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Bedside Evaluation of the Acute Stroke Patient

Bryan J. Eckerle, MD and Andrew M. Southerland, MD, MSc

Department of Neurology, University of Virginia Health System, Charlottesville, Virginia

Introduction

Emanating from the results of the original National Institute of Neurological Disorders and Stroke recombinant tissue plasminogen activator (NINDS rt-PA) trial [1], the management of acute stroke has evolved as a cornerstone of emergency medical care, hospital medicine, and clinical neurology. While the only treatment for acute ischemic stroke approved by the US Food and Drug Administration (FDA) remains intravenous (IV) rt-PA administered within 3 hours of symptom onset, the field continues to expand with a focus on more timely treatment, expanding the pool of patients eligible for treatment, and optimization of methods of reperfusion. These advances include the use of IV rt-PA beyond the 3-hour window, the direct administration of intra-arterial rt-PA, and implementation of a variety of devices aimed at mechanical thrombectomy and other interventional means of cerebrovascular recanalization. However, integrating all of the scientific evidence guiding the acute stroke paradigm is daunting, even for the most seasoned vascular neurologist. According to the National Guideline Clearinghouse, an initiative of the Agency for Healthcare Research and Quality in the De­­partment of Health and Human Services, there are ­currently 225 published guidelines related to “acute stroke” from various organizations and societies around the world [2]. The current standard of stroke care in the US is guided by the American Heart Association/American Stroke Association’s (AHA/ASA) Get With the Guidelines (GWTG) program [3].

While stroke therapeutics will be discussed in detail elsewhere in this book, the aim of this chapter is to offer a simple, practical approach to the bedside evaluation of the acute stroke patient. As the opinions and recommendations herein draw on experience treating acute stroke, they also reflect the literature and guiding evidence. The chapter will broadly highlight seminal studies, published AHA/ASA guidelines, FDA regulations, and The Joint Commission (TJC) certification requirements for primary/comprehensive stroke centers – links to further resources can be found in the Appendix, Chapter 9. Explored in detail will be the various issues facing neurologists or other physicians in acute stroke scenarios, including an accurate gathering of history, essentials of the acute stroke physical exam, radiological diagnosis, and potential hurdles precluding a treatment decision. While these necessary steps are very much protocol driven, the reality of the acute stroke setting dictates a somewhat simultaneous process in order to achieve the efficient delivery of treatment. Ultimately, the aim of the chapter is to further promote rapid diagnosis and timely management for all acute stroke patients, as the medical community continues to strive for the best possible outcomes from this disabling and deadly disease.

Is it a stroke?

Despite rapid advances in neuroimaging over the past 20 years, the bedrock of the evaluation of the acute stroke patient remains sound clinical diagnosis. The physician is frequently asked to see a patient in urgent consultation for treatment of acute stroke in the absence of a firmly established diagnosis. Even with the advent of highly advanced ­neuroimaging techniques, stroke remains a clinical diagnosis; as opposed to an infarct, which is an imaging or tissue-based diagnosis. Stroke is, by definition, the acute onset of a persistent focal neurological deficit or constellation of deficits referable to a specific cerebrovascular territory. The absence of abrupt onset of symptoms all but precludes acute stroke as the diagnosis. Symptoms that do not all fit into a specific vascular territory suggest either a diagnosis other than stroke or the ­possibility of multifocal ischemia as may be seen in cardioembolism. Additionally, stroke typically produces negative symptoms –that is to say, loss of strength, sensation, vision, or other neurological function. Presence of positive symptoms (pares­thesias, involuntary movements, visual pheno­mena) is uncommon in stroke, unless the patient with a cortical stroke is having a concurrent ­seizure or occasionally a triggered migraine – as in cervical artery dissection.

Ischemic stroke subtypes in specific vascular territories tend to produce fairly predictable constellations of signs and symptoms, or “syndromes” [4]. Rapid recognition of these syndromes is crucial in early diagnosis and timely treatment of acute stroke or, often of equal importance, the elimination of stroke as a potential diagnosis. In terms of broadly defined clinical stroke syndromes, one can consider large vessel versus small vessel presentations. Generally speaking, large vessel strokes tend to occur in the setting of atherosclerotic and/or embolic disease, whereas small vessel (lacunar) strokes tend to present in the setting of chronic small vessel occlusive disease related primarily to chronic hypertension and diabetes. The clinical manifestations of commonly encountered large vessel syndromes are described in Table 1.1.

Table 1.1 Large vessel stroke syndromes (laterality assumes left hemispheric dominance)

Vascular territory Signs and symptoms Internal carotid artery (ICA) Combined ACA/MCA syndromes; ipsilateral monocular visual loss secondary to central retinal artery occlusion (amaurosis); branch retinal artery occlusions may present as ipsilesional altitudinal field cuts Left anterior cerebral artery (ACA) Right leg numbness and weakness, transcortical motor aphasia, and possibly ipsilesional or contralesional ideomotor apraxia Right ACA Left leg numbness and weakness, motor neglect, and possibly ipsilesional or contralesional ideomotor apraxia Left middle cerebral artery (MCA) Right face/arm > leg numbness and weakness, aphasia, left gaze preference Right MCA Left face/arm > leg numbness and weakness, left hemispatial neglect, right gaze preference, agraphesthesia, stereoagnosia Left posterior cerebral artery (PCA) Complete or partial right homonymous hemianopsia, alexia without agraphia; if midbrain involvement, ipsilateral 3rd nerve palsy with mydriasis and contralateral hemiparesis (Weber syndrome) Right PCA Complete or partial left homonymous hemianopsia (same as above if midbrain involvement) Superior cerebellar artery (SCA) Ipsilesional limb and gait ataxia Anterior inferior cerebellar artery (AICA) Vertigo and ipsilesional deafness, possibly also ipsilesional facial weakness and ataxia Vertebral/posterior inferior cerebellar artery (PICA) Ipsilesional limb and gait ataxia; if lateral medullary involvement can have Wallenberg syndrome (see Table 1.4) Basilar artery (BA) Pontine localization with impaired lateral gaze, horizontal diplopia and dyscongugate gaze, nonlocalized hemiparesis, dysarthria

The syndromes above reflect classical neuroanatomy and may vary depending on individual variations in the circle of Willis or collateral vascular supply.

Cortical syndromes

Between large vessel and cardioembolic disease, there are several classic cortical syndromes that when presenting acutely are most often the result of an ischemic stroke. The classic hallmark of a left hemispheric cortical syndrome involves aphasia. Aphasia is defined as an acquired abnormality of language in any form. By and large, aphasia presents as a deficit of verbal language, but truly involves any medium of communication (e.g. reading and writing, or sign language in the hearing impaired). Specific linguistic properties that may be affected by aphasia include volume of speech, vocabulary, cadence, syntax, and phonics. Often, subtle aphasia is difficult to distinguish from encephalopathy and it is important for the bedside clinician to test specific domains of language – fluency, repetition, comprehension, naming, reading, and writing – in order to make the correct diagnosis.

Specific types of aphasia most often encountered in stroke patients (Table 1.2) classically include expressive/motor/nonfluent (Broca’s) and receptive/ sensory/fluent (Wernicke’s) types. Strokes causing expressive aphasia localize to the posterior inferior frontal lobe, or frontal operculum, whereas receptive aphasias commonly originate from lesions in the posterior superior temporal/inferior parietal lobe. Both of these types commonly affect naming and repetition. Broca’s patients are best identified by difficulties with word finding, speech initiation, volume of speech, and in making paraphasic errors (e.g. “hassock” instead of “hammock”). Wernicke’s patients have clearly impaired comprehension with non­sensical speech, but preserved speech volume and cadence. The transcortical aphasias mirror motor and sensory types except in preservation of repetition, due to lack of injury to the arcuate ­fasciculus linking Broca’s and Wernicke’s areas. Figure 1.1 ­displays the “aphasia...