Patient is an 87-year-old right-handed man with a history of hypertension, diabetes, and ischemic stroke (5 years ago) that presents with the onset of unsteady gait. He arrives to the hospital 4 h after the onset of his symptoms. On examination, the patient has rotary nystagmus at primary gaze, dysarthria, and right-sided dysmetria. His NIHSS is 2. The STAT head CT scan shows an area of early ischemic changes in the right cerebellum (Fig. 6.2). Despite a low NIHSS, the patient has disabling symptoms; however, his age (87 years) and comorbidities (history of diabetes and stroke) render him not a candidate for alteplase outside the 3 h time window. This patient is admitted to the stroke service for further diagnostic tests to understand the stroke etiology and to initiate secondary stroke prevention therapies. He is started on aspirin 81 mg daily, atorvastatin 80 mg daily and is deemed a candidate for physical and vestibular rehabilitation.

The primary focus for the initial treatment of acute ischemic stroke is determining whether a patient who presents with acute neurological deficits is a candidate for intravenous thrombolytic therapy. This chapter focuses on a review of the pathophysiology of acute ischemic stroke, the critical thinking algorithms that direct acute stroke care during the “golden hour” after presentation, and the role of the advanced practice clinician during the hyperacute, acute, and posttreatment recovery care process.

The two cases illustrate the diversity of acute stroke syndromes and their associated presentations, the importance of understanding neurovascular anatomy, the limitations of the currently recommended neurologic assessment (the National Institutes of Health Stroke Scale or NIHSS) in assessing posterior circulation strokes, the utility of imaging, and the criteria for IV alteplase treatment. Of the two stroke syndromes presented, the first patient has an anterior stroke syndrome and the second patient a posterior circulation syndrome. The significant contrast in the NIHSS assessments reflects the inadequacy of the NIHSS in appreciating disability caused by posterior circulation strokes.

A broad exposure to neuroanatomy and clinical correlation is important for prompt recognition of suspected acute stroke syndromes. Fortunately, many syndromes can be learned through pattern recognition (identifying specific symptoms that the patient presents with that can be correlated to and associated with loss of function in specific regions of the brain). For instance, strokes in the left hemisphere may be associated with aphasia and right-sided weakness. The patient from Case 1 had symptoms suggestive of right hemispheric dysfunction given that she had left-sided visual loss, left-sided weakness, and neglect. As shown in Case 2, posterior circulation strokes may be difficult to appreciate when depending on an NIHSS to make a diagnosis. A posterior circulation infarct must be considered if symptoms such as dysarthria, double vision, hemianopsia, and incoordination occur. Practitioners must also recognize a set of stroke syndromes that do not involve cortical signs on the examination. These strokes, called lacunar infarcts, occur in deeper brain perforating arteries commonly affecting the internal capsule, thalamus, and pons. The associated syndromes include focal motor weakness, focal sensory disturbances clumsy-hand dysarthria, and ataxic hemiparesis.

A stroke classification scheme worth reviewing and that requires a rudimentary knowledge of neurovascular anatomy includes Bamford’s Stroke Classification or the Oxfordshire Community Stroke Project [4]. Depending on the presence of cortical dysfunction and the extent of deficit, anterior strokes can be classified into a total anterior stroke or partial anterior stroke. If the patient has a cranial nerve palsy, bilateral motor deficits, conjugate eye movement problems, cerebellar dysfunction, or an isolated hemianopsia, patients can be classified as having a posterior circulation stroke. Pure sensory or motor deficits along with other small vessel syndromes described above can be categorized as a lacunar stroke.

Classification systems and scales are not a replacement for the neurological examination, which will refine localization and help the practitioner differentiate neurovascular from non-neurovascular presentations. The neurological examination will allow the stroke team to differentiate impairments stemming from the peripheral nervous system, such as hand weakness from a small cortical stroke as opposed to an ulnar neuropathy. It will also allow the advanced practice clinician to appreciate ocular findings, incoordination, and gait instability which are undervalued or not tested in the NIHSS.

Posterior circulation strokes are missed more frequently than anterior circulation strokes [5]. Vertigo evaluations can be challenging, especially when the patient has overwhelming nausea and head-motion intolerance. Additionally, focal signs on the exam may be absent in cerebellar strokes. For these cases, the neurologist and non-neurologist should be proficient in bedside testing that evaluates the vestibular-ocular reflex for corrective saccades, direction-changing nystagmus on eccentric gaze, and skew deviation. The acronym for the examination is called HINTS, which stands for head impulse testing, nystagmus, and test of skew deviation. A negative HINTS examination (which includes an abnormal head impulse finding, absence of nystagmus, and absence of a skew deviation) was found to be more sensitive than an early MRI of the brain for excluding stroke [6, 7].

It is estimated that up to 50% of acute presentations felt to be stroke are stroke mimics (Table 6.1) [8]. Most acute stroke responders will not have access to performing a brain MRI to confirm stroke, but will have to rely upon history, the neurological examination, and a head CT to determine whether to give IV alteplase [9]. Nevertheless, current practice supports have supported rapid treatment at the expense of a confirmatory diagnosis, citing that the risk of a complication from thrombolytics is very low.

For the purposes of understanding the time-sensitive nature of stroke, the assessment, stabilization, diagnosis, and management in the first few hours after symptom onset is referred to as the hyperacute phase of stroke care. This time window is more broadly defined as the first 24 h after contact with the healthcare system and includes interaction with the pre-hospital personnel (EMS) and with the emergency department staff and acute stroke team (which may also include neurosurgeons, neuro-interventionalists, and the critical care unit staff). The primary goal of care during this time frame is the rapid and efficient evaluation of patients presenting with neurological deficits that would benefit from early treatment therapies (to preserve the penumbra). Reference to the acute phase of stroke care includes the management of stroke patients during the early recovery stage and includes the time while hospitalized (several days) or the first 30 days after the index stroke, depending on the specific organization’s scope of practice [10]. During the acute phase of care, diagnostic tests to understand the possible stroke etiology are ordered; secondary stroke prevention strategies are implemented; and promotion of early recovery and prevention of complications are outlined. For the individualized care plan, a patient- and family-centered education module for post discharge recovery is initiated.

In addition to the above operational phases of care, a key time frame within the stroke care trajectory is the time window from when the patient’s symptoms begin (or when the patient was last known to be at his/her baseline) to the time when treatment is started. Depending on the available therapy options, patient-related variables, and clinical trial enrollment criteria, the treatment time window can vary from 3.0 h up to 12–24 h. The 3.0 h time window reflects the results of the 1995 NINDS trial which showed a significant outcome benefit for patients treated with intravenous alteplase [11]. The 4.5 h time window reflects the results of the 2008 ECASS III trial in which selected patients had a significantly improved outcome when treated with intravenous alteplase up to 4.5 h after symptom onset [12]. The stroke treatment time window that is extended out to 12–24 h reflects the additional treatment options such as mechanical thrombolysis and enrollment in acute stroke clinical trials for which specific pharmacologic or other experimental therapies might be offered. So for the clinicians involved in the acute stroke code process, this time window defines “acute,” it sets parameters for when the stroke code is activated, and it directs both the pre-hospital and stroke team efforts for early, efficient, and rapid evaluation.