Cerebral vascular accidents: Middle Cerebral Artery (CVAs –Stroke)

Posted on November 10, 2022 |

Cerebral vascular accidents: Middle Cerebral Artery (CVAs –Stroke) – Choose ONE of the following cerebral vascular accidents (CVAs – Stroke – in the brain) as your topic to present a comprehensive understanding of the material…

What You Will Learn hide

2.3 Structure of the Middle Cerebral Artery (MCA)

2.4 MCA Embryology

2.5 Middle Cerebral Artery (MCA) Strokes

2.6 Neurological Deficits Left Hemisphere (Dominant)

2.7 Apraxia

2.8 Right-Side Sensory Loss, Hemianopia, and Dysarthria.

2.9 Aphasia

2.10 Neurological Deficits Right Hemisphere (non-dominant)

2.11 Emotional Disorders

2.12 Evaluation of a Stroke

2.13 Risk factors of a Stroke

2.14 Treatment and Management of MCA Strokes

2.15 Conclusion

3 Health Care Systems Essay Examples

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Paper details

This written part of your practicum will entail a written submission, and it will demonstrate if you have been able to synthesize the material throughout the semester, and demonstrate how a lesion cascades throughout our bodies. Requirements that must be met to be given full credit are enumerated and not just content will receive full credit. You must understand the material and formatting, English, grammar, etc. all play a part in how you submit a comprehensive, synthesized, paper. This is an exercise in critical thinking PRIOR to having to execute a solution post injury.

Hence, the theory and anatomy are the central constructs, from this semester, and you must know before you can think of how to formulate a decision. Speaking to the nervous system, I want students to understand how a mild to severe lesion can have lasting effects throughout the kinematic chain of movement and all the human structures. Consider how a stroke changes the structure and/or the function of any one, or all, of them.

Choose ONE of the following cerebral vascular accidents (CVAs – Stroke – in the brain) as your topic to present a comprehensive understanding of the material:

· Anterior Cerebral Artery

· Middle Cerebral Artery

· Posterior Cerebral Artery

· Vertebral-Basilar Artery

By semester’s end, I will have covered, discussed, and/or touched on all constructs that the department requires, based on the department lab’s monthly calendar. We will HAVE identified, together, where all the structures are located. To begin, evaluate the anatomical structures that the artery affects, specifically. For example, the Anterior Cerebral Artery mainly affects the FRONTAL lobe and the LOWER extremities. Additionally, an ACA stroke does not generally affect the vision, but Broca’s Area, for speech, is central to the FRONTAL lobe. (This example will become clearer once these topics are covered).

Use resources such as Google Scholar, Wikipedia (to begin to know how the anatomy is affected), and the Miami Dade College Library. Use the college’s Writing Center, if you need help or need someone to review the final paper in terms of content and the structure of writing the actual paper. The Writing Center does not teach AMA citation format. Hence, I have posted examples and information on BB for your edification. No work will be accepted that does not follow the AMA citation guidelines. This is the medical field gateway and protocol is AMA style citations.

Required formatting is as follows:

· References must be cited in AMA style (American Medical Association) – Wikipedia included.

· NO OTHER FORMAT WILL BE ACCEPTED. (There are websites that you plug in the information and it formats the reference for you – this is not something to stress about – citations are annoying but they are necessary).

· Double spaced with 1-inch margins (double spaced takes up volume on your paper – do not stress about the number of pages). You’d be quite surprised at how quick a student can fill 10 pages, typed, double spaced)

· Times New Roman, in 10-point size

· The content must be no less than 10 pages with a separate title page (total pages = 11 and without the references).

· There must be at least 8 references (references are NOT part of your content though, you also cite them in text and at the end of the practicum.

· Peer reviewed journal articles (ie. Google scholar) – You must use AT A MINIMUM 8 references. These references help you understand lesions and the pervasiveness that strokes affect the CNS, PNS, & the Autonomic Nervous System (the ANS will be covered when the nervous system is formally introduced.

· Begin to read the “ABSTRACTS” to understand the study; don’t waste time reading the full article.

· This is a GREAT resource for students to use and read about clinical reasoning: www.teachmeanatomy.com

· Your lab book (you can use your book as an official resource – if cited correctly). It has a great amount of content.

You MUST submit a hard copy, to me, in person, NO LATER THAN April 16, 2020. NOT through E-mail or Blackboard. All practicums must be submitted in hard copy format, in class. Again, NOT through email or Blackboard. This due date is FINAL. I will not accept any work, on this practicum, past the ending of your class (#1495 by 9:40 am; #8529 by 2:40pm)

I am available to all students throughout the remaining of the semester, if you would like some feedback on your progress, or how to approach getting started and how to progress to the finished product, see me on campus or send me an email with the attachment and I can quickly review it and give you feedback. I am not planning on evaluating the whole thing but the general overview and can give feedback.

Be ORGANIZED.

It is the key to synthesizing your semester’s content. If you need help starting, ASK me. Two ways to approach this practicum would be to:

I. Start in the brain & CNS and what type of stroke it is. Deal with the sections of the brain that are affected, mostly. Then, work yourself out towards all topics covered this semester. In total, there are 15 topics that we will have worked on. Address how that section of the brain affects the axial and appendicular skeletal system as well as blend the topics into some order of organization. Such as, group all the special senses together which are in the last weeks of your semester.

An ACA stroke does not normally affect the upper extremities (UEs) but does the lower extremities (LEs) as a MCA stroke focuses more on the UEs. Vision is affect both in a MCA and a PCA stroke but not affected, for the most part by an ACA. Begin to reason when we discuss things in class and think about your own experiences. If you know someone, possibly, and if so, how was their life affected?

II. Address the topics in the order that the lab calendar is set up, ensuring you don’t forget any topics, possibly. And from there, begin to discuss topics that can be logically grouped together, such as bones and muscles, or cranial nerves in the brainstem.

Students should understand that topics can be grouped together. For example, when addressing muscle changes, this also includes bones, attachments, and relative nerve innervations. When discussing any muscle changes, for example in the lower extremities, these combined topics coalesce and produce an understanding as one evaluates changes to any one structure and how that change cascades to other structures.

Solution

Middle Cerebral Artery (CVAs –Stroke)

Introduction

Stroke is an acute compromise of cerebral perfusion, or vasculature that causes ischemia to an area of the brain. Strokes are categorized as ischemic, hemorrhagic, or subarachnoid. Ischemic strokes account for 85% of all strokes with the risk factors being age, family history, smoking, hypertension, hypercholesterolemia, and diabetes mellitus. These risk factors underlie the primary cause of Ischemic stroke, which is atherosclerosis.

Hemorrhagic strokes occur due to a rapture of an artery in the brain leading to the damage of brain cells. Strokes are the 5th leading cause of death and the leading cause of adult injury. It is imperative to examine the anatomical structures affected by a Middle Cerebral Artery stroke and understand how a lesion (mild or severe) can have lasting effects throughout the kinematic chain of movement and all human structures.

Brain & CNS

Vascular supply to the brain comes from a network of arteries that anastomose to form the circle of Willis. The brain, which consumes 15% of the total cardiac output, relies on anterior and posterior divisions of arteries for blood and energy supply, necessary for the well-functioning of the Central Nervous System (CNS). Hence, any blockage of blood flow leads to severe damage and a host of neurological pathologies. The supply is facilitated by four principal arteries, with the internal carotid artery (ICA), which formulates the anterior circulation division and the vertebral-basilar system, which forms the posterior circulation.

It is at the central cranial base that the anterior and posterior circulation join up to form the circle of Willis2. On the sides of the circle, we have the anterior cerebral arteries (ACA), the posterior cerebral arteries (PCA), together with anterior and posterior communicant arteries (Acom A and Pcom A) which also link the ICA and the PCA. The PCA, ACA, and MCA, contain branches that supply to critical areas such as the pituitary gland and its infundibular stalk, the optic chiasm, hypothalamus and thalamus, midbrain and basal ganglia.

Structure of the Middle Cerebral Artery (MCA)

The ICA comprises three terminal branches, which include the ACA, the Middle Cerebral Artery (MCA), and the anterior choroidal (artery ACh A). Focusing on the MCA, the subdivisions include M1, which is the Sphenoidal, M2- Insular, M3 opercula, and M4 cortical. M1 progresses on a lateral angle to the optic chiasm and the entrance of the Sylvian fissure. The subdivision contains branches that supply the caudate nucleus, internal capsule, basal ganglia as well as anterior pole of the temporal lobe. The M1 terminates at either the main bifurcation or at the genu adjacent to the limen insulae.

For M2, arteries form over the insula and on the upper side of the sulcus. The segment follows a course on the insular cleft and ends at the sulcus of insula. M3 proceeds from the circular sulcus of the insula follow through the frontoparietal operculum and end at the external surface of the Sylvain fissure2.

M4 is a distal branch that forms on the lateral side of the brain. It starts at the top surface of Sylvain fissure, follows through the lateral convexity, and ends at the final cortical territory. The 4 combine to form the MCA, which is the largest cerebral artery and also the most affected by a cerebrovascular accident. Its territory can be summarized by trifurcates into temporal, frontal, and parietal branches that supply most the parenchyma of these lobes.

The primary function of the MCA is to supply oxygenated blood to the brain parenchyma, with the cortical branches irrigating primary motor and somatosensory cortical areas of the face, trunk, and the upper extremities. Lenticulostriate vessels, in the form of small central branches, irrigate basal ganglia and internal capsule3. The lateral frontal lobes, which comprise of the non-fluent regions of speech production, language comprehension, and writing depend on the superior division. The inferior division, on the other hand, supplies the fluent region in charge of speech comprehension and language development3.

MCA Embryology

To better understand the structure and mechanisms of MCA, it is imperative to understand embryonic development. Blood vessel formation occurs through vasculogenesis, while angiogenesis takes a similar process in repairing damaged vessels. At 28 to 30 days, the ICA splits into the caudal and cranial branch. The ACA forms is an elongation of the cranial branch, and the MCA is still one of its collaterals.

At 31 to 33 days, the ICA formulates several braches with the primitive ACA being key. At 34 to 36 days, the truck of the MCA is formed through fusion and regression2. By day 41 of embryonic development, the MCA becomes prominent, and by day 45, the MCA attains near-adult configurations while the embryo is 40mm. Studies into MCA anomalies point out that they occur less frequently than anomalies of other intracranial arteries5.

MCA physiologic variants also play a critical role in explaining the aneurysm formation and stroke incidence. Common variants include bifurcations of the MCA before the genu and trifurcations before and after the genu. Studies point out that there is a higher risk of aneurysm formation in MCAs with specific MCA variants. The study also indicates that aneurysms have more in the M1 segment, even though they also appear in M2, some vessels, and near the cortical branches3.

Besides, variant anatomy includes MCA duplication with an incidence of 1.5% and supplies the temporal lobe parallel to the main MCA. Accessory MCA is also variant anatomy that stems from the ACA and has a prevalence of 2%3. Accessory MCA supplies some areas of the anterior frontal lobe. Though it is rare, MCA fenestration is also a variant manifested by the division of vessels into separate channels that rejoin distally. The variants increase the risk of aneurysm6.

Middle Cerebral Artery (MCA) Strokes

MCA strokes are the sudden onset of focal neurological deficit resulting from a brain infarction or ischemia in the territory covered by MCA. Ischemic strokes result in the sudden loss of blood circulation, leading to the loss of neurological function. Ischemic strokes, which account for 84% of all strokes, are caused by thrombotic or embolic occlusion. On further examination, thrombotic occlusion occurs due to the formation of a clot on the edges of plaque and may block lumen.

In the event of a thrombus break off, it becomes an embolus. The embolus then travels through the bloodstream until it reaches a narrow vessel where it causes a blockage, which results in neurological deficits. In specific manifestations such as atherosclerosis, there are deposits of cholesterol and plaque within the walls of the arteries leading to a narrow lumen and a reduced blood flow.

The MCA territory is the most affected during strokes. This is primarily due to the size of the territory and the direct flow of from the internal carotid artery, which provides a clear path for thromboembolism. Hence MCA strokes are common and are presented in a variety of ways. Factors that determine the severity of an MCA stroke include the initial degree of neurological deficit, size of the stroke, or the propensity to require further interventions3. Hence, MCA strokes often result in higher rates of disability, with more than half of MCA stroke survivors never regaining functional independence and higher mortality rates.

MCA strokes could also occur from lenticulostriate infarcts, which result from embolism of cardiac origin. In these infarcts, there is no cortical involvement and presentation occurs by pure limitation of motor movement. Besides, chronic hypertension in the vessels may also cause Charcot-Bouchard microaneurysms often associated with hemorrhages that cause tissue necrosis and affect regions of the basal ganglia and cerebellum6.

Malignant MCA infarction refers to deterioration due to the space-occupying cerebral edema following an MCA stroke. Even with sufficient treatment, malignant MCA still results in up to 80% mortality. The type of MCA stroke, is naturally severe, leading to quick progression of irreversible morphological damage, resulting in sizeable cytotoxic edema in the ischemic territory.

In a span of 6 hours, a combination of osmotic swelling, and terminal depolarization leads to irreversible damage due to the developing lesion that extends over the area, thus reducing blood flow. With difficulties in using noninvasive modalities, tracking of tissue damage is challenging7. Death eventually occurs due to transtentorial herniation and brainstem compression. Treatment occurs by either medication to limit the extent of edema and surgical decompression to relieve pressure effects.

Neurological Deficits Left Hemisphere (Dominant)

The clinical presentation of MCA strokes depends on the extent of the infarct and hemispheric dominance. Classified by the hemispheric dominance, MCA stroke left hemisphere (dominant) deficits are on the right hemiparesis, which involves the face and the upper and lower extremity6. Hemiparesis is the most common presenting form of strokes. MCA lesions affect the dominant sphere (left hemisphere); the stroke causes weakness of the arm and face on the upper extremities, which is worse than that of the lower limp MCA. However, there is a loss of motor skills leading to problems with balance due to limb weakness and the inability to shift weight7. This also leads to problems with daily activities and routines due to apraxia.

Apraxia

Left hemispheric patients display different classifications of apraxia. Motor or ideomotor apraxia, whose site of lesion is the left hemisphere, is manifested when the patient can perform a movement but cannot carry it out on command7. On gait apraxia, lesion located on frontal lobes, the patient finds it hard to initiate and maintain regular walking patterns even though motor and sensory patterns seem unimpaired7.

Right-Side Sensory Loss, Hemianopia, and Dysarthria.

It is also manifested on the right-sided sensory loss, in pattern with the right hemiparesis and upper and lower extremities. MCA also manifests on the contralateral through sensory loss in the face, in all modalities. This is also associated with left-right confusion, decreased vision on the right side of both eyes reduced timing and speed skills, and decreased analytical skills.

Furthermore, in the left hemisphere, visual field loss, also known as right homonymous hemianopia manifests as well as slow or slurred speech in the form of dysarthria. Dysarthria affects pronunciation, the loudness of the voice, and the ability to speak at an average rate with normal intonation. The effect and severity of dysarthria vary from person to person, depending on the severity of the stroke9. Visual loss in the form of hemianopia and anopsia on the contralateral side, as well as receptive aphasia, are in the lower division.

Aphasia

The left-sided stroke also results in Broca aphasia and Wernicke’s aphasia. Aphasia impedes communication as it affects a single aspect of language use, with the common manifestation being on the ability to retrieve the names of objects or construct and read sentences8. In the Broca form of aphasia, speech is limited to less than four words, and vocabulary access limited.

In Wernicke’s aphasia, the ability to grasp meaning is impaired while the speed of producing connected speech is less affected. Left-sided strokes also lead to Alexia, Agraphia, and Acalculia9. Agraphia is the impairment in the ability to produce written language and is often paired with aphasia. Alexia is the partial or complete inability to read and comprehend while Acalculia is the impairment in which the ability to perform calculations is limited.

Neurological Deficits Right Hemisphere (non-dominant)

On the non-dominant side, hemiparesis is on the left side and has the same manifestation as the right side. The clinical manifestations include visual-spatial perceptual disorders, unilateral spatial neglect, and emotional disorders intrinsically linked to communication challenges9. This includes left side sensory loss, left homonymous hemianopia, and dysarthria.
Visual-Spatial Perceptual Disorders

For over 90% of the population, the right hemisphere controls judgment, orientation, and constructional praxis9. Hence for right MCA, visual related disorders include left-sided neglect, figure-ground disorientation, constructional apraxia, and astereognosis. Differentially, strokes on the right side are associated with a lack of insight or Anosognosia, which affects the administration of treatment9. Further, Asomatognosia also manifests as the patient may fail to recognize or be aware of part of the body. This formulates the pattern of neglect and can be expressed verbally. The disorders are strongly linked to the rate of achieving independence.

Unilateral Spatial Neglect (USN) USN comprises of the failure response or reports to sensory stimuli. Found in 23% of stroke patients and is common with the right-sided lesions more than the left-sided lesions by 42% to 8%, respectively. While the left hemisphere modulates arousal and attention to the right visual field, the right hemisphere defines attention in the right and left visual fields, thereby increasing the risk of neglect. In the right MCA, USN is characterized with head to eye deviation to the left10. The manifestations also include neglect of the left side of the environment and flat affect, which limits emotional expressiveness.

Emotional Disorders

Typically, right MCA strokes may go unnoticed due to the absence of cognitive deficits such as language disturbance. Other manifestations such as neglect and reduced emotional awareness make it more challenging to determine right MCA strokes. Paradiso et al. point out neuropsychiatric images following a right MCA stroke may show alexithymia and apathy. Limitations in awareness and expressions of personal emotions are termed as alexithymia with the manifestation leading to significant interpersonal and psychiatric challenges.

Tissue damage in the insula or basal ganglia during the right MCA stroke elaborates apathy and lack of energy. The study investigates further and determines that a right MCA leads to a dysfunctional anterior cingulate cortex (ACC), leading to emotional blunting and emotional incontinence. Subsequent manifestation includes irritability, mood liability depression, anhedonia, and blunted affect11.

Evaluation of a Stroke

Radiography through CT and MRI offers to image for MCA infarcts. In evaluation, it is imperative to note that MCA strokes end up affecting perforator branches or one or more distal branches. To determine MCA occlusion, the first findings should indicate a hyperdense middle cerebral artery sign, which provides visualization for thromboembolism, and the presence of calcification is crucial as it nullifies angioplasty.

Parenchymal findings also include blurring, decreased attenuation, and swelling of the grey-white matter junction of affected areas. In the first hour of occlusion, the findings should also indicate the lentiform nucleus, which should be visible in 75% of patients at 3 hours. The insular ribbon and surface cortex also highlight the presence of an MCA stroke within the first 3 hours. On MRI, the findings correlate to those of other infarcts and fail to differentiate MCA infarctions with others. Hence CT angiography is an essential early diagnosis tool while MRI helps determine the infarct size early and could be coupled with magnetic resonance angiography to confirm the suspicion of occlusion.

Risk factors of a Stroke

There are modifiable and non-modifiable risk factors for stroke. The non-modifiable risk factors include age, gender, ethnicity, family history, and previous stroke. Studies dictate that the incidence of stroke doubles with age after 55 years. Even though incidence rates are increasing among the 20 to 54 years age group, the risk is at 18.2%. Furthermore, the relationship between sex and stroke incidence is also age. At younger ages, women have a significantly high risk of strokes compared to men due to risks associated with pregnancy, postpartum state, and hormonal issues. With age, the risk shifts tom men, even though strokes occur more in women than in men due to longer life spans.

On ethnic-related risks, African Americans have twice the risk of stroke incidence and a higher mortality rate compared to Hispanic and non-Hispanic Caucasians8. The higher risk is traced to young black adults who have a substantially higher risk for subarachnoid hemorrhage and intracerebral hemorrhage compared to peers of other ethnicities. The racial disparities can also be traced to social determinants of access, disease, language, and nativity. Genetic factors are hereditary and formulated through parental or family history14.

Modifiable risk factors include atrial fibrillation, hypertension, smoking, diabetes, and high cholesterol. Due to the link between blood pressure and strokes, hypertension stands out as a critical modifiable factor. Hence, the treatment of hypertension, either through behavioral change or medication, stands out as a practical approach to reducing strokes10. Besides, diabetes mellitus increases the risk of stroke by 2 fold and stroke accounts for 20% of all diabetes deaths.

A combination of behavioral therapy and medications in diabetes reduces the risk of strokes. Atrial fibrillation also a significant risk factor. Its treatment and management are associated with a decline in the risk for strokes. Sedentary behavior, obesity, metabolic structure, alcohol consumption, smoking, and substance abuse also significantly increase the risk as they formulate other risk factors such as hypertension and atherosclerosis14.

Treatment and Management of MCA Strokes

Like other types of strokes, a certified stroke center is highly recommended for treatment and management. These centers are associated with interdisciplinary care, improved outcomes such as length of stay, patient function, and the costs of care11. The approaches to care include the use of thrombolytic therapy, in appropriate and consistent measures, with the patient discharged to statin medication, antithrombotic therapy, and antihypertensive medication to prevent reoccurrence11.

Dysphagia screening and therapy should also be administered to manage impaired swallowing. Pulmonary embolism (PE), leading to 10-25 % of mortality after strokes, using pharmacological interventions and patient mobilization, is also imperative14. Treatment and management should also focus on modifiable risk factors, mainly hypertension management, smoking cessation, and stroke education.

Conclusion

MCA strokes are the most common type of CVA accident as it supplies two-thirds of the anterior cerebral hemisphere with blood including the lateral portion of the cerebral hemisphere, frontal, parietal, and the upper half of the temporal regions. With a mortality rate of up to 80%, this paper determines the clinical representations of MCA strokes, drawing from MCA structure, territory, embryology, variants, and manifestations of MCA strokes in both the dominant left hemisphere and the non-dominant right hemisphere. Left-sided lesions affect the upper extremities of the face and arm disproportionately to the leg weakness.

Moreover, left-sided occlusion differentially manifests through receptive aphasia and dysarthria. On the right-sided lesion, the manifestations specifically include more unilateral spatial neglect and emotional disorders coupled with visual-spatial perceptual disorders. MCA strokes can be differentially identified and evaluated early through CT angiography, and MRI can be used to determine the size of the infarct and the potential site of occlusion. Treatment involves mending modification factors couple with accurate thrombolytic therapy and dysphagia screening and therapy. With continued research into MCA strokes, it is imperative to determine how factors such as early mobilization could improve long-term patient outcomes.

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