Stroke : Clinical Presentation, Management, and Organization of Services


Introduction

Stroke and transient ischemic attacks (TIAs) are the most common clinical manifestations of disease of cerebral blood vessels. Other manifestations of cerebrovascular disease are subclinical and include cerebral white matter lesions, “silent” brain infarcts, and cerebral microbleeds. This chapter focuses mainly on stroke and TIA, with less emphasis on subclinical cerebrovascular disease. In terms of therapy, the chapter does not deal with primary prevention but, rather, with acute treatment, recovery, and secondary prevention.

Stroke and TIAs are the leading causes of acute neurologic admissions to hospitals throughout the world and tend to predominantly affect older people. Stroke is the second leading single cause of death worldwide. Approximately one third of stroke patients die within the first 6 months, and approximately 60% die within 5 years after stroke. Stroke ranks as the sixth most important cause of disability among survivors. Increasingly, in the developed world, patients admitted with stroke tend to be frail and have multiple comorbidities. The impact of a stroke on frail older people can be particularly devastating, often leading to a move from their home environment to residential care facilities. It is important to adopt a cohesive and multidisciplinary approach to minimize long-term stroke-related disability and enhance quality of life for the affected person. In the past decade significant improvements in stroke care, based on clinical trial evidence, have been made, and these improvements have resulted in measurable reductions in mortality and disability.

Definitions

Stroke and Transient Ischemic Attack

The American Heart Association recently defined ischemic stroke (or central nervous system infarction) as “brain, spinal cord, or retinal cell death attributable to ischemia, based on either pathologic, imaging, or other objective evidence of focal ischemic injury in a defined vascular distribution, or clinical evidence of focal ischemic injury based on symptoms persisting ≥24 hours or until death, and other etiologies excluded.” Intracerebral hemorrhage is the term applied to sudden focal neurologic symptoms and brain imaging evidence of brain parenchymal hemorrhage. TIAs refer to transient sudden focal neurologic symptoms lasting less than 24 hours and being of presumed vascular origin but without demonstrable infarction or hemorrhage on brain imaging. The type of brain imaging used can make a major difference as to whether a person is diagnosed as having a TIA or stroke. Computed tomography (CT) scans, although sensitive to intracerebral hemorrhage, are relatively insensitive to the presence of early or small infarctions. The use of acute diffusion-weighted magnetic resonance imaging (DWI-MRI) allows the detection of small infarcts in patients who may otherwise be labeled as having a TIA. Nonspecific symptoms such as faintness, loss of consciousness, dizziness, confusion, or falls are highly unlikely to be due to a TIA or stroke, unless they are accompanied by focal neurologic symptoms. Acute delirium, a common syndrome affecting older people, is unlikely to last only a few hours and is almost always not secondary to a TIA, although it can be an uncommon presentation of acute stroke.

Subclinical Cerebrovascular Lesions

Subclinical cerebrovascular lesions are abnormalities detected on MRI brain scans of older people in the absence of a history of acute stroke. They include silent brain infarcts, cerebral white matter lesions, and cerebral microbleeds. Silent brain infarcts are usually small subcortical infarcts seen in approximately 10% of the general population older than 65 years, which occur more frequently with increasing age and in the presence of traditional vascular risk factors such as hypertension, smoking, hypercholesterolemia, and diabetes mellitus. White matter lesions are visible as hyperintense (bright) signals seen on fluid-attenuated inversion recovery (FLAIR) sequences of MRI scans almost ubiquitously in people aged older than 65 years (their severity increasing with age) and in those with a history of hypertension. Cerebral microbleeds are small hypointense (dark) lesions seen on susceptibility weighted imaging MRI sequences and represent hemosiderin deposits adjacent to small vessels. Hypertension, low cholesterol, and the apolipoprotein epsilon 4 (ApoE4) allele are associated with the presence of cerebral microbleeds. All three manifestations of subclinical cerebrovascular disease commonly coexist in severe forms in frail older people, can lead to insidious cognitive and motor decline, and increase the risk of both ische­mic and hemorrhagic stroke.

Stroke Types

Strokes are either ischemic (80%) or hemorrhagic, each having different pathophysiologic mechanisms and treatments. The mechanisms of arterial occlusion are predominantly those of artery-to-artery embolism and cardioembolism rather than in situ vessel thrombosis. In the absence of arterial venous malformation, aneurysm and cavernous angioma, intracerebral hemorrhage occur in approximately 15% of all cases of stroke, and are either due to hypertensive small vessel disease or amyloid angiopathy. Distinguishing ischemic and hemorrhagic stroke is important as their treatments are quite different (thrombolysis and antiplatelet/anticoagulant treatments are used for the former). Some infarcts have hemorrhagic components and may be mistaken for primary intracerebral hemorrhage ( Figure 61-1 ). Separation of these two types of stroke requires careful consideration of the clinical features and their imaging findings.

Figure 61-1, Hemorrhagic infarct and not primary intracerebral hemorrhage.

Ischemic Stroke Subtypes

The most commonly used classification for ischemic stroke in observational epidemiology is the Oxfordshire Community Stroke Project (OCSP). This classification is based on clinical features and not advanced imaging findings, and hence it is not particularly useful in correctly identifying stroke mechanisms. In clinical trials, the most commonly used criteria for classification are the Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria. This is a classification of subtypes using a combination of clinical features and results of ancillary diagnostic studies. “Possible” and “probable” diagnoses can be made based on the physician's certainty of diagnosis based on all available clinical information. The TOAST classification denotes five categories of ischemic stroke: (1) large-artery atherosclerosis, (2) cardioembolism, (3) small vessel occlusion, (4) stroke of other determined cause, and (5) stroke of undetermined cause. A feature of this classification is that stroke is attributed to the offending carotid artery if the level of stenosis of that artery is greater than 50%. However, patients can have thromboembolic disease from carotid artery even when the level of stenosis is less than 50%. The degree of stenosis is important when deciding on whether carotid endarterectomy is required, rather than excluding large artery atherosclerosis as a mechanism.

Clinical Presentation of Stroke and Transient Ischemic Attack

The clinical features of TIA and stroke are the results of ischemia affecting eloquent brain areas. The classical patterns of stroke presentations are dealt with later in this chapter but cannot be exhaustively covered in this chapter alone. (For a detailed examination of this topic, see Stroke Syndromes , edited by Bogousslavsky and Caplan. ) However, it must be borne in mind that very old patients (>80 years of age) can have atypical presenting symptoms (e.g., falls or reduced mobility) and often have prestroke frailty, and a reasonable index of suspicion for stroke must be maintained for such people.

Clinical Features of Stroke

Motor weakness is the most common presenting feature in stroke, affecting about 80% of patients. The pattern of weakness is a clue to the location of the stroke lesion. Unilateral face, arm, and leg weakness often indicates involvement of the middle cerebral artery (MCA) territory, whereas bilateral weakness may indicate posterior circulation involvement. Pure unilateral motor weakness without cortical signs suggests involvement of the subcortical motor tracts (a “lacunar” syndrome). The presence of ideomotor dyspraxia (a disorder of higher cortical disorder of motor initiation) can sometimes mimic motor weakness. Weakness of the articulatory and swallowing muscles can lead to symptoms of dysarthria and dysphagia, respectively, and can occur from strokes affecting both anterior and posterior circulations.

Over 60% of stroke patients admitted to the hospital suffer some form of tactile sensory impairment, and smaller proportions either suffer loss of proprioception or have cortical sensory impairment. Sensory abnormalities may be associated with delayed but debilitating poststroke pain syndromes.

Higher cortical deficits that have the most important adverse impact on patients are dysphasia (usually dominant hemisphere stroke) and hemineglect. Broca aphasia (also termed expressive aphasia or motor aphasia) is most commonly caused by strokes involving the left frontal opercular and central cortex, with or without involvement of the subcortical striatocapsular region. It is characterized by effortful speech, word-finding difficulty, phonemic errors, and agrammatism, but comprehension is relatively preserved. Sensory aphasia with relatively fluent speech but poor language comprehension is usually associated with strokes involving the superior temporal lobe and includes Wernicke aphasia and conduction aphasia, among others. Global aphasia refers to severe impairment of motor speech, and comprehension and is usually a consequence of a major left MCA stroke.

Hemineglect is characterized by a reduction in attention to stimuli and events on one side of the body and can occur with either right or left hemisphere stroke. Hemineglect may affect visual, auditory, and somatosensory perceptual systems and is associated with poor outcome. Visual symptoms may arise from lesions affecting the visual pathway anywhere from the retinal to the occipital cortex. Retinal or ophthalmic artery occlusion occurs as a result of embolism from the carotid system and can lead to monocular blindness. Visual field defects are common, leading to either hemianopia or quadrantanopia, depending on the site of the lesion and the extent of damage to the optic radiation. Ocular movement abnormalities are commonly seen in stroke affecting the brainstem, but also less commonly seen with cerebellar and cerebral lesions. Diplopia is usually associated with eye movement abnormality and can be quite disabling. Detection and characterization of visual deficits in stroke patients are of extreme importance, given their potential impact on daily life and complex activities such as driving.

Vertigo or a disordered perception of motion of either the patient or the environment can be caused by strokes involving the vertebrobasilar circulation and is often accompanied by nystagmus. Ataxia of the trunk or limbs may be caused by strokes affecting the cerebellum and adjacent brainstem. Several auditory symptoms may also be associated with brainstem strokes including sudden hearing loss, hyperacusis, tinnitus, and auditory hallucinations.

Stroke is very commonly associated with neurocognitive syndromes at acute presentation as well as in the medium to long term. Close to 50% of survivors have some form of cognitive impairment at 3 months after stroke ; this can occur as a result of the effects of the stroke itself, or it may be a sign of worsening or unmasking of preexisting cognitive decline. Stroke is strongly associated with a twofold increase in the risk of dementia after stroke with the presence of prestroke cognitive decline explaining a large proportion of these cases. Up to 30% of patients may also suffer from depressed mood in the medium to long term after stroke. Urinary and fecal incontinence are common and disabling effects of stroke. The prevalence of urinary incontinence among survivors of stroke ranges from 36% to 83% within the first year. Incontinence may be a direct consequence of loss of neurogenic control or due to functional incapacitation secondary to immobility or cognitive loss, and is a marker for increased mortality after stroke and overall poor outcome among survivors.

Clinical Features of Transient Ischemic Attack

Features compatible with anterior circulation TIA commonly include unilateral motor, sensory or sensorimotor impairment, dysphasia, and amaurosis fugax. The diagnosis of amaurosis fugax is based on the patient's report of a transient unilateral visual loss, described on closer questioning as “a curtain coming down” over the affected eye with inability to see through this curtain. Features of posterior circulation TIA include vertigo and/or diplopia, or loss of balance, or unilateral weakness.

Investigations for Stroke

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