Author(s): Sofia Barchuk, DO, Rosanna Sabini, DO
Originally published: July 30, 2012 Last updated: February 8, 2024
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Disease/Disorder

Definition

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. 

Etiology

Of all strokes, 88% are ischemic and 13% are hemorrhagic.13,29

Ischemic stroke subtypes and underlying mechanisms are based on information by the TOAST (Trail of Org 10172 in Acute Stroke Treatment). The classification system includes five subtypes listed below.20 

  • Large-artery atherosclerosis: stenosis or occlusion of major brain artery or cortical artery
  • Cardioembolism: embolus arising from heart 
  • Small-artery occlusion: lacunar stroke, small vessel disease
  • Stroke of other determined etiology: nonatherosclerotic vasculopathies, hypercoagulable states, and/or hematologic disorders 
  • Stroke of undetermined etiology: stroke that cannot be determined with any degree of confidence  

Hemorrhagic strokes can be subdivided into intracerebral hemorrhage (within the brain) and subarachnoid hemorrhage (between the inner and outer layers of tissue covering the brain). Hemorrhagic strokes are most often caused by hypertension, with lesions typically located in the basal ganglia (50%), cerebral lobes (10-20%), thalamus (15%), pons and brainstem (10-20%). Cerebral amyloid angiopathy (CAA) is another important cause of primary lobar intracerebral bleeding in older adults. It is characterized by deposition of amyloid-B peptide in cerebral vasculature. Other risk factors for hemorrhagic stroke include, but are not limited to, dual antiplatelet therapy, chronic liver disease, sympathomimetics, old age, male sex, and tumors.12

Epidemiology including risk factors and primary prevention

Stroke is the leading cause of long-term adult disability and the fifth leading cause of death in the United States. Although stroke mortality has decreased in the past two decades research shows that it may be on the rise again.4

Risk factors for stroke can be broadly categorized as modifiable and non-modifiable, and treatment strategies often account the patient’s risk factor profile. The major modifiable risk factors, with increased relative risk of stroke that can be reduced with treatment, include hypertension, atrial fibrillation, diabetes, smoking, hyperlipidemia, and carotid artery stenosis.

The INTERSTROKE study identified 10 modifiable risk factors that explained 90% of strokes and 3 non-modifiable risk factors.4 Modifiable risk factors include hypertension, current smoking status, waist-to-hip ratio, diet, physical inactivity, hyperlipidemia, diabetes mellitus, alcohol consumption, cardiac causes, and apolipoprotein B to A1. Non-modifiable risk factors are age, sex, and race/ethnicity.4

Hypertension is the number one risk factor for both ischemic and hemorrhagic stroke.There are five American Heart Association blood pressure categories three of which are considered “high blood pressure”. Normal is defined as systolic blood pressure (SBP) less than 120 and diastolic blood pressure (DP) less than 80. Elevated is SBP ranging from 120-129 and DP less than 80. Hypertension stage 1, 2 and hypertensive crisis are categorized as “high blood pressure”. Hypertension stage 1 is SBP ranging from 130-139 or DP 80-89. Hypertension stage 2 is a SBP greater than or equal to 140 or a DP greater than 90. Hypertensive crisis is defined as a SBP greater than 180 and/or DP greater than 120.3

According to the European Society of Hypertension (ESH) Management of Arterial Hypertension 2023 Guidelines adults ages 18-79 yo primary SBP/DP goal is <140/90 mmHg. If treatment is well tolerated then target SBP/DP is < 130/80 mmHg, but not <120/70. In adults greater than 80 yo target is SBP/DP is < 140/90.17 In persons with elevated hypertension lifestyle modifications including diet and exercise to reduce BP are recommended.

The relationship between dyslipidemia and risk of stroke is intricate. Research shows that there is an increased risk for ischemic stroke with elevated total cholesterol levels and a decreased risk of ischemic stroke with increased levels of high-density lipoprotein (HDL).4 The association of each cholesterol subfraction with total stroke has shown inconsistent results therefore data are limited on associations with specific ischemic stroke subtypes.26 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 lipoprotein.7 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 risk.23

Diabetes mellitus presents as a stand-alone risk factor for stroke. The duration of diabetes mellitus is associated with a markedly increased likelihood of ischemic stroke compared to individuals without diabetes and accounts for about 20% of deaths in patients with the disease. (risk factors). In a subgroup analysis of the SHINE (Stroke Hyperglycemia Insulin Network Effort) Study published in 2022 intensive (target BG 80-130 mg/dL) vs standard (target BG 80-179mg/dL) insulin treatment of hyperglycemia in acute ischemic stroke did not affect 90-day functional outcomes measured by the modified Rankin Scale (mRS).11

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 thrombi.28

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 factors.14

Patho-anatomy/physiology

There are signs and symptoms characteristic of vascular lesions in the various arterial territories of the brain.20

  • 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.
  • Anterior cerebral: Contralateral loss of strength and sensation in the lower limb and, to a lesser extent, in the upper limb. Hand and face are usually spared.
  • Posterior cerebral: Homonymous hemianopsia, possibly confusion and aphasia if present in the dominant hemisphere.
  • 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.
  • 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.
  • 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 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.24

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

Medical complications following a stroke occur in 40%-96% of cases and are related to poor outcome. The most common neurologic complication following a stroke is recurrent stroke. Other complications are epileptic seizure, urinary tract infection, chest infection, pressure sores, falls, deep venous thrombosis, pulmonary embolus, shoulder pain, depression, anxiety and confusion.9

Essentials of Assessment

History

According to the 2018 AHA/ASA Stroke Early Management Guidelines, at initial evaluation IV tPA (tissue plasminogen activator) should be administered to eligible subjects with acute ischemic stroke within 3 hours of last known normal and to a more selective subgroup within 4.5 hours. Patients who are 18 years or older should undergo a mechanical thrombectomy with stent retriever if they have minimal pre-stroke disability, have a causative occlusion of the internal carotid artery or proximal middle cerebral artery, have National Institutes of Health Score (NIHS) of greater than or equal to 6, have a reassuring non-contrast CT head (ASPECT score greater than or equal to 6), and if they can be treated within 6 hours.30

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 treatments.16 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 performed.16

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).8

Imaging

Non-contrast computed tomography (NCCT) aids in ruling out hemorrhagic stroke, because blood will be hyperintense (bright) on imaging while acute ischemic strokes take longer to develop (within the first 24 hours) and will be hypointense (dark) on CT. Signs to look for on CT in patients with ischemic stroke include loss of grey/white differentiation, sulcal effacement, slit-like ventricles, and midline shift.

CT perfusion (CTP) scans are utilized to determine if there is a substantial amount of tissue that can be salvaged after reperfusion therapy. AHA stroke guidelines do not suggest utilizing CTP in the early time window which is defined as less than 6 hours after symptom onset. CTP is reasonable to obtain if NCCT +/- CTAngio are insufficient.  Endovascular therapy can usually be determined based on NCCT and CTAngio. Administration of tPA can often be implemented based on NCCT findings alone.10, 18,19

Magnetic resonance imaging (MRI) of the brain is more sensitive at identifying acute ischemic lesions compared to NCCT and can be seen within a few minutes of occlusion. Sequences include T1, T2, fluid-attenuated inversion-recovery (FLAIR), diffusion-weighted imaging (DWI), and apparent-diffusion coefficient (ADC). In acute ischemic stroke, comparison between DWI and ADC are utilized to confirm diagnosis. Acute lesions will be hyperintense (bright) on DWI and hypointense (dark) on ADC.10

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 is a rapid technique that determines flow velocity through the basilar arteries. It can be used to aid in the diagnosis of acute ischemic stroke, vasospasm, SAH, sickle cell disease, and brain death.1

Early predictions of outcomes

After stroke, females often have greater disability than males.6 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 conclusions.21

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 stay.6 

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 limb25. 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 care.7

Environmental

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.

References

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  3. The Facts About High&nbsp;Blood Pressure. www.heart.org. Accessed October 22, 2023. https://www.heart.org/en/health-topics/high-blood-pressure/the-facts-about-high-blood-pressure
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  28. Wang TJ, Massaro JM, Levy D, 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. 2003;290(8):1049-1056. doi:10.1001/jama.290.8.1049
  29. 2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline From the American Heart Association/American Stroke Association. doi:10.1161/STR.0000000000000375
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  31. 2018 AHA/ASA Stroke Early Management Guidelines. American College of Cardiology. Accessed October 24, 2023. https://www.acc.org/Latest-in-Cardiology/ten-points-to-remember/2018/01/29/12/45/http%3a%2f%2fwww.acc.org%2fLatest-in-Cardiology%2ften-points-to-remember%2f2018%2f01%2f29%2f12%2f45%2f2018-Guidelines-for-the-Early-Management-of-Stroke

Original Version of the Topic

Nneka L. Ifejika-Jones, MD MPH. Cerebrovascular Disorders Part 1 (Disease/Disorder, Principles of Assessment). 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. 4/19/2016

Nneka L. Ifejika, MD MPH. Cerebrovascular Disorders Part One: Disease/Disorder and Essentials of Assessment. 12/15/2020

Author Disclosure

Sofia Barchuk, DO
Nothing to Disclose

Rosanna Sabini, DO
Nothing to Disclose