A stroke, or cerebrovascular accident, is an abrupt onset of a neurologic deficit that is attributable to a focal vascular cause.
Modifiable Risk Factors
Hypertension
Obesity
Atrial fibrillation (AF) / cardiac disease
Diabetes
Dyslipidemia
Excessive alcohol intake
Physical inactivity
Smoking
Diet
Nonmodifiable risk factors:
Age
Gender
Family history
Ethnicity
Previous TIA or stroke
reduction in blood flow
Neurologic symptoms are manifest within seconds because neurons lack glycogen, so energy failure is rapid.
If the cessation of flow lasts for more than a few minutes, infarction or death of brain tissue results.
When blood flow is quickly restored, brain tissue can recover fully and the patient’s symptoms are only transient: this is called a transient ischemic attack (TIA). The definition of TIA requires that all neurologic signs and symptoms resolve within 24 h without evidence of brain infarction on brain imaging. Stroke has occurred if the neurologic signs and symptoms last for >24 h or brain infarction is demonstrated. A generalized reduction in cerebral blood flow due to systemic hypotension (e.g., cardiac arrhythmia, myocardial infarction, or hemorrhagic shock) usually produces syncope). If low cerebral blood flow persists for a longer duration, then infarction in the border zones between the major cerebral artery distributions may develop. In more severe instances, global hypoxia-ischemia causes widespread brain injury; the constellation of cognitive sequelae that ensues is called hypoxic-ischemic encephalopathy. Focal ischemia or infarction, conversely, is usually caused by thrombosis of the cerebral vessels themselves or by emboli from a proximal arterial source or the heart. Intracranial hemorrhage is caused by bleeding directly into or around the brain; it produces neurologic symptoms by producing a mass effect on neural structures, from the toxic effects of blood itself, or by increasing intracranial pressure.
Time last seen normal should be establish to decide whether to give
intravenous thrombolytics (dor to needle time of 60 minutes)
Treated with one or combination of IV alteplaseRapid evaluation is essential in order to possibly implement trombolysis or thrombectomy.1
++++++++++++0.9mg/kg (max 90 mg), thrombolysis-in-situ, mechanical thrombectomy.
loss of sensory and/or motor function on one side of the body (nearly 85% of ischemic stroke patients have hemiparesis); change in vision, gait, or ability to speak or understand; or a sudden, severe headache. The acronym FAST (Facial weakness, Arm weakness, Speech abnormality and Time) is simple and helpful to teach to the lay public about the common physical symptoms of stroke and to underscore that treatments are highly time-sensitive.
Other causes of sudden-onset neurologic symptoms that may mimic stroke include seizure, intracranial tumor, migraine, and metabolic encephalopathy. An adequate history from an observer that no convulsive activity occurred at the onset usually excludes seizure, although ongoing complex partial seizures without tonic-clonic activity can on occasion mimic stroke. Tumors may present with acute neurologic symptoms due to hemorrhage, seizure, or hydrocephalus. Surprisingly, migraine (Chap. 422) can mimic stroke, even in patients without a significant migraine history. When migraine develops without head pain (acephalgic migraine), the diagnosis can be especially difficult. Patients without any prior history of migraine may develop acephalgic migraine even after age 65. A sensory disturbance is often prominent, and the sensory deficit, as well as any motor deficits, tends to migrate slowly across a limb, over minutes rather than seconds as with stroke. The diagnosis of migraine becomes more secure as the cortical disturbance begins to cross vascular boundaries or if classic visual symptoms are present such as scintillating scotomata. At times, it may be impossible to make the diagnosis of migraine until there have been multiple episodes with no residual symptoms or signs and no changes on brain magnetic resonance imaging (MRI). Metabolic encephalopathies typically produce fluctuating mental status changes without focal neurologic findings. However, in the setting of prior stroke or brain injury, a patient with fever or sepsis may manifest a recurrent hemiparesis, which clears rapidly when the infection is treated. The metabolic process serves to “unmask” a prior deficit.
Once the diagnosis of stroke is made, a brain imaging study is necessary to determine if the cause of stroke is ischemia or hemorrhage (Fig. 419-1). Computed tomography (CT) imaging of the brain is the standard imaging modality to detect the presence or absence of intracranial hemorrhage (see “Imaging Studies,” below). If the stroke is ischemic, administration of recombinant tissue plasminogen activator (rtPA) or endovascular mechanical thrombectomy may be beneficial in restoring cerebral perfusion (Chap. 420). Medical management to reduce the risk of complications becomes the next priority, followed by plans for secondary prevention. For ischemic stroke, several strategies can reduce the risk of subsequent stroke in all patients, while other strategies are effective for patients with specific causes of stroke such as cardiac embolus and carotid atherosclerosis. For hemorrhagic stroke, aneurysmal subarachnoid hemorrhage (SAH) and hypertensive intracerebral hemorrhage are two important causes. The treatment and prevention of hypertensive intracerebral hemorrhage are discussed in Chap. 421. SAH is discussed in Chap. 302.
For completeness the nonmodifiable risk factors are listed below:
Age
Gender
Family history
Ethnicity
Previous TIA or stroke
Diet, sodium, exercise, weight, smoking, alcohol intake
All patients should receive information and counseling about possible strategies to modify their lifestyle and risk factors.
Encourage a balanced diet
High in fresh fruits, vegetables, low-fat dairy products, dietary and soluble fiber, whole grains and proteins from plant sources, and low in saturated fats, cholesterol, and sodium.
Most Americans consume excessive amounts of sodium leading to increasing prevalence of hypertension.4
One teaspoon of salt contains approximately 2300 mg (the upper limit recommended).
Encourage exercise—there are many reasons to do this
A meta-analysis published by Lee et al5 reviewed 23 studies (18 cohort and 5 case control studies), examining the association between exercise and stroke incidence and mortality.
Highly active people were reported as having a 27% lower risk of stroke than people who were designated as low active.
Moderately active people also demonstrated a significantly reduced risk of stroke when compared to the low active group. The benefits of both high and moderate levels of activity were reported for both ischemic and hemorrhagic strokes.
Maintain healthy weight—goal BMI of 18.5 to 24.9 kg/m2.
Stop smoking
Smokers who smoke 20 or more cigarettes per day have 2 to 4 times the risk of stroke as compared to nonsmokers. This risk is dose-dependent so the more you smoke, the greater the risk of stroke. Heavy smokers are more at risk than light smokers. Light smokers are more at risk than nonsmokers. Stopping smoking has been shown to reverse risk of cardiovascular disease. This highlights the cessation of smoking as a leading effective intervention available to reduce risk of stroke.
Alcohol (in moderation)6
A meta-analysis by Reynolds et al4 revealed that individuals who consumed 1 to 2 drinks per day had the least risk of stroke and those that had more than 5 drinks per day had the most risk of stroke when compared to a group of abstainers. (J-shaped relationship as abstaining had a higher risk than 1-2 drinks/day, making the first part of the J.)
Heavy drinking (more than 5 drinks per day) was associated with the risk of hemorrhagic stroke.
Irregular and binge drinking (more than 5 drinks at one time) have been associated with an increased risk of hemorrhagic stroke.
A. The diagnosis in this patient is stroke, characterized by the sudden onset of focal neurologic deficits that persist for at least 24 hours owing to an abnormality of the cerebral circulation. The focal symptoms and signs that result from stroke correlate with the area of the brain supplied by the affected blood vessel. In this case, the patient has weakness and sensory loss on the right side. These symptoms suggest involvement of the left middle cerebral artery or at least its associated vascular territory. The vascular territory supplied by the middle cerebral artery includes the lateral frontal, parietal, lateral occipital, and anterior and superior temporal cortex and adjacent white matter, as well as the caudate, putamen, and internal capsule.
B. Risk factors for stroke include age, male sex, hypertension, hypercholesterolemia, diabetes, smoking, heavy alcoholconsumption, and oral contraceptive use.
C. Stroke is classified as either ischemic or hemorrhagic in origin. Ischemic stroke may result from the thrombotic or embolic occlusion of the vessel. Hemorrhagic stroke may result from intraparenchymal hemorrhage, subarachnoid hemorrhage, subdural hemorrhage, epidural hemorrhage, or hemorrhage within an ischemic infarction. Given the CT scan result, it is likely that this man has sustained an ischemic, rather than a hemorrhagic, stroke. Hemorrhagic and ischemic strokes can be difficult to differentiate on clinical grounds, but the former often produce a less predictable pattern of neurologic deficits. This is because the neurologic deficits in hemorrhagic stroke depend both on the location of the bleed and on factors that affect brain function at a distance from the hemorrhage, including increased intracranial pressure, edema, the compression of neighboring brain tissue, and rupture of blood into the ventricles or subarachnoid space.
D. The most likely underlying cause of stroke in this patient is atherosclerosis. Atherosclerosis arises from vascular endothelial cell injury, often caused by chronic hypertension or hypercholesterolemia, both present in this man. Endothelial injury stimulates the attachment of circulating monocytes and lymphocytes that migrate into the vessel wall and stimulate the proliferation of smooth muscle cells and fibroblasts. This results in plaque formation. Damaged endothelium also serves as a nidus of platelet aggregation that further stimulates the proliferation of smooth muscle and fibroblasts. The plaques formed may enlarge and occlude the vessel, leading to thrombotic stroke, or they may rupture, releasing emboli and causing embolic stroke.
History of TIA
History of previous stroke
hypertension,
atherosclerosis, cardiac disease (eg, atrial fibrillation, myocardial infarction, and valvular disease),
diabetes,
carotid stenosis,
dyslipidemia,
hypercoagulable states,
tobacco, and
alcohol use.
Stroke occurs when
thrombosis,
embolism, or hemorrhage interrupts cerebral oxygenation and causes the death of neurons in the brain.
This leads to deficits in cognition and in motor and sensory function.
Ischemic Stroke Syndromes
Syndrome | Symptoms |
---|---|
Dominant hemisphere | Contralateral numbness and weakness, contralateral visual field cut, gaze preference, dysarthria, aphasia |
Nondominant hemisphere | Contralateral numbness and weakness, visual field cut, contralateral neglect, dysarthria |
Anterior cerebral artery | Contralateral weakness (leg > arm); mild sensory deficits; dyspraxia |
Middle cerebral artery | Contralateral numbness and weakness (face, arm > leg); aphasia (if dominant hemisphere) |
Posterior cerebral artery | Lack of visual recognition; altered mental status with impaired memory; cortical blindness |
Vertebrobasilar syndrome | Dizziness, vertigo; diplopia; dysphagia; ataxia; ipsilateral cranial nerve palsies; contralateral weakness (crossed deficits) |
Basilar artery occlusion | Quadriplegia; coma; locked-in syndrome (paralysis except upward gaze) |
Lacunar infarct | Pure motor or sensory deficit |
Syndrome | Symptoms |
---|---|
Intracerebral hemorrhage | May be clinically indistinguishable from infarction; contralateral numbness and weakness; aphasia, neglect (depending on hemisphere); headache, vomiting, lethargy, marked hypertension more common |
Cerebellar hemorrhage | Sudden onset of dizziness, vomiting, truncal instability, gaze palsies, stupor |
[It is possible, although challenging, to clinically infer the location of the anatomic insult to the clinical presentation by correlating symptoms with circulatory region.
Anatomy of brain and blood flow. (Modified, with permission, from Schwartz DT. Emergency Radiology: Case Studies. New York, NY: McGraw-Hill Education, 2008: 505.)
For instance, aphasia usually corresponds to a left hemispheric stroke; neglect generally indicates a right hemispheric stroke; crossed signs (eg, right-sided facial droop with left-sided extremity weakness) typically indicate brainstem involvement.
Middle Cerebral Artery
Infarction of the cerebral cortex in the region of the brain supplied by the middle cerebral artery (MCA) or one of its branches is most commonly responsible for stroke.
It supplies the area of the cerebral cortex responsible for hand function; the anterior cerebral artery supplies the area responsible for lower extremity motion.
Cerebral artery circulation.
The typical clinical picture following MCA stroke is contralateral hemianesthesia (decreased sensation), homonymous hemianopia (visual field deficit), and spastic hemiplegia with more paralysis in the upper extremity than in the lower extremity. Because hand function requires relatively precise motor control, even for activities with assistive equipment, the prognosis for the functional use of the hand and arm is considerably worse than for the leg. Return of even gross motor control in the lower extremity may be sufficient for walking.
Infarction in the region of the anterior cerebral artery causes paralysis and sensory loss of the opposite lower limb and, to a lesser degree, the arm.
Patients who have cerebral arteriosclerosis and suffer repeated bilateral infarctions are likely to have severe cognitive impairment that limits their general ability to function even when motor function is good.
After stroke, motor recovery follows a fairly typical pattern. The size of the lesion and the amount of collateral circulation determine the amount of permanent damage. Most recovery occurs within 6 months, although functional improvement may continue as the patient receives further sensorimotor reeducation and learns to cope with disability.
Initially after a stroke, the limbs are completely flaccid. Over the next few weeks, muscle tone and spasticity gradually increase in the adductor muscles of the shoulder and in the flexor muscles of the elbow, wrist, and fingers. Spasticity also develops in the lower extremity muscles. Most commonly, there is an extensor pattern of spasticity in the leg, characterized by hip adduction, knee extension, and equinovarus deformities of the foot and ankle.
Equinovarus deformities of the feet in a patient with spasticity.
In some cases, however, a flexion pattern of spasticity occurs, characterized by hip and knee flexion.
Whether the patient recovers the ability to move one joint independently of the others (selective movement) depends on the extent of the cerebral cortical damage. Dependence on the more neurologically primitive patterned movement (synergy) decreases as selective control improves. The extent to which motor impairment restricts function varies in the upper and lower extremities. Patterned movement is not functional in the upper extremity, but it may be useful in the lower extremity, where the patient uses the flexion synergy to advance the limb forward and the mass extension synergy for limb stability during standing.
The final processes in sensory perception occur in the cerebral cortex, where basic sensory information is integrated to complex sensory phenomena such as vision, proprioception, and perception of spatial relationships, shape, and texture. Patients with severe parietal dysfunction and sensory loss may lack sufficient perception of space and awareness of the involved segment of their body to ambulate. Patients with severe perceptual loss may lack balance to sit, stand, or walk. A visual field deficit further interferes with limb use and may cause patients to be unaware of their own limbs.
It is possible, although challenging, to clinically infer the location of the anatomic insult to the clinical presentation by correlating symptoms with circulatory region.
For instance, aphasia usually corresponds to a left hemispheric stroke; neglect generally indicates a right hemispheric stroke; crossed signs (eg, right-sided facial droop with left-sided extremity weakness) typically indicate brainstem involvement.1
Stroke is the fourth leading cause of death in the United States
Stroke is a serious and common disorder that affects over 795,000 persons in the United States each year. It remains the fourth leading cause of death in the United States after heart disease, cancer, and chronic lung disease.
Many surviving victims are left with neurologic deficits and may be unable to care for themselves. Symptoms vary widely depending on the type of infarct, the location, and the amount of brain involved.. Strokes are classified as either ischemic or hemorrhagic. Eighty percent of strokes are ischemic due to the blockage of a blood vessel secondary to thrombosis or embolism. They are generally seen in patients older than the age of 50 and present with the sudden onset of focal neurologic deficits. Hemorrhagic strokes are typically seen in younger patients and are due to intraparenchymal or subarachnoid cerebral vessel bleeding.
Strokes are more common in the elderly (75% occur in patients older than 75 years), males, and African Americans.
Symptoms vary widely depending on the type of infarct, the location, and the amount of brain involved (Tables 28–1 and 28–2). Strokes are classified as either ischemic or hemorrhagic. Eighty percent of strokes are ischemic due to the blockage of a blood vessel secondary to thrombosis or embolism. They are generally seen in patients older than the age of 50 and present with the sudden onset of focal neurologic deficits. Hemorrhagic strokes are typically seen in younger patients and are due to intraparenchymal or subarachnoid cerebral vessel bleeding.
Approximately 800,000 new strokes occur, as many as 30% of survivors permanently disabled and approximately 130,000 people die from stroke in the United States each year.
The incidence of stroke increases with age, The annual incidence of stroke is 1 in 1000, with cerebral thrombosis causing nearly three fourths of the cases. More than half of stroke victims survive and have an average life expectancy of approximately 6 years. Most survivors have the potential for significant function and useful lives if they receive the benefits of rehabilitation.
Modifiable risk factors for stroke include systolic or diastolic hypertension, , and
A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of Richard P. Usatine, MD.)
CTransient ischemic attack increases risk for 90-day stroke 10-fold.
Content 13
A 59-year-old man with a history of hypertension presents to the emergency department (ED) with right-sided paralysis and aphasia. The patient’s wife states he was in his normal state of health until 1 hour ago, when she heard a thud in the bathroom and walked in to find him collapsed on the floor. She immediately called emergency medical services, which transported the patient to your ED. En route, his fingerstick blood sugar was 108 mg/dL. On arrival in the ED, the patient is placed on monitors and an IV is established. His temperature is 36.8°C (98.2°F), blood pressure is 169/93 mm Hg, heart rate is 86 beats per minute, and respiratory rate is 20 breaths per minute. The patient has a noticeable left-gaze preference and is verbally unresponsive, although he will follow simple commands such as raising his left thumb. He has a normal neurologic examination on the left, but on the right he has a facial droop, no motor activity, decreased deep tendon reflexes (DTRs), and no sensation to light-touch.
Summary: This is a 59-year-old man with acute onset of aphasia and right-sided paralysis 60 minutes prior to arrival in the ED.
Obesity
Atrial fibrillation (AF) / cardiac disease
Diabetes
Dyslipidemia
Excessive alcohol intake
Physical inactivity
Smoking
Diet
If cost were NOT an issue, which of the following drugs/drug combinations would be the ideal regimen for the secondary prevention of stroke?
The correct answer is B. You answered D.
The correct answer is "B." Both clopidogrel and aspirin with extended release dipyridamole reduce the risk of stroke to a greater degree than aspirin alone in patients with a history of stroke. There is evidence to suggest that aspirin with extended release dipyridamole is the overall superior drug. Clopidogrel and aspirin should not be used together for secondary stroke prevention, as there is no significant benefit compared with clopidogrel alone.
Content 2
A 58-year-old man experienced a neurologic deficit and is diagnosed as having a stroke. Which of the following is the most likely etiology?
The correct answer is A. You answered A.
A. Ischemia is the most common etiology of stroke (due to thrombosis, embolism, or hypoperfusion) and is responsible for up to 80% of strokes.
Reference
https://www.ahajournals.org/doi/full/10.1161/STR.0000000000000158
Study Question
In a stroke affecting the territory of the middle cerebral artery–
A 62-year-old man presents with an asymptomatic abdominal aortic aneurysm (AAA) measuring 4.8 cm in diameter. The patient’s past medical history is significant for hypertension and stable angina. He has a 40-pack-year smoking history. His current medications include aspirin, a beta-blocker, and nitrates. The patient describes himself as an active man who just retired and plays 18-holes of golf two times a week. On examination, the carotid pulses and upper extremity pulses are normal. The abdomen is nontender with a prominent aortic pulse. Pulses in the femoral and popliteal regions are readily palpable and appear more prominent than usual.