dural sinuses and veins.
Vascular imaging can be performed using CT (CT angiography [CTA]) or MR (MR angiography [MRA]), or by using ultrasound. CTA and MRA images can be obtained concurrently with the respective primary brain imaging. CTA requires intravenous dye infusion. The neck and intracranial arteries and veins can be shown well by either technique. Duplex ultrasound, which includes a B-mode image combined with a pulsed Doppler spectrum analysis, can accurately show occlusive lesions within neck arteries. Transcranial Doppler ultrasound (TCD) involves insonation of intracranial arteries by measuring blood flow velocities using a probe placed on the orbit, temporal bone, and foramen magnum. Areas of narrowing or occlusion can be detected; these probes also provide a means to monitor for embolic materials passing under them. Dye contrast digital angiography shows neck and intracranial arteries in more detail than CTA and MRA and is now used to clarify vascular lesions not shown well by these screening techniques; it is also pursued at the time of intravascular interventions, such as coiling of aneurysms, stenting, and intra-arterial thrombolysis or mechanical clot extraction. In patients in whom strokes cause seizures, electroencephalography (EEG) can be helpful.
Treatment of acute stroke patients depends heavily on the type and cause of the stroke. In subarachnoid hemorrhage patients, aneurysms and vascular malformations can be controlled by cranial surgical clipping or coiling through an intravenous interventional approach. The vasoconstriction that follows bleeding and surgery also is a target for therapy. In patients who have had an intracerebral hemorrhage , blood pressure control, reversal of bleeding diatheses, and drainage of space-taking hematomas, especially those that are lobar and near the surface, are the major therapeutic strategies.
In patients with acute brain ischemia, attention is directed toward reperfusing ischemic zones. When a thromboembolus blocks an artery, intravenous or intra-arterial thrombolysis can be pursued; alternatively, mechanical devices or stenting of blocked arteries can also lead to recanalization. Maximizing collateral blood flow by attention to blood pressure and blood volume can augment perfusion of the ischemic zone. Anticoagulants (heparins, warfarin, and direct thrombin antagonists and factor X inhibitors) can be given to prevent propagation and embolization of clots.
In addition to treating the acute stroke, attention must be directed toward prevention of future strokes. Identifying and modifying potential risk factors is essential. Pharmacologic treatment using antihypertensives, statins, and agents that alter platelet function are the mainstays of prophylaxis of brain ischemia. In those patients who have residual deficits after stroke, recovery and rehabilitation are optimized.
Although atherosclerotic abnormalities of brain supplying arteries are the most frequent causes of stroke, many other etiologies need consideration, especially in young individuals and those who do not have risk factors for atherosclerosis. Evaluation of the heart, neck and intracranial arteries and veins, and the blood are important in all patients with stroke and transient ischemic attacks. The most common conditions are brain embolism arising from the heart, especially in patients with arrhythmias and valvular disease; dissections of neck and intracranial arteries; emboli from aortic plaques, various vascular anomalies and malformations, and blood disorders that promote excess clotting or bleeding. A partial list of conditions follows.
Cardiac. A variety of different heart conditions serve as donor sources for brain embolism. Cardiac pump failure can lead to ischemic brain damage through systemic hypoperfusion. Other cardiac lesions cause strokes by providing a source of embolism to the brain: valvular conditions —rheumatic, calcific, infectious endocarditis, and noninfective fibrotic lesions (Libman-Sacks endocarditis associated with systemic lupus erythematosus and similar valvular lesions in patients with cancer and antiphospholipid antibodies), mitral annulus calcifications, and artificial surgically implanted mechanical and biological valves; myocardial abnormalities —myocardial infarcts, myocarditis, myocardiopathies; arrhythmias —atrial fibrillation, sick sinus syndrome; neoplasms —myxomas, fibroelastomas; and septal abnormalities —atrial septal defects, patent foramen ovale.
Arteries. Vascular conditions can also predispose to artery-to-artery embolism as well as causing localized ischemia due to decreased perfusion. Some vascular lesions promote bleeding. Aortic atheromas, especially those that are mobile and protruding, may on occasion lead to a stroke. Arterial dissection in either the carotid or vertebral artery system requires careful consideration. These often occur related to seemingly benign problems, such as a paroxysm of vomiting, or athletic injuries, such as from wrestling, skiing accidents, falls from horses, and so forth. Other unusual primary vascular lesions include fibromuscular dysplasia, arteritis, moyamoya syndrome, Takayasu arteritis, and severe migraine. Certain quite rare genetic conditions require consideration in the differential diagnosis of stroke. These include CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), Ehlers-Danlos syndrome, pseudoxanthoma elasticum, progeria, and cerebral amyloid angiopathy. Vascular malformations —aneurysms, arteriovenous malformations, cavernous angiomas, developmental venous anomalies, varices—predispose to bleeding. Infections, such as with herpes zoster varicella virus, can invade blood vessels and cause stroke. Meningitis sometimes causes arterial inflammation and strokes.
Hematologic. Increase in coagulability is seen due to decreased amounts of usual inhibitors: protein S, protein C, antithrombin, activated protein C–resistance, sickle cell disease, and other hemoglobinopathies; severe anemia; thrombocythemia; thrombocytosis; and bleeding disorders —thrombocytopenia, hemophilia, and prescription of antithrombotic agents.
Veins. Thrombosis of the dural sinuses, especially the superior sagittal sinus and the lateral sinus, are often associated with brain infarction, brain edema, and brain hemorrhage. Occlusion of deep veins is an important cause of stroke in the young. Occlusion of veins on the surface of the brain can also cause infarction and seizures.
The most common etiology of internal carotid artery disease is atherosclerosis, predominantly occurring in Caucasians and the elderly. Other etiologies include arterial dissection, fibromuscular dysplasia, and giant cell arteritis.
Atherosclerosis causes stenosis or occlusion of extracranial and intracranial arteries and is directly responsible for a significant percentage of cerebral ischemic events. Atheroma formation involves the progressive deposition of circulating lipids and ultimately fibrous tissue in the subintimal layer of the large and medium arteries, occurring most frequently at branching points. Plaque formation is enhanced by blood-associated inflammatory factors as well as increased shear injury from uncontrolled blood pressure. Intraplaque hemorrhage, subintimal necrosis with ulcer formation, and calcium deposition can cause enlargement of the atherosclerotic plaque with consequent worsening of the degree of arterial narrowing.
Disruption of the endothelial surface triggers thrombus formation within the arterial lumen through activation of nearby platelets by the subendothelial matrix. When platelets become activated, they release thromboxane A 2 , causing further platelet aggregation. The development of a fibrin network stabilizes the platelet aggregate, forming a “white thrombus.” In areas of slowed or turbulent flow within or around the plaque, the thrombus develops further, enmeshing red blood cells (RBCs) in the platelet-fibrin aggregate to form a “red thrombs.” This remains poorly organized and friable for up to 2 weeks and presents a significant risk of propagation and embolization. Either the white or red thrombus, however, can dislodge and embolize to distal arterial branches.
The main risk factors for carotid artery atherosclerotic disease are arterial hypertension, diabetes, hypercholesterolemia, and smoking. Frequent sites for anterior circulation atherosclerosis are the origin of the internal carotid artery (ICA) , the carotid siphon, and the mainstems of the middle cerebral artery (MCA) and anterior cerebral artery (ACA) (see Plate 9-10 ). The internal carotid artery at or around the bifurcation is usually affected in Caucasians, whereas in Asian, Hispanic, and African-American populations, intracranial atherosclerosis is more common than carotid artery disease in the neck.
Dissection of the extracranial ICA usually occurs in patients between age 20 to 50 years and commonly involves its pharyngeal and distal segments. Dissection occurring between the intima and media usually causes stenosis or occlusion of the affected artery, whereas dissection between the media and adventitia is associated with aneurysmal dilation (see Plate 9-11, A and B ). Congenital abnormalities in the media or elastica of the arteries as seen in Marfan syndrome, fibromuscular dysplasia, osteogenesis imperfecta, and cystic medial necrosis can predispose patients to arterial dissection. Although often associated with acute trauma, arterial dissection may result from seemingly innocuous incidents, such as a fall while hiking or skiing, sports activities (particularly wrestling or diving into a wave), and paroxysms of coughing that stretch the artery.
Spontaneous intracranial ICA dissections are uncommon when compared with dissections of its cervical portion. Although early reports described a very poor prognosis with extensive strokes and very high mortality, more recent studies have shown a relatively better outcome, with patients surviving with few or moderate deficits. Imaging studies usually show narrowing of the supraclinoid ICA, with extension to the MCA or ACA and, less commonly, aneurysm formation (see Plate 9-11, C to F ).
Fibromuscular dysplasia is a nonatherosclerotic noninflammatory angiopathy characterized by fibrodysplastic changes of unclear etiology. It occurs predominantly in women of childbearing age and often affects the neck arteries, most often the pharyngeal portion of the internal carotid artery. Intracranial disease is much rarer. The lesions have a characteristic beaded appearance that can be detected on magnetic resonance angiography (MRA), computed tomography angiography (CTA), or conventional angiograms (see Plate 9-11, G ). Fibromuscular dysplasia is a predisposing factor for spontaneous cervical carotid dissections and consequent strokes; however, strokes can also be caused by thromboembolism secondary to the fibromuscular dysplasia.
Giant cell arteritis is a common form of systemic vasculopathy affecting patients older than 50 years. Although it typically involves the temporal, maxillary, and ophthalmic arteries, it can rarely affect the siphon of the internal carotid artery, sometimes producing bilateral stenosis.
TIAs in patients with carotid artery disease usually precede stroke onset by a few days or months. TIAs caused by intra-arterial embolism from a carotid source are not stereotypical, and symptoms vary depending on which ICA branch is involved. In contrast, hemodynamic “limb-shaking” TIAs are often stereotypical and posturally related and are usually seen in patients with high-grade ICA stenosis or occlusion. In this classic example of hemodynamic ischemia, patients have recurrent, irregular, and involuntary movements of the contralateral arm, leg, or both, usually triggered by postural changes and lasting a few minutes.
Another important clue to ICA disease is the development of episodes of transient monocular blindness (TMB) (see Plate 9-12 ). TMB refers to the occurrence of temporary unilateral visual loss or obscuration that is described by careful observers as a horizontal or vertical “shade being drawn over one eye,” but most frequently as a “fog” or “blurring” in the eye lasting 1 to 5 minutes. It often occurs spontaneously but at times is triggered by position changes. Positive phenomena, such as sparkles, lights, or colors evolving over minutes, are typical of migrainous phenomenon and help to differentiate such benign visual changes from the more serious TMB, a frequent harbinger of cerebral infarct within the carotid artery territory. Rarely, with critical ipsilateral internal carotid stenosis, gradual dimming or loss of vision when exposed to bright light, such as glare from snow on a sunlit background, can be reported and is due to limited vascular flow in the face of increased retinal metabolic demand.
Strokes from intra-arterial embolism from ICA disease are usually cortically based (see Plate 9-12 ). Symptoms depend on whether branches of the MCA, ACA, or both are involved (see Plate 9-13 ). The posterior cerebral artery (PCA) territory may rarely be affected by intra-arterial emboli from ipsilateral ICA stenosis or occlusion in patients with a persistent fetal PCA originating from the ICA.
Neurologic findings vary by the location of the occlusion and the adequacy of collateral circulation. A large MCA territory stroke is usually seen in patients with MCA mainstem occlusion without good collateral flow, whereas deep or parasylvian strokes are the most common presentation when enough collateral flow is present over the convexities. Contralateral motor weakness involving the foot more than the thigh and shoulder, with relative sparing of the hand and face, is the typical manifestations of distal ACA branch occlusion. Conversely, prominent cognitive and behavioral changes associated with contralateral hemiparesis predominate in patients with proximal ACA occlusions, due to involvement of the recurrent artery of Huebner.
Hemodynamic strokes usually involve the border zone territory between ACA and MCA (anterior border zone), MCA and PCA (posterior border zone), or between deep and superficial perforators (subcortical border zone) and cause the typical clinical symptoms outlined in Plate 9-12 .
Although TIAs can occur in intrinsic occlusive disease of the MCA and ACA , they are not as common as in patients with ICA disease and usually occur over a shorter period of hours or days. When strokes occur, initial symptoms are typically noticed on awakening and often fluctuate during the day, supporting a hemodynamic mechanism.
Isolated infarction of the anterior choroidal artery territory is not common. The classic clinical presentation includes hemiplegia, hemianesthesia, and homonymous hemianopsia, but incomplete forms of this syndrome are more frequently seen. Left-sided spatial neglect and mild speech difficulties may accompany right- and left-sided lesions, respectively. Small vessel disease is the most common mechanism of anterior choroidal strokes; however, large strokes in this territory have also been associated with cardioembolism and ipsilateral intracranial carotid artery disease.
Ipsilateral pain involving the eye, temple or forehead, and ipsilateral Horner syndrome secondary to involvement of sympathetic fibers along the wall of the internal carotid artery are common in patients with extracranial carotid dissection, and its presence helps with the clinical diagnosis. TIAs and/or strokes usually occur several days after onset of symptoms and are usually caused by intra-arterial embolism.
Severe retro-orbital or temporal headaches are also frequent in patients with intracranial dissections; however, the neurologic signs, most commonly a contralateral hemiparesis, tend to follow almost immediately the headache's onset. Neurologic deficits tend to fluctuate within the first two weeks of onset of symptoms, probably reflecting cerebral hypoperfusion.
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