Jump to:

Disease/ Disorder


Cerebrovascular disease refers to an abnormality of the brain, resulting from a pathologic process of the blood vessels. This chapter will focus on stroke or cerebrovascular accident, the abrupt onset of a focal neurologic deficit caused by cerebrovascular disease. 


Of  all strokes, 87% are ischemic, 10% are hemorrhagic and 3% are classified as subarachnoid hemorrhage1.

The Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification system2 for ischemic stroke is based on the underlying stroke mechanisms:

  1. Large artery atherosclerosis: Intracranial, extracranial (carotid, aortic arch)
  2. Cardioembolic: Atrial fibrillation, segmental wall akinesis, paradoxical embolus, patent foramen ovale, and congestive heart failure
  3. Small vessel: Lacunar infarction
  4. Other: Vessel dissection, venous thrombosis, drugs
  5. Cryptogenic

Hemorrhagic strokes are most often caused by hypertension, with lesions typically located in the basal ganglia, thalamus, pons, and cerebellum. Cerebral amyloid angiopathy is the second most common cause, with lesions more often in cortical locations. Other cause of stroke include medications (either iatrogenic, e.g., warfarin, novel or direct oral anticoagulant (NOAC/DOAC) agent, or drugs of abuse, e.g., cocaine), vascular malformations, cerebral venous thromboses, or tumors.

Epidemiology including risk factors and primary prevention

Stroke is the most common neurologic emergency, and it is a leading cause of disability in the United States1.

Modifiable risk factors include hypertension, hyperlipidemia, diabetes mellitus, obesity, atrial fibrillation, tobacco use, sedentary lifestyle and substance abuse.  Globally, 29% of stroke risk has been attributed to air pollution3.

Hypertension is the number one risk factor for both ischemic and hemorrhagic stroke.  There are four American Heart Association blood pressure categories:  normal (<120/80 mm Hg), elevated (120-129/<80 mm Hg), hypertension stage 1 (130-139/80/89 mm Hg), hypertension stage 2 (>140/90 mm Hg)4

Blood pressure should be lowered if ³140/90mm Hg and treated to a target <130/80 mm Hg (<140/80 in elderly patients)5.  In persons with elevated hypertension,(systolic BP of 120-129 mm Hg), lifestyle modifications (diet, exercise) to reduce BP are recommended.  Maintaining a blood pressure log increases awareness of blood pressure values and helps detect patterns. 

The association of each cholesterol subfraction with total stroke has shown inconsistent results therefore data are limited on associations with specific ischemic stroke subtypes 6.  A mendelian randomization study of lipid genetics suggested an increased risk of large artery ischemic stroke with increased low density lipoprotein (LDL), and a lower risk of small vessel ischemic stroke with increased high density lipoprotein7. A prospective study of over 480,000 first  stroke patients showed genetic markers predictive of increased LDL levels with ischemic stroke risk, and an inverse association with hemorrhagic stroke risk8.

Individuals with diabetes have a greater susceptibility to atherosclerosis and proatherogenic risk factors (hypertension and hyperlipidemia)9. The presence of hyperglycemia, or elevated blood sugars, can enlarge eventual stroke size and increase the risk of brain hemorrhage10, however, the SHINE study findings indicate treatment with intensive glucose control for up to 72 hours does not result in favorable functional outcomes at 3 months11.

Obesity is associated with an increased incidence of all listed modifiable risk factors. Excessive alcohol consumption, tobacco use, and other substance abuse leads to stroke predisposition. Nonvalvular atrial fibrillation is associated with a 4 to 5-fold increased risk of ischemic stroke because of embolism of stasis-induced thrombi12.

Nonmodifiable risk factors include a family history of cerebrovascular disease, sickle cell disease, or hypercoagulable states. Ethnic populations, such as African-Americans and Hispanics, are more likely to have cerebrovascular disease than Caucasians. Advanced age and male sex are also other nonmodifiable risk factors1.


There are signs and symptoms characteristic of vascular lesions in the various arterial territories of the brain.2

  1. Middle cerebral: Contralateral loss of strength and sensation in the face, upper limb, and to a lesser extent, the lower limb. Aphasia characterizes dominant hemisphere lesions, while neglect accompanies nondominant hemisphere lesions.
  2. Anterior cerebral: Contralateral loss of strength and sensation in the lower limb and, to a lesser extent, in the upper limb.
  3. Posterior cerebral: Contralateral visual field deficit, possibly confusion and aphasia if present in the dominant hemisphere.
  4. Penetrating branches (lacunar syndrome): Contralateral weakness or sensory loss (usually not both) in the face, arm, and leg. Dysarthria or ataxia may be present. Aphasia, neglect, or visual loss are not characteristic of lacunar syndromes.
  5. Basilar: Combinations of limb ataxia, dysarthria, dysphagia, facial and limb weakness, and sensory loss. Pupillary asymmetry, dysconjugate gaze, decreased responsiveness, and visual field loss may be present.
  6. Vertebral (or posterior inferior cerebellar): Truncal ataxia, dysarthria, dysphagia, ipsilateral sensory loss on the face, and contralateral sensory loss below the neck.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Presentation of ischemic strokes varies according to the underlying etiology:

Thrombotic/atherosclerotic strokes typically occur with a slow fluctuating clinical course, with deficits progressing over 24 to 48 hours. Thrombotic strokes are more likely to be preceded by transient ischemic attacks. Patients with large thrombotic strokes have an increased risk of cerebral edema development and herniation.  In those receiving hemicraniectomy after 72 hours, the odds of a poor outcome increase 13

In contrast, cardioembolic stroke has a sudden onset. Although the neurologic deficits can be severe with cardioembolism, as the embolus fragments into smaller pieces, these deficits can rapidly resolve 14.

Hypertensive hemorrhages symptoms include headache,  rapid deterioration (in large lesions), nausea or vomiting because of increased intracranial pressure 15.

Specific secondary or associated conditions and complications

The most common neurologic complications of cerebrovascular disease include recurrent stroke, with a 2 to 22% incidence during the five years, followed by hemorrhagic transformation, hydrocephalus, cerebral edema, and seizure.5 Cardiac complications include arrhythmia, acute coronary syndrome, and heart failure. Infectious complications include urinary tract infections and aspiration pneumonias. Thrombotic complications include deep venous thrombosis, pulmonary embolus, and thrombophlebitis1.

Essentials of Assessment


At initial evaluation, patients with ischemic stroke who present within the 0- to 4.5-hour time window may be eligible for intravenous thrombolysis with tissue plasminogen activator (t-PA) 16; 17.  Tenecteplase (TNK) is a single bolus fibrinolytic, which, like t-PA, acts on fibrin bound plasminogen within a thrombus.  It has a longer plasma half-life than t-PA and is not deactivated by the enzyme plasminogen activator inhibitor-1.  A recent study of TNK versus t-PA showed ischemic stroke patients who received TNK had better functional outcomes at 90 days;  22% of the patients treated with TNK versus 10% of those treated with t-PA also reperfused  >50% of the involved ischemic territory 18.  A meta-analysis of 5 randomized trials also added credence to TNK being non-inferior to t-PA 19

For patients with a large vessel occlusion of the anterior circulation (i.e., the M1 branch of the middle cerebral artery), mechanical thrombectomy with a stent retriever device is a second treatment for certain types of ischemic stroke within 24 hours from symptom onset 20; 21; 22; 23; 24; 25; 26. In all seven studies,  a significantly higher proportion of patients who received intra-arterial therapy via mechanical thrombectomy achieved a good functional outcome compared to medical management alone, without an increase in the incidence of symptomatic intracranial hemorrhage.  Used in conjunction with intravenous tissue plasminogen activator therapy, mechanical thrombectomy with a stent retriever in the anterior circulation improved functional outcomes at 90 days26.  The modified Thrombolysis in Cerebral Infarction (mTiCi) score details the percent and quality of reperfusion, divided into 5 categories:  Grade 0/1 (no/minimal reperfusion), Grade 2a (partial filling <50% of territory), Grade 2b (partial filling ³50% of territory), Grade 2c (near complete perfusion except slow flow or few distal cortical emboli) and Grade 3 (complete perfusion)27; 28

On admission to a rehabilitation unit, stroke distribution, type, and etiology should be documented.  Acute interventions, such as mechanical thrombectomy with mTiCi score, hemicraniectomy, carotid revascularization, or ventriculostomy placement should be listed. The patient’s hospital course and complications should also be reviewed. Medical history should focus on stroke risk factors. A thorough social history should discuss family support, home environment, and alcohol, tobacco, or drug use.

Physical examination

Vital signs should focus on temperature, pulse, respiratory rate, pulse oximetry with supplemental oxygen requirements, and blood pressure for the previous 24 hours. The patient’s level of arousal and responsiveness should always be documented. Head, ears, eyes, nose, and throat examination includes evaluation of incision sites, extraocular musculature and pupils, and the presence of a nasogastric tube.

Cardiovascular examination includes auscultation for the presence of a murmur, distant heart sounds, irregular rhythm, and a carotid bruit. The pulmonary examination includes careful auscultation both anteriorly and at the lung bases. The abdominal examination should document bowel sounds, abdominal tenderness, and the presence of a percutaneous endoscopic gastrostomy tube and urinary catheter.

A careful neurologic examination can often localize the region of brain dysfunction. The exam includes evaluation of mental status, cranial nerve, motor, cerebellar, and sensory function. Motor control, strength, balance, coordination, and gait should be evaluated. Examination of cortical function includes testing for aphasia, apraxia, neglect, and cortical sensation. Presence and severity of spasticity should be assessed. The extremity examination should include check for distal pulses, edema, color changes, and calf pain.

Functional assessment

The functional history documents the patient’s prestroke baseline and current status in order to aid in determining the prognosis.

This includes the prestroke ability to perform basic activities of daily living, ambulatory status, and use of durable medical equipment. Physical therapy and occupational therapy assessments are valuable for poststroke functional status.

Premorbid cognitive impairments, such as psychiatric disease, dementia, and learning disability, should be documented.

Speech/language pathologists can provide valuable input when managing any cognitive and communication deficits after stroke. A swallow assessment may include a bedside swallow evaluation, in addition to either a modified barium swallow or a fiberoptic endoscopic evaluation of swallow to evaluate dysphagia and to screen for aspiration risk.

If caregiver services were required prior to admission for either physical or cognitive impairments, the duration and frequency of this level of care should be documented.

Laboratory studies

Laboratory studies focus on both identification of stroke etiology and evaluation for acute treatments29. Serum electrolytes, cholesterol panel, liver function tests, complete blood count, and hemoglobin A1c are a part of standard practice.

If coagulopathy is suspected, a coagulation panel, D-dimer, and fibrinogen are performed. Hypercoagulable testing for arterial thromboses includes antiphospholipid antibody panel, lupus anticoagulant, Russell viper venom, and hemoglobin electrophoresis. Additional tests for venous thromboses are protein C and S, antithrombin III, Factor V Leiden, and Factor II G20210A. Autoimmune testing, such as erythrocyte sedimentation rate, antinuclear antibody, Complement components 3 and 4, SS-A, SS-B, and high-sensitivity C-reactive protein, should be performed29.

In patients with a concern for hereditary stroke, testing for mutations of the Notch 3 gene on chromosome 19 can help with the diagnosis of Cerebral Autosomal-Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)30.


Computed tomography (CT) scan of the brain without contrast will identify a hemorrhagic stroke, because blood is radiopaque (bright). However, CT may not show obvious changes in patients with acute ischemic stroke within the first 24 hours. Signs to look for on the CT in patients with ischemic stroke include loss of grey/white differentiation, sulcal effacement, slit-like ventricles, and midline shift.

For intra-arterial therapy within 6 and 24 hours of time last seen normal, Computed tomography (CT)-Perfusion or Diffusion Weighted-Magnetic Resonance Imaging (DW-MRI) with or without MRI Perfusion is used to select ischemic stroke patients for treatment based on –  core to penumbra ratio, core infarct volume and the time delay to perfusion of ischemic compared to unaffected brain 20; 21; 31.  For intra-arterial within 6 hours of last time seen normal, an Alberta Stroke Program Early Computed Tomography Score (ASPECTS) of ³ 6 and CT/CT angiogram or MR/MR Angiogram measuring infarct core and penumbra are recommended in preference to perfusion studies 24; 29; 32

Magnetic resonance imaging of the brain allows for identification of ischemic lesions. A set protocol includes T1, T2, fluid-attenuated inversion-recovery (FLAIR), diffusion-weighted imaging (DWI), and apparent-diffusion coefficient sequences. T1 shows possible subtle changes (appears dark) because of a decreased signal. On T2, ischemic lesions and cerebral edema appear white. With FLAIR, ischemic lesions appear white; the suppression of the cerebrospinal fluid (CSF) (dark) makes it easier to find pathology at the CSF/brain junction.

Ischemic lesions with DWI appear white, with maximal intensity at 40 hours33.  On apparent diffusion coefficient, ischemic lesions appear dark where the DWI is bright. It is maximally dark at 28 hours.

Supplemental assessment tools

Magnetic resonance angiography (MRA) evaluates the intracranial vessels and the extracranial vessels of the neck. MRA can detect arterial stenosis, aneurysms, and arteriovenous malformations.

Magnetic resonance venography can be used to identify venous sinus thrombosis. It can also detect atypical hemorrhagic infarcts located high in the convexity, with more associated edema.

Transcranial Doppler ultrasound detects left to right shunt (most common is the patent foramen ovale), emboli monitoring, diagnosis of intracranial stenosis or acute occlusion, and monitoring of acute thrombolytic therapy34.

Early predictions of outcomes

After stroke, females often have greater disability than males35.  A meta-analysis of > 25 studies examining sex differences in long-term outcomes among stroke survivors showed that females had worse functional recovery, and greater long-term disability.  Additional studies with less variability in the statistical approach to confounding can increase confidence in these conclusions36.  

Racial differences in early outcomes also exist.  A national study of inpatient rehabilitation after first stroke found African-Americans were younger, had a higher proportion of hemorrhagic stroke and more disabled on admission than non-Hispanic Whites.  After adjustment for age and stroke subtype, African-Americans had less improvement in functional status per day of  inpatient rehabilitation facility stay37

Additional risk factors for disability after stroke include severe stroke with minimal motor recovery at 4 weeks, evidenced by either a prolonged flaccidity, or a late return of the proprioceptive facilitation (>9d) of the proximal traction response in the arm (>13d).  The proximal traction response can be elicited through stretching the flexor muscles at one joint (shoulder, elbow, wrist, fingers), which evokes contraction of all flexor muscles in the limb38.  Other risk factors are bilateral lesions, low level of consciousness, previous stroke or functional disability, poor sitting balance, severe neglect, sensory and visual deficits, global aphasia, urinary or fecal incontinence (lasting >1-2wk), and delay in medical care39.


Environmental factors can significantly impact morbidity. In patients with limited bed mobility, a stage I pressure ulcer can form in as little as 2 hours. Turning/positioning schedules are integral to maintain skin integrity.

Orientation cues are important for patients with confusion or neglect. Dry-erase or virtual boards updated daily with the day, month, and year, as well as names of the care providers and scheduled test/procedures provide additional environmental support.

Social role and social support system

After a cerebrovascular event, it is common to see changes to the patient’s social role, both at home and in their community. There is a sense of loss, and it is appropriate for patients to grieve this loss. During this time, the support of family and friends is extremely important.

Professional Issues

The goal of providing acute stroke treatment and stroke rehabilitation is to restore as much independence as possible by improving physical, mental, and emotional function. This must be done in a way that preserves the dignity of the patient and motivates the patient to adjust and regain functional abilities.

Rehabilitation Management and Treatments

See Cerebrovascular Disorders Part 2.

Cutting Edge/ Emerging and Unique Concepts and Practice

See Cerebrovascular Disorders Part 2.

Gaps in the Evidence- Based Knowledge

See Cerebrovascular Disorders Part 2.


  1. VIRANI, S. S.  et al. Heart Disease and Stroke Statistics-2020 Update: A Report From the American Heart Association. Circulation, v. 141, n. 9, p. e139-e596, Mar 2020. ISSN 1524-4539. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/31992061
  2. ADAMS, H. P.  et al. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke, v. 24, n. 1, p. 35-41, Jan 1993. ISSN 0039-2499. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/7678184
  3. FEIGIN, V. L.  et al. Global burden of stroke and risk factors in 188 countries, during 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet Neurol, v. 15, n. 9, p. 913-924, 08 2016. ISSN 1474-4465. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/27291521
  4. CASEY, D. E.  et al. 2019 AHA/ACC Clinical Performance and Quality Measures for Adults With High Blood Pressure. Journal of the American College of Cardiology, v. 74, n. 21, p. 2661-2706,  2019.  Disponível em:https://www.jacc.org/doi/abs/10.1016/j.jacc.2019.10.001
  5. WILLIAMS, B.  et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension: The Task Force for the management of arterial hypertension of the European Society of Cardiology and the European Society of Hypertension. Journal of Hypertension, v. 36, n. 10, p. 1953-2041,  2018. ISSN 0263-6352. Disponível em:https://journals.lww.com/jhypertension/Fulltext/2018/10000/2018_ESC_ESH_Guidelines_for_the_management_of.2.aspx
  6. LEWINGTON, S.  et al. Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths. Lancet, v. 370, n. 9602, p. 1829-39, Dec 2007. ISSN 1474-547X. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/18061058
  7. HINDY, G.  et al. Role of Blood Lipids in the Development of Ischemic Stroke and its Subtypes: A Mendelian Randomization Study. Stroke, v. 49, n. 4, p. 820-827, 04 2018. ISSN 1524-4628. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/29535274
  8. SUN, L.  et al. Causal associations of blood lipids with risk of ischemic stroke and intracerebral hemorrhage in Chinese adults. Nat Med, v. 25, n. 4, p. 569-574, 04 2019. ISSN 1546-170X. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/30858617
  9. KHOURY, J. C.  et al. Diabetes mellitus: a risk factor for ischemic stroke in a large biracial population. Stroke, v. 44, n. 6, p. 1500-4, Jun 2013. ISSN 1524-4628. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/23619130
  10. LINDSBERG, P. J.; ROINE, R. O. Hyperglycemia in Acute Stroke. Stroke, v. 35, n. 2, p. 363-364,  2004.  Disponível em: https://www.ahajournals.org/doi/abs/10.1161/01.STR.0000115297.92132.84
  11. JOHNSTON, K. C.  et al. Intensive vs Standard Treatment of Hyperglycemia and Functional Outcome in Patients With Acute Ischemic Stroke: The SHINE Randomized Clinical Trial. Jama, v. 322, n. 4, p. 326-335, Jul 23 2019. ISSN 0098-7484 (Print) 0098-7484
  12. WANG, T. J.  et al. A risk score for predicting stroke or death in individuals with new-onset atrial fibrillation in the community: the Framingham Heart Study. JAMA, v. 290, n. 8, p. 1049-56, Aug 2003. ISSN 1538-3598. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/12941677
  13. DASENBROCK, H. H.  et al. Timing of Decompressive Hemicraniectomy for Stroke: A Nationwide Inpatient Sample Analysis. Stroke, v. 48, n. 3, p. 704-711, Mar 2017. ISSN 0039-2499
  14. ARBOIX, A.; ALIÓ, J. Cardioembolic stroke: clinical features, specific cardiac disorders and prognosis. Curr Cardiol Rev, v. 6, n. 3, p. 150-61, Aug 2010. ISSN 1573-403X (Print) 1573-403x
  15. HEMPHILL, J. C.  et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage. Stroke, v. 46, n. 7, p. 2032-2060,  2015.  Disponível em:https://www.ahajournals.org/doi/abs/10.1161/STR.0000000000000069
  16. GROUP, N. I. O. N. D. A. S. R.-P. S. S. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med, v. 333, n. 24, p. 1581-7, 12 1995. ISSN 0028-4793. Disponível em: https://www.ncbi.nlm.nih.gov/pubmed/7477192
  17. HACKE, W.  et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med, v. 359, n. 13, p. 1317-29, Sep 2008. ISSN 1533-4406. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/18815396
  18. CAMPBELL, B. C. V.  et al. Tenecteplase versus Alteplase before Thrombectomy for Ischemic Stroke. N Engl J Med, v. 378, n. 17, p. 1573-1582, Apr 26 2018. ISSN 0028-4793
  19. BURGOS, A. M.; SAVER, J. L. Evidence that Tenecteplase Is Noninferior to Alteplase for Acute Ischemic Stroke: Meta-Analysis of 5 Randomized Trials. Stroke, v. 50, n. 8, p. 2156-2162, 08 2019. ISSN 1524-4628. Disponível em: https://www.ncbi.nlm.nih.gov/pubmed/31318627
  20. NOGUEIRA, R. G.  et al. Thrombectomy 6 to 24 Hours after Stroke with a Mismatch between Deficit and Infarct. N Engl J Med, v. 378, n. 1, p. 11-21, Jan 4 2018. ISSN 0028-4793
  21. ALBERS, G. W.  et al. Thrombectomy for Stroke at 6 to 16 Hours with Selection by Perfusion Imaging. N Engl J Med, v. 378, n. 8, p. 708-718, Feb 22 2018. ISSN 0028-4793 (Print) 0028-4793
  22. GOYAL, M.  et al. Randomized assessment of rapid endovascular treatment of ischemic stroke. N Engl J Med, v. 372, n. 11, p. 1019-30, Mar 2015. ISSN 1533-4406. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/25671798
  23. JOVIN, T. G.  et al. Thrombectomy within 8 hours after symptom onset in ischemic stroke. N Engl J Med, v. 372, n. 24, p. 2296-306, Jun 2015. ISSN 1533-4406. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/25882510
  24. BERKHEMER, O. A.  et al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med, v. 372, n. 1, p. 11-20, Jan 2015. ISSN 1533-4406. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/25517348
  25. CAMPBELL, B. C.; MITCHELL, P. J.; INVESTIGATORS, E.-I. Endovascular therapy for ischemic stroke. N Engl J Med, v. 372, n. 24, p. 2365-6, 06 2015. ISSN 1533-4406. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/26061843
  26. SAVER, J. L.  et al. Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke. N Engl J Med, v. 372, n. 24, p. 2285-95, Jun 2015. ISSN 1533-4406. Disponível em: https://www.ncbi.nlm.nih.gov/pubmed/25882376
  27. DARGAZANLI, C.  et al. Modified Thrombolysis in Cerebral Infarction 2C/Thrombolysis in Cerebral Infarction 3 Reperfusion Should Be the Aim of Mechanical Thrombectomy: Insights From the ASTER Trial (Contact Aspiration Versus Stent Retriever for Successful Revascularization). Stroke, v. 49, n. 5, p. 1189-1196, May 2018. ISSN 0039-2499
  28. TUNG, E. L.  et al. Rethinking Thrombolysis in Cerebral Infarction 2b: Which Thrombolysis in Cerebral Infarction Scales Best Define Near Complete Recanalization in the Modern Thrombectomy Era? Stroke, v. 48, n. 9, p. 2488-2493, Sep 2017. ISSN 0039-2499
  29. POWERS, W. J.  et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke, v. 50, n. 12, p. e344-e418, 12 2019. ISSN 1524-4628. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/31662037
  30. JOUTEL, A.  et al. Notch3 mutations in CADASIL, a hereditary adult-onset condition causing stroke and dementia. Nature, v. 383, n. 6602, p. 707-10, Oct 1996. ISSN 0028-0836. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/8878478
  31. SARRAJ, A.  et al. Outcomes of Endovascular Thrombectomy vs Medical Management Alone in Patients With Large Ischemic Cores: A Secondary Analysis of the Optimizing Patient’s Selection for Endovascular Treatment in Acute Ischemic Stroke (SELECT) Study. JAMA Neurol, Jul 2019. ISSN 2168-6157. Disponível em:https://www.ncbi.nlm.nih.gov/pubmed/31355873
  32. BRACARD, S.  et al. Mechanical thrombectomy after intravenous alteplase versus alteplase alone after stroke (THRACE): a randomised controlled trial. Lancet Neurol, v. 15, n. 11, p. 1138-47, Oct 2016. ISSN 1474-4422
  33. EASTWOOD, J. D.  et al. Quantitative assessment of the time course of infarct signal intensity on diffusion-weighted images. AJNR Am J Neuroradiol, v. 24, n. 4, p. 680-7, Apr 2003. ISSN 0195-6108. Disponível em: https://www.ncbi.nlm.nih.gov/pubmed/12695203
  34. CAPLAN, L. R. Diagnosis and treatment of ischemic stroke. JAMA, v. 266, n. 17, p. 2413-8, Nov 1991. ISSN 0098-7484. Disponível em: https://www.ncbi.nlm.nih.gov/pubmed/1920747
  35. OTTENBACHER, K. J.  et al. Thirty-day hospital readmission following discharge from postacute rehabilitation in fee-for-service Medicare patients. JAMA, v. 311, n. 6, p. 604-14, Feb 2014. ISSN 1538-3598. Disponível em: https://www.ncbi.nlm.nih.gov/pubmed/24519300
  36. WHITSON, H. E.  et al. Chronic medical conditions and the sex-based disparity in disability: the Cardiovascular Health Study. J Gerontol A Biol Sci Med Sci, v. 65, n. 12, p. 1325-31, Dec 2010. ISSN 1758-535X. Disponível em: https://www.ncbi.nlm.nih.gov/pubmed/20675619
  37. OTTENBACHER, K. J.  et al. Racial and ethnic differences in postacute rehabilitation outcomes after stroke in the United States. Stroke, v. 39, n. 5, p. 1514-9, May 2008. ISSN 0039-2499 (Print) 0039-2499
  38. HOUGLUM, P. A.; BERTOTI, D.; BRUNNSTROM, S. Brunnstrom’s clinical kinesiology. 6th. Philadelphia: F.A. Davis, 2012. xxxiv, 704 p. ISBN 9780803623521
  39. CUCCURULLO, S. Physical medicine and rehabilitation board review. New York: DemosMedical,: 1 online resource p. 2019

Original Version of the Topic

Nneka L. Ifejika-Jones, MD MPH. Cerebrovascular Disorders Part 1 (Disease/Disorder, Principles of Assessment). Published 7/30/2012.

Previous Revision(s) of the Topic

Nneka L. Ifejika-Jones, MD MPH. Cerebrovascular Disorders Part One: Disease/Disorder and Essentials of Assessment. Published 4/19/2016

Author Disclosure

Nneka L. Ifejika, MD MPH
Nothing to Disclose