Stroke and Neurodegenerative Disorders: 1. Stroke Management in the Acute Care Setting

Stroke and Neurodegenerative Disorders

Stroke and Neurodegenerative Disorders: 1. Stroke Management in the Acute Care Setting Cara Camiolo Reddy, MD, Alex Moroz, MD, Steven R. Edgley, MD, Henry L. Lew, MD, PhD, John Chae, MD, Lisa A. Lombard, MD Objective: This self-directed learning module highlights management of stroke in the acute care setting. It is part of the study guide on stroke and neurodegenerative disorders in the Self-Directed Physiatric Education Program for practitioners and trainees in physical medicine and rehabilitation. Using a case vignette format, this article specifically focuses on initial assessment and management of acute ischemic and hemorrhagic stroke, descriptions of posterior circulation and lacunar stroke, and criteria for admission to acute inpatient rehabilitation after stroke and secondary stroke prevention. The goal of this article is to improve the learner’s ability to identify, treat and manage a patient with a stroke in the acute care setting. 1.1 Clinical Activity: A 65-year-old woman presents to the local hospital’s emergency department with a 2-hour history of right hemiparesis. Describe the initial assessment and management of acute stroke. Identify causes of acute mortality. Management of acute stroke necessitates timely organized care from all members of the care team. Response time is critical in the initial treatment of stroke; therefore, educational campaigns directed at the lay population have focused on the awareness of stroke symptoms and the need for quick response. Despite these efforts, less than 10% of patients with acute strokes arrive at the emergency department within 1 hour after stroke and less than 25% arrive in fewer than 3 hours [1]. The designation of medical centers as specialized stroke centers has improved delivery of care; however, the specialized services these centers provide are often limited to large academic settings. For example, recombinant tissue plasminogen activator (rt-PA), a now well-established treatment of ischemic stroke more commonly known as TPA, is given more frequently to patients at academic centers than nonacademic hospitals. Telemedicine technology, developed in response to these treatment barriers, is emerging as an effective way to extend stroke care into rural areas and small, community-based hospitals [2]. Any acute change in neurologic status warrants rapid assessment of the ABCs (Airway, Breathing, Circulation) upon arrival of the medical care team. Ensuring airway protection and adequate ventilatory support is critical. Cardiac assessment should include determination of cardiac rhythm, blood pressure (BP) and pulse. Vital signs are measured to assess for fever, high BP, or irregular heart rhythm. Cardiovascular physical assessment and electrocardiogram should be performed and cardiac monitoring should be done in all stroke patients for the first 24 hours, since cardiac abnormalities can both lead to and result from stroke. Evaluation of a patient with acute onset hemiparesis begins by determining that the symptoms are not due to a different neurologic disorder. A detailed history is imperative, including specific questions regarding onset of symptoms; recent events such as myocardial infarction (MI), stroke, trauma, or surgery; presence of comorbid diseases such as hypertension (HT) and diabetes mellitus (DM); and the use of insulin or anticoagulants. When assessing patients for possible treatment with thrombolytics, the time the patient was last observed to be symptom-free is assumed to be the time of onset. After historical details are obtained, a physical examination should be performed. The neurologic examination is one of the best predictors of stroke severity and it should be PM&R

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1934-1482/09/$36.00 Printed in U.S.A.

C.C.R. Department of Physical Medicine and Rehabilitation, University of Pittsburgh Medical Center, 3471 Fifth Ave, LKB Ste 201, Pittsburgh, PA 15213. Address correspondence to: C.C.R.; e-mail: [email protected] Disclosure: nothing to disclose A.M. NYU School of Medicine, Rusk Institute of Rehabilitation Medicine, New York, NY Disclosure: 2, IPRO S.R.E. University of Utah, Salt Lake City, UT Disclosure: 2, Northstar Neuroscience H.L.L. Harvard Medical School, VA Boston Healthcare System, Physical Medicine and Rehabilitation Service, Boston, MA Disclosure: nothing to disclose J.C. Case Western Reserve University, MetroHealth Medical Center, Department of Physical Medicine and Rehabilitation, Cleveland, OH Disclosure: nothing to disclose L.A.L. Santa Clara Valley Medical Center, Department of Physical Medicine and Rehabilitation, San Jose, CA Disclosure: nothing to disclose Disclosure Key can be found on the Table of Contents and at www.pmrjournal.org

© 2009 by the American Academy of Physical Medicine and Rehabilitation Suppl. 1, S4-S12, March 2009 DOI: 10.1016/j.pmrj.2009.01.015

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Table 1. National Institutes of Health Stroke Scale (NIHSS) Symptom

Scaled Description

Loss of consciousness 0 —alert 1— drowsy 2— obtunded 3— coma/unresponsive Orientation 0 —answers both correctly to questions 1—answers one correctly 2—answers neither correctly Response to 0 —performs both tasks correctly commands 1—performs one task correctly 2—performs neither correctly Gaze 0 —normal horizontal movements 1—partial gaze palsy 2— complete gaze palsy Visual fields 0 —no visual field defect 1—partial hemianopia 2— complete hemianopia 3— bilateral hemianopia Facial movement 0 —normal 1—minor facial weakness 2—partial facial weakness 3— complete unilateral palsy Motor function (arm) 0 —no drift, arm held at 45° Left 1— drift before 10 seconds Right 2—falls before 10 seconds 3—no effort against gravity 4 —no movement Motor function (leg) 0 —no drift, leg held at 30° Left 1— drift before 5 seconds Right 2—falls before 5 seconds 3—no effort against gravity 4 —no movement Limb ataxia 0 —no ataxia 1—ataxia in 1 limb 2—ataxia in 2 limbs Sensory function 0 —no sensory loss 1—mild sensory loss 2—severe sensory loss Language 0 —normal 1—mild aphasia 2—severe aphasia 3—mute or global aphasia Articulation 0 —normal 1—mild dysarthria 2—severe dysarthria Extinction or 0 —absent inattention 1—mild (loss of 1 sensory modality) 2—severe (loss of 2 sensory modalities) From Adams et al [2]. Reprinted with permission.

documented by a universally accepted assessment scale, such as the National Institutes of Health Stroke Scale (NIHSS; Table 1) [2]. Use of this standardized assessment scale, which has demonstrated reliability among non-neurologists, can assist in early prognostication, identification of patients appropriate for intervention, and communication among the medical team [2,3]. The NIHSS score is an excellent predictor of outcome: nearly 70% of patients with an NIHSS score less than 10 will have a favorable outcome at 1 year [4]. Conversely, those patients with an NIHSS greater than 20 have been shown to have a higher risk of hemorrhage following the administration of TPA [2].

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Table 2. Criteria for Administration of TPA ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ●

Age ⬎18 years Clinical diagnosis of ischemic stroke with measurable deficits “Last seen normal” or onset of symptoms is less than 3 hours Neurologic deficits not clearing spontaneously No seizure activity with postictal impairments Symptoms are not suggestive of subarachnoid hemorrhage No history of head trauma in previous 3 months No history of prior stroke or MI in previous 3 months No gastrointestinal or urinary tract hemorrhage in previous 3 weeks No major surgery in previous 2 weeks No arterial puncture at a noncompressible site in previous 1 week No history of intracranial hemorrhage Systolic blood pressure below 185 mm Hg, diastolic blood pressure below 110 mm Hg No active bleeding or acute trauma No use of anticoagulation or if on anticoagulation, INR ⬍ 1.7 No heparin within past 48 hours, aPTT within normal range Platelets above 100,000 mm3 Blood glucose above 50 mg/dL No CT evidence of intracranial hemorrhage No CT evidence of a large area of hypodensity greater than 1/3 MCA territory

aPTT ⫽ activated partial thromboplastin time; CT ⫽ computed tomography; INR ⫽ international normalized ratio; MCA ⫽ middle cerebral artery; MI ⫽ myocardial infarction; TPA ⫽ tissue plasminogen activator.

Further steps in the rapid sequence of assessment should include measures to exclude stroke mimickers, including seizure, electrolyte abnormalities and trauma. Laboratory tests include complete blood count with platelets, coagulation profile with prothrombin time and activated partial thromboplastin time, electrolytes, glucose, renal studies and toxicology screen. Hypoglycemia and hyperglycemia should also be investigated, as both can clinically mimic stroke. Additionally, hyperglycemia in the setting of acute neurologic deficits must be treated aggressively, because it is associated with a poor outcome after ischemic stroke [5]. Because the clinical picture of ischemic and hemorrhagic stroke can overlap, radiologic imaging is crucial to differentiate these distinct etiologies. Computed tomography (CT) without contrast should be performed in all patients. Though insensitive when compared with magnetic resonance imaging (MRI) for detection of small cortical and subcortical infarcts, CT is widely available, can be performed quickly, and can exclude intracranial hemorrhage. For TPA candidates, current guidelines suggest that the CT should be performed and read within 45 minutes after the person with suspected stroke arrives in the emergency department. An MRI with diffusion-weighted imaging is the most sensitive modality to pick up acute ischemia but is not routinely performed in the acute setting. Barriers to MRI include clearance due to metallic foreign bodies, availability of centers to perform MRI 24 hours a day, and time constraints [6].

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Eligibility criteria for administering intravenous TPA are listed in Table 2. Intravenous TPA is given at a dose of 0.9 mg/kg for a maximum dose of 90 mg. Ten percent of the dose is given as a bolus over 1 minute; the remainder is given over 1 hour. Frequent neurologic assessments and BP monitoring are recommended during the infusion of TPA and over the next 24 hours. Infusions are terminated if the patient develops headache, nausea, vomiting or hypertension. These changes warrant emergent CT. Because hypertension in persons treated with TPA increases the risk of hemorrhage, BP management is imperative in the first 24 hours of its administration. Pressure should be maintained at less than 185 mm Hg systolic and less than 110 mm Hg diastolic. Antihypertensives (hydralazine, labetalol, nicardipine, enalapril), can be used during TPA infusion in order to maintain blood pressure within these parameters [2]. In the landmark NINDS study [5], similar mortality rates were noted at 3 months and 1 year for the TPA and placebo arms. Further, favorable outcomes were noted both initially and at 1 year poststroke in the TPA group. Those with NIHSS scores less than 20 and the patients under age 75 had the most benefit. The risk of symptomatic intracranial hemorrhage was approximately 6.4% in the TPA group, compared with 0.6% in the placebo group, despite the similar mortality rates [7]. Of note, the rate of asymptomatic intracerebral hemorrhage was similar in the 2 groups. Those patients with large areas of hypodensity on initial scan have a greater incidence of hemorrhagic conversion after TPA [6]. For patients presenting outside of the 3-hour onset window, CT angiography of the head and neck can evaluate occlusion in large vessels, such as the proximal middle cerebral artery (MCA), carotid terminus, and basilar artery. In this setting, MRI can also be used to define the degree of irreversible neurologic damage and to delineate which patients might benefit from late revascularization. If large vessel occlusion is present, intra-arterial therapy can be considered, including mechanical revascularization by means of angiography and possible stenting, clot retrieval by mechanical embolus removal in cerebral embolism (MERCI) and intraarterial thrombolytics [8]. Intra-arterial thrombolytics, an off-label alternative, can be considered for patients presenting within 6 hours from symptom onset who have contraindications to TPA, including recent surgery. The PROACT II trial confirmed higher recanalization rates in MCA occlusions after 3 hours with intra-arterial prourokinase; however, symptomatic hemorrhage rates were higher than those for intravenous TPA [9]. Outcome, as measured by the ability to live independently at 3 months, was significantly improved in the prourokinase intervention arm. Current guidelines set forth by the American Stroke Association and American Heart Association suggest that intraarterial therapies should only be performed at specialized stroke centers and only by interventionalists who have cerebral angiography immediately available to them [2]. For patients who do not receive thrombolytic therapy, aspirin at 325 mg, when given within the first 24 to 48 hours poststroke, has shown to improve morbidity and mortality

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by reducing recurrent events in patients. Anticoagulation with heparin and antiplatelet agents, including ticlopidine, clopidogrel or dipyridamole, has not shown any significant benefit in acute stroke management [2]. Acute causes of death in stroke patients include preexisting heart failure, arrhythmias, myocardial infarction, and respiratory failure. For cases of malignant middle cerebral artery (MCA) syndrome, marked by cerebral edema causing subsequent herniation, the mortality rate approximates 80% in patients who receive medical management alone [10]. Surgical decompression with evacuation of the infarcted tissue can be a life-saving intervention, potentially lowering the mortality rate to 24% [11,12]. Outcome data regarding quality of life and disability following hemicraniectomy have been less definitive, although there is evidence that younger patients can achieve good functional recovery [13]. 1.2 Clinical Activity: A 59-year-old woman with longstanding history of poorly controlled hypertension is found unresponsive at home by her daughter. Initial CT findings reveal right basal ganglia hemorrhage. Discuss the initial assessment and management of hemorrhagic stroke. Identify the indications for surgical intervention. Intracerebral hemorrhage (ICH) accounts for 10% to 15% of acute strokes. The rate of mortality at 1 month approaches 50%, half occurring within the first 48 hours [14]. Due to risk of rapid neurologic deterioration and high rates of early mortality, prompt evaluation and close neurological monitoring in an intensive care unit are imperative. Evaluation begins with the assessment of ABCs. The need for intubation and ventilatory support is higher in individuals with ICH than it is for patients with ischemic stroke. Cardiovascular assessment and monitoring is obligatory in initial management. For patients with Glasgow Coma Scale scores less than 9, intracranial pressure (ICP) monitoring is warranted, since persistent elevation in ICP is associated with herniation and poorer outcomes. Important historical details include history of head trauma, prior intracranial hemorrhage, and presenting symptoms. “Classic symptoms” of ICH such as headache, nausea and vomiting are unreliable for differentiating hemorrhagic from ischemic injuries. It is important to ascertain any history of coagulopathy, drug use, or liver disease. Coagulopathy or thrombocytopenia warrants correction with intravenous vitamin K and fresh frozen plasma (FFP). Factor VII has not be proven to be significantly better in reducing morbidity and mortality at 90 days when given in the first 3 hours of onset and has been associated with increased rates of thromboembolism [14]. Radiologic assessment with head CT can reveal acute hemorrhage and is the gold standard for evaluation. Volume of hemorrhage has been shown to be a strong predictor of outcome [15]. MRI is not warranted acutely due to time constraints and, often, medical acuity.

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Hypertension is the leading cause of ICH and persistently elevated blood pressure is associated with poorer outcome; however, BP correction in the setting of ICH remains controversial. Similar to ischemic stroke, concern exists that aggressive correction of BP can decrease cerebral perfusion and increase the risk of ischemia. Conversely, there is evidence to suggest that after ICH, lowering the BP can reduce the amount of hemorrhagic extension [16,17]. Consensus guidelines suggest that if systolic pressure is greater than 200 mm Hg, intravenous antihypertensives should be employed. If the systolic pressure is greater than180 mm Hg with elevated intracranial pressure, medications should be used to keep cerebral perfusion pressures between 60 and 80 mm Hg. When systolic pressure is greater than 180 mm Hg and intracerebral pressure is within normal limits, aggressive treatment is not needed and conservative intervention can be used for a target BP of 160/90 mm Hg [14]. Neurosurgical consultation and surgical intervention are recommended for patients with evidence of cerebellar hemorrhage greater than 3 cm with neurological deterioration, brain stem compression or ventricular obstruction. The STICH trial revealed that early surgical intervention for ICH greater than 9 mL with significant neurologic impairment showed no clinical benefit over routine medical management [18], although more recent meta-analyses reveal trends toward reduction in mortality [19]. 1.3 Clinical Activity: A 71-year-old man presents with 1-day history of nausea, vomiting, and dizziness. Initial workup reveals posterior circulation infarct. Describe the anatomy and clinical manifestations of common stroke syndromes of the posterior circulation. The vertebrobasilar system, including the vertebral arteries, basilar artery, posterior inferior cerebellar arteries, anterior inferior cerebellar arteries, superior cerebellar arteries, and posterior cerebral arteries, provides the posterior cerebral circulation to the cerebellum, medulla, pons, thalamus, and portions of the occipital, parietal and temporal lobes. Ischemic strokes of the posterior circulation most commonly occur at the proximal portions of the basilar artery. Of note, cerebellar infarctions more commonly arise from cardioembolic disease while infarctions of the pons and thalamus result from stenotic occlusions [20]. Stroke syndromes of the posterior circulation (Figure 1) have been well classified, because clear correlations exist between vascular supply and brainstem anatomy; however, clinical presentations of such syndromes are rarely as distinct (Table 3). Locked-in syndrome resulting from occlusion of the basilar artery to the ventral pons bilaterally produces a classic picture of maintained consciousness with paresis of all movement except vertical gaze and eyelid control. Involvement of the bilateral cortical spinal tracts results in weakness of the bilateral upper and lower extremities, corticobulbar tract involvement results in bilateral facial weakness, cranial nerve

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VI involvement causes bilateral lateral gaze weakness, and corticobulbar tract involvement causes dysarthria. Due to sparing of the reticular activating system and supranuclear ocular motor pathways, consciousness is spared and the patient has control over vertical eye motion and eye blinking. 1.4 Clinical Activity: A 75-year-old woman presents with a 6-hour history of dysarthria and incoordination of her left hand. Identify lacunar syndromes, associated anatomy and management. Lacunar strokes are subcortical infarctions occurring with occlusion of single small-diameter penetrating vessels. The lacuna results from macrophage activity absorbing necrotic brain tissue leaving a small cavity. Radiographically, these lesions are hypodense with diameters less than 20 mm [21]. The basal ganglia, thalamus, internal capsule and brain stem are the most common sites of occlusion. Pure motor lacunar stroke results from involvement of the posterior limb of the internal capsule. Weakness in the face, arm and leg are noted and recovery tends to be good. Lacunar infarcts of the thalamus may present with pure sensory symptoms involving the face, arm or leg in the absence of other symptoms. Dysarthria clumsy-hand syndrome includes facial weakness, dysarthria, and dysphagia with weakness and clumsiness of the hand. The lesion is located at the base of the pons and occurs without sensory deficits. Sensorimotor lacunae occur in the thalamus and posterior limb of the internal capsule and, as the name implies, produce sensory and motor symptoms. Ataxic hemiparesis refers to a combination of ataxia and weakness on the same side of the body due to involvement of the corona radiata and anterior limb of the internal capsule. In these cases, the weakness generally improves more readily than the ataxia [22]. Compared to individuals with nonlacunar strokes, patients with lacunar strokes had lower 1-month and 1-year mortalities, secondary to cerebrovascular events. Conversely, long-term risk of death and stroke recurrence was similar to those with nonlacunar strokes, emphasizing the need for risk factor management in this population, particularly in patients with diabetes mellitus and hypertension [23,24]. Diabetes mellitus and hypertension have been identified in several studies as independent risk factors for lacunar and non-lacunar ischemia, although no synergy between these factors appears to exist. Diffuse small vessel occlusive disease is a well-documented consequence of DM and subgroup analyses reveal a relation between DM and multiple lacunae [24]. The prevalence of hypertension in lacunar ischemia has been variable across studies; however, evidence indicates a significant relationship between diastolic hypertension, microangiopathy and multiple lacunae [21,24]. No clear relations between smoking history, hypercholesterolemia, alcohol consumption, or prior transient ischemic attack have been found for lacunar strokes over non-lacunar strokes [25].

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(A)

Paramedian arteries to midbrain and thalamus (via posterior perforated substance) Posterior cerebral artery (PCA) Superior cerebellar artery (SCA)

Oculomotor nerve (CN III)

Short and long circumferential pontine arteries Basilar artery

Abducens nerve (CN VI)

Internal auditory (labyrinthine) artery Anterior inferior cerebellar artery (AICA) Posterior inferior cerebellar artery (PICA) Vertebral artery Anterior spinal artery

(B)

Posterior cerebral artery (PCA)

Superior cerebellar artery (SCA) Short and long circumferential pontine arteries Basilar artery Internal auditory (labyrinthine) artery Anterior inferior cerebellar artery (AICA)

Posterior inferior cerebellar artery (PICA) Vertebral artery Anterior spinal artery

Figure 1. Anatomy of the brain’s posterior circulation. From Blumenfeld [44]. Reprinted with permission.

1.5 Clinical Activity: On the consultation service, you are asked to see a 65-year-old woman who sustained a stroke 2 days prior. Outline recommendations for determining appropriate levels of rehabilitation care.

The American Academy of Physical Medicine and Rehabilitation recently published Standards for Assessing Medical Appropriateness Criteria for Admitting Patients to Rehabilitation Hospitals or Units [26], which outline patient characteristics for appropriate rehabilitation admission (Table 4). These

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Table 3. Brainstem Syndromes Region Medial medulla

Lateral medulla

Syndrome Name Medial medullary syndrome

Wallenberg syndrome (lateral medullary syndrome)

Medial pontine basis

Pure motor hemiparesis

Medial pontine basis and tegmentum

Millard-Gubler syndrome

Lateral caudal pons

AICA syndrome

Dorsolateral rostral pons

Midbrain basis

Midbrain tegmentum

SCA syndrome

Weber syndrome

Claude syndrome

Vascular Supply Paramedian branches of vertebral and anterior spinal arteries Vertebral artery or PICA

Paramedian branches of basilar artery, ventral territory Paramedian branches of basilar artery, ventral and dorsal territories AICA

SCA

Branches of PCA and top of basilar artery Branches of PCA and top of basilar artery

Midbrain basis and tegmentum

Benedikt syndrome

Thalamus

Dejerine-Roussy syndrome

Branches of PCA

Occipital cortex

Anton syndrome

Occipital cortex

Alexia without agraphia Locked-in syndrome

Bilateral PCAs or top of the basilar artery PCA

Ventral pons, bilateral

Branches of PCA and top of basilar artery

Basilar artery

Anatomical Structures Pyramidal tract Medial lemniscus Hypoglossal nucleus and CN 12 fascicles Inferior cerebellar peduncle, vestibular nuclei Trigeminal nucleus and tract Spinothalamic tract Descending sympathetic fibers Nucleus ambiguous Corticospinal and corticobulbar tracts Corticospinal and corticobulbar tracts Fascicles of facial nerve Middle cerebellar peduncle Spinothalamic tract Superior cerebellar peduncle and cerebellum Other lateral tegmental structures Oculomotor nerve fascicles Corticospinal tracts/ cerebellar peduncle Oculomotor nerve fascicles Red nucleus, superior cerebellar peduncle fibers Oculomotor nerve fascicles Cerebral peduncle Red nucleus, substantia nigra, superior cerebellar peduncle fibers Thalamic nuclei

Clinical Features Contralateral arm or leg weakness Contralateral decreased position and vibration sense Ipsilateral tongue weakness Ipsilateral ataxia, vertigo, nystagmus, nausea Ipsilateral decreased pain and temperature sense on face Contralateral decreased pain and temperature sense on body Ipsilateral Horner syndrome Hoarseness, dysphagia Contralateral face, arm and leg weakness; dysarthria Contralateral arm and leg weakness Ipsilateral face weakness Ipsilateral ataxia Contralateral body decreased pain and temperature sense Ipsilateral ataxia

Variable features of lateral tegmental involvement Ipsilateral third nerve palsy Contralateral hemiparesis Ipsilateral third nerve palsy Contralateral ataxia

Ipsilateral third nerve palsy Contralateral hemiparesis Contralateral ataxia, tremor, and involuntary movements

Primary visual cortex

Contralateral hemisensory loss to all sensory modalities Contralateral hemibody pain Cortical blindness, anosognosia

Optic pathway

Able to write, unable to read

Corticospinal tracts Corticobulbar tracts

Quadriplegia Bilateral facial weakness, dysarthria Lateral gaze weakness

Bilateral CN 6 fascicles

From Blumenfeld [44]. Adapted with permission. AICA ⫽ anterior inferior cerebellar artery; CN ⫽ cranial nerve; PCA ⫽ posterior cerebellar artery; PICA ⫽ posterior inferior cerebellar artery; SCA ⫽ superior cerebellar artery.

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Table 4. Characteristics of Patients Deemed Appropriate for Admission to a Rehabilitation Facility 1. Regardless of diagnosis, the patient has significant functional deficits and medical and nursing needs that require a. close medical supervision by a physiatrist or other physician qualified by training and experience; b. 24-hour availability of nurses skilled in rehabilitation; c. treatment by multiple other licensed rehabilitation professionals (physical therapists, occupational therapists, speech language pathologists, psychologists), as needed, in a time-intensive and medically coordinated program. 2. The patient’s medical stability and medical or surgical comorbidities are considered to be a. manageable in the rehabilitation hospital; b. sufficiently under control that the patient can participate in the rehabilitation program concurrently with their prescribed management. 3. The patient presents as capable of fully participating in the inpatient rehabilitation program. (In unusual situations, when it is unclear whether the patient is able to fully participate in the program, a brief period of inpatient care may be required to make a final determination. These circumstances may be referred to as an evaluative admission or a trial admission). 4. Admission is warranted because clear functional goals have been set and these goals a. are realistic; b. offer practical improvements; and c. are expected to be achieved within a reasonable time. 5. The patient has a high probability of benefiting from the program of care. 6. The patient has a home and available family or care providers in most circumstances that support a likelihood of returning the patient to home or a community-based environment. Adapted from the Medical Inpatient Rehabilitation Criteria Task Force [26]. Reproduced with permission.

criteria are based in physiatric philosophy, which emphasizes quality of life and function. Further, they underscore the important role of the physiatric consultant. The standards suggest that “although the cost of care is certainly a consideration in evaluating alternative treatment options, price comparisons only become appropriate once it has been determined that the options being considered are similar (ie, similar clinical capacities, similar resources, and capability of achieving similar outcomes in reasonable, comparable time frames)” [26]. This recommendation necessitates that the benefits of rehabilitation be evaluated. More specifically, it requires that the benefits of stroke rehabilitation units be assessed in comparison to other available levels of care. There is a significant amount of data in the European literature to support the benefits of stroke units [27]. Stroke units, in the European model, are similar to American rehabilitation units in that they are comprised of a multidisciplinary team of physicians, nurses, physical therapists, occupational therapists, speech therapists, and neuropsychologists. In one prospective study of over 1200 stroke patients randomized to either a specialized stroke unit or general neurological/medical ward,

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significant reductions were noted in mortality (in-hospital, 6-month, and 1-year), length of stay, and discharges to nursing home. Further, a 1313 bed-day saving per 100 patients indicated a significant economic benefit [28]. De Wit et al [29] directly compared 4 European rehabilitation centers and found significantly higher motor and functional recovery in the centers that provided more therapy per day. In the United States, comparisons of acute inpatient rehabilitation versus skilled nursing facilities (SNF)-based rehabilitation have also been undertaken. One study showed that patients who were admitted to rehabilitation units after stroke were more likely to be younger, have a caregiver after discharge, and had a significantly better premorbid level of function prior to their injury, compared to individuals admitted to SNF. At 6 months, after adjusting for demographics and other baseline differences, those patients who had a stroke and were admitted to rehabilitation facilities had better functional status and were more likely to have returned to the community [30]. Although data demonstrate that stroke survivors treated in stroke units experience significantly better outcomes than those treated in a less organized manner, stroke patients with more severe impairments, functional deficits, and older age appear to benefit most [31]. For individuals who had milder impairments and functional deficits, intact cognitive function, and availability of 24-h supervision and assistance, home rehabilitation was just as effective as stroke unit care [32,33]. The timing of rehabilitation, with regard to maximizing functional recovery, has also been investigated. Concern arose from animal studies revealing an increase in lesion volume with early forced overuse of the affected limb [5,34,35]. However, evidence exists that in the first 2 weeks after stroke, neurotrophic proteins are induced to facilitate plasticity—which makes the initial postevent period optimal for induction of rehabilitative efforts. In a rodent study, early initiation of rehabilitation after ischemia resulted in significant functional gains and plasticity when compared to similar therapy initiated 1 month later [36]. 1.6 Clinical Activity: A 65-year-old man is admitted to your rehabilitation facility after a right MCA infarct and new-onset of an irregularly irregular heart rate. Outline the measures for secondary stroke prophylaxis. Cardioembolism accounts for 20% of ischemic strokes. For patients with atrial fibrillation and documented cardioembolic disease, anticoagulation with warfarin has well documented benefit for stroke prevention [37]. In patients with noncardioembolic stroke, including those with atherosclerotic disease, lipohyalinosis, or cryptogenic stroke, antithrombotic interventions are the mainstay of current treatment guidelines for secondary prevention. The WARSS trial supports the use of aspirin, extended release dipyridamole plus aspirin, and clopidogrel as effective means for secondary stroke prevention after noncardioembolic events [37]. In this

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study, no benefit was found with warfarin over aspirin in secondary stroke prevention or in mortality. Clinical studies, including the MIRACL, SPARCL, GREACE, LIPID, and CARE trials, have indicated that the use of statins can significantly lower the risk of cerebrovascular accident in patients as primary prevention with known high-risk vascular disease, including those with DM and HTN, and also as secondary prevention for those with history of stroke [38-40]. Tight control of blood glucose levels with the goal of preventing micro- and macrovascular complications should be a component of risk factor management in this population. Hypertension accelerates the formation of atherosclerotic vessel lesions; consequently, controlling BP in an effort to prevent primary and secondary stroke has shown significant reduction in stroke rate. This finding emphasizes the need for close monitoring of BP in persons with known cerebrovascular disease [41]. Clear relationships between obstructive sleep apnea (OSA) and hypertension, atherosclerosis, and acute coronary symptoms have been found, and OSA occurs with increased prevalence in the stroke population. Given these relationships, OSA screening and treatment are recommended in the stroke population [42]. Patients should receive counseling on smoking cessation and healthy diet and exercise habits, topics to be discussed further in chapter 4. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) [43] found a significant reduction in ipsilateral stroke in patients with severe grade stenosis of 70% or more who had undergone endarterectomy. This reduction extended at least 5 years postoperatively. Additional guidelines recommend that the procedure be performed at institutions with experienced surgeons. For patients with moderate (50% to 60%) stenosis, results were not as robust and current guidelines recommend weighing the patient’s other stroke risk factors when considering surgery, since risk may outweigh benefit [43].

REFERENCES 1. Audebert HJ, Kukla C, Vatankhah B, et al. Comparison of tissue plasminogen activator administration management between Telestroke Network hospitals and academic stroke centers: the Telemedical Pilot Project for Integrative Stroke Care in Bavaria/Germany. Stroke 2006; 37:1822-1827. 2. Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early management of patients with ischemic stroke. Stroke 2007;38:1655-1711. 3. Goldstein LB, Samsa GP. Reliability of the NIH Stroke Scale. Extension to non-neurologists in the context of a clinical trial. Stroke 1997;8:307-310. 4. Adams HP, Davis PH, Leira EC, et al. Baseline NIH Stroke Scale score strongly predicts outcome after stroke: a report of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Neurology 1999;53:126-131. 5. Bruno A, Levine SR, Frankel MR, et al. Admission glucose level and clinical outcomes in the NINDS rt-PA Stroke Trial. Neurology 2002;59: 669-774. 6. Mullins ME. Modern emergent stroke imaging: pearls, protocols, and pitfalls. Radiol Clin N Am 2006;44:41-62. 7. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995;333:1581-1587.

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