Stroke and Other Vascular Disorders


Introduction

Stroke is the most common serious neurologic disorder, the fifth leading cause of death in the United States and second in the world, and the most common cause of neurologic disability in adults. Over 800,000 strokes occur each year in the United States, which is more than one each minute. Many additional, small strokes, perhaps as many as 11 million per year in the United States, may be asymptomatic, but the accumulated effects can lead to vascular dementia.

A stroke is a focal abnormality of brain function, caused by either an obstruction in blood flow from occlusion of an artery (ischemic stroke) or hemorrhage from a ruptured blood vessel (hemorrhagic stroke). About 80% to 85% of strokes are ischemic, and 15% to 20% are hemorrhagic. The management of the stroke patient begins with diagnosis based on symptoms and signs. Stroke must be understood in terms of the risk factors for the condition, prior transient ischemic attacks (TIAs), prior strokes, and the developing symptoms and mode of evolution of the stroke itself. The neurologic examination serves to localize the lesion. The diagnosis is then confirmed by imaging studies. Treatment includes acute stroke management, including intravenous tissue plasminogen activator (tPA), mechanical thrombectomy, secondary prevention measures, and finally stroke rehabilitation.

Clinical Presentation: Symptoms and Signs

In general, stroke symptoms reflect dysfunction of focal areas of the brain that are affected by either ischemia or hemorrhage. This presentation of a focal deficit in a conscious patient, especially a patient of older age or with known risk factors, is instantly recognizable as a stroke to most people, including family members who are not medically trained.

TIAs involve temporary focal ischemia that resolves completely within minutes or hours. TIAs can be warning signs of stroke. Carotid distribution TIAs include transient obscuration of the vision of one eye (transient monocular blindness or amaurosis fugax) or symptoms of hemisphere ischemia, such as slurred speech or language difficulty and weakness or numbness of the contralateral side of the body. TIAs in the vertebrobasilar artery distribution are associated with combinations of dizziness, diplopia, slurred speech, numbness or weakness on one or both sides of the body, ataxia, and decreased level of consciousness. Symptoms of TIA resolve within 24 hours. A recent modification of the concept of TIA states that if transient symptoms are associated with an acute infarction on magnetic resonance imaging (MRI) scan, then the event is considered a stroke rather than a TIA. TIA is a major warning sign of stroke and is associated with a major risk of impending stroke.

The American Heart Association also lists sudden, severe headache as a warning sign of stroke. A sudden, severe headache, especially the worst headache of a patient’s life, should raise the concern of a subarachnoid hemorrhage (SAH), which is usually caused by rupture of a cerebral aneurysm. Stiff neck makes the diagnosis of SAH even more likely. Although most headaches do not reflect SAH, this diagnosis is a medical emergency and one that clinicians should strive not to miss.

The symptoms of stroke are, in general, the same as those of TIAs. Patients presenting to an emergency department 1 to 2 hours after the onset of ischemic symptoms are very likely to have a stroke because most TIAs begin to resolve within minutes to a few hours.

In the case of a hemorrhage, the location of the bleed is of importance in determining the stroke syndrome. Intracranial hemorrhage (ICH) can occur into one of four separate spaces: the extradural, subdural, subarachnoid, and intracerebral spaces. Extradural hemorrhage usually occurs after head trauma in a young patient; the most common occurrence is a skull fracture that tears a dural artery such as the middle meningeal artery. This is a rapidly progressive, acute syndrome that often requires emergency neurosurgical evacuation. Sometimes a lucid interval occurs between the head injury and the development of symptoms, as the blood accumulates. Progression can then be rapid, and prompt diagnosis and neurosurgical consultation are critical.

Subdural hemorrhage (SDH) also occurs most often after trauma, but SDH may be either acute or chronic. Symptoms of a subacute or chronic SDH may develop gradually, sometimes without a clear history of trauma. Chronic SDH is more common in elderly patients in whom brain atrophy leaves a space between the brain and the skull, which is traversed by fragile bridging veins. Drowsiness and subtle neurologic symptoms and signs are the hallmark of SDH, and the clinician must have a high index of suspicion to send patients for diagnostic computed tomography (CT) or MRI scans.

SAH most commonly results from a ruptured aneurysm, although there are many patients with traumatic SAH. Headache and stiff neck are the most common symptoms of SAH, although a variety of other syndromes can occur.

The fourth type of hemorrhage, ICH, occurs directly into the substance of the brain. This is the type of hemorrhage that most closely mimics the presentation of an ischemic stroke. The most common cause of ICH, hypertension, tends to produce bleeds deep in the brain, in the putamen and basal ganglia most commonly and then the thalamus, brainstem, and cerebellum. Cerebellar hemorrhage is the most amenable to neurosurgical treatment and is therefore especially crucial to diagnose early. This hemorrhage syndrome often causes seemingly nonspecific symptoms such as dizziness, nausea, vomiting, and headache. The key to diagnosis is early gait ataxia. Patients who are dizzy from vestibular function can usually walk, but patients with cerebellar hemorrhage typically cannot. CT scan will then be diagnostic. Hemorrhage in the pons tends to cause bilateral hemiparesis and often coma. The prognosis is poor, unless the hemorrhage is small. Hemorrhage into the basal ganglia usually causes hemiparesis. Occasionally, hemorrhage in the caudate or thalamus breaks into the ventricular system and causes symptoms of increased intracranial pressure (ICP), without obvious focal symptoms and signs. Hemorrhage into the cortical-subcortical areas of the brain, termed lobar hemorrhage, may occur with hypertension but is more characteristic of a bleed related to coagulopathies (e.g., anticoagulation) or structural changes in small arteries that occur with aging (cerebral amyloid angiopathy).

Ischemic stroke, the result of an obstruction of blood flow to the brain, can have several mechanisms. The most common ones, by a widely used classification, are (1) large vessel, atherothrombotic strokes; (2) small vessel or lacunar thrombotic strokes; (3) cardioembolic strokes; (4) strokes caused by a variety of clinically definite, but less common mechanisms; and (5) cryptogenic strokes, or those for which a precise mechanism or cause is not discovered. In this last category, strokes that appear embolic, meaning sudden in onset, cortical-subcortical in distribution, and for which no source of embolus is found, are sometimes referred to as embolic strokes of unknown source or ESUS.

Localization of Specific Stroke Syndromes

The functional anatomy of the specific regions of the brain including cerebrum, basal ganglia, thalamus, brainstem, and cerebellum were discussed in previous chapters. This chapter presents the features that can help localize and diagnose specific stroke syndromes.

Vascular Anatomy

In terms of vascular anatomy, the two internal carotid arteries (ICAs) supply most of the blood flow to the cerebral hemispheres. The carotid artery distribution is the anterior circulation, whereas the vertebrobasilar distribution is the posterior circulation.

The bifurcation of the common carotid artery into the ICA and external carotid artery (ECA) is a frequent site of lipid plaque accumulation in atherosclerosis, and disease at this location is often the cause of large vessel, thrombotic TIA, and stroke. Less commonly, stenosis of the ICA develops higher up in the intracranial portions of the ICA.

Intracranial large vessel disease develops with advanced atherosclerosis in patients with chronic risk factors such as hypertension, diabetes mellitus, hyperlipidemia, obstructive sleep apnea, and smoking. Intracranial atherosclerosis is more common in those of African and Asian descent. The ICA bifurcates into the anterior cerebral artery (ACA) and middle cerebral artery (MCA). Because the MCA takes a straighter course from the ICA, emboli more commonly travel there, although occasionally emboli involve the ACA or posterior cerebral artery (PCA) territories. In general, disease of the MCA is more commonly caused by emboli than by local atherosclerotic disease, whereas disease of the ACA is more equally distributed between embolic and local disease. MCA territory strokes are much more common than ACA territory strokes. The ICA also gives rise to a posterior communicating artery, joining the carotid circulation with the PCA, that arises from the basilar artery of the posterior circulation. Occasionally, the posterior communicating artery supplies most of the blood supply to the PCA on one or both sides; this is a normal variant sometimes referred to as a fetal PCA.

Middle Cerebral Artery Infarction

The MCA bifurcates into an upper division and a lower division; the upper division of the left MCA supplies the motor speech area (Broca area), the motor strip in the precentral gyrus (face and arm areas), and the sensory strip in the postcentral gyrus, leading to the common syndrome of Broca aphasia and right hemiparesis in left MCA stroke. If only single branches are involved, more restricted deficits, such as Broca aphasia with only right facial weakness, may occur. Involvement of the inferior division branches causes a fluent, Wernicke aphasia (see Chapter 5.2 ), sometimes accompanied by a right upper quadrant visual field defect. Involvement of both upper and lower divisions of the left MCA, as in an embolus in the left MCA stem, produces global aphasia and right hemiplegia, which is a severe and disabling stroke syndrome. Visuospatial deficits and neglect behavior are commonly associated with right MCA. Involvement of deep branches of the MCA on either side also produces weakness of the leg and the arm because the descending fibers from the cortical leg area descend through the MCA territory and into the internal capsule, which is also largely supplied by deep branches of the MCA. Over time, however, the leg usually improves more than the arm after a left MCA stroke.

Internal Capsule Infarction

Small vessel, lacunar infarctions in the territory of the deep, lenticulostriate branches of the MCA produce localized infarctions of the posterior limb of the internal capsule, resulting in the stroke syndrome of pure motor hemiparesis, without sensory signs, cortical behavioral or cognitive deficits, or visual field abnormalities. Larger infarctions in the lenticulostriate territory produce more complex syndromes including combined motor and sensory deficits, dysarthria, and even cognitive and language deficits.

Thalamic Infarction

Lacunar infarctions in the thalamus which typically receives arterial supply from perforating vessels from the PCA, produce a pure sensory stroke with paresthesias and numbness on the contralateral side, sometimes followed by neuropathic pain (Dejerine-Roussy syndrome).

Basal Ganglia Infarction

The basal ganglia receives arterial supply predominately from the MCA lenticulostriate branches. Lacunes in the basal ganglia can produce contralateral weakness and clumsiness.

Small infarctions in the basal ganglia, sparing the internal capsule, may be relatively silent and are noted on brain imaging studies of patients without a clinical history of stroke.

Vertebrobasilar Anatomy

The posterior circulation is comprised of the two vertebral arteries, arising from the subclavian artery on each side and merging within the skull to form the single, unpaired basilar artery. The vertebral arteries can be affected by atherosclerosis in their proximal portions, at the origin from the subclavian artery, or distally. The vertebral arteries are also a site of dissection, usually in more distal portions.

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