Cerebral infarction

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Cerebral infarct
Infarction.svg
CT scan slice of the brain showing a right-hemispheric cerebral infarct (left side of image).
Specialty Neurology

Cerebral infarction, also known as an ischemic stroke, is the pathologic process that results in an area of necrotic tissue in the brain (cerebral infarct). [1] In mid to high income countries, a stroke is the main reason for disability among people and the 2nd cause of death. [2] It is caused by disrupted blood supply (ischemia) and restricted oxygen supply (hypoxia). This is most commonly due to a thrombotic occlusion, or an embolic occlusion of major vessels which leads to a cerebral infarct . [3] [4] In response to ischemia, the brain degenerates by the process of liquefactive necrosis. [1]

Contents

Classification

There are various classification systems [5] for cerebral infarcts, some of which are described below.

Stroke recognition

There are many tests that can be done to prescreen a patient who may be showing stroke-like symptoms. No one test is better than the other and they all have room for improvement. One of these tests that is used by prehospital personnel is the Cincinnati Pre Hospital Stroke scale (CPSS). This test looks for facial droop, arm drift, and a change in the person's speech pattern. Another test that can be used and is a modification to the CPSS is the Face Arm Speech Test (FAST). This checks for facial weakness, arm weakness, and speech disturbances. The ROSIER (Recognition of Stroke in The ER), is a test used by an ER physician. Each variable is rated from a -2 to a +5. Loss of consciousness (-1), convulsive fit (-1), facial weakness (+1), arm weakness (+1), leg weakness (+1), abnormal speech patterns (+1), and visual defect (+1). [9] In recent years, a study has been done to show how AI can aid in diagnosis of cerebral infarct and improve patient outcomes in areas that may not have stroke trained physicians. [10]

Symptoms

Cerebral infarction Cerebral infarction.jpg
Cerebral infarction
Hemodynamic changes seen using an IOS camera specific for hemoglobin volume changes where we see the occlusion of a Middle Cerebral Artery (MCA) and how Spreading Depolarizations appear and spread over the cortex. Middle Cerebral Artery occlusion. Kentar et al Acta Neuroch 2020.gif
Hemodynamic changes seen using an IOS camera specific for hemoglobin volume changes where we see the occlusion of a Middle Cerebral Artery (MCA) and how Spreading Depolarizations appear and spread over the cortex.
Histopathology at low magnification of a cerebral infarction on H&E stain, showing pallor in the infarcted area due to edema. Histopathology of thalamus infarction at approximately 24 hours, low magnification, annotated.jpg
Histopathology at low magnification of a cerebral infarction on H&E stain, showing pallor in the infarcted area due to edema.
Histopathology at high magnification of a normal neuron, and a cerebral infarction at approximately 24 hours on H&E stain: The neurons become hypereosinophilic and there is an infiltrate of neutrophils. There is slight edema and loss of normal architecture in the surrounding neuropil. Histopathology of thalamus infarction at approximately 24 hours, high magnification, annotated.jpg
Histopathology at high magnification of a normal neuron, and a cerebral infarction at approximately 24 hours on H&E stain: The neurons become hypereosinophilic and there is an infiltrate of neutrophils. There is slight edema and loss of normal architecture in the surrounding neuropil.

Ischemic strokes usually present as a problem with nerve, spinal cord, or brain function. Depending on where the stroke is located in the brain, symptoms may start within minutes, or they make take hours to present themselves. Most strokes occur without warning. Some common symptoms include one sided weakness, facial paralysis or numbness, vision problems, trouble speaking, problems with walking and keeping balanced. A person can show one or more of these symptoms during a stroke. If person has a decrease in consciousness, they may be suffering from a stroke in more than one part of the brain or in the brain stem. [12]

Symptoms of cerebral infarction can help determine which parts of the brain are affected. If the infarct is located in the primary motor cortex, contralateral hemiparesis is said to occur. With brainstem localization, brainstem syndromes are typical: Wallenberg's syndrome, Weber's syndrome, Millard–Gubler syndrome, Benedikt syndrome or others.

Risk factors

Major risk factors for cerebral infarction are generally the same as for atherosclerosis. These include high blood pressure, diabetes mellitus, tobacco smoking, obesity, and dyslipidemia. [13] There are also risks that a person can't control. These include a person's age, family history of strokes, being African American, and being born a male. A person's risk of a stroke doubles each decade after the age of 55. [14] The American Heart Association/American Stroke Association (AHA/ASA) recommends controlling these risk factors in order to prevent stroke. [15] The AHA/ASA guidelines also provide information on how to prevent stroke if someone has more specific concerns, such as sickle-cell disease or pregnancy. It is also possible to calculate the risk of stroke in the next decade based on information gathered through the Framingham Heart Study. [16]

Pathophysiology

Cerebral infarction is caused by a disruption to blood supply that is severe enough and long enough in duration to result in tissue death. The disruption to blood supply can come from many causes, including:

  1. Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
  2. Embolism (obstruction due to an embolus from elsewhere in the body), [17]
  3. Systemic hypoperfusion (general decrease in blood supply, e.g., in shock) [18]
  4. Cerebral venous sinus thrombosis. [19]
  5. Unusual causes such as gas embolism from rapid ascents in scuba diving. [20]

Even in cases where there is a complete blockage to blood flow of a major blood vessel supplying the brain, there is typically some blood flow to the downstream tissue through collateral blood vessels, and the tissue can typically survive for some length of time that is dependent upon the level of remaining blood flow. [21] If blood flow is reduced enough, oxygen delivery can decrease enough to cause the tissue to undergo the ischemic cascade. The ischemic cascade leads to energy failure that prevents neurons from sufficiently moving ions through active transport which leads the neurons to first cease firing, then depolarize leading to ion imbalances that cause fluid inflows and cellular edema, then undergo a complex chain of events that can lead to cell death through one or more pathways. [22] [23] [24]

Diagnosis

Computed tomography (CT) and MRI scanning will show damaged area in the brain. A CT scan will rule out a hemorrhagic stroke, is cheaper for the patient, and can be found in almost all hospitals unlike an MRI machine. [25] [26] Once the Doctor rules out a hemorrhagic stroke, rTPA can be given. [25] An MRI can help to diagnose an acute cerebral infarct as quickly as 6 hours from start of symptoms, [25] It can also help time when the stroke happened. [27] The biggest problem with an MRI is it can't be done on a patient with certain metallic implants or if the patient is claustrophobic. [28] A head and neck CT angiogram can be performed within 6 hours of onset of symptoms to see where the occlusion may be located which can help in determining the cause of the stroke. [29] In people who die from a stroke an autopsy can reveal additional diseases or conditions beyond the stroke itself, as well as uncover uncommon causes of a stroke. [30]

Treatment

In the last decade, similar to myocardial infarction treatment, thrombolytic drugs were introduced in the therapy of cerebral infarction. The use of intravenous rtPA therapy can be advocated in patients who arrive to stroke unit and can be fully evaluated within 3 hours of the onset. The quicker rTPA is started, the better the outcome for the patient. [29]

If cerebral infarction is caused by a thrombus occluding blood flow to an artery supplying the brain, definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die. [31] In increasing numbers of primary stroke centers, pharmacologic thrombolysis with the drug tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery. Giving rTPA lessens the chance of disability after 3 months by 30%. [29] Another intervention for acute cerebral ischemia is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive thrombolytic drugs or for whom the drugs were ineffective, [32] [33] [34] [35] though no differences have been found between newer and older versions of the devices. [36] The devices have only been tested on patients treated with mechanical clot embolectomy within eight hours of the onset of symptoms.

Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute cerebral ischaemia. In a systematic review of six uncontrolled, single-center trials, involving a total of 300 patients, of intra-cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical success (reduction to stenosis of <50%) ranged from 90 to 98%, and the rate of major peri-procedural complications ranged from 4-10%. The rates of restenosis and/or stroke following the treatment were also favorable. [37] This data suggests that a large, randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this treatment.

If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after cerebral infarction. Carotid endarterectomy is also indicated to decrease the risk of cerebral infarction for symptomatic carotid stenosis (>70 to 80% reduction in diameter). [38]

In tissue losses that are not immediately fatal, the best course of action is to make every effort to restore impairments through physical therapy, cognitive therapy, occupational therapy, speech therapy and exercise.

Permissive hypertension - allowing for higher than normal blood pressures in the acute phase of cerebral infarction - can be used to encourage perfusion to the penumbra. [39]

Related Research Articles

A transient ischemic attack (TIA), commonly known as a mini-stroke, is a minor stroke whose noticeable symptoms usually end in less than an hour. A TIA causes the same symptoms associated with a stroke, such as weakness or numbness on one side of the body, sudden dimming or loss of vision, difficulty speaking or understanding language, slurred speech, or confusion.

<span class="mw-page-title-main">Cerebrovascular disease</span> Condition that affects the arteries that supply the brain

Cerebrovascular disease includes a variety of medical conditions that affect the blood vessels of the brain and the cerebral circulation. Arteries supplying oxygen and nutrients to the brain are often damaged or deformed in these disorders. The most common presentation of cerebrovascular disease is an ischemic stroke or mini-stroke and sometimes a hemorrhagic stroke. Hypertension is the most important contributing risk factor for stroke and cerebrovascular diseases as it can change the structure of blood vessels and result in atherosclerosis. Atherosclerosis narrows blood vessels in the brain, resulting in decreased cerebral perfusion. Other risk factors that contribute to stroke include smoking and diabetes. Narrowed cerebral arteries can lead to ischemic stroke, but continually elevated blood pressure can also cause tearing of vessels, leading to a hemorrhagic stroke.

<span class="mw-page-title-main">Ischemia</span> Restriction in blood supply to tissues

Ischemia or ischaemia is a restriction in blood supply to any tissue, muscle group, or organ of the body, causing a shortage of oxygen that is needed for cellular metabolism. Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue i.e. hypoxia and microvascular dysfunction. It also implies local hypoxia in a part of a body resulting from constriction.

<span class="mw-page-title-main">Infarction</span> Tissue death due to inadequate blood supply

Infarction is tissue death (necrosis) due to inadequate blood supply to the affected area. It may be caused by artery blockages, rupture, mechanical compression, or vasoconstriction. The resulting lesion is referred to as an infarct (from the Latin infarctus, "stuffed into").

<span class="mw-page-title-main">Stroke</span> Death of a region of brain cells due to poor blood flow

Stroke is a medical condition in which poor blood flow to a part of the brain causes cell death. There are two main types of stroke: ischemic, due to lack of blood flow, and hemorrhagic, due to bleeding. Both cause parts of the brain to stop functioning properly.

Mechanical thrombectomy, or simply thrombectomy, is the removal of a blood clot (thrombus) from a blood vessel, often and especially endovascularly as an interventional radiology procedure called endovascular thrombectomy (EVT). It thus contrasts with thrombolysis by thrombolytic medications, as either alternative or complement thereto. It is commonly performed in the cerebral arteries as treatment to reverse the ischemia in some ischemic strokes. Open vascular surgery versions of thrombectomy also exist. The effectiveness of thrombectomy for strokes was confirmed in several randomised clinical trials conducted at various medical centers throughout the United States, as reported in a seminal multistudy report in 2015.

<span class="mw-page-title-main">Cerebral hypoxia</span> Oxygen shortage of the brain

Cerebral hypoxia is a form of hypoxia, specifically involving the brain; when the brain is completely deprived of oxygen, it is called cerebral anoxia. There are four categories of cerebral hypoxia; they are, in order of increasing severity: diffuse cerebral hypoxia (DCH), focal cerebral ischemia, cerebral infarction, and global cerebral ischemia. Prolonged hypoxia induces neuronal cell death via apoptosis, resulting in a hypoxic brain injury.

<span class="mw-page-title-main">Carotid endarterectomy</span> Surgical procedure

Carotid endarterectomy is a surgical procedure used to reduce the risk of stroke from carotid artery stenosis. In endarterectomy, the surgeon opens the artery and removes the plaque. The plaque forms and thickens the inner layer of the artery, or intima, hence the name of the procedure which simply means removal of part of the internal layers of the artery.

<span class="mw-page-title-main">Desmoteplase</span> Medication

Desmoteplase is a novel, highly fibrin-specific "clot-busting" (thrombolytic) drug in development that reached phase III clinical trials. The Danish pharmaceutical company, Lundbeck, owns the worldwide rights to Desmoteplase. In 2009, two large trials were started to test it as a safe and effective treatment for patients with acute ischaemic stroke. After disappointing results in DIAS-3, DIAS-4 was terminated, and in December 2014 Lundbeck announced that they would stop the development of desmoteplase.

Vertebrobasilar insufficiency (VBI) describes a temporary set of symptoms due to decreased blood flow (ischemia) in the posterior circulation of the brain. The posterior circulation supplies the medulla, pons, midbrain, cerebellum and supplies the posterior cerebellar artery to the thalamus and occipital cortex. As a result, symptoms vary widely depending which brain region is predominantly affected.

<span class="mw-page-title-main">Watershed stroke</span> Medical condition

A watershed stroke is defined as a brain ischemia that is localized to the vulnerable border zones between the tissues supplied by the anterior, posterior and middle cerebral arteries. The actual blood stream blockage/restriction site can be located far away from the infarcts. Watershed locations are those border-zone regions in the brain supplied by the major cerebral arteries where blood supply is decreased. Watershed strokes are a concern because they comprise approximately 10% of all ischemic stroke cases. The watershed zones themselves are particularly susceptible to infarction from global ischemia as the distal nature of the vasculature predisposes these areas to be most sensitive to profound hypoperfusion.

Animal models of ischemic stroke are procedures inducing cerebral ischemia. The aim is the study of basic processes or potential therapeutic interventions in this disease, and the extension of the pathophysiological knowledge on and/or the improvement of medical treatment of human ischemic stroke. Ischemic stroke has a complex pathophysiology involving the interplay of many different cells and tissues such as neurons, glia, endothelium, and the immune system. These events cannot be mimicked satisfactorily in vitro yet. Thus a large portion of stroke research is conducted on animals.

<span class="mw-page-title-main">Carotid stenting</span>

Carotid artery stenting is an endovascular procedure where a stent is deployed within the lumen of the carotid artery to treat narrowing of the carotid artery and decrease the risk of stroke. It is used to treat narrowing of the carotid artery in high-risk patients, when carotid endarterectomy is considered too risky.

<span class="mw-page-title-main">Hemorrhagic infarct</span> Medical condition

A hemorrhagic infarct is determined when hemorrhage is present around an area of infarction. Simply stated, an infarction is an area of dead tissue or necrosis. When blood escapes outside of the vessel (extravasation) and re-perfuses back into the tissue surrounding the infarction, the infarction is then termed a hemorrhagic infarct (infarction). Hemorrhagic infarcts can occur in any region of the body, such as the head, trunk and abdomen-pelvic regions, typically arising from their arterial blood supply being interrupted by a blockage or compression of an artery.

<span class="mw-page-title-main">Lacunar stroke</span> Medical condition

Lacunar stroke or lacunar cerebral infarct (LACI) is the most common type of ischemic stroke, resulting from the occlusion of small penetrating arteries that provide blood to the brain's deep structures. Patients who present with symptoms of a lacunar stroke, but who have not yet had diagnostic imaging performed, may be described as having lacunar stroke syndrome (LACS).

<span class="mw-page-title-main">Leptomeningeal collateral circulation</span>

The leptomeningeal collateral circulation is a network of small blood vessels in the brain that connects branches of the middle, anterior and posterior cerebral arteries, with variation in its precise anatomy between individuals. During a stroke, leptomeningeal collateral vessels allow limited blood flow when other, larger blood vessels provide inadequate blood supply to a part of the brain.

In pathology and anatomy the penumbra is the area surrounding an ischemic event such as thrombotic or embolic stroke. Immediately following the event, blood flow and therefore oxygen transport is reduced locally, leading to hypoxia of the cells near the location of the original insult. This can lead to hypoxic cell death (infarction) and amplify the original damage from the ischemia; however, the penumbra area may remain viable for several hours after an ischemic event due to the collateral arteries that supply the penumbral zone.

A silent stroke is a stroke that does not have any outward symptoms associated with stroke, and the patient is typically unaware they have suffered a stroke. Despite not causing identifiable symptoms, a silent stroke still causes damage to the brain and places the patient at increased risk for both transient ischemic attack and major stroke in the future. In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of these strokes were symptomatic and 11 million were first-ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as MRI. The risk of silent stroke increases with age but may also affect younger adults. Women appear to be at increased risk for silent stroke, with hypertension and current cigarette smoking being amongst the predisposing factors.

Remote ischemic conditioning (RIC) is an experimental medical procedure that aims to reduce the severity of ischaemic injury to an organ such as the heart or the brain, most commonly in the situation of a heart attack or a stroke, or during procedures such as heart surgery when the heart may temporary suffer ischaemia during the operation, by triggering the body's natural protection against tissue injury. Although noted to have some benefits in experimental models in animals, this is still an experimental procedure in humans and initial evidence from small studies have not been replicated in larger clinical trials. Successive clinical trials have failed to identify evidence supporting a protective role in humans.

A cerebroprotectant is a drug that is intended to protect the brain after the onset of acute ischemic stroke. As stroke is the second largest cause of death worldwide and a leading cause of adult disability, over 150 drugs have been tested in clinical trials to provide cerebroprotection.

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