Exhibits a penumbra,
Highly reproducible,
No craniectomy
The intraluminal suture MCAo model : The middle cerebral artery (MCA) is vulnerable to ischemic insult and occlusion in humans, accounting for 70% of stroke-related disability. This disease model has been widely studied in rat and mouse models, with more than 2600 experiments conducted [ 76 , 77 ]. The MCAo procedure is minimally invasive; it involves occlusion of the carotid artery by insertion of a suture until it interrupts blood flow to the MCA. This procedure is applied for time periods such as 60 or 90 min or permanently, to induce infarction, and has a success rate of 88–100% in rats and mice [ 78 ]. The most commonly used animal for studying pre-clinical stroke is the Sprague–Dawley rat, which has a small infarct volume [ 79 ]. In mice, C57BL/6 and SV129 are commonly used to introduce MCA infarction. The reproducibility of the technique depends on a multitude of factors, such as the animal strain, suture diameter, body weight and age. The advantage of this model is that it mimics the human ischemic stroke and displays similar penumbra [ 80 ]. The MCAo model is appropriate for reproducing ischemic stroke and associated clinical manifestations such as neuronal cell death, cerebral inflammation and blood–brain barrier damage [ 75 ].
Craniectomy model : This model uses a surgical procedure for inducing occlusion in the artery. In this technique, a neurological deficit can be induced in mice by electrocoagulation causing permanent insult or a microaneurysm until blood flow is interrupted. Alternatively, three-vessel occlusion is used, reducing the blood flow and resulting in damaged tissue. The infarct volume differs depending on whether the occlusion is permanent or transient [ 81 , 82 , 83 ]. A study conducted in neonatal P14–P18 rats mimicked pediatric stroke in a younger human population; a 3-h occlusion was performed to induce lesions affecting 40–50% of the brain [ 84 ]. Similarly, in P7 rats, oedema formation was observed in the MCA, followed by microglial infiltration. The P12 CB-17 is another animal model used for stroke research, mainly due to low variability in occlusion insult to the brain [ 85 ]. The other advantages of this model include reproducible infarct size and neurofunctional deficits, reduced mortality and visual ratification. The CB-17 model was successfully used to reproduce cerebral infarction and long-term survival rate, and to study ischemic reperfusion. Researchers showed that reperfusion supports neuron survival, rescues vascular phenotypes and is associated with functional recovery after stroke [ 86 ].
The Levine–Rice model : It involves histological examination and behavioral tests in rat pups, and it is used to study neonatal hypoxic-ischemic stroke [ 87 ]. In this model, a unilateral ligation is followed by reperfusion and recovery. Later, the animal is placed in a hypoxic chamber to understand neonatal stroke pathophysiology as well as regenerative and rehabilitative therapeutic possibilities. P7 rat animal models are commonly used to study the clinical manifestations of hypoxic-ischemic injury [ 88 , 89 , 90 ].
Photo-thrombosis model : This model is based on photo-oxidation of the vasculature leading to lesion formation in the cortex and striatum. In this method, the skull is irradiated with a photoactive dye that causes endothelial damage, intraparenchymal vessel aggregation and platelet stimulation in the affected area. It is injected intraperitoneally in mice and intravenously in rats [ 91 ]. This model is highly reproducible, with a low mortality rate and no surgery. The pathophysiology of this method is slightly different to that seen in human stroke due to little collateral blood flow or formation of ischemic penumbra. However, recent researchers modified the photothrombotic ischemia model to include hypoperfusion in an attempt to mimic penumbra. It has also been deployed in freely moving mice to evaluate the development of motor cortex ischemia and motor deficits. This model permits assessment of the ongoing infarction and improves our understanding of the neuronal insult and repair process [ 92 , 93 ].
Endothelin-1 model: Endothelin-1 (ET-1) : ET-1 is a small peptide molecule produced by smooth muscle cells and the endothelium. It is a paracrine factor that restricts the vascular system through cell-specific receptors. Ischemic lesion is induced by stereotaxic injection of ET-1 directly into the exposed MCA in the intracerebral or cortex region [ 94 ]. ET-1 administration was observed to cause 70–90% reduction in cerebral blood flow, followed by reperfusion [ 95 ]. This technique is minimally invasive, has a low death rate and can be applied to deep and superficial brain regions. It is appropriate for long-term lesion studies, and the lesion size can be controlled by regulating ET-1 concentration, which is critical for reproducibility [ 95 ]. ET-1 is expressed by both neurons and astrocytes, which may decrease the stringency of interpretation of neuronal dysfunction in stroke [ 96 ]. A study in juvenile P21 rats used ET-1 to induce focal lesion in the striatum [ 97 ]. Similarly, aged P12 and P25 rats showed neuronal damage and lesion formation after injection of ET-1 into the hippocampus [ 98 ].
The embolic stroke model : It includes microsphere, macrosphere and thromboembolic models. The microsphere model involves introduction of spheres of diameter 20–50 μm into the circulatory system using a microcatheter to form multifocal infarcts [ 99 ]. Macrospheres are 100–400 μm in diameter and introduced into the intracerebral artery (ICA) to produce reproducible lesions in the MCA [ 100 ]. In the thromboembolic model, thrombin is directly injected to form clots in the ICA or MCA. The volume of the infarct depends upon the size of the clot formed [ 101 ]. This model closely resembles the type of stroke seen in humans. Prior study of clots induced by this model in mice have showed that they are mainly comprised of polymerized fibrin with few cells and platelets present, and 75% of clots exhibit platelet/fibrin build-up and deposition of neutrophils, monocytes and erythrocytes [ 102 ].
Neurorehabilitation in animal models : Various rehabilitative devices and forced training strategies have been deployed in stroke-affected animals to study neurological behavior. Robotic and electric devices have also been developed for training purposes in animal models to evaluate the functionality and effectiveness of the rehabilitation process. Similarly, forced exercise regimes, such as running on a treadmill or task-oriented motor training, are used to study rehabilitation scope in humans. Housing environments that provide social, motor and sensory stimuli and support cell engraftment, creating a more realistic approximation of human treatment, can be tested using animal models [ 103 , 104 , 105 ].
Animal models in biomaterial testing : Animal models have been well characterized for the study of brain tissues via brain atlases ( http://www.med.harvard.edu/AANLIB/ , https://portal.brain-map.org ) for the required species. Stereotaxic techniques are utilized to introduce biomaterials or cells into particular coordinates of the target tissue. Microlesions can be studied precisely, and targeted localization can be confirmed using magnetic resonance imaging (MRI)-based lesion cartography [ 106 , 107 , 108 ].
Stroke prevention involves modifying risk factors within a population or individuals, while stroke management depends on treating its pathophysiology. Despite an enormous amount of research into stroke over the last two decades, no simple means of treating or preventing all the clinical causes of stroke has been established. The overall direction of current stroke research is to generate novel therapies that modulate factors leading to primary and secondary stroke. Recent and current strategies for stroke prevention and treatment are discussed below ( Figure 3 ).
Stroke therapy. This represents the overall process to manage the incidence of stroke.
Excitotoxicity : Neuronal death is a key manifestation of stroke. A key reason for this phenomenon is neuronal depolarization and inability to maintain membrane potential within the cell. This process is mediated by glutamate receptors N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), which were among the first neuroprotective agents tested in stroke prevention. However, the untimely release of glutamate overpowers the system that removes glutamate from the cell and causes abnormal release of NMDA and AMPA molecules, leading to uninhibited calcium influx and protein damage. As a result, these agents have not been shown to reduce neuronal death in human subjects. Targeting the molecular pathways downstream of excitotoxicity signaling, rather than directly targeting glutamatergic signaling, might reduce the side effects of the process [ 109 , 110 ].
Gamma aminobutyric acid (GABA) agonists : Clomethiazole is a GABA agonist that has been tested for its ability to improve stroke symptoms in patients, but failed to reduce the toxicity induced by the glutamate receptor [ 111 ].
Sodium (Na + ) channel blockers : Na + channel blockers have been used as neuroprotective agents in various animal models of stroke. They prevent neuronal death and reduce white matter damage. Many voltage-gated Na + channel blockers have been tested in clinical trials, but most have proved to be ineffective [ 112 ]. Mexiletine is a neuroprotectant and Na + channel blocker that proved effective in grey and white matter ischemic stroke, though further evaluation is required to confirm its role [ 113 ]. Lubeluzole was shown to reduce mortality in stroke in initial clinical trials, but successive trials failed to reproduce similar outcomes. Similarly, sipatrigine is a Na + and Ca 2+ channel blocker which failed in a Phase II clinical trial in stroke patients. Amiodarone was shown to aggravate brain injury due to defective transportation and accumulation of Na + ions in the brain after stroke [ 114 ].
Calcium (Ca 2+ ) channel blockers : Voltage-dependent Ca 2+ ion channel blockers have been shown to decrease the ischemic insult in animal models of brain injury. The Ca 2+ ion chelator DP-b99 proved efficient and safe in Phase I and II clinical trials when administered to stroke patients. Similarly, Phase II trials significantly improved clinical symptoms in stroke patients treated within 12 h of onset [ 115 ]. In another study, Ca 2+ channel blockers reduced the risk of stroke by 13.5% in comparison to diuretics and β-blockers [ 116 ].
Antioxidants : Reactive oxygen species produced in the normal brain are balanced by antioxidants generated in a responsive mechanism. However, in the ischemic stroke model, excess production of free radicals and inactivation of detoxifying agents cause redox disequilibrium. This phenomenon leads to oxidative stress, followed by neuronal injury. Therefore, antioxidants are employed in treatment of acute stroke to inhibit or scavenge free radical production and degrade free radicals in the system. In one study, antioxidant AEOL 10,150 (manganese (III) meso-tetrakis (di-N-ethylimidazole) porphyrin) effectively regulated the gene expression profiles specific to inflammation and stress response to decrease the ischemic damage and reperfusion in stroke patients [ 117 ]. In another, deferoxamine was shown to regulate the expression of hypoxia-inducible factor-1, a transcriptional factor regulated by oxygen levels, which in turn switched on other genes like vascular endothelial growth factor and erythropoietin. This mechanism, studied in an animal stroke model, proved beneficial in reducing lesion size and improving sensorimotor capabilities [ 118 , 119 ]. Similarly, NXY-059 compound acts as a scavenger to eliminate free radicals and decrease neurological deficits. The Stroke-Acute-Ischemic-NXY-Treatment-I (SAINT) clinical trial showed the efficacy and safety of NXY-059, but SAINT II failed to reproduce the positive effect of this drug in stroke patients [ 120 , 121 ]. In another study, researchers employed intravenous injection of antioxidants directly into mice brains to understand the benefits of route of administration. This method reduced neurological defects, but had minimal influence on brain damage [ 122 ].
The intravenous thrombolytics (IVT) : The IVT treatment paradigm was originally developed to treat coronary thrombolysis but was found to be effective in treating stroke patients. The efficiency of thrombolytic drugs depends on factors including the age of the clot, the specificity of the thrombolytic agent for fibrin and the presence and half-life of neutralizing antibodies [ 123 ]. The drugs used in IVT treatment aim to promote fibrinolysin formation, which catalyzes the dissolution of the clot blocking the cerebral vessel. The most effective IVT drug, recombinant tissue plasminogen activator (rt-PA, or alteplase), was developed from research conducted by the US National Institute of Neurological Disorders and Stroke (NINDS) [ 124 ]. However, European Cooperative Acute Stroke Study (ECASS and ECASS II) researchers were unable to reproduce NINDS’ results. Later, it was found that this drug was effective in reducing clot diameter in stroke patients within three hours of incidence. The Safe Implementation of Thrombolysis in Stroke Monitoring Study (SITS-MOST) confirmed the efficacy and safety of alteplase within the designated time frame [ 125 ]. Another category of thrombolytics, consisting of fibrin and non-fibrin drugs, is used for treatment of stroke symptoms. Fibrin activators like alteplase, reteplase and tenecteplase convert plasminogen to plasmin directly, whereas non-fibrin activators like the drugs streptokinase and staphylokinase do so indirectly [ 123 ].
Intra-arterial thrombolysis (IAT) : IAT is another approach designed to combat acute stroke. This treatment is most effective in the first six hours of onset of MCA occlusion, and requires experienced clinicians and angiographic techniques [ 115 ]. Prolyse in Acute Cerebral Thromboembolism II (PROACT II) and Middle Cerebral Artery Embolism Local Fibrinolytic Intervention (MELT) were randomized clinical trials (RCTs) undertaken to test the efficacy and safety of a recombinant pro-urokinase drug [ 126 , 127 ], but did not produce any data useful for stroke treatment. Thrombolytics and glycoprotein IIb/IIIa antagonists were combined in two small clinical trials; this approach was helpful in treating atherosclerotic occlusions but less effective for cardioembolism [ 128 , 129 ]. The Interventional Management of Stroke (IMS) III trial tested IVT and IAT together to assess the benefits of combining rapid administration of therapy (IVT) and a superior recanalization methodology for faster relief (IAT) [ 130 ]. The IMS III trial was fruitful with bridging therapy (combination of IVT and IAT) as compared to IVT alone. There was an increase of 69.6% in the recanalization rate using bridging therapy in stroke patients [ 131 , 132 ].
Fibrinogen-depleting agents : Research has found a strong correlation between high fibrinogen levels in stroke patients and poor diagnosis for clinical outcomes. Fibrinogen-depleting agents decrease blood plasma levels of fibrinogen, hence reduce blood thickness and increase blood flow. They also remove the blood clot in the artery and restore blood flow in the affected regions of the brain. However, although some RCTs of defibrinogen therapy identified beneficial effects of fibrinogen-depleting agents in stroke patients, others failed to show positive effects on clinical outcomes after stroke [ 133 ]. Moreover, some studies reported bleeding after treatment with defibrinogen agents. Ancrod is a defibrinogenating agent derived from snake venom that has been studied for its ability to treat ischemic stroke within three hours of onset [ 134 ]. The European Stroke Treatment with Ancrod Trial (ESTAT) concluded that controlled administration of ancrod at 70 mg/dL fibrinogen was efficacious and safe, and achieved lower prevalence of ICH than observed at lower fibrinogen levels [ 135 ].
Antihypertensive therapy : Hypertension is a risk factor for stroke. There are many reasons for high BP in stroke, including a history of hypertension, acute neuroendocrine stimulation, increased intracranial pressure, stress linked to hospital admission and intermittent painful spells [ 136 ]. Correct treatment of high BP during stroke is uncertain due to contradictory outcomes of clinical studies. Some research shows positive correlations between high BP and stroke-related mortality, hematoma expansion or intracerebral damage, suggesting that high BP should be treated. In other studies, low BP levels led to tissue perfusion and increased lesion size, thereby worsening the clinical outcome [ 137 , 138 ]. The multi-center Acute Candesartan Cilexetil Therapy in Stroke Survivors (ACCESS) Phase II study proved that taking medication (candesartan) for BP during stroke was safe, with no orchestrated cerebrovascular events reported due to hypotension. Similar research has been performed with antihypertensive drugs, such as the Continue Or Stop post Stroke Antihypertensives Collaborative Study (COSSACS) to study the efficacy of antihypertensive therapy in stroke; the Control of Hypertension and Hypotension Immediately Post Stroke (CHHIPS) study, designed to determine the cut-off value for BP during an attack; and the Scandinavian Candesartan Acute Stroke Trial (SCAST), which aimed to measure the effectiveness of the drug candesartan on stroke and cardiovascular disease [ 115 , 139 ]. In the COSSACS study, continuing antihypertensive drugs for a two-week period produced no extra harm as compared to stopping it and might be associated with reduced two-week mortality in patients with ischemic stroke [ 140 ]. The CHHIPS study demonstrated that a relatively moderate reduction in blood pressure lowered the mortality rate [ 141 ], whereas the SCAST study suggested that a careful BP-lowering treatment was associated with a higher risk of poor clinical outcome [ 142 ].
Glucose management : Hyperglycemia (elevated blood glucose) is common in stroke patients, so targeting blood glucose levels is an efficient stroke management strategy. Hyperglycemia > 6.0 mmol/L (108 mg/dL) is observed in most stroke patients; it initiates lipid peroxidation and cell lysis in compromised tissue, leading to stroke complications. An experimental study conducted in a rat model of collagenase-induced ICH found that hyperglycemia worsens edema formation and increases cell death, accelerating the course of ischemic injury. Increased blood glucose level is also associated with progression of infarction, reduced recanalization and poor clinical outcome [ 143 ]. Continuous glucose monitoring systems have been deployed to reduce stroke-related risks in both diabetic and non-diabetic stroke patients [ 144 ].
Antiplatelet therapy : This therapy is used for acute ischemic stroke management and for prevention of stroke incidence. It is also vital in controlling non-cardioembolic ischemic stroke and TIA. Antiplatelet agents like aspirin, clopidogrel and ticagrelor are the most widely used drugs administered to stroke sufferers within the first few days of attack [ 145 ]. Dual antiplatelet therapy, which involves a combination of clopidogrel, prasugrel or ticagrelor with aspirin, has become popular; many studies have tested the efficacy and safety of this dual therapy. It has been claimed that clopidogrel and aspirin combination therapy is most beneficial if introduced within 24 h of stroke and continued for 4–12 weeks [ 146 ].
Stem cell therapy : It offers promising therapeutic opportunities, safety and efficacy to stroke patients. Research on embryonic stem cells, mesenchymal cells and induced pluripotent stem cells has assessed their potential for tissue regeneration, maintenance, migration and proliferation, rewiring of neural circuitry and physical and behavioral rejuvenation [ 147 ]. Recently, a new type of mesenchymal stem cells (MSCs), called multilineage differentiating stress-enduring (Muse) cells, has been found in connective tissue. These cells offer great regenerative capacity and have been tested as a stroke treatment. After intravenous transplantation of Muse cells in a mouse model, they were found to engraft into the damaged host tissue and differentiate to provide functional recovery in the host [ 148 ]. Neovascularization is another mode of action of cell therapies in stroke; studies conducted in vitro and in vivo have shown that transplanted cells promote angiogenesis [ 149 , 150 ]. Furthermore, multiple stroke studies have reported that MSCs stimulate neurogenesis; this was confirmed in human embryonic neural stem cells using BrdU-labelling [ 151 , 152 ]. Stem cell therapy enhances the proliferation of neural stem cells and neuritogenesis [ 153 ]. Careful experimental design and clinical trials of stem cell therapies are likely to usher in a new era of treatment for stroke by promoting neurogenesis, rebuilding neural networks and boosting axonal growth and synaptogenesis.
Neural repair : This is an alternative therapy to neuroprotection. It is used to rejuvenate the tissue when the damage is already done and is therefore not time-bound but is most effective when administered 24 h after stroke attack. Many animal models have been used in attempts to stimulate neurogenesis and initiate the neuronal repair process [ 154 ]. Neural repair utilizes stem cell therapy to initiate repair mechanisms through cell integration into the wound or use of neurotrophic factors to block neuronal growth inhibitors. These cells may be channeled to any injured region to facilitate greater synaptic connectivity. Clinical trials using neural stem cells have proven beneficial in stroke patients. However, trials of myelin-associated glycoprotein, neurite outgrowth inhibitor (NOGO) proteins and chondroitin sulphate proteoglycans have shown these agents to be insufficiently effective; more clinical trials are required to increase treatment efficacy [ 155 ]. Biological intrusions may foster regeneration of newer cells, improve axonal guidance and enhance neural circuitry. Pharmacological and immunological interventions may target receptors to provide signaling cues for regeneration or block inhibitory factors in stroke-affected regions of the brain [ 156 ].
Rehabilitation : Stroke can leave individuals with short- and long-term disabilities. Daily activities like walking and toileting are often affected, and sensorimotor and visual impairment are common. Rehabilitation aims to reinforce the functional independence of people affected by stroke [ 157 ]. It includes working with patients and families to provide supportive services and post-stroke guidance after 48 h of stroke attack in stable patients. Stroke rehabilitation may involve physical, occupational, speech and/or cognitive therapy. It is designed to assist patients to recover problem-solving skills, access social and psychological support, improve their mobility and achieve independent living. Rehabilitation may also include neurobiological tasks designed to lessen the impact of cognitive dysfunction and induce synaptic plasticity, as well as long-term potentiation [ 158 , 159 ]. Neuromodulators play a vital role in triggering expression of specific genes that promote axon regeneration, dendritic spine development, synapse formation and cell replacement therapy. Task-oriented approaches, like arm training and walking, help stroke patients to manage their physical disability, and visual computer-assisted gaming activities have been used to enhance visuomotor neuronal plasticity [ 160 ].
The incidence of stroke-related emergencies has decreased substantially over recent years due to improved understanding of the pathophysiology of stroke and identification of new drugs designed to treat the multitude of possible targets. Technological advancements like telestroke [ 161 ] and mobile stroke [ 162 ] units have reduced mortality and morbidity. Therefore, stroke management systems should include post-stroke care facilities on top of existing primary care and access to occupational, speech or any physical therapy following hospital discharge. Hospitals should develop standardized policies to handle emergencies in a timely fashion to avoid casualties and prevent secondary stroke [ 163 ]. Recently, the role of physiotherapists has emerged as an important aspect of post-stroke care management. Physiotherapists have initiated clinical trials of stroke recovery processes and rehabilitation therapy sessions. One ongoing study includes a strategy to manage disability by improving mobility using treadmill exercise, electromechanical device therapy and circuit class therapy [ 164 , 165 ]. Stroke Recovery and Rehabilitation Roundtables bring physiotherapists and other experts together to recommend research directions and produce guidance for the post-stroke healthcare system. Optimized delivery of stroke care systems and access to rehabilitation services are the future of healthcare for stroke [ 166 ].
Animal models used in stroke research reflect only a portion of the consequences of the condition in human subjects. Moreover, experiments conducted within a single laboratory are often constrained in terms of their research output. In vivo animal models of stroke should include aged populations to maximize their relevance, but most recent studies involve young and adult animals. Stroke studies should be conducted in both male and female subjects to exclude gender bias, and should take account of other confounders like hypertension, diabetes and obesity. All these issues make stroke research complex and expensive, and imply that it should be carried out collaboratively, across multiple labs. Ideally, an international multicenter platform for clinical trials would be established to increase the validity of research outcomes with respect to efficacy, safety, translational value, dose–response relationships and proof-of-principle. This strategy will help to overcome the current hurdles in transforming laboratory data into therapeutics for stroke.
Advancements in stem cell technologies and genomics have led to regenerative therapy to rebuild neural networks and repair damaged neurons due to ischemic insult [ 167 , 168 ]. The WIP1 gene is a regulator of Wnt signaling and a promising target for drug development. Studies in mice models showed that knockdown of WIP1 downregulates the stroke functional recovery process after injury, and that the presence of this gene regulates neurogenesis through activation of β-Catenin/Wnt signaling [ 169 ]. Similarly, NB-3 (contactin-6) plays a vital role in neuroprotection, as shown by knockdown of NB-3 in mice after stroke attack. NB-3-deficient mice had increased brain damage after MCAo, which also affected neurite outgrowth and neuronal survival rate. NB-3 is believed to have therapeutic benefits for ischemic insult [ 170 ]. Therefore, WIP1 and NB-3 are promising candidates for future drug trials. This is a vast field, and more research must be conducted in the coming years to enable the development of therapeutic drugs.
Numerous natural compounds have proven to be beneficial for stroke prevention and treatment. They can be synthesized at a lower cost than synthetic compounds and offer competitive efficacy and safety. Honokiol is a natural product that showed neuroprotective effects in animal models, and appears to have a role in reducing oxidative stress and inhibiting inflammatory responses [ 171 ]. Gastrodin, a compound extracted from Gastrodia elata , is a promising candidate in stroke treatment. In a mouse model, it improved neurogenesis and activated β-Catenin-dependent Wnt signaling to provide neuroprotection after ischemic insult. It also has antioxidative effects which protects the neural progenitor cells from neuron functional impairment. Gastrodin’s safety has been proved in clinical trials, hence it is an option for stroke management in the coming years [ 172 ].
The Utstein methodology is a process of standardizing and reporting research on out-of-hospital stroke and defining the essential elements of management tools. Its growing popularity led to the establishment of the Global Resuscitation Alliance (GRA), an organization that governs best practices. The primary aim of GRA is to facilitate stroke care from pre-hospital admission to rehabilitation and recovery. It has developed 10 guidelines to ensure smooth transitioning of services during and after attack. It has implemented a stroke registry, public awareness and educational programs, promoted techniques for early stroke recognition by first responders, sought to optimize prehospital and in-hospital stroke care, advocated the use of advanced neuroimaging techniques and promoted a culture of excellence. The Utstein community has developed comprehensive plans to improve early diagnosis and treatment of stroke patients globally [ 173 ].
Future clinical trials should aim not only to determine the efficacy and safety of drugs but to characterize recovery and clinical outcomes. Clinical trials of pharmacological therapies for post-stroke recovery should adhere to the following guidelines [ 174 ]. Patients should be enrolled within two weeks of stroke whenever possible. Studies should include sampling from a multicenter platform and include global scale criteria for data analysis. The underlying mechanism of action of the tested drugs on target molecules should be thoroughly understood. Secondary measurements like day-to-day progress of recovery, length of rehabilitation, treatment endpoint analysis and any other compounding factors should also be recorded. Overall, research on stoke management has advanced rapidly in recent years and is certain to make additional valuable discoveries through the application of new technologies in hypothesis-driven clinical trials.
Stroke research has seen fundamental advancements over recent years. The improvements in the selection of animal models, imaging techniques and methodological progress have led to immense drug targets and therapeutic interventions. In spite of this, the subsequent clinical trials failed to prove pre-clinical outcomes. Recanalization therapy showed some promising results in the clinical trials but only a small section of stroke patients benefited from this treatment [ 175 ]. Hence, the translational potential of stroke research is still under-investigated.
The key challenges that hinder the smooth transition of pre-clinical research into successful drugs include relevant endpoint selection, confounding diseases models like hypertension and diabetes, modelling age and gender effects in stroke patients, development of medical devices, investigating medical conditions that co-exist during stroke incidence, reproducibility of pre-clinical stroke research data and modelling functional and behavioral outcome [ 176 , 177 , 178 ]. Multiple causality of the stroke occurrence is another problem that is often over-looked. Homogeneity in stroke models to exhibit the broad spectrum of stroke pathophysiology associated with ischemic lesions or cortical or intracerebral damage is critical. Therefore, stroke animal models that target specific causes of stroke should be included. Latent interaction between comorbidities and stroke treatment should be identified to increase the safety and efficacy of the clinical outcome [ 179 ]. Short-term experimental trials often result in failed therapeutic development due to false-negative outcomes in the clinical settings [ 180 ]. Understanding the functional and behavioral output which might mislead true recovery is problematic in clinical trials wherein animal models have greater ability to mask the functional benefits [ 181 ]. This affects the affecting translational capability of the research. Adapting a combined approach to model recovery and rehabilitation is also important for successful transition.
One of the other problems with the clinical trials for stroke is the lack of efficient data management. The impact of large data generated from numerous clinical experiments is over-whelming and there should be a standardized system to manage such data. Moreover, these data should be deposited into a public data repository for easy access.
Industry and academic corroborations in stroke research are critical to improve the translational value [ 182 ]. A consensus between industry and academic interests is vital for successful transition. The industry collaborations are mostly monetary driven and have time constraints which might compromise the pre-clinical study protocol design, appropriate sample sizes and overestimation of treatment effects. IP protection and publication of research data may discord between these groups. A multicenter approach, long-term collaborations, effective project management, use of advanced methodologies and establishment of functional endpoints will probably advance the translational roadblocks in stroke research [ 183 ].
Stroke is the second leading cause of death and contributor to disability worldwide and has significant economic costs. Thus, more effective therapeutic interventions and improved post-stroke management are global health priorities. The last 25 years of stroke research has brought considerable progress with respect to animal experimental models, therapeutic drugs, clinical trials and post-stroke rehabilitation studies, but large gaps of knowledge about stroke treatment remain. Despite our increased understanding of stroke pathophysiology and the large number of studies targeting multiple pathways causing stroke, the inability to translate research into clinical settings has significantly hampered advances in stroke research. Most research has focused on restoring blood flow to the brain and minimizing neuronal deficits after ischemic insult. The major challenges for stroke investigators are to characterize the key mechanisms underlying therapies, generate reproducible data, perform multicenter pre-clinical trials and increase the translational value of their data before proceeding to clinical studies.
Conceptualization, D.K.; writing—original draft preparation, D.K.; writing—review and editing, Z.X.; funding acquisition, Z.X. All authors have read and agreed to the published version of the manuscript.
This research and The APC was funded by Apex Biotech Research.
The authors declare no conflict of interest.
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Many health experts have discovered that stroke is the main reason of deaths in the world, which may also cause disability in case a person survives. Due to the brain damage accompanied by the stroke, the victim needs long-term personal care to increase his/her chances to live a long life (Evashwick, 2005).
Although stroke victims rarely recover, there are some cases when it takes at least two years to get over it. Stroke completely disables a victim as the one is unable to do a thing, and therefore, the patient is useless for a long period or the entire lifetime. During this period, the person will need intensive personal care and attention. Therefore, the only people able to help the stroke victim are the family members or the guardians.
The most important step in handling a stroke survivor is to prepare him or her psychologically for any eventual outcome of the disability. Medical experts associate stroke with frequent back pains. It is important for the patient to understand all the possible outcomes of the stroke (Bogousslavsky, 2002).
The family members should closely monitor the patient since isolating a patient on the basis of his/her disability worsens the state of health and does not contribute to the improving. Stroke patient is likely to recover faster when he or she feels appreciated in the society than becomes alienated from the world.
To improve the standards of care of the patient, the family should consider buying some important equipment for use by the patient so that he or she can at least perform some tasks on his/her own. Such equipments include the wheelchair, handheld urinal and bedside commode.
The wheelchairs are very essential as they give a person an opportunity to move anywhere within their ability. The handheld urinal and the bedside commode are very important for individual wellbeing as they help an individual to answer the call of nature when no one is within to help. Though these equipments are very expensive, they are very resourceful in the long run in assisting the stroke patient within the family (Bogousslavsky, 2002).
Long-term care will aid the stroke patients because they are no longer able to do any task on their own. There are several services that the stroke patient will need in the long run. These are nursing, medical, community, social and custodial services. Moreover, these services can also be provided at nursing homes or personal homes. Family members must note that stroke patients who are not well attended to are prone to deteriorating health eventually shortening their life span.
It is also important to note that a person providing a personal care to stroke patients should know that the stroke survivors cannot express themselves freely regarding their urgent needs. For example, bathing, grooming and dressing require a close family member to assist a patient in most occasions (Evashwick, 2005). Moreover, helping the patient use the toilet and eat are the most essential activities that promote the stroke victims’ health standards and wellbeing.
In some cases, it is possible for a family to hire a specialized caregiver to attend to the patient when the family is not able to attend to a person. Stroke survivors need a specialized attention all the time which will also call for more resources to be used.
The family may ask for a help from a professional nurse or take the patient to a nursing home for more specialized care. Moreover, specialized medication is also needed to help the patient to get over, which calls for taking concerted actions to ensure the stroke victim receives the best health care (Evashwick, 2005).
Bogousslavsky, J. (2002). Long-term effects of stroke . New York: M. Dekker.
Evashwick, C. (2005). The continuum of long-term care . New York: Thomson/Delmar Learning.
IvyPanda. (2018, December 19). Care Process of the Stroke Patients. https://ivypanda.com/essays/care-of-the-stroke-patients/
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IvyPanda . "Care Process of the Stroke Patients." December 19, 2018. https://ivypanda.com/essays/care-of-the-stroke-patients/.
Jeirym Miranda; Fareeha S. Alavi; Muhammad Saad
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Case review, case discussion, clinical symptoms.
A 59-year-old Hispanic man presented with right upper and lower extremity weakness, associated with facial drop and slurred speech starting 2 hours before the presentation. He denied visual disturbance, headache, chest pain, palpitations, dyspnea, dysphagia, fever, dizziness, loss of consciousness, bowel or urinary incontinence, or trauma. His medical history was significant for uncontrolled type 2 diabetes mellitus, hypertension, hyperlipidemia, and benign prostatic hypertrophy. Social history included cigarette smoking (1 pack per day for 20 years) and alcohol intake of 3 to 4 beers daily. Family history was not significant, and he did not remember his medications. In the emergency department, his vital signs were stable. His physical examination was remarkable for right-sided facial droop, dysarthria, and right-sided hemiplegia. The rest of the examination findings were insignificant. His National Institutes of Health Stroke Scale (NIHSS) score was calculated as 7. Initial CT angiogram of head and neck reported no acute intracranial findings. The neurology team was consulted, and intravenous recombinant tissue plasminogen activator (t-PA) was administered along with high-intensity statin therapy. The patient was admitted to the intensive care unit where his hemodynamics were monitored for 24 hours and later transferred to the telemetry unit. MRI of the head revealed an acute 1.7-cm infarct of the left periventricular white matter and posterior left basal ganglia. How would you manage this case?
This case scenario presents a patient with acute ischemic cerebrovascular accident (CVA) requiring intravenous t-PA. Diagnosis was based on clinical neurologic symptoms and an NIHSS score of 7 and was later confirmed by neuroimaging. He had multiple comorbidities, including hypertension, diabetes, dyslipidemia, and smoking history, which put him at a higher risk for developing cardiovascular disease. Because his symptoms started within 4.5 hours of presentation, he was deemed to be a candidate for thrombolytics. The eligibility time line is estimated either by self-report or last witness of baseline status.
Ischemic strokes are caused by an obstruction of a blood vessel, which irrigates the brain mainly secondary to the development of atherosclerotic changes, leading to cerebral thrombosis and embolism. Diagnosis is made based on presenting symptoms and CT/MRI of the head, and the treatment is focused on cerebral reperfusion based on eligibility criteria and timing of presentation.
Symptoms include alteration of sensorium, numbness, decreased motor strength, facial drop, dysarthria, ataxia, visual disturbance, dizziness, and headache.
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Chapter 1 Introduction Title: EFFECT OF INTENSIVE STRENGTH TRAINING EXERCISES ON BALANCE AND MOBILITY IN POST STROKE HEMIPLEGICS – A PROBE STUDY. 1. Introduction Stroke is a leading neurological disorder and causes long-term disability worldwide. The definition of stroke was recently updated by 2009 task committee endorsed by American heart and stroke associations as follows. Stroke refers to a CNS infarction. “A CNS infarction is brain , spinal cord, or retinal cell death attributable to ischemia, based on (a) Pathological imaging, or other objective evidence of cerebral, spinal cord or retinal focal ischemic injury in a defined vascular distribution; …show more content…
The CVA can be a hemorrhage or thrombus and the severity of the lesion determines the loss of function. In extensive disease, neighboring neurons may also be affected. Following a stroke, the oxygen supply to brain cells is blocked and cells start to die within minutes. This will be reflected by symptoms like sudden weakness, paralysis or numbness of the face, arms, or legs, difficulty in communication, loss of consciousness etc. The loss of function in stroke is dependent on the number of neurons involved and how long the blood flow to the brain has been interrupted. Early diagnosis, underlying cause and time taken for the commencement of treatment play the main role in determining whether the deficit is stable, progressive, or completely …show more content…
Ischemic stroke is more common type of stroke, occurs around 80% of all strokes (Feigin et al., 2003), of which 60% are involved with large-artery ischemia. Following ischemia there is a local reduction in oxygen supply or nutrients, results in failure of energy production such as adenine triphosphate (ATP). This harmfully influences the tissue cell survival, and leads to cellular damage and death. The amount of cellular injury depends upon extend of illness, severity, and area involved (Deb P,
A stroke is the sudden death of brain cells due to the lack of oxygen, caused by blockage of blood flow or a rupture of an artery to the brain. Sudden loss of speech, weakness, or in Bolton’s case, paralysis of one side of the body can be the symptoms of a stroke. A suspected stroke can be confirmed by scanning the brain with special x-ray tests, such as CAT scans. The death rate and level of disability resulting from strokes can be dramatically reduced by immediate and appropriate medical care.
The Blood Brain Barrier or (BBB), is a protective
Imagine being a competitive athlete that can do almost anything and in a matter of seconds never being able to hug love ones or do the simple everyday tasks many take for granted. That’s how life is when a person is diagnosed with Amyotrophic Lateral Sclerosis (ALS) it’s a fatal disease that causes a person to lose complete control of their body and constantly need assistance. Having ALS also means having to watch the body deteriorate when the mind is perfectly aware of its own demise. Being diagnosed with Chronic Traumatic Encephalopathy (CTE) is a progressive degenerative disease caused by multiple severe concussions to the head.
A unneeded brain surgery could cause someone to die or go brain dead. Also as Charlie’s intelligence wore off, he got sick, staying in bed for weeks not eating. He went into emotional instability. Finally Charlie could die like Algernon died. Algernon died after his surgery wore off due to smoothing of the cerebral convolutions.
When the motor neurons start to die, the ability of the brain to start and control muscle movement is eventually stopped. With muscle action
The condition is often fatal, and almost everyone who is not killed is severely disabled. The cause of SIS is uncertain,but it is thought that the brain's arterioles lose their ability to regulate
If untreated cerebral edema can cause death. When treated it may still have lingering effects on the body such as: loss of vision, cerebral atrophy with cognitive decline, and altered mental
- If an individual has poor cognition, suffering from a stroke and in general has a lack of mental capacity this will affect them on how they understand death and
Symptoms may include dizziness, nausea and confusion. Although the loss of consciousness is possible, it is usually brief. The diagnosis of mild brain injury such as a concussion, usually made based on symptoms and a CT scan, which is used to rule out more serious injuries. The treatment is often not necessary.
Brain Aneurysm Four major blood vessel supply blood to the brain. They join together at the circle of willis at the base of the brain. Smaller arteries leave the circle and branch out to supply brain cells with oxygen and nutrients. Artery junction points may become weak causing a ballooning of the blood vessel wall to potentially form a small sac or aneurysm. Cerebral aneurysms are common but most are asymptomatic and are found incidentally at autopsy.
What is it like to have ALS or a CTE? Either a progressive neurological disease that attacks your motor skills or one that attacks the cognitive parts of the brain. Each one has its own particular attack strategy. On one hand the body is rendered completely motionless while being completely conscious of the outside environment. On the other, the body stays unharmed while it slowly loses the mind, both are equally devastating.
False 7. According to one small study mentioned in the article, the volume of ischemic tissue can be determined by MRI within how many hours of stroke onset? a. 12 hours b. 24 hours c. 36 hours d. 48 hours 8. Acute occlusion of the cervical internal carotid artery, basilar artery, or a large intracranial artery is associated with a(n) ______________ risk of poor outcome.
Stroke may be somewhat unlikely to happen in children but when it does happen it has a significant impact because it can cause morbidity and mortality. Children’s strokes can present differently than adult. Also according to the “Pediatric Stroke: A Review”, “The reported incidence rate of both ischemic and hemorrhagic pediatric stroke ranges from 1.2 to 13 cases per 100,000 children under 18 years of age”(Tsze & Valente 1). Nevertheless, Pediatric CVA is more familiar than we can imagine, because of the misdiagnoses. In one report, it is said that 19 out of 45 children with a stroke did not obtain the accurate diagnosis until 15 hours to 3 months after initial presentation.
A Transient Ischemic Attack, also known as a mini stroke, is an acute illness where blood flow to a certain part of the brain gets blocked which most of the time is caused by a blood clot (Webmd n.d.). After a couple minutes the clot dissolves, blood flow continues again and symptoms disappear. It is called a mini stroke because all the signs and symptoms are the same as a stroke, but the symptoms last a shorter period of time and there is no permanent damage done to the cells. According to the website mayoclinic.org, About 1 in 3 people who have a transient ischemic attack will eventually have a stroke, with half occurring within a year after the transient ischemic attack (Mayo Clinic Staff 2014). Overall, even though it is considered a mini stroke and the symptoms last shorter time, it is still a serious condition and need medical attention immediately.
This study would be useful in studying about early onset of AD, as it informs on the direction of diagnosing early-onset
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Introduction A stroke occurs when there is a sudden decrease in blood flow to a localized area in the brain (Trakalo, 2015, p.1234). This can occur in different ways such as a thrombus, an embolus, a stenosis, or a hemorrhage - all of which can cause devastating neurological effects depending on the extent of ischemia and necrosis resulting from the decreased oxygen carried by the blood. According to The Stroke Association of the UK, an individual that smokes is 3 times more susceptible to suffering from a stroke than that of a person who does not smoke. With that being said, the more cigarette smoke inhaled per day places an individual at an even higher risk (“ Smoking and the risk of stroke,” 2012, para. 2). National Institute of Neurological …show more content…
The client must know that quitting betters and lengthens a person’s life by a number of years. The following material corresponds with each objective listed above. 1. Teach the client how smoking directly compares with the added risk of having a stroke. Smokers should know that smoking cigarettes could cause a stroke to happen in many ways. One of these ways is that chemicals in cigarette smoke damage the cells in a person’s body. Also, smoking can raise the bad cholesterol (which is fat) in the blood. When there is more fat in the blood, it causes arteries (vessels that carry blood to the heart) to become blocked. If arteries are blocked, then the oxygen that is needed cannot get through to the brain. Just like any other organ in the body, oxygen is important for the brain to work. Lastly, smoking increases platelets in the blood. Platelets cause the blood to become thicker and clot. A clot can block a blood vessel anywhere in the body, and if the clot moves to the brain, then it will block the vessel there causing oxygen to not be able to pass through (“Smoking and the risk of stroke,” 2012, “How does smoking cause stroke”, para.
Justine Morgan (2014) divulge that Nicotine which is contained in e-cigarettes is an addictive drug that affects the brain, nervous system, and the heart. It also increases blood pressure, causes abnormal heart rate and blood clotting, a leading factor to stroke. Nicotine though may not be harmful if taken within the prescribed limit but narrow the blood vessels (Amanda & Woerner, 2014) and this could lead to stroke and other health issues.
The harmful effects of smoking are well known. Smoking increases the chances of chronic disease’s for example Lung Cancer, with 90% of these cases being caused by smoking (Cancer Research UK 2009). Responsible for 5200 lives per year, the huge financial burden on the National
According to a recent research (http://www.thehealthsite.com/news/passive-smoking-just-as-harmful-ups-stroke-risk-in-non-smokers-i715/), passive smoking increased the risk of stroke by 30/% in non-smoking
Cerebral vascular accident or a stroke is the destruction of brain substance, resulting from thrombosis, intracranial hemorrhage, or embolism, which causes vascular insufficiency. In addition, it is an area of the brain denied blood and oxygen that is required and damage is done to a part of the cells. The effect of the patient depends upon where the damage occurs and the severity of the stroke.
Tobacco Use ¡V Cigarette smoking is a major, preventable risk factor for stroke. Smoking contributes to plaques in your arteries. Also, nicotine raises blood pressure.
A cerebrovascular accident more commonly known as a stroke or brain attack is the term used to describe the sudden death of brain cells in a localized area due to inadequate blood flow. In order to woke the brain needs a constant supply of oxygen and nutrients. This supply is carried to the brain
Stroke affects everybody differently, and it is difficult to say how much of a recovery is possible. Many stroke survivors experience the most dramatic recovery during their stay in hospital in the weeks after their stroke.
A stroke is a type of cardiovascular disease that affects the cerebral arteries, those blood vessels that carry blood to the brain. A stroke occurs when one of those blood vessels in the brain is obstructed or ruptures flooding the brain with blood. Depriving blood and oxygen to the brain results in those immediate cells death, causing the brain not to function properly. Once parts of the brain stop functioning, it can directly affect the areas of the body controlled (1).
Acheson 1998; Marmot 2010; Scientific Committee on Tobacco and Health (1998), Smith (2013). The goal is to review the evidence-based recommendations for the stroke risk factors. A modification in a person’ current and future health status can be credited to antecedent health care. The overall long-term impact of health interventions are both on populations as a whole and on individuals in particular (Wolfe et al., 1996). Cerebrovascular diseases can be prevented by addressing known, modifiable risk factors. It is important to identify risk factors for stroke and sources in order to take steps towards preventing stroke and provides concrete actions to reduce the burden of stroke within a population (Mohr et al.,
Lung disease, COPD, Heart disease, and many cancers are just a few examples of the effects smoking has on a person. COPD is one of the most major diseases smoking can cause. The effects of COPD can range anywhere from long-term disability to an early death. A loss of sense of smell and taste, decaying teeth, eye cataracts, and increased risk of stroke are other terrible things that can occur from smoking. A smoker may not think of these dangerous possibilities while smoking, but the danger of smoking will never cease until awareness of its harm is
Cigarette smokers are two to four times more likely to develop coronary heart disease than non-smokers, and tobacco use doubles risk for stroke. It also causes reduced circulation by narrowing the blood vessels, and it causes premature wrinkles because it constricts the oxygen and warmth from all parts of the body so the skin ages faster.
Regardless of consumer belief, smoking dramatically increases the chances of contracting many diseases - such as heart disease or high blood pressure. Although not every user experiences these diseases, it is well known that smoking can decrease one’s life time dramatically. The information given states, “It’s virtually impossible to escape the effects of tobacco” (Jordan). This stated, Jordan expresses that essentially if you use tobacco, there is a fairly high chance that one will damage his/her body in some way. Furthermore, there are many more diseases that can be contracted and the ones stated are only the most common. Continuing, the author explains the affects of smoking, “Expose to specific elements of secondhand smoke causes blood clot more easily and damages arterial lining” (Jordan). As stated, certain components in tobacco increase the chances of high blood pressure and blood clots to form in the body. Concluding, respiratory problems in young children can occur through second hand smoking, these include asthma. Children that asthma effect increases from smoke, “Asthma turns out to be about twice as common in children exposed to high levels of second hand smoke” (Secondhand Smoke: Is it a Hazard). Not only does tobacco smoke increase other diseases, it also increases the severity of diseases already contracted as shown in the previous quote. To conclude, tobacco smoke
The Surgeon General has called it "the leading preventable cause of disease and deaths in the United States." Smoking is among the top preventable risk factors of heart disease amongst many other health problems. Coronary heart disease and strokes are the primary types of cardiovascular disease caused by smoking. They rank as the first and third leading causes of death in the United States. More than 61 million Americans suffer from some form of cardiovascular disease. Smoking increases your risk for high blood pressure, coronary heart disease, stroke, congestive heart failure, and aneurysms to name a few. More than 2,600 Americans die every day from cardiovascular diseases.
Smoking increases the risk of suffering from heart diseases, stroke, other lung diseases and other respiratory illnesses. The body develops horrific reactions to the daily onslaught of smoking. It damages the blood vessels in the legs and arms for example, which lead to restricted circulation and even amputation of the limbs. Also, a smoker addict will eventually start getting eye irritations (which leads to blindness), foul smelling hair, hair loss and even start developing a loss of smell. All of these reactions are due to the dangerous chemicals cigarettes contain.
Another cardiovascular malfunction that cigarette smoking may cause are strokes. A stroke is damage to the brain caused by leakage from a ruptured blood vessel or an interruption in blood supply. Nicotine and carbon monoxide in cigarette smoke affect the adhesives of blood platelets, the main clotting factor in blood. This can cause blood vessels to harden and form blood clots that can flow to the brain, a major cause of strokes. Nicotine can also cause the blood vessels to constrict. When a smokers arteries become too constricted,
A 66-year-old man was admitted to hospital with a right frontal cerebral infarct producing left-sided weakness and a deterioration in his speech pattern. The cerebral infarct was confirmed with CT imaging. The only evidence of respiratory symptoms on admission was a 2 L oxygen requirement, maintaining oxygen saturations between 88% and 92%. In a matter of hours this patient developed a greater oxygen requirement, alongside reduced levels of consciousness. A positive COVID-19 throat swab, in addition to bilateral pneumonia on chest X-ray and lymphopaenia in his blood tests, confirmed a diagnosis of COVID-19 pneumonia. A proactive decision was made involving the patients’ family, ward and intensive care healthcare staff, to not escalate care above a ward-based ceiling of care. The patient died 5 days following admission under the palliative care provided by the medical team.
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https://doi.org/10.1136/bcr-2020-235920
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SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) is a new strain of coronavirus that is thought to have originated in December 2019 in Wuhan, China. In a matter of months, it has erupted from non-existence to perhaps the greatest challenge to healthcare in modern times, grinding most societies globally to a sudden halt. Consequently, the study and research into SARS-CoV-2 is invaluable. Although coronaviruses are common, SARS-CoV-2 appears to be considerably more contagious. The WHO figures into the 2003 SARS-CoV-1 outbreak, from November 2002 to July 2003, indicate a total of 8439 confirmed cases globally. 1 In comparison, during a period of 4 months from December 2019 to July 2020, the number of global cases of COVID-19 reached 10 357 662, increasing exponentially, illustrating how much more contagious SARS-CoV-2 has been. 2
Previous literature has indicated infections, and influenza-like illness have been associated with an overall increase in the odds of stroke development. 3 There appears to be a growing correlation between COVID-19 positive patients presenting to hospital with ischaemic stroke; however, studies investigating this are in progress, with new data emerging daily. This patient report comments on and further characterises the link between COVID-19 pneumonia and the development of ischaemic stroke. At the time of this patients’ admission, there were 95 positive cases from 604 COVID-19 tests conducted in the local community, with a predicted population of 108 000. 4 Only 4 days later, when this patient died, the figure increased to 172 positive cases (81% increase), illustrating the rapid escalation towards the peak of the pandemic, and widespread transmission within the local community ( figure 1 ). As more cases of ischaemic stroke in COVID-19 pneumonia patients arise, the recognition and understanding of its presentation and aetiology can be deciphered. Considering the virulence of SARS-CoV-2 it is crucial as a global healthcare community, we develop this understanding, in order to intervene and reduce significant morbidity and mortality in stroke patients.
A graph showing the number of patients with COVID-19 in the hospital and in the community over time.
A 66-year-old man presented to the hospital with signs of left-sided weakness. The patient had a background of chronic obstructive pulmonary disease (COPD), atrial fibrillation and had one previous ischaemic stroke, producing left-sided haemiparesis, which had completely resolved. He was a non-smoker and lived in a house. The patient was found slumped over on the sofa at home on 1 April 2020, by a relative at approximately 01:00, having been seen to have no acute medical illness at 22:00. The patients’ relative initially described disorientation and agitation with weakness noted in the left upper limb and dysarthria. At the time of presentation, neither the patient nor his relative identified any history of fever, cough, shortness of breath, loss of taste, smell or any other symptoms; however, the patient did have a prior admission 9 days earlier with shortness of breath.
The vague nature of symptoms, entwined with considerable concern over approaching the hospital, due to the risk of contracting COVID-19, created a delay in the patients’ attendance to the accident and emergency department. His primary survey conducted at 09:20 on 1 April 2020 demonstrated a patent airway, with spontaneous breathing and good perfusion. His Glasgow Coma Scale (GCS) score was 15 (a score of 15 is the highest level of consciousness), his blood glucose was 7.2, and he did not exhibit any signs of trauma. His abbreviated mental test score was 7 out of 10, indicating a degree of altered cognition. An ECG demonstrated atrial fibrillation with a normal heart rate. His admission weight measured 107 kg. At 09:57 the patient required 2 L of nasal cannula oxygen to maintain his oxygen saturations between 88% and 92%. He started to develop agitation associated with an increased respiratory rate at 36 breaths per minute. On auscultation of his chest, he demonstrated widespread coarse crepitation and bilateral wheeze. Throughout he was haemodynamically stable, with a systolic blood pressure between 143 mm Hg and 144 mm Hg and heart rate between 86 beats/min and 95 beats/min. From a neurological standpoint, he had a mild left facial droop, 2/5 power in both lower limbs, 2/5 power in his left upper limb and 5/5 power in his right upper limb. Tone in his left upper limb had increased. This patient was suspected of having COVID-19 pneumonia alongside an ischaemic stroke.
A CT of his brain conducted at 11:38 on 1 April 2020 ( figure 2 ) illustrated an ill-defined hypodensity in the right frontal lobe medially, with sulcal effacement and loss of grey-white matter. This was highly likely to represent acute anterior cerebral artery territory infarction. Furthermore an oval low-density area in the right cerebellar hemisphere, that was also suspicious of an acute infarction. These vascular territories did not entirely correlate with his clinical picture, as limb weakness is not as prominent in anterior cerebral artery territory ischaemia. Therefore this left-sided weakness may have been an amalgamation of residual weakness from his previous stroke, in addition to his acute cerebral infarction. An erect AP chest X-ray with portable equipment ( figure 3 ) conducted on the same day demonstrated patchy peripheral consolidation bilaterally, with no evidence of significant pleural effusion. The pattern of lung involvement raised suspicion of COVID-19 infection, which at this stage was thought to have provoked the acute cerebral infarct. Clinically significant blood results from 1 April 2020 demonstrated a raised C-reactive protein (CRP) at 215 mg/L (normal 0–5 mg/L) and lymphopaenia at 0.5×10 9 (normal 1×10 9 to 3×10 9 ). Other routine blood results are provided in table 1 .
CT imaging of this patients’ brain demonstrating a wedge-shaped infarction of the anterior cerebral artery territory.
Chest X-ray demonstrating the bilateral COVID-19 pneumonia of this patient on admission.
Clinical biochemistry and haematology blood results of the patient
Interestingly the patient, in this case, was clinically assessed in the accident and emergency department on 23 March 2020, 9 days prior to admission, with symptoms of shortness of breath. His blood results from this day showed a CRP of 22 mg/L and a greater lymphopaenia at 0.3×10 9 . He had a chest X-ray ( figure 4 ), which indicated mild radiopacification in the left mid zone. He was initially treated with intravenous co-amoxiclav and ciprofloxacin. The following day he had minimal symptoms (CURB 65 score 1 for being over 65 years). Given improving blood results (declining CRP), he was discharged home with a course of oral amoxicillin and clarithromycin. As national governmental restrictions due to COVID-19 had not been formally announced until 23 March 2020, and inconsistencies regarding personal protective equipment training and usage existed during the earlier stages of this rapidly evolving pandemic, it is possible that this patient contracted COVID-19 within the local community, or during his prior hospital admission. It could be argued that the patient had early COVID-19 signs and symptoms, having presented with shortness of breath, lymphopaenia, and having had subtle infective chest X-ray changes. The patient explained he developed a stagnant productive cough, which began 5 days prior to his attendance to hospital on 23 March 2020. He responded to antibiotics, making a full recovery following 7 days of treatment. This information does not assimilate with the typical features of a COVID-19 infection. A diagnosis of community-acquired pneumonia or infective exacerbation of COPD seem more likely. However, given the high incidence of COVID-19 infections during this patients’ illness, an exposure and early COVID-19 illness, prior to the 23 March 2020, cannot be completely ruled out.
Chest X-ray conducted on prior admission illustrating mild radiopacification in the left mid zone.
On the current admission, this patient was managed with nasal cannula oxygen at 2 L. By the end of the day, this had progressed to a venturi mask, requiring 8 L of oxygen to maintain oxygen saturation. He had also become increasingly drowsy and confused, his GCS declined from 15 to 12. However, the patient was still haemodynamically stable, as he had been in the morning. An arterial blood gas demonstrated a respiratory alkalosis (pH 7.55, pCO 2 3.1, pO 2 6.7 and HCO 3 24.9, lactate 1.8, base excess 0.5). He was commenced on intravenous co-amoxiclav and ciprofloxacin, to treat a potential exacerbation of COPD. This patient had a COVID-19 throat swab on 1 April 2020. Before the result of this swab, an early discussion was held with the intensive care unit staff, who decided at 17:00 on 1 April 2020 that given the patients presentation, rapid deterioration, comorbidities and likely COVID-19 diagnosis he would not be for escalation to the intensive care unit, and if he were to deteriorate further the end of life pathway would be most appropriate. The discussion was reiterated to the patients’ family, who were in agreement with this. Although he had evidence of an ischaemic stroke on CT of his brain, it was agreed by all clinicians that intervention for this was not as much of a priority as providing optimal palliative care, therefore, a minimally invasive method of treatment was advocated by the stroke team. The patient was given 300 mg of aspirin and was not a candidate for fibrinolysis.
The following day, before the throat swab result, had appeared the patient deteriorated further, requiring 15 L of oxygen through a non-rebreather face mask at 60% FiO 2 to maintain his oxygen saturation, at a maximum of 88% overnight. At this point, he was unresponsive to voice, with a GCS of 5. Although, he was still haemodynamically stable, with a blood pressure of 126/74 mm Hg and a heart rate of 98 beats/min. His respiratory rate was 30 breaths/min. His worsening respiratory condition, combined with his declining level of consciousness made it impossible to clinically assess progression of the neurological deficit generated by his cerebral infarction. Moreover, the patient was declining sharply while receiving the maximal ward-based treatment available. The senior respiratory physician overseeing the patients’ care decided that a palliative approach was in this his best interest, which was agreed on by all parties. The respiratory team completed the ‘recognising dying’ documentation, which signified that priorities of care had shifted from curative treatment to palliative care. Although the palliative team was not formally involved in the care of the patient, the patient received comfort measures without further attempts at supporting oxygenation, or conduction of regular clinical observations. The COVID-19 throat swab confirmed a positive result on 2 April 2020. The patient was treated by the medical team under jurisdiction of the hospital palliative care team. This included the prescribing of anticipatory medications and a syringe driver, which was established on 3 April 2020. His antibiotic treatment, non-essential medication and intravenous fluid treatment were discontinued. His comatose condition persisted throughout the admission. Once the patients’ GCS was 5, it did not improve. The patient was pronounced dead by doctors at 08:40 on 5 April 2020.
SARS-CoV-2 is a type of coronavirus that was first reported to have caused pneumonia-like infection in humans on 3 December 2019. 5 As a group, coronaviruses are a common cause of upper and lower respiratory tract infections (especially in children) and have been researched extensively since they were first characterised in the 1960s. 6 To date, there are seven coronaviruses that are known to cause infection in humans, including SARS-CoV-1, the first known zoonotic coronavirus outbreak in November 2002. 7 Coronavirus infections pass through communities during the winter months, causing small outbreaks in local communities, that do not cause significant mortality or morbidity.
SARS-CoV-2 strain of coronavirus is classed as a zoonotic coronavirus, meaning the virus pathogen is transmitted from non-humans to cause disease in humans. However the rapid spread of SARS-CoV-2 indicates human to human transmission is present. From previous research on the transmission of coronaviruses and that of SARS-CoV-2 it can be inferred that SARS-CoV-2 spreads via respiratory droplets, either from direct inhalation, or indirectly touching surfaces with the virus and exposing the eyes, nose or mouth. 8 Common signs and symptoms of the COVID-19 infection identified in patients include high fevers, severe fatigue, dry cough, acute breathing difficulties, bilateral pneumonia on radiological imaging and lymphopaenia. 9 Most of these features were identified in this case study. The significance of COVID-19 is illustrated by the speed of its global spread and the potential to cause severe clinical presentations, which as of April 2020 can only be treated symptomatically. In Italy, as of mid-March 2020, it was reported that 12% of the entire COVID-19 positive population and 16% of all hospitalised patients had an admission to the intensive care unit. 10
The patient, in this case, illustrates the clinical relevance of understanding COVID-19, as he presented with an ischaemic stroke underlined by minimal respiratory symptoms, which progressed expeditiously, resulting in acute respiratory distress syndrome and subsequent death.
Our case is an example of a new and ever-evolving clinical correlation, between patients who present with a radiological confirmed ischaemic stroke and severe COVID-19 pneumonia. As of April 2020, no comprehensive data of the relationship between ischaemic stroke and COVID-19 has been published, however early retrospective case series from three hospitals in Wuhan, China have indicated that up to 36% of COVID-19 patients had neurological manifestations, including stroke. 11 These studies have not yet undergone peer review, but they tell us a great deal about the relationship between COVID-19 and ischaemic stroke, and have been used to influence the American Heart Associations ‘Temporary Emergency Guidance to US Stroke Centres During the COVID-19 Pandemic’. 12
The relationship between similar coronaviruses and other viruses, such as influenza in the development of ischaemic stroke has previously been researched and provide a basis for further investigation, into the prominence of COVID-19 and its relation to ischaemic stroke. 3 Studies of SARS-CoV-2 indicate its receptor-binding region for entry into the host cell is the same as ACE2, which is present on endothelial cells throughout the body. It may be the case that SARS-CoV-2 alters the conventional ability of ACE2 to protect endothelial function in blood vessels, promoting atherosclerotic plaque displacement by producing an inflammatory response, thus increasing the risk of ischaemic stroke development. 13
Other hypothesised reasons for stroke development in COVID-19 patients are the development of hypercoagulability, as a result of critical illness or new onset of arrhythmias, caused by severe infection. Some case studies in Wuhan described immense inflammatory responses to COVID-19, including elevated acute phase reactants, such as CRP and D-dimer. Raised D-dimers are a non-specific marker of a prothrombotic state and have been associated with greater morbidity and mortality relating to stroke and other neurological features. 14
Arrhythmias such as atrial fibrillation had been identified in 17% of 138 COVID-19 patients, in a study conducted in Wuhan, China. 15 In this report, the patient was known to have atrial fibrillation and was treated with rivaroxaban. The acute inflammatory state COVID-19 is known to produce had the potential to create a prothrombotic environment, culminating in an ischaemic stroke.
Some early case studies produced in Wuhan describe patients in the sixth decade of life that had not been previously noted to have antiphospholipid antibodies, contain the antibodies in blood results. They are antibodies signify antiphospholipid syndrome; a prothrombotic condition. 16 This raises the hypothesis concerning the ability of COVID-19 to evoke the creation of these antibodies and potentiate thrombotic events, such as ischaemic stroke.
No peer-reviewed studies on the effects of COVID-19 and mechanism of stroke are published as of April 2020; therefore, it is difficult to evidence a specific reason as to why COVID-19 patients are developing neurological signs. It is suspected that a mixture of the factors mentioned above influence the development of ischaemic stroke.
If we delve further into this patients’ comorbid state exclusive to COVID-19 infection, it can be argued that this patient was already at a relatively higher risk of stroke development compared with the general population. The fact this patient had previously had an ischaemic stroke illustrates a prior susceptibility. This patient had a known background of hypertension and atrial fibrillation, which as mentioned previously, can influence blood clot or plaque propagation in the development of an acute ischaemic event. 15 Although the patient was prescribed rivaroxaban as an anticoagulant, true consistent compliance to rivaroxaban or other medications such as amlodipine, clopidogrel, candesartan and atorvastatin cannot be confirmed; all of which can contribute to the reduction of influential factors in the development of ischaemic stroke. Furthermore, the fear of contracting COVID-19, in addition to his vague symptoms, unlike his prior ischaemic stroke, which demonstrated dense left-sided haemiparesis, led to a delay in presentation to hospital. This made treatment options like fibrinolysis unachievable, although it can be argued that if he was already infected with COVID-19, he would have still developed life-threatening COVID-19 pneumonia, regardless of whether he underwent fibrinolysis. It is therefore important to consider that if this patient did not contract COVID-19 pneumonia, he still had many risk factors that made him prone to ischaemic stroke formation. Thus, we must consider whether similar patients would suffer from ischaemic stroke, regardless of COVID-19 infection and whether COVID-19 impacts on the severity of the stroke as an entity.
Having said this, the management of these patients is dependent on the likelihood of a positive outcome from the COVID-19 infection. Establishing the ceiling of care is crucial, as it prevents incredibly unwell or unfit patients’ from going through futile treatments, ensuring respect and dignity in death, if this is the likely outcome. It also allows for the provision of limited or intensive resources, such as intensive care beds or endotracheal intubation during the COVID-19 pandemic, to those who are assessed by the multidisciplinary team to benefit the most from their use. The way to establish this ceiling of care is through an early multidisciplinary discussion. In this case, the patient did not convey his wishes regarding his care to the medical team or his family; therefore it was decided among intensive care specialists, respiratory physicians, stroke physicians and the patients’ relatives. The patient was discussed with the intensive care team, who decided that as the patient sustained two acute life-threatening illnesses simultaneously and had rapidly deteriorated, ward-based care with a view to palliate if the further deterioration was in the patients’ best interests. These decisions were not easy to make, especially as it was on the first day of presentation. This decision was made in the context of the patients’ comorbidities, including COPD, the patients’ age, and the availability of intensive care beds during the steep rise in intensive care admissions, in the midst of the COVID-19 pandemic ( figure 1 ). Furthermore, the patients’ rapid and permanent decline in GCS, entwined with the severe stroke on CT imaging of the brain made it more unlikely that significant and permanent recovery could be achieved from mechanical intubation, especially as the damage caused by the stroke could not be significantly reversed. As hospitals manage patients with COVID-19 in many parts of the world, there may be tension between the need to provide higher levels of care for an individual patient and the need to preserve finite resources to maximise the benefits for most patients. This patient presented during a steep rise in intensive care admissions, which may have influenced the early decision not to treat the patient in an intensive care setting. Retrospective studies from Wuhan investigating mortality in patients with multiple organ failure, in the setting of COVID-19, requiring intubation have demonstrated mortality can be up to 61.5%. 17 The mortality risk is even higher in those over 65 years of age with respiratory comorbidities, indicating why this patient was unlikely to survive an admission to the intensive care unit. 18
Regularly updating the patients’ family ensured cooperation, empathy and sympathy. The patients’ stroke was not seen as a priority given the severity of his COVID-19 pneumonia, therefore the least invasive, but most appropriate treatment was provided for his stroke. The British Association of Stroke Physicians advocate this approach and also request the notification to their organisation of COVID-19-related stroke cases, in the UK. 19
SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) is one of seven known coronaviruses that commonly cause upper and lower respiratory tract infections. It is the cause of the 2019–2020 global coronavirus pandemic.
The significance of COVID-19 is illustrated by the rapid speed of its spread globally and the potential to cause severe clinical presentations, such as ischaemic stroke.
Early retrospective data has indicated that up to 36% of COVID-19 patients had neurological manifestations, including stroke.
Potential mechanisms behind stroke in COVID-19 patients include a plethora of hypercoagulability secondary to critical illness and systemic inflammation, the development of arrhythmia, alteration to the vascular endothelium resulting in atherosclerotic plaque displacement and dehydration.
It is vital that effective, open communication between the multidisciplinary team, patient and patients relatives is conducted early in order to firmly establish the most appropriate ceiling of care for the patient.
Contributors SB was involved in the collecting of information for the case, the initial written draft of the case and researching existing data on acute stroke and COVID-19. He also edited drafts of the report. MH was involved in reviewing and editing drafts of the report and contributing new data. SP oversaw the conduction of the project and contributed addition research papers.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent for publication Next of kin consent obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
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Open Access
Peer-reviewed
Research Article
Roles Formal analysis, Investigation, Methodology, Writing – original draft
* E-mail: [email protected]
Affiliation Department of Occupational Therapy, Tokyo Bay Rehabilitation Hospital, Narashino, Chiba, Japan
Roles Writing – review & editing
Affiliation Department of Occupational Therapy, Teikyo Heisei University, Toshima, Tokyo, Japan
Affiliation Department of Occupational Therapy, Saitama Medical Center, Kawagoe, Saitama, Japan
Affiliation Faculty of Human Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Ibaraki, Japan
This study aimed to explore the stressors experienced by older patients with stroke in convalescent rehabilitation wards in Japan. Semi-structured interviews were conducted with four stroke patients aged > 65 years who experienced a stroke for the first time in their lives. The interviews were analyzed using the Steps for Coding and Theorization method for qualitative data analysis. The results of the qualitative analysis demonstrated that patients experienced specific stressors, such as, difficulty in movement of the paralyzed hand, fear of stroke recurrence, and dietary problems. Some stressors were manageable through healthcare professionals’ active and sensitive communication strategies. These stressors were derived from the theoretical framework of “stressors related to hospitalization” and “stressors related to the illness”. Additional stressors emerged from the interaction between these two types within the theoretical framework. The results of this study contribute to a deeper understanding of the specific stressors experienced by older stroke patients during the recovery process.
Citation: Asada Y, Nishio K, Iitsuka K, Yaeda J (2024) A qualitative study of stressors faced by older stroke patients in a convalescent rehabilitation hospital. PLoS ONE 19(8): e0309457. https://doi.org/10.1371/journal.pone.0309457
Editor: Chinh Quoc Luong, Bach Mai Hospital, VIET NAM
Received: February 24, 2024; Accepted: August 13, 2024; Published: August 26, 2024
Copyright: © 2024 Asada et al. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Data Availability: All relevant data are within the manuscript and its Supporting Information files.
Funding: The author(s) received no specific funding for this work.
Competing interests: The authors have declared that no competing interests exist.
Stress is a nonspecific response of the body to external stimuli [ 1 ]. Stress varies as the stressors faced by individuals differ depending on their age, sex, and social role [ 2 ]. Stressors include physical, biological, chemical, psychological, and social factors. The accumulation of these stressors causes stress, which, if not adequately addressed, can lead to physical or mental health problems, such as cardiovascular disease and depression, respectively [ 3 ]. To prevent these stress-related diseases, it is imperative to identify and address the stressors.
Patients often face various stressors in inpatient settings as their physical and human environments differ significantly from those of their regular home settings [ 4 ]. As the length of the hospital stay increases, patients may become particularly vulnerable to stressors such as “concern for family” and “anxiety about financial situation” [ 4 ]. The severity of a stroke, the age of the patient, and the presence of underlying medical conditions are factors that tend to extend the duration of hospitalization [ 5 ]. The incidence of stroke increases with age and is more common among older adults [ 6 ]. Moreover, patients present with a variety of symptoms, such as motor paralysis and higher brain dysfunction, and their ability to perform activities of daily living (ADL) becomes more limited. In particular, convalescent rehabilitation hospitals have a prolonged hospital stay [ 7 ] as one of their goals is to help patients return to the community and their homes.
Much of what is known about stressors related to stroke involves the risk of stroke onset [ 8 , 9 ], and there are insufficient studies on the stressors faced by older stroke patients in hospitals. Clarifying these unspoken stressors can contribute to reducing the stress of hospitalization for older stroke patients during convalescent rehabilitation, meeting their true needs, and enriching their lives after discharge. Few studies have elicited patients’ true feelings regarding stressors in convalescent rehabilitation wards. The purpose of this study is to provide a deeper understanding of the specific stressors experienced by older stroke patients in convalescent rehabilitation wards during their hospital stay.
We conducted a qualitative study and interviewed each participant separately. The interview transcripts were analyzed according to the “Steps for Coding and Theorization” method (SCAT), a sequential and thematic qualitative data analysis technique [ 10 – 12 ].
This study was conducted in accordance with the Consolidated Criteria for Reporting Qualitative Research (COREQ), a checklist designed to improve the transparency and reliability of qualitative research [ 13 ] (S1 Table in S1 File ).
The first author (hereafter, “the author”) is a M.S. student in comprehensive human sciences and male occupational therapist with six years of clinical experience in recovery rehabilitation. Before this study was conducted, the author reviewed the literature on SCAT, conducted an analysis, and attended a workshop for SCAT developers to deepen his understanding of the analysis methods to ensure the accuracy of the analysis [ 10 – 12 ].
Patients aged 65 years or older, experiencing stroke for the first time, and hospitalized in a recovery center were included in the study. Patients who had difficulty answering the interview questions owing to the effects of aphasia, hospitalized patients in the charge of an interviewer, patients diagnosed with dementia or psychiatric disorders, and patients who were hospitalized for a short period of approximately one month were excluded.
Patients were asked to cooperate in the study and fully informed about the purpose and significance of the study, research methods, voluntary nature of research cooperation and freedom to withdraw, and handling of personal information. Signing a consent form indicated patients’ willingness to cooperate in the study.
Three interviews were conducted between June and November, 2022. The interviewer asked questions according to an interview guide. Semi-structured in-person interviews were conducted in a private room in the hospital that the author is affiliated with, involving the patients and interviewer only. The first interview was conducted at the time of hospital admission, and subsequent interviews were conducted several times, with a gap of approximately one month. The interviews were recorded with the participants’ consent using the voice recorder function of an iPad and transcribed afterwards. The interview transcripts were not returned to participants for comments or correction. The interviewer recited the patients’ statements to them and made efforts to confirm the content of the statements to ensure data accuracy.
The interview guide was developed based on a preliminary survey of two stroke patients to determine ease of response. The content of the interview guide was first explained to the participants through specific examples to help them fully understand the difference between “stress” and “stressors.” The guide began by explaining, through specific examples, what the stressors in this study were. To investigate the stressors faced by older stroke patients in recovery, we asked, “What comes to mind when you hear the term ‘stressors in hospitalization’?”
We predicted that the outcome of the interviews would be strongly influenced by the participants’ individual characteristics. Therefore, to obtain objective results, we used the SCAT technique that specializes in coding and theorization and can be applied to a small amount of data. The SCAT method consists of the following steps [ 10 – 12 ]:
Step 1: Focus words from within the interview texts.
Step 2: Words outside the text that can replace the words from Step 1.
Step 3: Words that explain the words in Step 1 and Step 2.
Step 4: Themes and constructs, including the process of writing a story and offering theories that weave the themes and constructs together.
As this study was designed to create multiple storylines from a single participant, we integrated those multiple storylines into a single storyline and wrote a theoretical description, ensuring no loss of chronological contextuality and individuality of the storylines. The data analysis and confirmation process were conducted by the author and three other authors who were not involved in the interview process.
This study was approved by the Ethical Review Committee (Approval No. 289–2) of Tokyo Bay Rehabilitation Hospital.
Five participants who met the inclusion criteria were recruited for the study. One participant (female) was excluded owing to early discharge from the hospital on short notice. Thus, four patients (two male and two female) were included in the study. The participants’ average age was 79.3 years (range: 71–88 years). Their disabilities included cerebral hemorrhage (one patient) and cerebral infarctions (three patients).
The average duration of the series of 12 interviews was 20.3 minutes, ranging from 7.5 to 32.7 minutes.
In the sections below, the storylines and theoretical descriptions as well as quotes from each participant, are described.
At the time of the first interview, Mr. A experienced stress owing to an inconvenient situation during hospitalization. He was unable to perform the activities he did before the onset of the disease, especially owing to the psychological burden caused by the inability to eat and drink according to his preferences. He also expressed dissatisfaction with the current situation, limitations in leisure-time activities, inconvenience of activities, and a sense of shame caused by assistance with bathing. Limited leisure-time activities resulted from challenges in moving his paralyzed hands. He specifically encountered difficulties in willingly engaging them to act. Furthermore, he was separated from his family as a result of hospitalization. Thus, he faced restrictions in eating and drinking luxury foods, lack of freedom in daily life, and lack of family time.
“ Not being able to do things freely is the biggest stressor. All in all, there’s nothing better than that. I can’t eat what I like, or drink a lot. Even if I have a computer, I can’t use my right hand. I can’t even do my own hobbies. And, it is still significant whether or not you have a wife nearby.”
At the time of the second interview, Mr. A experienced stress regarding eating and drinking, including dissatisfaction with the variety of meals compared to before the disease onset, and the psychological burden owing to meals not being replaced on a daily basis. This was also the minimum element that Mr. A looked for during hospitalization. Other stress factors included a feeling of disappointment owing to limited leisure-time activities, and feelings of activity limitation and resignation owing to the inability to walk independently.
“ The most important thing is the food. Anyway, there’s nothing to do, so at least a meal, you’d think, wouldn’t you? The food is different from when we’re at home. It doesn’t help that I can’t walk. And, I think it’s a bit hard not to have hobbies.”
At the time of the third interview, Mr. A expressed that his biggest stress factor was difficulty moving his paralyzed dominant hand. This significantly impacted his daily self-care, including toileting and grooming. He also encountered limitations in various leisure activities, such as reading books. Eating and drinking induced a significant psychological burden. He felt dissatisfied with the lack of variety in meals as he could not manage to eat as well as previously.
“ Whatever I do, my hands don’t work. For example, when you brush your teeth. It’s the same when you go to the toilet and wipe your bottom. I can’t use my right hand. Also, I like books and I want to read, but I can’t turn the pages. And, unlike in the past, I eat rice and side dishes every day. My eating habits have changed drastically.”
At the time of the first interview, Ms. B faced stressors related to basic lifestyle habits, such as falling asleep and toileting, in the hospital. Variations in individual lifestyles and environmental factors, like noise and room brightness, contributed to sleep deprivation in shared living arrangements. Furthermore, inadequate management of the paralyzed side during sleep led to anxiety and sleep deprivation. Problems related to toileting needs arose owing to overlap in toilet timings with roommates and assisted by staff of the opposite sex.
“ I sometimes have trouble sleeping well at night because of noises or brightness. Everyone is trying to go to the toilet before rehabilitation, so the timing is… And with male nurses, there was a bit of resistance to using the toilet. After all, in shared living arrangements, everyone has a different rhythm of life.”
During the second interview, Ms. B continued to face stress owing to communal living. Stressors included abnormal breathing noises caused by roommates when falling asleep, noise problems during roommates’ movements, and nocturnal awakenings caused by physical environmental factors such as differences in depth of sleep. Additionally, there were case of sleep problems caused by the staff’s response to a roommate’s problematic behavior, and case of nocturnal awakenings caused by noise from staff responses. Other issues included self-perceived persistent distress over defecation problems and dealing with defecation needs in a time-constrained environment, with a roommate.
“ Like last time, in shared living arrangements, everyone has a different rhythm of life, but it can’t be helped. Sleep, you know, because some people go to the toilet at night or early in the morning, so it’s quite noisy and you can’t sleep well. And the nurse puts the patient next to me to sleep, and there are all sorts of noises when she does that. We all have the same desire to go to the toilet before rehabilitation, so we don’t make it in time. Toilets are a perpetual problem.”
At the time of the third interview, Ms. B had problems with how he interacted with his roommates and stressors related to falling asleep at night. Ms. B was dissatisfied with differences in personal characteristics in communal living, and concerned about the deterioration of his relationship with his roommates over defecation. Furthermore, stress was caused by differences in lifestyle in communal living affecting sleep and awakening during the night owing to physical environmental factors such as noises made by roommates. Sudden changes in training hours also caused dissatisfaction.
“ Like how to communicate with people in the room. Like sleeping. Because of the lights and noise when my roommate goes to the toilet at night. Roommates have different living patterns. In rehabilitation, though, there were some questionable things like time changes.”
At the time of the first interview, Ms. C faced the problem of excrement in communal living. Dissatisfaction was caused by the suppression of excretory behavior and rejection of excretion in communal living, leading to anxiety. There were also conflicts and a psychological burden caused by the staff’s lack of information sharing, which led to restraining from defecating after unpleasant experiences.
“ I don’t like the situation of one toilet for four people. I and others are suffering. I thought it was hard. I didn’t know that you have to press the nurse call. Then I wished they had told me from the beginning. That was a bit of a shock.”
At the time of the second interview, Ms. C expressed dissatisfaction with their lack of independence in elimination. This led to a sense of aversion caused by dealing with the need to defecate frequently during the night and self-consciousness about requests for nighttime defecation assistance, which, in turn, led to resisting the need to defecate, a distressing experience unique to the patient.
“ I feel bad because I have to go to the toilet in the middle of the night. But I try to be patient. If it was during the day, I would ask the nurse to help me, but at night I would still feel sorry. It’s painful. You have to be experienced to understand.”
At the time of the third interview, Ms. C was anxious about the gap between their life at home after discharge and their life in the hospital and about the gradual decline of their brain functions. They also experienced anxiety owing to the fear of stroke recurrence and an undecided medical support system for the prevention of recurrence. These stressors were related to worry caused by a lack of information sharing by the staff and delays in sharing information about discharge from the hospital.
“ I have a little bit of anxiety about my future and my life. Because I’ve got comfortable here. And I don’t know what I would do if I fell ill again. No one is going to talk to me about it. I’m a bit worried about that. That’s what I’m most worried about.”
At the time of the first interview, Mr. D expressed their stress that they had to hold their toileting until the hospital staff arrived when they needed to defecate. This occurred as the hospital staff were extremely busy, and they experienced failure in excretory management. However, at the time of the interview, they were able to use the toilet independently.
“ I’ve had a leak before the nurse came. She can’t come right away, she’s too busy. It’s gone now.”
At the time of the second interview, Mr. D had a low appetite owing to low-temperature meals and refused to eat as a result of inappropriate meal temperature. Additionally, there were difficulties with grooming movements around the use of the wash basin and dealing with the need to defecate in communal living.
“ The rice and side dishes are cold. So I feel sorry to leave it. I can eat it beautifully when it’s warm. But when it’s cold, I just can’t. After the meal, I can’t wash my hands because some people wash their hands in their rooms first. When I want to go into the toilet, there are people ahead of me. It can’t be helped.”
In the third interview, Mr. D felt stress when the meal was not hot enough to eat and lost their appetite. He also felt stress when his mealtime was delayed as it that cause would take time for them to do their personal grooming after returning to their room where their roommate occupied t the wash basin.
“ Side dish is cold. Wish it was room temperature. I eat my meals late, so I’m the last one to go back to my room. So, I can’t wash my hands first.”
In this study, semi-structured interviews were conducted to identify the stressors faced by older patients with stroke during convalescent rehabilitation, throughout hospitalization; data analysis was conducted using SCAT.
Based on the storylines and theoretical descriptions, the stressors experienced by stroke patients were categorized into “stressors related to hospitalization” and “stressors related to the illness” [ 4 ].
The results of this study revealed that older stroke patients in convalescent rehabilitation face stressors related to ADLs, such as eating, sleeping, grooming, and toileting; leisure activities; problems with roommates in communal living; and inability to be with their family members. In this study, the first interview was conducted at the time of admission, and stressors were reported by all participants. Stress during hospitalization is caused by the fact that patients are forced to live a life with less freedom than before [ 4 ].
The psychological burden is particularly high for older adults as they have a reduced ability to adapt to changes in the external environment compared with younger patients [ 14 ]. In light of the above, older stroke patients may face a variety of stressors from the early stages of hospitalization compared with younger patients; therefore, intervention against these stressors is necessary from the early stages of hospitalization.
Factors such as relationships with roommates may lead patients to experience discomfort [ 15 ], and the way patients relate to their roommates is considered important. In this study, physical environmental factors caused by differences in lifestyle and the timing of toilet and wash basin use with roommates emerged as stressors. Additionally, these factors affected the participants’ ADL, such as grooming, toileting, and sleeping. Considering these findings, it is important for patients living together to consider each other’s needs. Therefore, it is necessary for patients to communicate with each other to deepen their understanding, and healthcare professionals are expected to play a role in building such relationships.
Furthermore, stressors such as meal variations and meal temperature emerged rather than stressors such as taste and preference. Older people tend to experience a decline in dietary variety owing to a decline in physical and oral functions and appetite [ 16 ]. Moreover, older patients undergoing treatment for cerebrovascular disease are more likely to experience changes in food preferences than younger patients [ 17 ], which is not consistent with the results of the present study. Given that the amount of food intake in a hospital setting is linked to the quality of food, including taste and the dining environment [ 18 , 19 ], there is a need for further research on qualitative aspects of meal preparation, such as food variations and appropriate temperatures. However, studies on meal variations and temperature are limited. In the future, these should be investigated in detail as characteristic stressors faced by older stroke patients during convalescent rehabilitation.
The results revealed that older stroke patients in rehabilitation face stressors such as difficulty moving the hand affected by motor paralysis, recurrent strokes, lack of information given by healthcare providers, and inappropriate actions or words of healthcare providers. Approximately 50% of stroke survivors experience unilateral motor paralysis [ 20 ]. Improvement in motor paralysis of the upper limbs and fingers contributes to greater independence in ADL [ 21 , 22 ]. It not only affects ADL but a wide range of activities, such as housework and leisure activities [ 23 , 24 ].
In this study, there were patients whose hobbies were limited by difficulty in moving the paralyzed hand. Additionally, based on the interviews at the time of admission, activity limitation caused by paralysis was a stressor faced from the time of admission itself. Therefore, early interventions and psychological support are needed for patients with paralysis.
A lack of information about the disease may also increase patient anxiety and cause dissatisfaction among healthcare providers [ 4 ]. Stroke recurs at a rate of 2.2% to25.4% within one year of disease onset, 12.9% within two years, and approximately 16% within five years [ 25 ]. Therefore, it is important to support stroke patients to prevent recurrence [ 26 ]. The participants were interviewed before discharge from the hospital about stressors such as recurrent stroke and lack of information provided by healthcare providers. This suggests that providing information to older patients with stroke undergoing convalescent rehabilitation to prevent recurrence is very important, especially for patients who are about to be discharged from the hospital, and that a lack of information can cause stress. Furthermore, communication between stroke patients and healthcare professionals does not always match [ 27 ]. Efforts should be made to prevent a lack of information, considering the patient’s cognitive function and the degree of higher brain dysfunction.
Additionally, stressors such as the personal care of patients by healthcare professionals of the opposite sex, and behaviors and words caused by misunderstandings on the part of healthcare professionals emerged. Patients may experience discomfort and high psychological distress owing to factors such as the attitudes and actions of healthcare workers [ 16 , 28 ]. An inadequate explanation or lack of consideration of shame may also arouse anger in patients [ 29 ]. Stroke patients are placed in a situation where they are prone to feelings of shame owing to assistance with ADL such as bathing and toileting. Therefore, healthcare professionals must be sensitive to patients when providing daily care. Stress can be prevented through appropriate attitude and information sharing.
Various symptoms, such as motor paralysis, sensory disturbance, higher brain dysfunction, and cognitive decline, appear as post-effects of stroke. The complex interplay between these symptoms causes a decline in the ability to perform ADL [ 30 – 32 ]. In this study, there were patients for whom difficulty in achieving independence in ADL was a stressor. Patients with higher levels of ADL independence had higher self-efficacy, and successful experiences were effective in forming self-efficacy [ 33 ]. This principle should be applicable to older stroke patients in convalescent rehabilitation hospitals. The positive outcomes of their hospital experience may be partially attributed to reduced stress.
Additionally, some patients faced limitations in self-care, stressors related to hospitalization owing to the aftereffects of stroke, and stressors related to illness. Given these findings, it was suggested that stroke patients may have been stressed by the interaction of “stressors related to the disease” and “stressors related to hospitalization.” However, if one of these stressors can be adequately addressed, it is likely that related stressors can be reduced.
In conclusion, we clarified the stressors faced by older stroke patients in convalescent for rehabilitation. However, this study has some limitations. First, the study was severely limited by the small number of patients, which prevents us from drawing some important conclusions. The SCAT method can be used to analyze data from a small number of people because it provides a theoretical description from the participants’ storylines; however, the number of participants in this study was not sufficient to generalize the findings. Second, this study did not fully consider the participants’ individual characteristics, such as personality and background, nor did it analyze the patients in terms of their pathology and sequelae. Therefore, the results obtained should be interpreted carefully, as individual bias was not sufficiently eliminated. In future, it is necessary to select other participants and data analysis methods that consider participants’ individual characteristics and the aftereffects of stroke and recruit more participants to elucidate the stressors faced by older stroke patients in convalescent rehabilitation.
Stressors specific to older stroke patients were identified, including difficulty moving the paralyzed hand, recurrent stroke, and diet-related stressors. Stressors identified in this study can be broadly classified into “stressors related to hospitalization” and “stressors related to the disease,” consistent with previous studies [ 4 ]. However, it was found that stress is also caused by the interaction between “stressors related to hospitalization” and “stressors related to the disease.” To the best of our knowledge, thus far, no reports have identified the specific stressors faced by older stroke patients. Therefore, this study provides valuable information from a first-hand perspective that will lead to a deeper understanding of the specific stressors experienced by older stroke patients during recovery. Future studies should explore how various stressors lead to stress in older stroke patients at various types of rehabilitation hospitals.
S1 file. consolidated criteria for reporting qualitative studies (coreq): a 32-item checklist..
https://doi.org/10.1371/journal.pone.0309457.s001
We thank all the participants who agreed to be interviewed for this study. We also thank the members of the Rehabilitation Science Degree Program, Graduate School of Comprehensive Human Sciences, University of Tsukuba, for their guidance and encouragement during this study.
Introduction Stroke is described as a common disease, which is as well referred to as CVA (Cerebrovascular Accident). The condition is typified by extraordinary injury of the function of the brain because of hindered supply of blood to the tissues of the brain. Usually, the disease is managed as a medical emergency, which can at times cause the death of a person. The resultant hindrances of blood flow to the tissues of brain limit the brain of sufficient nutrients that as a result makes the brain incapable of carrying out its vibrant activities as a consequence of the incapability of receiving adequate blood (Agbor-Etang & Setaro, 2015; Boorstein 2011). This paper focuses on the case study of Mrs. Greta Balodis, a 75 year-old widow who has been experiencing deterioration in her health over the past two years incapacitating her normal activities. She is diagnosed with right-sided cerebrovascular accident (CVA). Background Information Greta presented with headache, drooping of her face and mouth on the side, weakness of her left arm and leg, dizziness and nauseous. She was then diagnosed with Right cerebral vascular accident (CVA) and atrial fibrillation. After spending two weeks in the acute care hospital and six weeks at the specialist stroke rehabilitation, she was discharged with mild residual Left sided hemiplegia and resolving dysphagia. On discharge, she was put on Aspirin PO 100mg daily Clopidogrel PO 75mg daily Digoxin 125mcg PO daily. Currently she is doing fine. She is on home rehabilitation program receiving regular in-home physiotherapy with a nurse visiting her once a week. She manages to mobilize short distances with a three-pronged stick. Pathophysiology of Cerebrovascular Accident (Stroke) and How It Affects the Central Nervous System (CNS) The CNS is often is affected by cardiac conditions or by very similar pathologic processes, which affect the heart. Many diverse heart diseases are capable of producing CNS dysfunctions signs and symptoms (Mohr et al. 2011). Due to Gretas presentation and history, definitely he was suffering from an embolic stroke. Cerebral embolism patients typically present with an acute, neurologic deficit. Occasionally, headache may ensue just earlier or together with the development of the deficit. Emboli lodge in the vessels supplying blood to the brain reducing supply of blood. Frequently seizures are the common initial presentation (Mohr 2011). Greta for instance had a history of falls (three in last six months) and TIA in 2012. Often, cerebral embolism ensues during vigorous activity. Apart from Gretas arterial fibrillation, other causes of cerebral embolism include MI (Myocardial infarction); Left-ventricular aneurysm; RHD (Rheumatic heart disease); infectious endocarditis; cardiomyopathy; thyrotoxicosis; cardiac cancers; mitral valve prolapse; and CHD (Congenital heart disease) among others. Pathophysiology of Embolic Stroke Ischemic stroke is usually is as a result of blood supply to a part of the brain that ultimately stops working. Ischemia is capable of being caused in the brain as a result of thrombotic plaque, which prevents the blood vessels blocking communication via the blood vessel (Gasecki, Karaszewski & Narkiewicz 2016). On the other hand, embolism may result to blockage of blood vessels. Perhaps emboli may be moved from whichever body part and dislocated in a substantial portion of the brain thus stopping blood flow to the brain. Moreover, decreased the supply of blood similar to shock; may lead to a person to CVA. Ischemic stroke is capable of being extremely acute in definite instances. Nonetheless, cryptogenic stroke (unknown type) also leads to a huge percentage of the whole strokes types (Mohr et al. 2011). The etiology of Ischemic strokes is blood clots. Ischemic stroke is of two types: thrombotic and embolic. An embolic CVA takes place at the time a blood clot, which forms somewhere else in the body (embolus), is dislodged and moves to the brain through the circulation. Ultimately, the embolus lodges in vessels and blocks blood the flow resulting to CVA (Campbell2010). Pathophysiology Blood clots resulting to embolic CVA can form in any part of human body, but usually originate from the heart or upper chest and neck arteries. Following dislodge the clot moves via the circulation to the brain. However, after entering a small brain vessel, it stuck obstructing the blood flow to the brain (Grotta et al. 2015). Emboli can result from fat globules, air bubbles, or an arterial plaque. However, emboli can as well arise from abnormal heartbeat (for instance atrial fibrillation); a disorder that the heart fails to beat efficiently, resulting to pooling and clotting of blood (Siniscalchi et al. 2015). Gretas CVA was as a result of this. In most cases, the mechanism ischemic stroke is a significant characteristic and aids in the prediction of results after stroke and consider stroke recurrence risk. There are five classification structures of ischemic strokes etiologies, which has turned out to be extensively acknowledged: embolism, large-artery atherosclerosis, CVA of other determined cause, small-vessel disease, as well as stroke of undetermined cause (Galvagno 2013). In the case of Greta, the cause of facial drooping and weakness was as a result of cardiac embolism. This is referred to as Bells palsy: is a type of transitory facial paralysis due to damage to the facial nerves. Turbulent or still flow conditions in the heart causes thrombi formation. The thrombi dislodge and block vessels in the intracranial flow past downstream. The significant cardioembolic stroke cause is atrial fibrillation (Galvagno 2013). Risk Factors Persons with heart diseases are at higher risk of developing embolic stroke. Consistent withGrotta et al. (2015), atrial fibrillation forms 15% of embolic CVAs. Persons with a familial history of CVA, or who have before experienced a mini-stroke remain at higher risk (Grotta et al. 2015).Other risk factors are older age (Greta Balodis 75 years old);Hypertension (Greta Balodis is Hypertensive); high cholesterol; diabetes; autoimmune diseases; smoking (Greta Balodis is a passive smoker); and obesity (J??rgense, Nakayama, Raaschou, Pedersen, Houth & Olsen 2015). In short, factors that may have precipitated Gretas stroke are previous history of TIA, hypertension, atrial fibrillation, passive smoking, and obesity (Greta is obese her BMI is 34.96: height 1.55m and weight 84kg). Management of Stroke Medical treatment Anticoagulation; patients with cerebral embolism episode are required to be anti-coagulated primarily with heparin (7-10 days) and later on warfarin provided the predisposing heart disease lasts. Anti-coagulation should be avoided in patients with infectious and infectious endocarditis or cardiac cancers. TIAs patients often respond well from daily aspirin, 650 mg BD; clopidogrel, 75mg OD; or Aggrenox) (Spence & Hammond 2016). Also, TIA patients will have less attack in case they are managed with warfarin; nevertheless, warfarin treatment has an increased bleeding complications risk compared to aspirin (Aiyagari & Gorelick 2011). For reduction of risk factors, patients are given therapy targeted at reducing the risk factors for instance management of hypertension. Greta Balodis was discharged with Aspirin PO 100mg OD and Clopidogrel PO 75mg OD for TIA and Digoxin 125mcg PO OD to manage hypertension. However, the current medication Atenolol PO 50mg daily is for the management of hypertension and Panadol PO 500mg prn is for the management of pain. Pharmacology Thrombolytic, more precisely, fibrinolytic agents convert captured plasminogen to plasmin as well as binding to clot fibrin leading local fibrinolysis. Alteplase is a t-PA utilized in the management of acute MI, acute pulmonary embolism, and ischemic stroke. However, aspirin administration prevents prostaglandin synthetase activity that later on bars synthesis of prostaglandin and prevents the creation of platelet-aggregating thromboxane A2 (Jones & Riazi 2011). Similarly, it works on the hypothalamic heat-regulating centre to diminish fever. On the other hand, Clopidogrel prevents aggregation of platelet and is utilized for the prevention secondary CVA (Gasecki, Karaszewski, & Narkiewicz, 2016). Acetaminophen lessens high temperature by acting on hypothalamic heat-regulating centres directly by raising the body heat dissipation through sweating and vasodilation. Atenolol, an adrenergic receptor-blocking agent produces dose-related reductions in hypertension without bringing down reflex tachycardia (Aiyagari & Gorelick 2011). Conclusion Greta presented with headache, drooping of mouth and eye, dizziness and nausea. Sudden trouble in walking, dizziness occurs as a result of injury to inner-ear nerves. Similarly, this may cause nausea, wobbliness on the feet, a propensity to turn to one side or the other, or a mysterious fall. Headache result from due to meningeal stretching or irritation. The present management of Greta with Atenolol PO 50mg OD and paracetamol when necessary were prescribed for the management of hypertension and pain respectively. Aspirin was given 100mg along with Clopidogrel 75mg per oral for the management of TIA. On the same note, the earlier prescription of Digoxin was to manage hypertension. Bibliography Agbor-Etang, BB, & Setaro, JF 2015, Management of hypertension in patients with ischemic heart disease, Current cardiology reports, vol. 17, no. 12, pp. 1-7. Aiyagari, V, & Gorelick, PB 2011, Hypertension and stroke: Pathophysiology and management, Humana Press/Springer, New York. Boorstein, S 2011, Different strokes: An intimate memoir for stroke survivors, families, and caregivers, Skyhorse Pub, New York, NY. Campbell, J 2010, Different strokes, different people, Lulu Com, S.l. Galvagno, SM 2013, Emergency pathophysiology: Clinical applications for prehospital care: Samuel M, Teton NewMedia, Galvagno Jr. Jackson, Wyo. Gasecki, D, Karaszewski, B, & Narkiewicz, 2016, Management of High Blood Pressure in Acute Ischaemic Stroke, In Hypertension and Brain Damage (pp. 143-158), Springer International Publishing. Gasecki, D, Karaszewski, B, & Narkiewicz, K 2016, Management of High Blood Pressure in Intracerebral Haemorrhage, In Hypertension and Brain Damage (pp. 159-171), Springer International Publishing. Grotta, JC, Albers, GW, Broderick, JP, Kasner, SE, Lo, EH?? & Sacco, RL?? & Wong, LK, 2015, Stroke: pathophysiology, diagnosis, and management, Elsevier Health Sciences, London. Jones, F, & Riazi, A 2011, Self-efficacy and self-management after stroke: a systematic review, Disability and rehabilitation, vol. 33, no. 10, pp. 797-810. J??rgense, HS., Nakayama, H, Raaschou, HO, Pedersen, PM, Houth, J, & Olsen, TS 2015, Functional and neurological outcome of stroke and the relation to stroke severity and type, stroke unit treatment, body temperature, age, and other risk factors: The Copenhagen Stroke Study, Topics in stroke rehabilitation. Mohr, JP, 2011, Stroke: Pathophysiology, diagnosis, and management, PA: Elsevier/Saunders, Philadelphia. Mohr, JP, Grotta, JC, Wolf, PA, Moskowitz, MA, Mayberg, MR, & Von Kummer, R 2011, Stroke: pathophysiology, diagnosis, and management, Elsevier Health Sciences, London. Siniscalchi, A, Bonci, A, Biagio Mercuri, N, De Siena, A, De Sarro, G, Malferrari, G., ?? & Gallelli, L 2015, Cocaine dependence and stroke: pathogenesis and management, Current neurovascular research, Vol. 12, no. 2, pp. 163-172. Spence, JD, & Hammond, R 2016, Hypertension and stroke, In Hypertension and the Brain as an End-Organ Target (pp. 39-54), Springer International Publishing.
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CASE 1. A 20 year old man with no past medical history presented to a primary stroke center with sudden left sided weakness and imbalance followed by decreased level of consciousness. Head CT showed no hemorrhage, no acute ischemic changes, and a hyper-dense basilar artery. CT angiography showed a mid-basilar occlusion.
Impact of Stroke Case Study. Introduction. Jithra is now 68 years of age. Her family consists of husband, daughter, nephew and nephew's wife. She has been living with left side hemiplegia caused by stroke since she was 64. As this interview went, Jithra was holding her daughter's hand and slowly elaborated her word by word experience in tears.
Other hypothesised reasons for stroke development in COVID-19 patients are the development of hypercoagulability, as a result of critical illness or new onset of arrhythmias, caused by severe infection. Some case studies in Wuhan described immense inflammatory responses to COVID-19, including elevated acute phase reactants, such as CRP and D-dimer.
Amani Baidwan, Kendyl Egizi and Alysha Payne. Darrell Jackson, 81 year old male, came to the Emergency Department at Los Robles Hospital by ambulance after he collapsed in a coffee shop. Upon arrival he presented with left sided weakness, facial drooping, and aphasia. He was diagnosed with an ischemic stroke, right humerus head fracture, and ...
Abstract. Increasing evidence reports a greater incidence of stroke among patients with Coronavirus disease 2019 (COVID-19) than the non-COVID-19 population and suggests that SARS-CoV-2 infection represents a risk factor for thromboembolic and acute ischemic stroke. Elderly people have higher risk factors associated with acute ischemic stroke or embolization vascular events, and advanced age ...
A case study conducted in the US showed that people with high financial status had better stroke treatment options than ... Annoni V., Merli M.F., Ablondi F., Valenti G. The role of lipid profile in determining the risk of ischemic stroke in the elderly: A case-control study. Arch. Gerontol. Geriatr. 2003; 37:51-62. doi: 10.1016/S0167-4943 ...
Care Process of the Stroke Patients Case Study. Many health experts have discovered that stroke is the main reason of deaths in the world, which may also cause disability in case a person survives. Due to the brain damage accompanied by the stroke, the victim needs long-term personal care to increase his/her chances to live a long life ...
To our knowledge, the adoption of Learning Health System (LHS) concepts or approaches for improving stroke care, patient outcomes, and value have not previously been summarized. This topical review provides a summary of the published evidence about LHSs applied to stroke, and case examples applied to different aspects of stroke care from high and low-to-middle income countries. Our attempt to ...
MLA Citation Miranda J, Alavi FS, Saad M. Miranda J, & Alavi F.S., & Saad M Miranda, Jeirym, et al. "10 Real Cases on Transient Ischemic Attack and Stroke: Diagnosis, Management, and Follow-Up." Patient Management in the Telemetry/Cardiac Step-Down Unit: A Case-Based Approach Saad M, Bhandari M, Vittorio TJ.
Shubham Avadhesh Pandey, 2Dr. Manjit Kumar. siotherapy Intern, 2Assistant ProfessorAbstract: This case study focuses on the comprehensive physiotherapy management of Ram S. gar, a 59-year-old patient who experienced a stroke. The study outlines the assessment, treatment plan, and interventions employed to aid Ram's functional.
Stroke Case Study. 6954 Words28 Pages. Chapter 1 Introduction. Title: EFFECT OF INTENSIVE STRENGTH TRAINING EXERCISES ON BALANCE AND MOBILITY IN POST STROKE HEMIPLEGICS - A PROBE STUDY. 1. Introduction. Stroke is a leading neurological disorder and causes long-term disability worldwide. The definition of stroke was recently updated by 2009 ...
Stroke Case Study Essay. Better Essays. 1812 Words; 8 Pages; Open Document. Shorter lengths of stay in the hospital can mean that the stroke survivors' caregiver and family will inevitably face a lot of stress and burden from home care; therefore, in order to prevent a re-current stroke, more efficient treatments, such as long-term education ...
This paper will discuss the case study relating to the patient, Mrs Amelia Middleton, and answer a series of questions relating to the pathophysiology of stroke, nursing care of the patient, and response to pharmacological issues with her treatment. Question 1. Farrell & Dempsey (2014b) define the pathophysiological characteristics of an ...
Stroke Case Study Essay. Decent Essays. 1101 Words; 5 Pages; Open Document. The prior health history and current findings that put A.J. at risk for a stroke includes a history of left-sided weakness and tingling of the hand, face and arm three months prior to the ischemic stroke she just suffered.
MC study case Abnormal blood results recommendations • For major bleeding (e.g. intracerebral) within 48 h of administration of R-tpa we recommend: • All patients should be discussed with haematology team urgently • Stop infusion of fibrinolytic drugs and other antithrombotic drugs . • Administer FFP 12 ml/kg. • Administer intravenous tranexamic acid 1 g tds .
Approximately 800,000 people in the United States experience a stroke each year. Stroke ranks as the fifth leading cause of death and the leading cause of disability, with over $40 billion annual cost.1 The nurse practitioner (NP) may significantly impact patient outcomes during the prehospital, acute, and posthospital phase of care. This article addresses preischemic stroke, acute, and ...
Stroke Case Study Essay. A stroke occurs when there is a sudden decrease in blood flow to a localized area in the brain (Trakalo, 2015, p.1234). This can occur in different ways such as a thrombus, an embolus, a stenosis, or a hemorrhage - all of which can cause devastating neurological effects depending on the extent of ischemia and necrosis ...
Stroke Case Study. Case Study Assignment #1- Stroke Patient Assessment. Introduction. Stroke is the single leading cause of adult disability in Canada, also accounting for one third of all deaths (Ontario Stroke Network, 2017). Approximately 14,000 Canadians die from strokes annually, and around 430,000 Canadians live with the debilitating ...
A 66-year-old man was admitted to hospital with a right frontal cerebral infarct producing left-sided weakness and a deterioration in his speech pattern. The cerebral infarct was confirmed with CT imaging. The only evidence of respiratory symptoms on admission was a 2 L oxygen requirement, maintaining oxygen saturations between 88% and 92%. In a matter of hours this patient developed a greater ...
Case study, Pages 11 (2543 words) Views. 2206. Stroke is Australia's single greatest killer and a leading cause of disability. Stroke is a serious and deadly condition involving cerebral circulation within the brain and can seriously affect a person maintaining a safe environment, communication and mobility as well as other activities of living.
Stroke Case Study. 1. The man has had an ischaemic stroke, identify the biological changes that would have occurred in his brain during the process. Arnold's ischaemic stroke would be initiated when a lack of blood supply (ischaemia) is prevented from reaching the brain (NHS, 2016). The lack of oxygen causes the neurons within the brain to ...
This study aimed to explore the stressors experienced by older patients with stroke in convalescent rehabilitation wards in Japan. Semi-structured interviews were conducted with four stroke patients aged > 65 years who experienced a stroke for the first time in their lives. The interviews were analyzed using the Steps for Coding and Theorization method for qualitative data analysis.
Introduction Stroke is described as a common disease, which is as well referred to as CVA (Cerebrovascular Accident). The condition is typified by extraordinary injury of the function of the brain because of hindered supply of blood to the tissues of the brain. Usually, the disease is managed as a medical emergency, which can at … Continue reading "Stroke Case Study Academic Essay"