










































American Journal Of Biomedical Science & Pharmaceutical Innovation 1 https://theusajournals.com/index.php/ajbspi 

 
 

 VOLUME Vol.05 Issue03 2025 

PAGE NO. 1-6 

 
 
 
 
 

Dysbiosis and Gastrointestinal Dysfunction in Ischemic 

Stroke: A New Frontier for Treatment 
 

Ahmed Ibrahim Hassan 

Department of Medical Physiology, Faculty of Medicine, Suez Canal University, Ismailia, Egypt 

 

Rana Mohamed Sabry 

Department of Medical Physiology, Faculty of Medicine, Suez Canal University, Ismailia, Egypt 

 

Received: 03 January 2025; Accepted: 02 February 2025; Published: 01 March 2025 

 

Abstract: Background: Ischemic stroke (IS) is a leading cause of mortality and disability worldwide. Recent 
evidence suggests that gastrointestinal (GI) dysfunction and dysbiosis, an imbalance in the gut microbiome, may 
play a significant role in stroke pathophysiology. This article explores the relationship between gastrointestinal 
dysfunction, dysbiosis, and ischemic stroke, highlighting the potential for therapeutic interventions to improve 
patient outcomes. 

Methods: A comprehensive review of the literature was conducted to explore the mechanisms linking ischemic 
stroke to GI dysfunction and dysbiosis. Studies published between 2000 and 2024 were examined for evidence of 
GI involvement, alterations in the gut microbiota, and potential therapeutic strategies targeting these factors. 

Results: GI dysfunction, including impaired gut motility, intestinal permeability, and gut microbial imbalances, has 
been observed in ischemic stroke patients. Dysbiosis may contribute to stroke-related inflammation, immune 
responses, and long-term complications. Preclinical and clinical studies suggest that restoring gut microbiota 
balance through probiotics, dietary interventions, and gut-targeted drugs may offer promising therapeutic 
avenues. 

Conclusion: Gastrointestinal dysfunction and dysbiosis represent important areas of research in ischemic stroke 
pathophysiology. Targeted interventions aimed at the gut microbiome hold promise for improving outcomes in 
ischemic stroke patients, though further clinical studies are needed to confirm these findings and optimize 
treatment strategies. 

 

Keywords: Ischemic stroke, gastrointestinal dysfunction, dysbiosis, gut microbiome, neuroinflammation, 
therapeutic interventions, probiotics, prebiotics, gut-brain axis, stroke recovery, intestinal permeability, immune 
modulation, gut-targeted therapies, fecal microbiota transplantation, dietary interventions. 

 

Introduction: Ischemic stroke (IS) remains one of the 
leading causes of disability and death worldwide, with 
limited therapeutic options for improving recovery 
post-stroke. Recent studies have uncovered a 
surprising link between the gut microbiome, 
gastrointestinal (GI) dysfunction, and the 
pathophysiology of ischemic stroke. The gut microbiota 
plays a crucial role in maintaining intestinal 
homeostasis, modulating immune responses, and 
influencing systemic inflammation. Dysbiosis, an 
imbalance in gut microbial composition, has been 

implicated in several neurological disorders, including 
stroke. Additionally, ischemic stroke has been 
associated with GI dysfunction, such as impaired gut 
motility, increased intestinal permeability, and 
alterations in gut microbiota composition. 
Understanding the mechanisms that link GI dysfunction 
and dysbiosis to ischemic stroke could provide novel 
therapeutic opportunities to improve patient 
outcomes. 

This article reviews the current literature on the 
relationship between GI dysfunction, dysbiosis, and 

 



American Journal of Applied Science and Technology 2 https://theusajournals.com/index.php/ajast 

American Journal of Applied Science and Technology (ISSN: 2771-2745) 
 

 

ischemic stroke, emphasizing how interventions 
targeting the gut microbiome may serve as potential 
therapeutic strategies for stroke patients. 

METHODS 

A systematic literature search was conducted using 
databases such as PubMed, Google Scholar, and 
Scopus. The search included studies published from 
2000 to 2024, using keywords like “ischemic stroke,” 
“gastrointestinal dysfunction,” “dysbiosis,” “gut 
microbiota,” and “therapeutic interventions.” Studies 
focusing on the pathophysiology of GI dysfunction in 
stroke, the role of dysbiosis in stroke recovery, and 
potential therapeutic approaches targeting the gut 
microbiome were selected for inclusion. Preclinical 
studies, clinical trials, and meta-analyses were 
reviewed to assess the current understanding of these 
topics and identify future research directions. 

RESULTS 

Gastrointestinal Dysfunction in Ischemic Stroke 

Gastrointestinal dysfunction is common in patients 
who have suffered from ischemic stroke. The 
gastrointestinal system is closely connected to the 
brain through the gut-brain axis, a bidirectional 
communication pathway that involves the nervous, 
endocrine, and immune systems. After ischemic stroke, 
patients often experience several GI disturbances, 
including: 

1. Gut Motility: Stroke survivors commonly 
experience impaired gastrointestinal motility, which 
leads to constipation, delayed gastric emptying, and 
bowel dysfunction. The disruption of autonomic 
control of the GI system, particularly following a stroke 
that affects the brainstem or autonomic centers, 
contributes to this dysfunction. 

2. Increased Intestinal Permeability: The 
intestinal barrier is compromised in stroke patients, 
leading to a phenomenon known as "leaky gut." This 
condition allows for the translocation of harmful 
bacteria and toxins into the bloodstream, which can 
trigger systemic inflammation and contribute to stroke-
related complications. 

3. Altered Gut Microbiota: Dysbiosis, 
characterized by an imbalance in gut microbial 
composition, has been observed in stroke patients. 
Specific changes in the abundance of certain microbial 
species may exacerbate inflammation and negatively 
influence stroke recovery. Studies suggest that stroke 
can alter the diversity and richness of gut microbiota, 
leading to reduced levels of beneficial bacteria such as 
Lactobacillus and Bifidobacterium and an overgrowth 
of pathogenic species like Firmicutes and 
Proteobacteria. 

Linking Dysbiosis and Ischemic Stroke 

Recent studies have highlighted the role of the gut 
microbiome in modulating the immune response and 
inflammatory pathways following ischemic stroke. 
Dysbiosis in stroke patients may contribute to: 

1. Neuroinflammation: The gut microbiome 
influences systemic inflammation, which plays a pivotal 
role in the progression of ischemic stroke. Dysbiosis can 
enhance the production of pro-inflammatory 
cytokines, which, in turn, promote neuroinflammation 
and exacerbate neuronal injury. 

2. Immune System Activation: Dysbiosis has been 
shown to affect the function of immune cells, including 
microglia and T-cells. These immune cells play a crucial 
role in the brain's response to injury. Dysbiosis may 
disrupt the immune homeostasis, making the brain 
more susceptible to inflammation and cell death 
following ischemic events. 

3. Post-Stroke Recovery: Alterations in the gut 
microbiota composition have been linked to poorer 
post-stroke recovery outcomes. A healthy gut 
microbiome is associated with better immune 
modulation, reduced systemic inflammation, and 
improved neural repair. Dysbiosis, on the other hand, 
may impair these processes, resulting in longer 
recovery times and worse functional outcomes for 
stroke survivors. 

Therapeutic Interventions Targeting the Gut 
Microbiome 

Given the emerging evidence linking gastrointestinal 
dysfunction and dysbiosis to ischemic stroke, several 
therapeutic interventions are being explored to restore 
gut health and improve stroke outcomes: 

1. Probiotics: Probiotic supplementation has 
been shown to help restore gut microbiota balance. 
Studies have suggested that probiotics, such as 
Lactobacillus and Bifidobacterium, may reduce 
intestinal permeability, improve gut motility, and 
modulate immune responses. Clinical trials are 
underway to determine the efficacy of probiotics in 
improving outcomes in ischemic stroke patients. 

2. Dietary Interventions: Dietary changes, 
including the incorporation of fiber-rich foods, 
prebiotics, and fermented foods, may help support gut 
health. A diet rich in polyphenols and other bioactive 
compounds can enhance microbial diversity and 
promote the growth of beneficial bacteria. Nutritional 
interventions aimed at maintaining a balanced gut 
microbiome could offer a complementary approach to 
stroke rehabilitation. 

3. Gut-Targeted Drugs: Emerging research 
suggests that gut-targeted drugs may have therapeutic 



American Journal of Applied Science and Technology 3 https://theusajournals.com/index.php/ajast 

American Journal of Applied Science and Technology (ISSN: 2771-2745) 
 

 

potential for stroke patients. These drugs could target 
the gut microbiota directly to restore its balance, 
modulate immune responses, and reduce 
inflammation. For instance, short-chain fatty acids 
(SCFAs), produced by gut bacteria during fermentation 
of dietary fiber, have been shown to have anti-
inflammatory properties and could be utilized 
therapeutically. 

4. Fecal Microbiota Transplantation (FMT): FMT 
involves transferring fecal material from a healthy 
donor to the recipient’s gastrointestinal tract to restore 
a healthy microbiome. While still in the experimental 
stages for stroke recovery, preliminary studies have 
suggested that FMT may help in modulating the 
immune system and reducing neuroinflammation. 

DISCUSSION 

The relationship between ischemic stroke, 
gastrointestinal dysfunction, and dysbiosis represents a 
novel and promising area of research. While the 
pathophysiology is still not fully understood, the 
evidence points to a critical role for the gut microbiome 
in influencing stroke outcomes. Restoring gut health 
through probiotics, dietary changes, and novel 
microbiome-targeted therapies may offer a potential 
avenue for improving recovery and reducing the long-
term impact of ischemic stroke. 

Despite these promising findings, much more research 
is needed to understand the mechanisms underlying 
the gut-brain axis and how dysbiosis contributes to 
stroke pathology. Clinical trials evaluating the efficacy 
of probiotic and prebiotic interventions in stroke 
patients are essential to confirm their therapeutic 
potential. 

Additionally, the development of gut-targeted drugs 
and more advanced microbiome therapies could 
revolutionize post-stroke care, offering personalized 
treatment options based on the patient’s gut 
microbiome composition. 

The relationship between gastrointestinal (GI) 
dysfunction, dysbiosis, and ischemic stroke (IS) is an 
emerging area of research that offers novel insights 
into the pathophysiology of stroke and presents 
potential therapeutic avenues. While ischemic stroke is 
primarily considered a cerebrovascular event, 
increasing evidence points to the profound and 
complex effects of stroke on the gastrointestinal 
system. Additionally, the gut microbiome, which plays 
a critical role in maintaining homeostasis, modulating 
immune responses, and regulating systemic 
inflammation, appears to be significantly affected by 
stroke. The discussion will delve deeper into the 
mechanisms connecting ischemic stroke to 
gastrointestinal dysfunction and dysbiosis, the clinical 

implications of these findings, and the potential 
therapeutic interventions that may offer improved 
outcomes for stroke patients. 

Gastrointestinal Dysfunction and Ischemic Stroke 

Gastrointestinal dysfunction in ischemic stroke patients 
has multifaceted origins, influenced by both direct and 
indirect mechanisms. The brain-gut axis, which is the 
bidirectional communication between the gut and the 
brain, is of critical importance in understanding the role 
of GI dysfunction following a stroke. Disruption of this 
axis after a cerebrovascular event leads to a range of 
gastrointestinal problems. 

1. Impaired Gut Motility: Stroke patients often exhibit 
a decrease in gastrointestinal motility, which can lead 
to symptoms such as constipation, delayed gastric 
emptying, and bloating. The brain's role in regulating GI 
motility is well documented, as brain regions 
responsible for autonomic function, such as the 
brainstem, are involved in controlling digestive 
processes. Ischemic damage to these areas, particularly 
in the case of brainstem strokes or large strokes 
affecting multiple vascular territories, impairs 
autonomic function. Moreover, dysregulation of the 
enteric nervous system (the "second brain" of the gut) 
in the aftermath of a stroke can exacerbate these 
motility issues. 

2. Intestinal Barrier Dysfunction: In addition to motility 
issues, ischemic stroke has been linked to increased 
intestinal permeability, often referred to as "leaky gut." 
This condition allows endotoxins and harmful 
microorganisms from the intestines to translocate into 
the bloodstream. In stroke patients, systemic 
inflammation is a major concern, and the increased 
permeability of the intestinal barrier serves as a route 
for further inflammatory mediators to enter 
circulation. This phenomenon can contribute to both 
local and systemic inflammatory responses, worsening 
the overall stroke outcome and complicating recovery. 
Notably, this impaired gut permeability can further 
exacerbate ischemic brain injury by promoting 
neuroinflammation. 

3. Dysbiosis and Gut Microbiota Alterations: Emerging 
research has highlighted the role of the gut microbiome 
in modulating both local and systemic inflammation, 
which is particularly relevant in the context of ischemic 
stroke. The gut microbiota comprises trillions of 
bacteria that interact with the immune system and the 
central nervous system. Dysbiosis, or an imbalance in 
the composition of the gut microbiome, has been 
identified as a key factor in promoting systemic 
inflammation, which may influence the severity of 
ischemic stroke and recovery outcomes. 

Ischemic stroke is associated with significant shifts in 



American Journal of Applied Science and Technology 4 https://theusajournals.com/index.php/ajast 

American Journal of Applied Science and Technology (ISSN: 2771-2745) 
 

 

gut microbiota composition. Studies have shown a 
reduction in microbial diversity and a shift towards an 
overgrowth of pro-inflammatory bacteria such as 
Firmicutes and Proteobacteria, while beneficial 
bacteria like Lactobacillus and Bifidobacterium are 
diminished. This alteration in gut microbial 
composition can result in increased production of 
inflammatory cytokines, which may amplify 
neuroinflammation and worsen the ischemic injury to 
the brain. The gut microbiome, by influencing both 
immune cells and neuronal activity, has the potential to 
modify the course of the stroke and recovery. 

Mechanisms Linking Dysbiosis and Ischemic Stroke 

The connection between dysbiosis and ischemic stroke 
is multifactorial and is largely mediated through 
systemic inflammation, immune modulation, and 
alterations in the gut-brain axis. 

1. Neuroinflammation: Neuroinflammation plays a 
central role in the pathophysiology of ischemic stroke, 
and dysbiosis has been shown to enhance this 
inflammatory response. Pro-inflammatory cytokines 
such as TNF-α, IL-6, and IL-1β are elevated after stroke, 
and dysbiosis can contribute to an exaggerated 
production of these molecules. The imbalance in the 
gut microbiome leads to the activation of innate 
immune cells such as macrophages and dendritic cells, 
which in turn produce inflammatory cytokines. This 
inflammatory cascade can directly impact the brain, 
worsening ischemic damage and impeding recovery. 
Furthermore, the gut microbiome affects microglial 
cells (the brain's resident immune cells) by stimulating 
them to produce pro-inflammatory molecules that 
enhance the neuroinflammatory response post-stroke. 

2. Immune System Activation: The gut microbiota is 
integral in shaping immune responses, and its 
imbalance can disturb immune cell function. In stroke 
patients, dysbiosis may contribute to immune 
dysregulation, leading to an exaggerated inflammatory 
response both locally (in the gut) and systemically. This 
immune dysregulation can impair neuroprotective 
mechanisms and hinder recovery. For instance, 
dysbiosis can impact the function of T cells, which have 
been shown to influence stroke outcomes. The altered 
gut microbiome may lead to excessive activation of 
immune responses, which can contribute to increased 
neuronal injury, swelling, and tissue damage in the 
brain. 

3. Impact on Post-Stroke Recovery: Dysbiosis not only 
influences the acute response to ischemic stroke but 
may also affect long-term recovery. A balanced gut 
microbiome is essential for immune regulation, tissue 
repair, and the resolution of inflammation. Dysbiosis 
can disrupt these processes, potentially impairing the 

brain's capacity for repair and regeneration. Animal 
studies have shown that the restoration of gut 
microbial diversity after stroke can improve 
neurological recovery, suggesting that modifying the 
gut microbiome might accelerate recovery and 
functional recovery. 

Therapeutic Interventions Targeting the Gut 
Microbiome 

Given the significant role of the gut microbiome in 
ischemic stroke outcomes, targeting dysbiosis 
represents a promising therapeutic strategy. A variety 
of interventions have been explored to restore a 
healthy gut microbiota and potentially improve stroke 
recovery. 

1. Probiotics and Prebiotics: Probiotics, which are live 
microorganisms that confer health benefits when 
administered in adequate amounts, may help restore 
gut microbial balance. Specific strains, such as 
Lactobacillus and Bifidobacterium, have been shown to 
enhance gut barrier integrity, reduce inflammation, 
and support immune function. Prebiotics, which are 
non-digestible food components that promote the 
growth of beneficial bacteria, may also be used to 
support gut health. Clinical trials examining the effects 
of probiotics in stroke patients are promising, though 
additional research is needed to determine the optimal 
strains, dosages, and duration of treatment. 

2. Dietary Interventions: Diet plays a crucial role in 
shaping the gut microbiome, and a well-balanced, 
fiber-rich diet has been associated with a healthier gut 
microbiome. In ischemic stroke patients, dietary 
interventions that include fiber, polyphenols, and 
antioxidants could support gut microbiota composition 
and reduce inflammation. Diets rich in fermented 
foods, such as yogurt, kefir, and kimchi, can introduce 
beneficial microorganisms into the gut, potentially 
restoring microbial balance. Moreover, dietary 
interventions targeting specific gut microbes or 
metabolic pathways involved in neuroinflammation 
may offer personalized therapeutic strategies. 

3. Fecal Microbiota Transplantation (FMT): FMT is an 
emerging therapy that involves transferring fecal 
material from a healthy donor to a patient to restore a 
healthy microbiome. Though primarily used for 
conditions like Clostridium difficile infection, FMT has 
shown promise in preclinical models of ischemic stroke. 
By rebalancing the gut microbiome, FMT may reduce 
inflammation, improve immune function, and enhance 
post-stroke recovery. However, FMT remains 
experimental in stroke therapy, and its safety and 
efficacy need to be validated in large-scale clinical 
trials. 

4. Gut-Targeted Drugs: Research into gut-targeted 



American Journal of Applied Science and Technology 5 https://theusajournals.com/index.php/ajast 

American Journal of Applied Science and Technology (ISSN: 2771-2745) 
 

 

drugs aims to directly modulate the gut microbiome 
and its effects on systemic inflammation. For example, 
short-chain fatty acids (SCFAs) such as butyrate, which 
are produced by gut bacteria during fermentation of 
dietary fiber, possess anti-inflammatory properties and 
could be used to reduce neuroinflammation in stroke 
patients. Other molecules that influence gut-brain 
signaling, such as gut peptides or selective probiotics, 
could also be investigated for their therapeutic 
potential. 

Challenges and Future Directions 

Despite the promising potential of gut microbiome-
targeted therapies, several challenges remain in their 
implementation in ischemic stroke management. The 
complexity of the gut microbiome, interindividual 
variability in microbial composition, and the long-term 
effects of interventions must be carefully considered. 
Furthermore, the safety and efficacy of these 
interventions in stroke patients need to be evaluated in 
larger clinical trials to better understand their potential 
impact on outcomes and recovery. 

Future research should focus on identifying specific 
microbial signatures that are predictive of stroke 
severity and recovery, as well as developing 
personalized therapeutic strategies based on an 
individual's microbiome. Additionally, clinical trials 
assessing the efficacy of probiotic, prebiotic, and 
dietary interventions should be conducted to confirm 
their potential as adjunctive therapies in stroke 
rehabilitation. 

Gastrointestinal dysfunction and dysbiosis are 
emerging factors that significantly influence the 
pathophysiology and recovery of ischemic stroke. The 
connection between the gut microbiome, systemic 
inflammation, and brain injury opens new therapeutic 
avenues, including probiotics, prebiotics, dietary 
interventions, and gut-targeted drugs. Though 
promising, these interventions need further 
investigation in clinical trials to optimize their use in 
stroke recovery. Addressing GI dysfunction and 
dysbiosis could become an integral part of 
comprehensive stroke management, offering a novel 
and potentially effective approach to improving post-
stroke outcomes. 

CONCLUSION 

Gastrointestinal dysfunction and dysbiosis represent 
significant factors in the pathophysiology of ischemic 
stroke. Restoring a balanced gut microbiome through 
targeted interventions, such as probiotics, dietary 
changes, and gut-specific therapies, holds promise as a 
novel therapeutic strategy to enhance recovery and 
improve long-term outcomes for stroke patients. 
However, further research and clinical trials are 

necessary to validate these interventions and optimize 
their use in stroke rehabilitation. 

REFERENCES 

CDC Stroke Facts|Cdc.Gov. Availabl online: 
https://www.cdc.gov/stroke/facts.htm (accessed on 
16 September 2022). 

Katan, M.; Luft, A. Global Burden of Stroke. Semin. 
Neurol. 2018, 38, 208–211. [Google Scholar] [CrossRef] 

WHO EMRO. Stroke, Cerebrovascular Accident|Health 
Topics. Available online: 
http://www.emro.who.int/health-topics/stroke-
cerebrovascular-accident/index.html (accessed on 30 
December 2024). 

Gomes, J.; Wachsman, A.M. Types of Strokes. In 
Handbook of Clinical Nutrition and Stroke; Corrigan, 
M.L., Escuro, A.A., Kirby, D.F., Eds.; Nutrition and 
Health; Humana Press: Totowa, NJ, USA, 2013; pp. 15–
31. ISBN 978-1-62703-380-0. [Google Scholar] 

Nogueira, R.G.; Haussen, D.C.; Liebeskind, D.S.; Jovin, 
T.G.; Gupta, R.; Saver, J.L.; Jadhav, A.P.; Budzik, R.F.; 
Baxter, B.; Krajina, A.; et al. Clinical Effectiveness of 
Endovascular Stroke Treatment in the Early and 
Extended Time Windows. Int. J. Stroke 2022, 17, 389–
399. [Google Scholar] [CrossRef] [PubMed] 

Treatment of Acute Stroke: Current Practices and 
Future Horizons-ClinicalKey. Available online: 
https://www.clinicalkey.com/#!/content/playContent/
1-s2.0-
S1553838922008934?returnurl=null&referrer=null 
(accessed on 2 January 2023). 

Wang, J.; Zhang, J.; Ye, Y.; Xu, Q.; Li, Y.; Feng, S.; Xiong, 
X.; Jian, Z.; Gu, L. Peripheral Organ Injury After Stroke. 
Front. Immunol. 2022, 13, 901209. [Google Scholar] 
[CrossRef] [PubMed] 

Pongmoragot, J.; Rabinstein, A.A.; Nilanont, Y.; Swartz, 
R.H.; Zhou, L.; Saposnik, G.; Investigators of the Registry 
of the Canadian Stroke Network (RCSN) and University 
of Toronto Stroke Program for the Stroke Outcomes 
Research Canada (SORCan [www.sorcan.ca]) Working 
Group. Pulmonary Embolism in Ischemic Stroke: 
Clinical Presentation, Risk Factors, and Outcome. J. Am. 
Heart Assoc. 2013, 2, e000372. [Google Scholar] 
[CrossRef] [PubMed] 

Prosser, J.; MacGregor, L.; Lees, K.R.; Diener, H.-C.; 
Hacke, W.; Davis, S. VISTA Investigators Predictors of 
Early Cardiac Morbidity and Mortality after Ischemic 
Stroke. Stroke 2007, 38, 2295–2302. [Google Scholar] 
[CrossRef] 

Bieber, M.; Werner, R.A.; Tanai, E.; Hofmann, U.; 
Higuchi, T.; Schuh, K.; Heuschmann, P.U.; Frantz, S.; 
Ritter, O.; Kraft, P.; et al. Stroke-induced Chronic 



American Journal of Applied Science and Technology 6 https://theusajournals.com/index.php/ajast 

American Journal of Applied Science and Technology (ISSN: 2771-2745) 
 

 

Systolic Dysfunction Driven by Sympathetic 
Overactivity. Ann. Neurol. 2017, 82, 729–743. [Google 
Scholar] [CrossRef] [PubMed] 

Joundi, R.A.; Rabinstein, A.A.; Nikneshan, D.; Tu, J.V.; 
Fang, J.; Holloway, R.; Saposnik, G.; Stroke Outcomes 
Research Working Group (SORCan-www.sorcan.ca). 
Cardiac Arrest in Acute Ischemic Stroke: Incidence, 
Predisposing Factors, and Clinical Outcomes. J. Stroke 
Cerebrovasc Dis. 2016, 25, 1644–1652. [Google 
Scholar] [CrossRef] [PubMed] 

Colivicchi, F.; Bassi, A.; Santini, M.; Caltagirone, C. 
Cardiac Autonomic Derangement and Arrhythmias in 
Right-Sided Stroke with Insular Involvement. Stroke 
2004, 35, 2094–2098. [Google Scholar] [CrossRef] 

Laowattana, S.; Zeger, S.L.; Lima, J.A.C.; Goodman, S.N.; 
Wittstein, I.S.; Oppenheimer, S.M. Left Insular Stroke Is 
Associated with Adverse Cardiac Outcome. Neurology 
2006, 66, 477–483, discussion 463. [Google Scholar] 
[CrossRef] 

Shrestha, P.; Thapa, S.; Shrestha, S.; Lohani, S.; BK, S.; 
MacCormac, O.; Thapa, L.; Devkota, U.P. Renal 
Impairment in Stroke Patients: A Comparison between 
the Haemorrhagic and Ischemic Variants. 
F1000Research 2017, 6, 1531. [Google Scholar] 
[CrossRef] 

Tsagalis, G.; Akrivos, T.; Alevizaki, M.; Manios, E.; 
Stamatellopoulos, K.; Laggouranis, A.; Vemmos, K.N. 
Renal Dysfunction in Acute Stroke: An Independent 
Predictor of Long-Term All Combined Vascular Events 
and Overall Mortality. Nephrol. Dial. Transplant. 2009, 
24, 194–200. [Google Scholar] [CrossRef] 

Duan, H.; Cheng, Z.; Yun, H.J.; Cai, L.; Tong, Y.; Han, Z.; 
Geng, X.; Ding, Y. Serum Bilirubin Associated with 
Stroke Severity and Prognosis: Preliminary Findings on 
Liver Function after Acute Ischemic Stroke. Neurol. Res. 
2023, 45, 62–69. [Google Scholar] [CrossRef] 

Muscari, A.; Collini, A.; Fabbri, E.; Giovagnoli, M.; 
Napoli, C.; Rossi, V.; Vizioli, L.; Bonfiglioli, A.; Magalotti, 
D.; Puddu, G.M.; et al. Changes of Liver Enzymes and 
Bilirubin during Ischemic Stroke: Mechanisms and 
Possible Significance. BMC Neurol. 2014, 14, 122. 
[Google Scholar] [CrossRef] [PubMed] 

Chelluboina, B.; Vemuganti, R. Chronic Kidney Disease 
in the Pathogenesis of Acute Ischemic Stroke. J. Cereb. 
Blood Flow Metab. 2019, 39, 1893–1905. [Google 
Scholar] [CrossRef] [PubMed] 

Sarfo, F.S.; Agyei, M.; Ogyefo, I.; Opare-Addo, P.A.; 
Ovbiagele, B. Factors Linked to Chronic Kidney Disease 
Among Stroke Survivors in Ghana. J. Stroke 
Cerebrovasc. Dis. 2021, 30, 105720. [Google Scholar] 
[CrossRef] [PubMed] 

Kanis, J.; Oden, A.; Johnell, O. Acute and Long-Term 

Increase in Fracture Risk after Hospitalization for 
Stroke. Stroke 2001, 32, 702–706. [Google Scholar] 
[CrossRef] [PubMed] 

Pang, M.Y.; Eng, J.J. Muscle Strength Is a Determinant 
of Bone Mineral Content in the Hemiparetic Upper 
Extremity: Implications for Stroke Rehabilitation. Bone 
2005, 37, 103–111. [Google Scholar] [CrossRef] 

Meng, H.; Liu, T.; Borjigin, J.; Wang, M.M. Ischemic 
Stroke Destabilizes Circadian Rhythms. J. Circadian 
Rhythm 2008, 6, 9. [Google Scholar] [CrossRef] 

 

 


