Posterior Cerebral Artery and Cerebral Vascular Accidents -Solved

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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 howa stroke changes the structure and/or the function of any one, or all, of them.  

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Solution

Posterior Cerebral Artery and Cerebral Vascular Accidents (CVAs –Stroke)

Introduction

Strokes are the number one leading cause of disability, the second most common cause of dementia and the third-highest cause of mortality. Strokes, in general, have substantial clinical, social, and economic effects requiring sustained efforts from research scientists and clinical practitioners in their quest for understanding the underlying pathogenic mechanisms. The subsequent understanding facilitates the adoption of preventive measures and effective therapies. By definition, a stroke (also known as a cerebral vascular accident (CVA) refers to the sudden loss of brain function as a result of interruption of blood supply to the central nervous system (CNS).[1]Physiologically speaking, normal cerebral blood flow falls between 50 to 60 ml/100g/min.  If the CBF falls below 20ml/100g/min, this fall triggers an electrical silence while falling below 10ml/100g/min leads to irreversible neuronal damage. Inadequate blood circulation to the brain denies the neurons needed glucose and oxygen¹. More than 85% of strokes are of ischemic origin, usually caused by a blockage of one or more cerebral arteries[2]. The major arteries are anterior cerebral artery (ACA), middle cerebral artery (MCA) posterior cerebral artery (PCA), and vertebral basilar artery (VBA). The blockage occurs due to blood clots leading to cerebral perfusion.  The remaining 15% causes of stroke are hemorrhagic meaning they result from either intracerebral or subarachnoid bleeding¹. Consequently, the goal of this essay is to examine the post cerebral artery stroke (PCA) and the sections of the brain, which this type of stroke mostly affects.

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PCA Structure

According to Kuybu, Okkes, Prasanna Tadi, and Rimal H. Dossani[3] a comprehensive understanding of the pathophysiology of PCA stroke and the syndrome connected to it demands enough knowledge of the structures as well as the brain’s vascular anatomy. Suffice it to say that anterior and posterior circulation offers the brain its primary blood circulation. The posterior communication arteries (PCOM) connect both ACA and PCA to form the circle of Willis³. The circle of Willis and collateral circulations supplies blood to the occluded areas in case there is blood circulation interruption in the cerebral vasculature. The vertebral arteries (VA) posterior inferior cerebellar arteries (PICA) basilar artery (BA), pontine branches of BA, anterior cerebellar arteries (AICA), and superior cerebellar arteries (SCA) contribute to posterior circulation⁴. The vertebral arteries originate from the subclavian arteries and join the BA in the cranium. The BA conventionally divides into PCAs around the pituitary stock. In 70% of the time, PCAs originate from BA, 20 % from PCOM, and 10% from a mix of the two. The PCA is divided into five segments namely P1, P2, P3, P4, and P5[4].The P1 segment is found within the inter-pendicular cistern running from the end of BA to the posterior communicating artery. Embolism to the rare anatomical variant where the PCA branches of at the artery of Percheron results in bilateral paramediam thalamic lesions. The P1 PCA stroke manifests through memory impairment, altered senses, and vertical gaze palsy. The P2 segment commences at the posterior communicating artery and forms a loop around the ambient cistern of the midbrain and runs above the tentorium cerebelli³. The P3 segment describes the part of the artery that courses through the quadrigeminal cistern and usually branches off into anterior and posterior inferior temporal arteries. The P4 segment forms the last segment of the PCA terminating in the calcimine sulcus. Lastly, the end branches of parieto-occipital and the calcarine arteries from the P5 segment.

PCA Etiology and Epidemiology and Pathophysiology

            The mechanism of PCA stroke comprises of diseases and conditions like significant artery disease, migraine, embolism, thrombosis of either PCA, BA or VA and small artery disease, among others. Despite all these causes, the leading causes of PCA stroke remain small artery disease, embolism, and atherosclerosis. In the US, stroke is a leading cause of adult disability and the fifth leading cause of death. According to Kuybu, Tadi & Dosani³ there are over 140 000 fatalities besides 800 000 individuals who experience new or recurrent strokes. Of these, 5 to 10 % are related to PCA stroke. When PCA stroke disrupts the supply of blood to many regions of the brain, the resulting signs and symptoms depend on the location and severity of the obstruction. For example, if a deep. Proximal occulion occurs; the ischemic stroke may happen in the thalamus or midbrain and the cortex. In case a superficial or distal occlusion happens, the stroke may only happen in cortico structures. Due to these occlusions, the health care provider must understand the mechanism of PCA stroke, its acute and chronic management, and the preventive measures that need to be instituted³. Large artery disease may trigger artery to artery embolism, complete branch blockage, in situ blockage, and hemodynamic stability. The main atherosclerotic arteries, namely VA, BA, and proximal PCA primary, generate thrombosis. On the other hand, PCA stroke of small artery disease like lipophyhlinosis and hyaline arteriolosclerosis could be to complications arising from diseases like hypertension and diabetes or even ageing.

PCA Embryology

      Around the first month of development, the internal carotid artery divides into the anterior ad posterior segments. It is from the anterior segment that anterior choroidal artery together with anterior cerebral artery and the middle cerebral artery emerge⁴. Similarly, the posterior segment gives rise to the fetal posterior cerebral artery.  In its formative stages of fetal development, the vertebra-basilar anastomosis gives posterior circulation about the whole of its blood supply. With time and as the contents of the posterior fossa and occipital lobe continue to grow, the posterior circulation stops relying on anterior circulation leading to the annihilation of anterior-posterior anastomoses^{3, 4}. The reduction annihilation leaves the posterior communicating arteries as the only mature anastomoses present within the anterior-posterior circulation. If the fetal posterior cerebral artery survives and continues to grow from the internal carotid artery, it may give rise to a smaller calibre basilar artery a phenomenon which according to Kinan and Das⁴ happens to between 10and 29% of the population.

      Furthermore, the persistence of fetal PCA can be described as complete or partial, depending on whether the P1 segment of the PCA is hypoplastic. The medical significance of this is that patients with ipsilateral persistence of a fetal PCA cannot adequately establish leptomeningeal anastomoses within the ACA, MCA, and PCA⁴. Subsequently, patients having ipsilateral fetal PCA may be prone to ischemia due to ICA stenosis or thrombosis.

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Clinical Manifestations of PCA Strokes

      Some of the signs and symptoms associated with PCA strokes include visual field defects, memory impairment, consciousness alterations, diplopia, vertigo, and dysphagia. The visual impairment due to PCA strokes arises from the fact that a substantial portion of the CNS ensures good vision[5] experiencing transient vision problems could indicate vision loss after a cerebral infarction or be a harbinger of an impending PCA.  Visual challenges after an individual have experienced stroke manifest in the form of transient monocular vision Dloss (TMVL) visual field deficits in addition to ocular dysmotility^{4, 5}. For one to fully understand the varied PCA stroke syndrome, one should be aware of the physiological framework of the visual system in connection to its blood supply.

      To begin with, visual the prechiasmal visual network comprises the axons from the retina’s layer of nerve fiber which join to form the optic nerves[6]. These nerves fibres extend medially towards the optic canals. The ophthalmic artery and internal carotid artery supply blood to the prechiasmaloptic nerves. The central retina artery, an offshoot of the ophthalmic artery, supplies blood to the retina. The optic nerves rejoin to make the optic chiasm of which the Circle of Willis supplies^{3, 6}. On the other hand, the retrochiasmal visual network embraces the part from the optic chiasm to the visual context. The anterior choroidal artery extends to the lateral geniculate body. Be that as it may, the terminal anastomosis s still vulnerable to ischemia.

Visual stroke Syndromes

      The medical practitioner can utilize the anatomical; understanding of the visual landmarks and the matching blood supply so that they can clinically localize a stroke affecting vision because they can recognize the effects of its defects immediately after clinical examination.

Prechiasmal Ischemia and Monocula Visual loss

      Retina ischemia secondary to occlusion in the region around ophthalmic artery vascular supply can cause prechiasmal vision loss. Symptoms that occur before non- visual strokes include TMVL where more than three-quarters of the patients encounter decreased visual acuity. Retina ischemia car happens because of temporary amaurosis fugax or permanently due to retinal artery occlusion (BRAO), the central retinal artery (CRAO), or in rare circumstances ophthalmic artery occlusion⁵. Irrespective of the type of occlusion, each of them can cause permanent loss of vision with decreased visual acuity or deficits in the visual field. A confirmatory diagnosis of CRAO is the cherry-red spot within the macula. At this juncture, it is essential to remember that transient binocular visual loss (TBVL is not a result of a prechiasmal process but that of the vertebra –basilar ischemia⁶. The medical practitioner should also remember that since TVBL generates homonymous visual defects and can, therefore, be a warning sign of stroke, just like atrial fibrillation.

Chiassmal Ischemia and Bitemporasl Hemianopia

            The rich supply of collateral circulation facilitated by the Circle of Willis to the optic chiasm makes chiasmal strokes a very rare occurrence. However, when they do occur, chiasmal strokes make the patient t experience acute onset bitemporal hemianopia. Unusual presentations can also happen with a case of the right temporal visual loss with total contralateral monocular vision loss⁶. Other vision loss defects caused by PCA stroke include homonymous hemianopia whose cause is postchiamal ischaemia and efferent visual dysfunction due to lesions outside the visual afferent pathways.

Cognitive and Behavioral Dysfunctions

      Infarction of the hippocampus and parahippocampus cause memory impairment. At the same time, an infarction large enough to affect the parietal lobe or temporal lobe has the potential to cause aphasia where transcortical sensory aphasia emanates from the infarctions to the left side of the parietal, occipital region. Zhang, Duoduo, Wei Zhang, Chunyang Wei, and Jingjing Kong.  Note that the general belief both mental and behavioral disorders can result from acquired frontal and temporal lesions is medically true.  The caudate nucleus plays an important function in modulating motor functions.  Despite these facts, the final consequences of the damage to the caudate nucleus and the impact the damage has on cognitive and behavioral abnormalities are not clearly understood currently.  Studies though have established that the caudate nucleus plays a vital function in the control of behavioral processes. Reports from the previously mentioned study demonstrate that patients having cognitive and behavioral abnormalities as the chief complaints face the likelihood of being misdiagnosed with an intracranial infection like encephalitis. The rarity of the caudate stroke means this type of stroke receives inadequate attention in medical practice. As a result, this paper calls for further investigations of caudate stroke so that the research findings can enrich our understanding of caudate functions.  Be that as it may, the most frequent clinical manifestations of caudate nucleus stroke is abulia.  Over 50% of the caudate nucleus stroke displayed lowered spontaneous activity and language.

      Similarly, these patients lacked initiative, had psychic akinesia and displayed extended latency in responding to questions or other stimuli. The mechanism of abulia is currently unclear and probably interrelates with the impairment of the frontal –striatal- thalamic cortical circuits. Studies have also found that other causes which lead to damage of the frontal lobe also result in abnormal behavior, implying that the frontal lobe may play a key role in some abnormal behavior and abulia. Additionally, some clients with caudate nucleus lesions exhibited hyperactivity, confusion and restlessness among other cognitive dysfunctions. In some cases, the patients also had affective symptoms with psychotic features. Depression in some of the patients suggesting that the caudate nucleus probably also regulates emotions. Hallucination is rare but may emerge after PCA strokes to any side of the brain with palinopsia or the seeing of persistent images long after, and the image has been removed was also noted. PCA can also lead to other dysfunctions lie Anton syndrome, which results from the spontaneous onset of bilateral occipital strokes, causing cortical blindness. Balint syndrome which results from the bilateral occipitoparietal border infarction presents with optic ataxia, oculomotor apraxia and simultagnosia³.

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Evaluation of a Stroke

      The primary method used to evaluate an acute stroke is a non-contrast enhanced computed Tomogram (CT). While contrast may improve the quality of a CT image, it is not recommended because of the possibility of the stroke emanating from a hemorrhagic instead of an ischemic cause. Medical practitioners should be aware that giving a contrast CT to a patient with hemorrhagic stroke would exacerbate the hemorrhage and cause further damage because that contrast is poisonous to the human cell. Javed and Das⁴ point out that a stroke can be categorized into three phases. The acute phase lasts less than 24 hours) subacute (is between 1 and 5 days) or chronic extends for several weeks. Cytotoxic edema occurring in acute stroke enables the physician to visualize hyper attenuation with effacement of cortico sulci and the absence of differentiation between the gray and white matter.

      On the other hand, vasogenic edema occurs with a sub-acute stroke, and it is within this phase that mass effect and the herniation that follows are at the highest risk of happening. Chronic strokes while also having hypo-attenuation are accompanied by loss of brain tissue. A  CT angiogram (CTA) may also enable the physician to visualize the whole cerebral circulation starting from the aortic arch so that the doctor can establish the specific etiology of the stroke⁶.  A CTA has the same drawback of contrast as the CT, although it is a useful technique that can determine etiologies like aneurysm or artery- venous malformations. Magnetic resonance imaging (MRI may be the gold standard of detecting various etiologies, but their use in acute stroke is not common. The reasons why MRIs are not used are several. Some of these reasons include but are not limited to the fact that MRIs take a longer time to process compared to CT scans. They are also ineffective in detecting intracellular edema as seen in the acute phase of the stroke.

Causes of PCA Strokes

       A point to bear in mind is that when an ischemic event happens within the posterior circulation, the main causative factors are arterial dissection, embolism and atherosclerosis. Beginning with atherosclerosis, large vessel atherosclerotic disease leads to thromboembolism but may also have the potential to cause hemodynamic imbalance resulting in ischemia.  Large vessel atherosclerosis within the posterior usually manifests in the vertebral arteries. 35% of the PCA strokes are caused by large vessel atherosclerotic disease, while the small vessel disease contributed to 13% of these types of strokes. Arterial dissection is a very rare cause of PCA and conventionally does not present without the concomitant involvement of the basilar or vertebral arteries. The rationale behind this is that dissection in the PCA is due to cervical trauma. This condition presents in patients of motor vehicle accidents or active young adults. The symptoms are a history of trauma, neck pain and occipital headache. The third and last cause of posterior circulatory strokes is cardioembolism. Unlike the vertebral and basilar arteries, PCA stroke can be caused by embolism from the heart, aorta or ventral arteries. Cardio embolism can be associated with several causative factors like among them delayed cardiomyopathy, atrial fibrillation, prosthetic heart valves, congestive heart failure and valvular disease[7].

Treatment and Management of PCA Stroke

      Treatment of ischemic stroke includes using t-PA (tissue plasminogen activator) within four and a half hours since its onset. However, the healthcare provider should be sure that no hemorrhagic etiology was present. The fact that PCA strokes produce several symptoms which overlap with those of other diseases implies the proper diagnosis is delayed most of the times.  In their case report Yamamoto, Taiki, Tomotaka Ohshima, Masaki Sato, Shunsaku Goto, Kojiro et al., report, the case of a patient who was successfully treated with endovascular clot aspiration[8]. The researchers note that due to progress in endovascular treatment. Statistics indicate that between 5 and 10% of all acute ischemic stroke occurs within the PCA area. In the cited case, physicians did not use t-PA as the patient’s NHSS score was very low. The successful treatment led the physicians to observe that if a patient with PCA stroke has no contraindications, he or she can be treated within four and half hours from the onset of the symptoms-PA can be used. With EVT remaining uncertain at present, healthcare providers and patients should stick to recurrent stroke prevention techniques. The prevention strategies should consider controlling risk factors like blood pressure lowering, use of satin to lower the lipids.

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Conclusion

In conclusion, this research paper has established that adequate knowledge of the pathophysiology of PCA requires a sufficient understanding of the structures and vascular anatomy of the brain. The author has outlined an anatomical structure of the PCA right from fetal stages development exploring how a PCA stroke impacts on visual system cognitive impairment and other dysfunctions The essay has also determined that both anterior and posterior circulations supply the primary blood circulation to the brain.  The paper has also found that cerebral vasculature is distinct in that the Circle of Willis provides collateral circulation to the brain. Additionally, the essay has explored the various diagnostic instruments that can be used to make a PCA stroke diagnosis before examining how PCA strokes can be treated. Finally, the paper acknowledges the fact that the role of acute endovascular revascularization remains uncertain at present.

References

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[1]  Coupland AP, Thapar A, Qureshi MI, Jenkins H, Davies AH. The definition of stroke. J R Soc Med. 2017; 110(1):9–12. doi:10.1177/0141076816680121

[2] Marnane M, Duggan CA, Sheehan OC, et al. Stroke subtype classification to mechanism-specific and undetermined categories by TOAST, A-S-C-O, and causative classification system: direct comparison in the North Dublin population stroke study. Stroke. 2010; 41(8):1579–1586. doi:10.1161/STROKEAHA.109.575373

[3] Kuybu O, Tadi P, Dossani RH. Posterior Cerebral Artery Stroke. [Updated 2019 May 6]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532296/

[4] Javed K, Reddy V, M Das J. Neuroanatomy, Posterior Cerebral Arteries. [Updated 2020 Apr 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538474/

[5] Pula JH, Yuen CA. Eyes and stroke: the visual aspects of cerebrovascular disease. Stroke Vasc Neurol. 2017; 2(4):210–220. Published 2017 Jul 6. doi:10.1136/svn-2017-000079

[6] Zhang, Duoduo, Wei Zhang, Chunyang Wei, and Jingjing Kong. “Case Report Cognitive and behavioral dysfunctions caused by caudate infarction: a case report and literature review.” Int J Clin Exp Med 10, no. 11 (2017): 15615-15618

[7] Sciascia A, Monaco M. When Is the Patient Truly “Ready to return,” a.k.a. Kinetic Chain Homeostasis? Elite Techniques in Shoulder Arthroscopy. 2015:317-327. doi:10.1007/978-3-319-25103-5_25.

[8] Yamamoto T, Ohshima T, Sato M, et al. A Case of Acute Isolated Posterior Cerebral Artery Occlusion Successfully Treated with Endovascular Clot Aspiration. NMC Case Rep J. 2017; 4 (2):55–58. Published 2017 Mar 8. doi:10.2176/nmccrj.cr.2016-0214

Question – Posterior Cerebral Artery and Cerebral Vascular Accidents

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 howa 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

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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.

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