Stroke

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2] Khizer Yaseen, M.B.B.S.[3]

Stroke is the rapidly developing loss of brain functions due to a disturbance in the blood vessels supplying blood to the brain. This can be due to ischemia (lack of blood supply) caused by thrombosis or embolism, or due to a hemorrhage. Stroke is a medical emergency and can cause permanent neurological damage, complications and death if not promptly diagnosed and treated. It is the third leading cause of death and the leading cause of adult disability in the United States and Europe. It is predicted that stroke will soon become the leading cause of death worldwide.

.Patent foramen ovale is associated with ischemic stroke of undetermined source, particularly in patients younger than 60 years. Evaluation focuses on determining whether the PFO is causally related to the index stroke and on excluding alternative etiologies.^[1]

The history of stroke goes back to the 5th century B.C. as apoplexy. In 17th century it was discovered that the cause is sudden disruption of blood supply to the brain.

Ischemic stroke may be classified according to the duration of onset of symptoms and causative agent. The major classification system of ischemic stroke include toast classification system, causative classification of stroke system (CCS),and sparkle classification of ischemic stroke.

The pathophysiology of ischemic stroke may depend on the underlying cause of ischemia. Ischemic infarct may be categorized into two types depending on the area of the brain involved as focal ischemic stroke or global ischemic stroke. Hemodynamic changes in ischemic stroke results from cerebral auto regulation dysfunction as brain tissue is highly sensitive to mild changes in oxygen levels. Several minutes of hypoxia leads to irreversible injury. Cerebral auto regulation maintains the perfusion pressure in the brain between the pressure range of 60-150 mm Hg via vasoconstriction and vasodilatation. Prolonged ischemia decreases oxygen delivery to the cells causing anaerobic glycolysis and increased production of free oxygen and nitrate radicals which in turn causes cell membrane, DNA damage and cell death.

There are several causes for stroke. Some may cause hemorrhage and some causes ischemia. Among all of them there are several lethal causes which we need to be more cautious about them.

Patent foramen ovale may permit paradoxical embolism, allowing venous thrombi to bypass the pulmonary circulation and enter the arterial system, resulting in ischemic stroke.^[1]

The differential diagnosis of ischemic stroke may include brain tumour, hemorrhagic stroke, subdural hemorrhage, neurosyphilis, complex or atypical migraine, hypertensive encephalopathy, wernicke’s encephalopathy, CNS abscess, drug toxicity, conversion disorder, electrolyte disturbance, meningitis or encephalitis, multiple sclerosis exacerbation, seizure and hypoglycemia. There are also some conditions which may cause muscle weakness and paralysis such as Botulism, Myasthenia gravis, Guillian-Barre syndrome, Eaton Lambert syndrome, Electrolyte disturbance, Organophosphate toxicity, Multiple sclerosis exacerbation, Amyotrophic lateral sclerosis, Inflammatory myopathy. It is necessary to differentiate these conditions from stroke.

The worldwide incident of stroke is about 68 percent and it increases with age. It is more common in men. However, the mortality is more in women. the incident and mortality rates are high in African-American population and developing countries.

Younger patients with ischemic stroke are more likely to have a pathogenic patent foramen ovale, particularly in the absence of traditional vascular risk factors.

Risk factors for stroke are divided into modifiable and non modifiable risk factors. Modifiable risk factors include hypertension, diabetes mellitus, cardiac disease, cigarette smoking, alcohal consumption, hyperhomocysteinemia, hyperlipidemia, obesity, sedentary life style and oral contraceptive usage. Some of the non modifiable risk factors include advanced age, male gender, family history of ischemic stroke, african-american and hispanic race, and genetic diseases such as sicke cell disease.

Clinical features associated with PFO-related ischemic stroke include younger age, absence of vascular risk factors, and embolic cortical infarction patterns.^[2]

The Risk of Paradoxical Embolism (RoPE) score is used to estimate the probability that a detected patent foramen ovale is causally related to ischemic stroke.^[2]The PFO-Associated Stroke Causal Likelihood (PASCAL) classification integrates anatomical and clinical features to guide management decisions.^[1]

There are several screening tests for high risk patients to detect and prevent stroke: Carotid Artery Ultrasound, Abdominal Aortic Aneurysm Screening, Atrial Fibrillation, Peripheral Artery Disease.

Stroke can cause temporary or permanent complications based on the location and time to appropriate treatment. Delayed treatment or sever hemorrhagic or ischemic stroke can lead to death. Other may suffer from Dysphagia, Pneumonia, Myocardial infarction and arrhythmias, need for mechanical ventilation, pulmonary edema, central sleep apnea, urinary incontinence, falls, Musculoskeletal spasticity, Post-stroke seizure, Bowel incontinence, cognitive impairment. Prognosis depends on patient’s age and stroke severity based on clinical evaluation and imaging.

Ischemic stroke due to paradoxical embolism is a recognized complication of patent foramen ovale.^[3]Prognosis is influenced by patient age, absence of vascular risk factors, and anatomical characteristics of the PFO.^[2]

A systematic review found that acute facial paresis, arm drift, or abnormal speech are the best findings.^[4]

Electrocardiogram (ECG) may be performed to determine the underlying etiology such as arrhythmias which may result in clots in the heart that may spread to the brain vessels through the bloodstream. Holter monitor may be used to identify intermittent arrhythmias.

Electrocardiography and prolonged rhythm monitoring are mandatory to exclude atrial fibrillation in patients with ischemic stroke of undetermined source..^[1]At least 30 days of cardiac rhythm monitoring is recommended.^[5]

Echocardiography may be performed to determine the underlying etiology such as arrhythmias and the resultant clots in the heart that may spread to the brain vessels through the bloodstream.

Echocardiographic evaluation may identify structural cardiac abnormalities associated with embolic stroke mechanisms, including patent foramen ovale.^[1] Transesophageal echocardiography with contrast may be used to detect right-to-left shunting. Transesophageal echocardiography allows detection of high-risk PFO features, including large right-to-left shunt, atrial septal aneurysm, long PFO tunnel, and the presence of a Eustachian valve.^[6]

Transesophageal echocardiography with contrast and provocative maneuvers is the preferred diagnostic study for identifying patent foramen ovale and for anatomical risk stratification in ischemic stroke. Evaluation should exclude alternative cardioembolic sources.^[6]

Transcranial Doppler ultrasonography is a sensitive screening modality for detecting right-to-left shunting but lacks detailed anatomic resolution.^[1]

Ultrasound/doppler study of the carotid arteries can be used to detect carotid stenosis or dissection of the precerebral arteries.

When a stroke has been diagnosed, various other studies may be performed to determine the underlying etiology. With the current treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli. Test selection may vary, since the cause of stroke varies with age, comorbidity and the clinical presentation. An angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation)

Magnetic resonance imaging findings of embolic cortical infarcts or infarcts involving multiple vascular territories support a cardioembolic mechanism, including PFO-associated stroke.^[7]

Laboratory evaluation is performed to exclude hypercoagulable states and alternative stroke etiologies. Evidence of venous thromboembolism supports paradoxical embolism as a stroke mechanism.^[7]

Early recognition of the signs of stroke is generally regarded as important. Only detailed physical examination and medical imaging provide information on the presence, type, and extent of stroke, and hence hospital attendance — even if the symptoms were brief — is advised.

Studies show that patients treated in hospitals with a dedicated Stroke Team or Stroke Unit and a specialized care program for stroke patients have improved odds of recovery.

Treatment of stroke is occasionally with thrombolysis (“clot buster”), but usually with supportive care (physiotherapy and occupational therapy) and secondary prevention with antiplatelet drugs (aspirin and often dipyridamole), blood pressure control, statins and anticoagulation (in selected patients).^[8]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2]

The history of stroke goes back to the 5th century B.C. as apoplexy. In 17th century it was discovered that the cause is sudden disruption of blood supply to the brain.

Stroke is documented in the Hippocrates notes in the 5th century B.C. as apoplexy, meaning “struck down by violence”, which refers to a person who suddenly falls and becomes unconscious. In 1658, Dr. Johann Jacob Wepfer, pathologist and pharmacologist, discovered that the apoplexy is caused by sudden disruption of blood supply to the brain. He identified that the blood supply to the brain was disrupted either due to bleeding in the brain or blocking of the arteries by blood clots. At this time, physicians also believed that excessive food consumption would cause a person to strain with a bowel movement. This straining was thought to have a possible connection with the occurrence of apoplexy, so purging with enemas and stimulants was used frequently. Exercising and proper body position with the neck and head extension were encouraged to ensure proper blood flow to the brain. Finally, bloodletting had become a common practice, but at this point, restrictions were now being discussed. New guidelines recommended the use of bloodletting judiciously when physicians believed that congestion was the cause of apoplexy in a patient.

It is believed that actors Luke Perry, Cary Grant and Bill Paxton; actresses Debbie Reynolds, Della Reese and Grace Kelly; former presidents Franklin Roosevelt, Richard Nixon and Gerald Ford; director John Singleton; baseball player Kirby Puckett; former British prime minister Winston Churchill; former Russian dictator Josef Stalin were all the victims of a fatal stroke. In addition, singers Loretta Lynn and Randy Travis; actresses Sharon Stone (“Basic Instinct”) and Marla Gibbs (TV’s “The Jeffersons”); former NFL New England Patriots player Tedy Bruschi; sprinter Michael Johnson; actors Tim Curry (“Rocky Horror Picture Show”) and Frankie Muniz (TV’s “Malcolm In The Middle”); rock singer Bret Michaels have also had the experience of a stroke but have survived.^[1][2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2]Seyedmahdi Pahlavani, M.D. [3]Aysha Anwar, M.B.B.S[4],Tarek Nafee, M.D. [5],Sara Mehrsefat, M.D. [6]

Ischemic stroke may be classified according to the duration of onset of symptoms and causative agent. The major classification system of ischemic stroke include toast classification system, causative classification of stroke system (CCS), and sparkle classification of ischemic stroke.

Ischemic stroke may be classified according to the duration of onset of symptoms and causative agent. The major classification system of ischemic stroke include: ^{[1][2][3][4][5][6][7]}

• Toast classification system^[1]
• Causative classification of stroke system (CCS)^[4]
• Sparkle classification of ischemic stroke^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2],Aysha Anwar, M.B.B.S[3]

The pathophysiology of ischemic stroke may depend on the underlying cause of ischemia. Ischemic infarct may be categorized into two types depending on the area of the brain involved as focal ischemic stroke or global ischemic stroke. Hemodynamic changes in ischemic stroke results from cerebral auto regulation dysfunction as brain tissue is highly sensitive to mild changes in oxygen levels. Several minutes of hypoxia leads to irreversible injury. Cerebral auto regulation maintains the perfusion pressure in the brain between the pressure range of 60-150 mm Hg via vasoconstriction and vasodilatation. Prolonged ischemia decreases oxygen delivery to the cells causing anaerobic glycolysis and increased production of free oxygen and nitrate radicals which in turn causes cell membrane, DNA damage and cell death.

The brain receives blood from two sources: the internal carotid arteries, which arise at the point in the neck where the common carotid arteries bifurcate, and the vertebral arteries. The internal carotid arteries branch to form two major cerebral arteries, the anterior and middle cerebral arteries. The right and left vertebral arteries come together at the level of the pons on the ventral surface of the brainstem to form the midline basilar artery. The basilar artery joins the blood supply from the internal carotids in an arterial ring at the base of the brain (in the vicinity of the hypothalamus and cerebral peduncles) called the circle of Willis. The posterior cerebral arteries arise at this confluence, as do two small bridging arteries, the anterior and posterior communicating arteries. Conjoining the two major sources of cerebral vascular supply via the circle of Willis presumably improves the chances of any region of the brain continuing to receive blood if one of the major arteries becomes occluded. The physiological demands served by the blood supply of the brain are particularly significant because neurons are more sensitive to oxygen deprivation than other kinds of cells with lower rates of metabolism. In addition, the brain is at risk from circulating toxins, and is specifically protected in this respect by the blood-brain barrier. As a result of the high metabolic rate of neurons, brain tissue deprived of oxygen and glucose as a result of compromised blood supply is likely to sustain transient or permanent damage. Brief loss of blood supply (referred to as ischemia) can cause cellular changes, which, if not quickly reversed, can lead to cell death. Sustained loss of blood supply leads much more directly to death and degeneration of the deprived cells.

The pathogenesis of ischemic stroke may depend on the underlying cause of ischemia. Ischemic infarct may be categorized into two types depending on the area of the brain involved:^{[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][6][8]}

Traditionally, stroke has been classified into 2 broad categories of stroke syndrome: hemorrhagic (bleeding) stroke and thrombotic (ischemic) stroke. These 2 phenotypes are considered to be diametrically opposite conditions because hemorrhage is characterized by bleeding into the brain tissue resulting in hematoma and brain tissue shift while ischemia is due to thrombosis characterized by “blood clots” within intracranial vasculature leading to hypoxia to a certain part of the brain due to reduced blood supply. Both may result in different clinical brain syndromes even in the same locality.^[17][18]

Pathologies affecting large extracranial vessels include:

• Atherosclerosis
• Giant cell arteritis
• Dissection
• Takayasu arteritis
• Fibromuscular dysplasia

Pathologies affecting large intracranial vessels include:

• Atherosclerosis
• Dissection
• Arteritis/vasculitis
• Noninflammatory vasculopathy
• Vasoconstriction

Embolic strokes are divided into four categories:

• Those with a known source that is cardiac
• Those with a possible cardiac or aortic source based upon transthoracic and/or transesophageal echocardiographic findings
• Those with an arterial source (artery to artery embolism)
• Those with a truly unknown source in which tests for embolic sources are negative

• Hemodynamic changes in ischemic stroke results from cerebral auto regulation dysfunction as brain tissue is highly sensitive to mild changes in oxygen levels
• Several minutes of hypoxia leads to irreversible injury^[6][8]
• Cerebral auto regulation maintains the perfusion pressure in the brain between the pressure range of 60-150 mm Hg via vasoconstriction and vasodilatation.^[8]
• Pressure changes below 60 mm Hg and more than 150 mm Hg disrupts the normal auto regulation.
• Below 60 mm Hg, initially there is extensive vasodilatation of the affected vessels to increase blood flow to the affected area. This is mediated by increase in endothelial nitric oxide production.
• Extensive increase in nitric oxide production due to sustained hypoxia results in massive vasodialation and formation of large amounts of nitric oxide free radicals causing damage to cellular structures.
• Drop in blood flow rates below 30ml/100gm results in inhibition of protein synthesis and increase in anaerobic glycolysis
• Blood flow rates below 20ml/100gm results in extensive membrane damage causing cell death.

The sequence of molecular changes that may result due to ischemia include:^[2][6]

• Prolonged ischemia- decrease in oxygen delivery to the cells
• Anaerobic glycolysis with decline in ATP production
• Increased lactic acid production
• Increased free oxygen and nitrate radicals-cell membrane and DNA damage^[1]
• Excitatory neurotransmitter –glutamate is increased in neuronal synapses leading to NMDA receptor activation^[5][6]
• NMDA receptor activation causes opening of ion channels in the cell membrane causing K+ efflux and Na+, Ca2+ and water influx
• Increased Ca2+ influx activates apoptotic cell death pathways
• ATP required for final steps of apoptosis, hence massive decline in ATP results in necrosis of cells

The sequence of cellular changes during ischemic stroke results in loss of structural integrity of brain causing disruption of blood brain barrier and cerebral edema.

• Release of proteases (matrix metalloproteinases, MMP) due to cell membrane damage-ATP depletion + free radicals^[1][2]
• MMP causes degradation of collagen and laminins in the basement membrane of the cells and blood vessels
• Disruption of blood brain barrier may lead to hemorrhage
• Cerebral edema due to increased Na+, Ca2+ and water influx into the cells.

Advances in sequencing technology have facilitated the discovery of single-gene disorders associated with stroke beyond classic syndromes, such as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and sickle-cell disease. In addition, heterozygous mutations within the 3ʹ untranslated region of COL4A1 (the gene encoding collagen 4A1) is identified as a cause of pontine autosomal dominant microangiopathy with leukoencephalopathy (PADMAL). Heterozygous mutations (in particular, glycine substitutions) in the triple helical domains of COL4A1 or COL4A2 cause a different syndrome characterized by hemorrhagic stroke along with additional neurological and non-neurological manifestations.^[19]

The following gene loci may also increase the risk for stroke:

• PITX2 and ZFHX3- atrial fibrillation and cardio embolic stroke
• HDAC9- large vessel disease
• ABO- ischemic stroke

• Central necrotic tissue is called umbra
• Peripheral tissue which surrounds area of necrosis and can be salvaged with increased blood flow is called pneumbra^[4]

• Within 1-6 min of ischemia, red neurons and vacoulation results ^[13]
• If ischemia lasts > 6 min, karryorhexis and cell death occurs

Gross and microscopic changes that may occur due to ischemia with the passage of time is tabulated below: ^[13][20]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2],Seyedmahdi Pahlavani, M.D. [3]Aysha Anwar, M.B.B.S[4],Tarek Nafee, M.D. [5],Sara Mehrsefat, M.D. [6] Khizer Yaseen, M.B.B.S.[7]

There are several causes for stroke. Some may cause hemorrhage and some causes ischemia. Among all of them there are several lethal causes which we need to be more cautious about them.

Patent foramen ovale is a potential cause of stroke through paradoxical embolism, in which embolic material from the venous circulation enters the arterial system via a right-to-left intracardiac shunt, resulting in ischemic stroke.^[1]

The following table lists causes for stroke.^{[2][3][4][5][6][7][8][9][10][11]}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2],Aysha Anwar, M.B.B.S[3]

The differential diagnosis of ischemic stroke may include brain tumor, hemorrhagic stroke, subdural hemorrhage, neurosyphilis, complex or atypical migraine, hypertensive encephalopathy, Wernicke’s encephalopathy, CNS abscess, drug toxicity, conversion disorder, electrolyte disturbance, meningitis or encephalitis, multiple sclerosis exacerbation, seizure and hypoglycemia. There are also some conditions which may cause muscle weakness and paralysis such as Botulism, Myasthenia gravis, Guillian-Barre syndrome, Eaton Lambert syndrome, Electrolyte disturbance, Organophosphate toxicity, Multiple sclerosis exacerbation, Amyotrophic lateral sclerosis, Inflammatory myopathy. It is necessary to differentiate these conditions from stroke.

Stroke, must be differentiated from other diseases that may cause, altered mental status, motor and or somatosensory deficits. The table below, summarizes the differential diagnosis for stroke:^{[1][2][3][4][5][4][5][6][7][8][9][10][11]}

Stroke should be differentiated from other causes of muscle weakness and paralysis. The differentials include the following:

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2],Seyedmahdi Pahlavani, M.D. [3]Aysha Anwar, M.B.B.S[4],Tarek Nafee, M.D. [5],Sara Mehrsefat, M.D. [6] Khizer Yaseen, M.B.B.S.[7]

The worldwide incident of stroke is about 68 percent and it increases with age. It is more common in men. However, the mortality is more in women. the incident and mortality rates are high in African-American population and developing countries.

• Worldwide, the incidence of ischemic stroke is estimated to be 68 percent.^[1]
  • Stroke is the third leading cause of death in the Western world, after heart disease and cancer, and causes 10% of deaths worldwide.^[2]
• The incidence of stroke increases exponentially from 30 years of age, and etiology varies by age.^[3]

Younger patients with ischemic stroke are more likely to have a pathogenic patent foramen ovale, particularly in the absence of traditional vascular risk factors.^[4]

• Stroke can occur in all age groups. However, the incidence of stroke is less among individuals age less than 40 years of age and the risk increases with increasing age. ^[5]
• According to National Health Interview survey data, there is increased number of hospitalizations in patients aged 5-44 years for ischemic stroke.
• 95% of strokes occur in people age 45 and older; two-thirds of strokes occur in those over the age of 65.^[6]
• A person’s risk of dying if he or she does have a stroke also increases with age.
  • However, stroke can occur at any age, including in fetuses.
• According to WHO, stroke also occurs in about 8% of children with sickle cell disease. Stroke is the second leading killer of people under 20 years age who suffer from sickle-cell anemia.^[7].
• The incidence of stroke in people aged 18 to 50 years is estimated to be approximately 10%. ^[8]

• Men are 1.25 times more likely to suffer cerebral vascular accidents than women.
  • However, 60% of deaths from stroke occur in women: Since women usually live longer, they are usually older when they suffer from strokes and are more often killed).^[6]
• Some risk factors for stroke apply only to women
  • Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT).

• The risk of incidence of first stroke is twice in African-American population as compared to Caucasians with increased mortality rates.^[5]

• There is increased incidence and mortality rates of stroke in developing countries as compared to developed countries due to low socioeconomic status and heath facilities.
• In the USA, the highest death rates from stroke are in the southeastern United States.^[5]

• Stroke is a leading cause of serious long-term disability
• In USA, the incidence and mortality rates of stroke has significantly decreased compared to previous years.
• From year 2003 to 2013, the mortality rates due to stroke declined by 18.5%.^[8]
• In 2013, stroke became the fifth leading cause of death.
• The case fatality rate of stroke is estimated to be 41.7 deaths per 100, 000 population^[8]
• The incidence of new (610, 000) or recurrent stroke (185, 000) is estimated to be 795000 people annually or 250 cases per 100, 000.^[8]
• It is estimated that one incidence of stroke happens every 4 sec with death occurs every 4 min.^[8]
• About 87% of all strokes are ischemic strokes^[5]
• Stroke costs the United States an estimated $34 billion each year^[5]

• According to WHO, the incidence of stroke is estimated to be 15 million people annually, worldwide.^[7].
• Out of these, 5 million die and 5 million are left permanently disabled.^[7].

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2] Khizer Yaseen, M.B.B.S.[3]

Risk factors for stroke are divided into modifiable and non-modifiable risk factors. Modifiable risk factors include hypertension, diabetes mellitus, cardiac disease, cigarette smoking, alcohol consumption, hyperhomocysteinemia, hyperlipidemia, obesity, sedentary life style and oral contraceptive usage. Some of the non-modifiable risk factors include advanced age, male gender, family history of ischemic stroke, African-American and Hispanic race, and genetic diseases such as sickle cell disease.

Identification of risk factors for stroke is complicated by the fact that strokes come in many varieties. Risk factors for hemorrhagic and ischemic stroke are similar, but there are some notable differences; there are also differences in risk factors among the etiologic categories of ischemic stroke.^[1][2] According to Framingham cohort and later research, the risk factors for ischemic stroke are as follows:

• Modifiable risk factors
  • Hypertension
  • cigarette smoking
  • diet
  • Physical Inactivity
  • Hyperlipidemia
  • Diabetes
  • Alcohol Consumption
  • Cardiac disease (Atrial fibrillation, Coronary artery disease)
  • Apolipoprotein B to A1
  • Hyperhomocysteinemia
  • Hyperlipidemia
  • Oral contraceptive usage
• Non-modifiable risk factors
  • Age
  • Sex
  • Race/Ethnicity
  • Sickle cell disease

There is a similar classification for the risk factors of hemorrhagic stroke, which is:

• Modifiable risk factors
  • Hypertension
  • Alcohol Consumption
  • Diet
• Non-modifiable risk factors
  • Age
  • Sex
  • Race/Ethnicity

Clinical features associated with PFO-related ischemic stroke include younger age, absence of vascular risk factors, and embolic cortical infarction patterns.^[3]

The Risk of Paradoxical Embolism (RoPE) score is used to estimate the probability that a detected patent foramen ovale is causally related to ischemic stroke.^[4]The PFO-Associated Stroke Causal Likelihood (PASCAL) classification integrates anatomical and clinical features to guide management decisions.^[5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2]

There are several screening tests for high-risk patients to detect and prevent stroke: Carotid Artery Ultrasound, Abdominal Aortic Aneurysm Screening, Atrial Fibrillation, Peripheral Artery Disease.

It is suggested to use a variety of tests and assessments to detect high-risk patients and prevent stroke events. The tools are as follows:

• Carotid Artery Ultrasound: Ultrasound is used to image the carotid arteries in the neck to detect blockages that may lead to a stroke.
• Abdominal Aortic Aneurysm Screening: This screening looks at abnormal bulging in the wall of the main artery in the abdomen. Abnormal bulging may lead to rupture if not detected. Less than 40% of individuals survive a ruptured aneurysm.
• Atrial Fibrillation: A limited ECG (rhythm strip) is performed to detect an abnormal heart rhythm called atrial fibrillation. The risk of stroke increases five times for those individuals with atrial fibrillation.
• Peripheral Artery Disease: This screening test uses ankle-brachial index to predict blockage in leg arteries that may cause deep vein thrombosis or other thrombotic events, including stroke. Peripheral Artery Disease affects about 8 million Americans, and is associated with significant morbidity and mortality.

^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2]

Stroke can cause temporary or permanent complications based on the location and time to appropriate treatment. Delayed treatment or severe hemorrhagic or ischemic stroke can lead to death. Others may suffer from Dysphagia, Pneumonia, Myocardial infarction and arrhythmias, need for mechanical ventilation, pulmonary edema, central sleep apnea, urinary incontinence, falls, Musculoskeletal spasticity, Post-stroke seizure, Bowel incontinence, cognitive impairment. Prognosis depends on patient’s age and stroke severity based on clinical evaluation and imaging.

Given the ability to alter the natural history of stroke with endovascular thrombectomy, early identification of patients with vessel occlusion is critical. Differentiating acute ischemic stroke (AIS) patients with large vessel occlusions from those without based on clinical presentation is nonetheless challenging due to the variable nature of collateral vasculature and the potential for unique “at risk” and symptomatic tissue patterning across patients with the same anatomical site of occlusion. Vessel occlusions can also commonly manifest with minimal symptomology. While not pathognomonic, the clinical presentation of patients with vessel occlusion is nonetheless often stereotyped and anatomically matched to the site of occlusion and downstream affected cerebrum. Specifically, ICA or proximal MCA occlusions often present with contralateral hemi body and face weakness and/or numbness, contralateral homonymous hemianopsia, and ipsilateral gaze deviation, as well as aphasia for dominant hemispheric lesions and neglect for lesions of the nondominant hemisphere. More nuanced presentations of variable clinical severity and importance are observed with more distal occlusions. One notable distal occlusion site is the M3 branch to the angular gyrus of the dominant hemisphere. Due to the involvement of this vascular territory in speech processing and complex cognition, focal occlusions in this location are sometimes more aggressively pursued for thrombectomy in an attempt to preserve speech and cognition as compared to similarly distant blockages in arteries supplying less eloquent cortex.^[1][2]

The early complications of patients, survived from a stroke is as follows:^[3][4][5]

• Dysphagia
• Venous thromboembolism
• Pneumonia
• Urinary tract infection
• Myocardial infarction
• Arrhythmias
• Neurogenic cardiac damage
• Need for mechanical ventilation
• Neurogenic pulmonary edema
• Central sleep apnea
• Gastrointestinal bleeding
• Urinary incontinence
• Falls and bone fractures
• Depression
• Post-stroke fatigue

There are also some long-term complications including:

• Musculoskeletal spasticity
• Hemiplegic shoulder pain
• Post-stroke seizure
• Bowel incontinency
• Cognitive impairment

In the acute phase of stroke, the strongest predictors of outcome are stroke severity and patient age. Stroke severity can be judged clinically, based upon the degree of neurologic impairment (e.g., altered mentation, language, behavior, visual field deficit, motor deficit) and the size and location of the infarction on neuroimaging with magnetic resonance imaging (MRI) or computed tomography (CT). In addition, presence of anemia, atrial fibrillation, cancer, coronary artery disease, dementia, diabetes, heart failure, renal dysfunction, and poor nutrition are among other comorbidities, which can make the prognosis poorer.^[6][7][8]

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