4
27
The arterial supply to the brain consists of four large vessels – two (right and left) internal carotid arteries and two vertebral arteries (Fig. 4.1). The brain itself is per-fused by two kinds of arteries, large-diameter arteries that lead from the inferior por-tion of the brain over the lateral surfaces of the cerebral hemispheres, brain stem, and cerebellum, and penetrating arteries that branch from these large surface arteries and enter the brain parenchyma to supply specific areas. There are also interconnecting arteries at the base of the brain that form the circle of Willis (Fig. 4.2).
Internal carotid
Basilar
Vertebral Middle
cerebral
Figure 4.1 Schematic lateral view of the brain showing the major arterial vessels. The internal carotid gives rise to the anterior and middle cerebral arteries. The vertebral–basilar arteries constitute the posterior circulation including the posterior cerebral hemispheres, brain stem, cerebellum, and medial subcortical structures.
Carotid system
The carotid arteries supply anterior portions of the brain. The right common carotid artery branches from the innominate artery while the left common carotid artery branches directly from the aortic arch. These vessels course upward in the neck and bifurcate approximately at the angle of the jaw to form the internal and external carotid arteries. The internal carotid artery then passes up to the base of the skull and through the carotid canal. It traverses the cavernous sinus after enter-ing the skull and sends tiny branches to the eye and the optic nerve as well as the pituitary, trigeminal nerve, and middle ear.
The posterior communicating artery is the next branch and runs posteriorly con-necting with the posterior cerebral artery (Fig. 4.2). The anterior choroidal artery sup-plies portions of the hippocampus, caudate nucleus, and amygdala as well as portions of the basal ganglia (Fig. 4.3). The internal carotid artery then bifurcates into two main branches: the middle cerebral artery and the anterior cerebral artery (Fig. 4.2). These two arteries provide the blood supply for all of the anterior cerebral hemispheres.
The anterior cerebral arteries course forward into the interhemispheric fissure just above the optic chiasma and then pass upward and around the corpus callosum over the medial surface of the cerebral hemispheres (Fig. 4.4). These branches
28 Introduction
Anterior cerebral
Medial striate
Anterior communicating Internal carotid Middle cerebral
Posterior communicating
Superior cerebellar
Posterior cerebral
Basilar
Figure 4.2 The circle of Willis connecting the anterior internal carotid circulation with the posterior circulation. The posterior communicating arteries lie at the base of the brain and allow internal carotid artery to supply some posterior cerebral brain regions (modified from R. G. Clark, Clinical Neuroanatomy and Neurophysiology, FA Davis, Philadelphia, 1975, with permission).
29 Vascular anatomy and classification of stroke
Lateral ventricle Caudate nucleus Thalamus Putamen Globus pallidus Third ventricle
Anterior cerebral artery Middle cerebral artery
Anterior choroidal artery Posterior cerebral artery
Figure 4.3 A schematic coronal view of the brain taken through the temporal and parietal cortex and thalamus. The overlapping regions subserved by anterior and middle cerebral arteries (internal carotid circulation) and posterior cerebral arteries (posterior circulation) are demonstrated.
Anterior cerebral
Middle cerebral Lenticulostriate Anterior communicating Bifurcation of
internal carotid
Figure 4.4 The anterior and middle cerebral artery circulation demonstrating the medial course of the anterior cerebral artery along the interhemispheric separation and the lenticulostriate arteries which penetrate the brain to provide circulation to the basal ganglia (modified from R. G. Clark, Clinical Neuroanatomy and Neurophysiology, FA Davis, Philadelphia, 1975, with permission).
supply blood to the anterior medial and superior portions of the frontal lobes.
A large branch of the anterior cerebral artery, called the medial striate or Heubner’s artery, penetrates the brain substance and often supplies the internal capsule and anterior portions of the basal ganglia.
The anterior communicating artery connects the two anterior cerebral arteries (Fig. 4.4). Penetrating branches of the anterior cerebral artery may reach the ante-rior thalamus and anteante-rior portions of the basal ganglia.
The middle cerebral artery courses laterally along the base of the hemisphere emerging through the Sylvian fissure where its branches spread over the lateral surface of the cerebral hemispheres (Fig. 4.1). The middle cerebral artery usually divides into two or three large branches which course over the cerebral hemispheres and give rise to as many as 20 penetrating branches. These are called the lenticulos-triate arteries which supply the lateral portion of the basal ganglia, the lateral por-tion of the thalamus, and the posterior limb of the internal capsule (Fig. 4.4).
The middle cerebral artery supplies the bulk of the cerebral hemispheres, including the motor and sensory cortex for the hand, arm, shoulder, face, tongue, and portion of the leg (Fig. 4.1). Most strokes occur within the distribution of the middle cerebral artery and occlusion may cause varying degrees of weakness and sensory loss in the shoulder, arm, hand, face, and lower extremity on the opposite side of the body. When the dominant cerebral hemisphere (usually the left hemi-sphere) is damaged by middle cerebral artery occlusion, speech may be impaired.
Occlusion of the penetrating branches of the middle cerebral artery gives rise to a variety of clinical syndromes, depending on the size of the artery and the specific area of brain infarcted.
Vertebral–basilar system
The posterior portion of the brain is supplied by the vertebral system. The verte-bral arteries arise from the subclavian arteries and ascend through the verteverte-bral canal and the foramen magnum to enter the skull. At the rostral end of the medulla, they unite to form the basilar artery which courses the full length of the pons to the midbrain (Fig. 4.2). Connections between the posterior circulation (i.e., the vertebral–basilar system) and the anterior circulation (i.e., the carotid sys-tem) occur by way of the posterior communicating arteries. The basilar–vertebral arteries supply the brain stem and cerebellum. The vertebral–basilar system sup-plies both midline brain stem structures as well as circumferential arteries which pass around the brain stem and supply the dorsal portions of the brain stem.
The posterior–inferior cerebellar artery is usually the last branch of each verte-bral artery while the anterior–inferior cerebellar artery arises from the basilar artery. The superior cerebellar artery arises close to the rostral end of the basilar
30 Introduction
artery and supplies large portions of the cerebellar hemispheres. The posterior cerebral arteries become the terminal branches of the basilar artery (Fig. 4.2). The two posterior cerebral arteries encircle the brain stem and supply branches to the cerebellar peduncles, the geniculate bodies, posterior portions of the thalamus, the medial portion of the occipital lobes, and the inferior–medial portion of the temporal lobes (Fig. 4.3). The most distal branches supply the calcarien cortex (primary visual cortex).
Venous system
The venous drainage consists of a superficial system and a deep system. Both of these venous drainage systems enter into a collecting system of large channels called sinuses which in turn drain into the internal jugular veins that leave the skull through the jugular foramina and eventually empty into the superior vena cava.
The superficial venous system consists of surface veins that carry blood into the superior saggital sinus, the cavernous sinus, and the transverse and petrosal sinuses.
The deep venous system generally empties into large veins in the interventricu-lar foramen of Monroe, several veins join to form the internal cerebral vein which joins the inferior saggital sinus. The inferior saggital sinus also collects blood from basal areas of the preoptic region and hypothalamus. The superior saggital sinus courses over the brain between the hemispheres, the inferior saggital sinus forms the straight sinus, while the transverse sinus is located in the fixed lateral margin of the tentorium cerebella. The cavernous sinuses are paired venous spaces in the dura on either side of the sella turcica receiving blood from the orbit by way of the thalamic veins.
The most clinically important abnormalities of the venous system include thrombolic occlusion of the superior saggital sinus which may impair acceptance of cerebral spinal fluid. Thrombosis of the transverse sinus may be caused by dis-ease of the temporal bone. Occlusion of the deep cerebral veins may be caused by hemorrhage of deep cerebral structures. Infections may enter the brain through the venous system, such as sepsis within the orbit or nasal bacteria entering the cavernous sinus leading to swelling of orbital brain tissue.
Classification of cerebrovascular disease
There are many ways to classify the wide range of disorders that are called stroke.
On the one hand, cerebrovascular disease can be understood as an anatomical–
pathological process of the blood vessels that have been discussed. This would lead to a classification based on the etiologies of underlying anatomical–pathological processes. Such a classification would include an extensive list of diseases, including 31 Vascular anatomy and classification of stroke
those with infectious, connective tissue, neoplastic, hematological, pharmacologi-cal, and traumatic causes. Alternatively, a classification of stroke could be based on the mechanism by which these vascular pathological processes manifest themselves.
For example, the interactive effects of systemic hypertension and atherosclerosis on the resilience of large arteries, integrity of vessel lumens, and production of end-organ ischemia might be one mechanistic classification of stroke. Another might be the formation of aneurysm dilatations or vascular disease or the effect of cardiac arrhythmias on the propagation of thromboemboli.
From the perspective of schematizing the emotional disorders associated with stroke, however, probably the most pragmatic way of classifying cerebrovascular disease is not to focus on the anatomical–pathological process or the interactive mechanisms but to examine the means by which parenchymal changes in the brain occur (Table 4.1). Using this classification, the first major category is ischemia which occurs in about 80–85% of patients with symptomatic cerebrovascular dis-ease. Ischemia may occur either with or without infarction of parenchyma, and includes transient ischemic attacks (TIAs), atherosclerotic thrombosis, cerebral embolism, and small lacunar infarction. The second major category is hemorrhage which occurs in about 15–20% of patients with symptomatic cerebrovascular dis-ease. Hemorrhage may cause either direct parenchymal damage by extravasation of blood into the surrounding brain tissues as in intracerebral hemorrhage (ICH),
32 Introduction
Table 4.1. Classification of cerebrovascular disease Ischemic disorders
• Infarction
1. Atherosclerotic thrombosis 2. Cerebral embolism 3. Lacunae
4. Other causes: arteritis (e.g., infectious or connective tissue disease), cerebral thrombophlebitis, fibromuscular dysplasia, and venous occlusions
• TIAs
Hemorrhagic disorders
• Intraparenchymal hemorrhage 1. Primary (hypertensive) ICH
2. Other causes: hemorrhagic disorders (e.g., thrombocytopenia and clotting disorders) and trauma
• Subarachnoid or intraventricular hemorrhage 1. Ruptured saccular aneurysm or AVM 2. Other causes
• SDH or epidural hematoma
or indirect damage by hemorrhage into the ventricles, subarachnoid space, extra-dural area, or subextra-dural area. These changes result in a common mode of expression, defined by Adams and Victor (1985) as a sudden, non-convulsive, focal neurological deficit – or stroke.
Expanding on this categorization (i.e., the means by which parenchymal changes occur), there are four major categories of ischemic cerebral infarction. These include atherosclerotic thrombosis, cerebral embolism, lacunae, and other more rare condi-tions. Studies of the incidence of cerebrovascular disease (e.g., Wolf et al. 1977) found that the ratio of infarcts to hemorrhages is about 5:1. Atherosclerotic throm-bosis and cerebral embolism each account for approximately one-third of all strokes.
Atherosclerotic thrombosis
Atherosclerotic thrombosis is often the result of a dynamic interaction between hypertension and atherosclerotic deposition of hyaline-lipid material in the walls of peripheral, coronary, and cerebral arteries. Risk factors in the development of atherosclerosis include hyperlipidemia, diabetes mellitus, hypertension, and ciga-rette smoking. Atheromatous plaques tend to propagate at the branchings and curves of the internal carotid artery, in the carotid sinus, in the cervical part of the vertebral arteries and their junction to form the basilar artery, in the posterior cerebral arteries as they wind around the midbrain, and in the anterior cerebral arteries as they curve over the corpus callosum. These plaques may lead to stenosis of one or more of these cerebral arteries or to complete occlusion. TIAs, defined as periods of transient focal ischemia associated with reversible neurological deficits, almost always indicate that a thrombotic process is occurring. Only rarely is embolism or ICH preceded by transient neurological deficits. Thrombosis of virtually any cerebral or cerebellar artery can be associated with TIAs.
TIAs, therefore, although not listed among the main causes of stroke, may pre-cede, accompany, or follow the development of stroke or may occur by themselves without leading to complete occlusion of a cerebral or cerebellar artery. Most com-monly, TIAs have a duration of 2–15 min, with a range from a few seconds to up to 12–24 h. Since the neurological examination between successive episodes of this thrombotic process shows entirely normal findings, the existence of permanent neurological deficits indicates that infarction has occurred. The progression of events leading to the completed thrombotic stroke, however, can be quite variable.
Cerebral embolism
Cerebral embolism, which accounts for approximately one-third of all strokes, is usually caused by a fragment breaking away from a thrombus within the heart and traveling up the carotid artery. Less commonly, the source of the embolism may be from an atheromatous plaque within the lumen of the carotid sinus or from the 33 Vascular anatomy and classification of stroke
distal end of a thrombus within the internal carotid artery, or it may represent a fat, tumor, or air embolus within the internal carotid artery. The causes of thrombus formation within the heart can include cardiac arrhythmias, congenital heart dis-ease, infectious processes (e.g., syphilitic heart disdis-ease, rheumatic valvular disdis-ease, and endocarditis), valve prostheses, postsurgical complications, or myocardial infarction with mural thrombus. Of all strokes, those due to cerebral embolism develop most rapidly. In general, there are no warning episodes; embolism can occur at any time. A large embolus may occlude the internal carotid artery or the stem of the middle cerebral artery producing a severe hemiplegia. More often, however, the embolus is smaller and passes into one of the branches of the middle cerebral artery, producing infarction distal to the site of arterial occlusion, charac-terized by a pattern of neurological deficits consistent with the vascular distribu-tion, or producing a transient neurological deficit that resolves as the embolus fragments and travels into smaller, more distal arteries.
Lacunae
Lacunae, which account for nearly one-fifth of all strokes, are the result of occlu-sion of small penetrating cerebral arteries. They are infarcts that may be so small as to produce no recognizable deficits, or, depending on their location, they may be associated with pure motor or sensory deficits. There is a strong association between lacunae and both atherosclerosis and hypertension, suggesting that lacu-nar infarction is the result of the extension of the atherosclerotic process into small-diameter vessels.
Hemorrhage
Intracranial hemorrhages, which account for about one-seventh of all strokes, is the fourth most frequent cause of stroke. The main causes of intracranial hemor-rhage that present as acute strokes include ICH, usually associated with hyperten-sion; rupture of saccular aneurysms or arteriovenous malformations (AVMs);
a variety of hemorrhagic disorders of assorted etiology; and trauma-producing hemorrhage. Primary (hypertensive) ICH occurs within the brain tissue. The extravasation of blood forms a roughly circular or oval-shaped mass that disrupts and displaces the parenchyma. Adjacent tissue is compressed, and seepage into the ventricular system usually occurs, producing bloody spinal fluid in more than 90%
of cases. ICH can range in size from massive bleeds of several centimeters in diam-eter to petechial hemorrhages of a millimdiam-eter or less, most commonly occurring within the putamen, in the adjacent internal capsule, or in various portions of the white matter underlying the cortex. Hemorrhages of the thalamus, cerebellar hemispheres, or pons are also common. Severe headache is generally considered to be a constant accompaniment of ICH, but this occurs in only about 50% of cases.
34 Introduction
The prognosis for ICH is grave, with 70–75% of patients dying within 1–30 days (Adams and Victor 1985).
Aneurysms and AVMs
Ruptured aneurysms and arterial venous malformations (AVMs) are the next most common type of cerebrovascular disease after thrombosis, embolism, lacunae, and ICH. Aneurysms are usually located at arterial bifurcations and are presumed to result from developmental defects in the formation of the arterial wall; rupture occurs when the intima bulges outward and eventually breaks through the adventi-tia. AVMs consist of a tangle of dilated vessels that form an abnormal communica-tion between arterial and venous systems. They are developmental abnormalities consisting of embryonic patterns of blood vessels. Most AVMs are clinically silent but will ultimately bleed. Hemorrhage from aneurysms or AVMs may occur within the subarachnoid space, leading to an identifiable presentation as a bleeding vessel anomaly, or may occur within the parenchyma, leading to hemiplegia or even death.
Subdural and epidural hematomas
Although it could be contended that subdural hematomas (SDH) and epidural hematomas do not represent forms of cerebrovascular disease, nonetheless their behavior as vascular space-occupying lesions that produce many of the signs and symptoms of stroke warrants a brief description here.
Chronic SDHs are frequently (60%), but not exclusively, caused by head trauma, followed by a gradual progression of signs and symptoms during the subsequent days to weeks. Traumatic chronic SDH may be caused by tears of bridging veins in the subdural space. Non-traumatic causes include ruptured aneurysms or AVMs of the pial surface or rapid deceleration injuries. The most common symptom of chronic SDH is headache as well as a variety of neuropsychiatric manifestations which paral-lel the gradual increase in intracranial pressure. These include confusion, inatten-tion, apathy, memory loss, drowsiness, and coma. Chronic SDH is also one of the many conditions in the differential diagnosis of treatable causes of dementia.
Fluctuations in the level of consciousness predominate over any focal or lateralizing signs, which may include hemiparesis, hemianopsia, cranial nerve abnormalities, aphasia, or seizures. Chronic SDH may continue to expand if left unchecked, or may reabsorb spontaneously.
Acute SDH and epidural hematomas, although frequently manifested by similar changes in level of consciousness and focal neurological deficits (as in chronic SDH), are associated with severe head trauma. They may occur simultaneously or in combination with cerebral laceration or contusion, and progress rapidly over a period of a few hours to days, rather than days to weeks. Epidural hematomas usu-ally follow temporal or parietal skull fracture that causes a laceration or avulsion of 35 Vascular anatomy and classification of stroke
the middle meningeal artery or vein or a tear of the dural venous sinus; acute SDH is usually caused by the avulsion of bridging veins or laceration of pial arteries. Both conditions produce loss of consciousness or a brief period of lucidity followed by a loss of consciousness, hemiparesis, cranial nerve palsies, and death, usually second-ary to respiratory compromise, if the hematoma is not emergently evacuated.
Other types of cerebrovascular disease
One of the other causes of cerebrovascular disease is fibromuscular dysplasia, which leads to narrowed arterial segments caused by degeneration of elastic tissue, disruption and loss of the arterial muscular coat, and an increase in fibrous tissue.
Inflammatory diseases of the arterial system can also lead to stroke; these include meningovascular syphilis, pyogenic or tuberculous meningitis, temporal arteritis, and systemic lupus erythematosus.
There are many other less common causes of cerebrovascular disease that have not been cited here due to lack of space. It appears obvious, however, that examin-ing the many causes and types of cerebrovascular disease in relation to specific neuropsychiatric disorders is a very formidable task. Few studies have compared the emotional disorders associated with thromboembolic stroke to those associ-ated with hemorrhagic (Robinson et al. 1983a). In general, our studies have included lesions caused by both ischemia and hemorrhage and have found that the associ-ated mood disorders are similar, depending on the size and location of the lesion and the time elapsed since injury. This issue, however, has never been systemati-cally investigated. As indicated previously, the type or pattern of neuronal damage may be different, depending on the cause of the cerebrovascular disease. Resultant neuropsychiatric disorders may also vary depending on the nature of the vascular disorder.
In summary, whether emotional changes are directly or indirectly produced by stroke, they are ultimately dependent upon the brain’s structural and vascular anatomy. The most frequent location for cerebral infarctions is the distribution of the middle cerebral artery. Thrombosis or emboli which occlude the large-diameter vessels on the lateral surface of the brain produce the largest lesions. Posterior cir-culation lesions affecting the brain stem or penetrating arterial lesions affecting subcortical structures usually produce small focal or lacunar lesions.
Classification of cerebrovascular disease may be based on either the cerebral ves-sels occluded, the cause of the vessel disease or the means by which tissue damage occurs. I have outlined a classification of stroke based on the cause of tissue dam-age. The most frequent type of stroke is thromboembolic infarction followed by ICH. These vascular disorders lead to permanent damage of cerebral tissue and the physical and cognitive impairments produced by stroke.
36 Introduction
As discussed in Chapter 3, emotional disorders are thought to be associated with dysfunction in the limbic system. Limbic structures are supplied by anterior cere-bral (i.e., orbitofrontal cortex), posterior cerecere-bral (i.e., thalamus and the medial portion of temporal lobe) as well as penetrating branches of the middle cerebral arteries (i.e., septum, accumbens, as well as portions of temporopolar cortex and orbital–frontal cortex). Thus, strokes which lead to emotional disorders may occur within any of the anterior, middle, or posterior cerebral arteries, and may occur in large surface arteries or deep penetrating arteries. The infarct may be large or small depending upon the artery affected and may be either hemorrhagic or ischemic in nature. Vascular anatomy and stroke classification give us a basis for understand-ing where and how the stroke occurred but do not predict the likelihood of an emotion disorder which may be a consequence.
R E F E R E N C ES
Adams, R. D., and Victor, M. Principles of Neurology. McGraw-Hill, New York, 1985.
Robinson, R. G., Kubos, K. L., Starr, L. B., et al. Mood changes in stroke patients: relationship to lesion location. Compr Psychiatr (1983) 24:555–566.
Wolf, P. A., Dawber, T. R., Thomas, H. E., et al. Epidemiology of stroke. In R. A. Thompson and J. R. Green, eds., Advances in Neurology. Raven Press, New York, 1977, 5–19.
37 Vascular anatomy and classification of stroke