scholarly journals Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

2010 ◽  
Vol 31 (1) ◽  
pp. 17-35 ◽  
Author(s):  
Martin Lauritzen ◽  
Jens Peter Dreier ◽  
Martin Fabricius ◽  
Jed A Hartings ◽  
Rudolf Graf ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurological Disorders ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Neuronal Damage ◽  
Ion Homeostasis ◽  
Large Body ◽  
Treatment Strategies ◽  
Pathophysiological Mechanism

Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. The implications of these findings are widespread and suggest that intrinsic brain mechanisms have the potential to worsen the outcome of cerebrovascular episodes or brain trauma. The consequences of these intrinsic mechanisms are intimately linked to the composition of the brain extracellular microenvironment and to the level of brain perfusion and in consequence brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders. The findings have implications for monitoring and treatment of patients with acute brain disorders in the intensive care unit. Drawing on the large body of experimental findings from animal studies of CSD obtained during decades we suggest treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves.

scholarly journals Hyponatremia in the Neurologically Ill Patient: A Review

2020 ◽  
Vol 10 (3) ◽  
pp. 208-216
Author(s):  
David P. Lerner ◽  
Starane A. Shepherd ◽  
Ayush Batra
Keyword(s):  
Traumatic Brain Injury ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Early Diagnosis ◽  
Neurological Disorders ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Treatment Strategies ◽  
Diagnosis And Treatment ◽  
Systemic Complications ◽  
Acute Presentation

Hyponatremia is a well-known disorder commonly faced by clinicians managing neurologically ill patients. Neurological disorders are often associated with hyponatremia during their acute presentation and can be associated with specific neurologic etiologies and symptoms. Patients may present with hyponatremia with traumatic brain injury, develop hyponatremia subacutely following aneurysmal subarachnoid hemorrhage, or may manifest with seizures due to hyponatremia itself. Clinicians caring for the neurologically ill patient should be well versed in identifying these early signs, symptoms, and etiologies of hyponatremia. Early diagnosis and treatment can potentially avoid neurologic and systemic complications in these patients and improve outcomes. This review focuses on the causes and findings of hyponatremia in the neurologically ill patient and discusses the pathophysiology, diagnoses, and treatment strategies for commonly encountered etiologies.

Cortical Spreading Depression in the Setting of Traumatic Brain Injury

2020 ◽  
Vol 134 ◽  
pp. 50-57 ◽  
Author(s):  
Sauson Soldozy ◽  
Khadijeh A. Sharifi ◽  
Bhargav Desai ◽  
Daniel Giraldo ◽  
Michelle Yeghyayan ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cortical Spreading Depression ◽  
Spreading Depression

Cortical Spreading Depression in Migraine

Cephalalgia ◽  
2001 ◽  
Vol 21 (7) ◽  
pp. 757-760 ◽  
Author(s):  
M Lauritzen
Keyword(s):  
Amino Acids ◽  
Excitatory Amino Acids ◽  
Cortical Spreading Depression ◽  
Animal Studies ◽  
Spreading Depression ◽  
Neurological Diseases ◽  
Ion Homeostasis ◽  
Large Body ◽  
Experimental Findings ◽  
Reliable Methods

Cortical spreading depression (CSD) is associated with a dramatic failure of brain ion homeostasis as well as efflux of excitatory amino acids from nerve cells and increased energy metabolism. There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine. This paper will, based on the experience related to the detection of CSD in humans, discuss pitfalls and possible strategies for detection of CSD in man. Development of reliable methods for detection of CSD in humans will determine the extent to which the large body of experimental findings from animal studies of CSD can be applied to the investigation and treatment of human brain disease. The paper is based on the experience that has been gained from two decades of studies of CSD in relation to clinical neurological diseases.

FGF10 Attenuates Experimental Traumatic Brain Injury through TLR4/MyD88/NF-κB Pathway

2021 ◽  
pp. 1-9
Author(s):  
Qinhan Hou ◽  
Hongmou Chen ◽  
Quan Liu ◽  
Xianlei Yan
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Protein Expression ◽  
Water Content ◽  
Neurological Deficit ◽  
Neuronal Apoptosis ◽  
Neuronal Damage ◽  
Intraventricular Injection ◽  
Brain Water Content ◽  
Brain Water

Traumatic brain injury (TBI) can induce neuronal apoptosis and neuroinflammation, resulting in substantial neuronal damage and behavioral disorders. Fibroblast growth factors (FGFs) have been shown to be critical mediators in tissue repair. However, the role of FGF10 in experimental TBI remains unknown. In this study, mice with TBI were established via weight-loss model and validated by increase of modified neurological severity scores (mNSS) and brain water content. Secondly, FGF10 levels were elevated in mice after TBI, whereas intraventricular injection of Ad-FGF10 decreased mNSS score and brain water content, indicating the remittance of neurological deficit and cerebral edema in TBI mice. In addition, neuronal damage could also be ameliorated by stereotactic injection of Ad-FGF10. Overexpression of FGF10 increased protein expression of Bcl-2, while it decreased Bax and cleaved caspase-3/PARP, and improved neuronal apoptosis in TBI mice. In addition, Ad-FGF10 relieved neuroinflammation induced by TBI and significantly reduced the level of interleukin 1β/6, tumor necrosis factor α, and monocyte chemoattractant protein-1. Moreover, Ad-FGF10 injection decreased the protein expression level of Toll-like receptor 4 (TLR4), MyD88, and phosphorylation of NF-κB (p-NF-κB), suggesting the inactivation of the TLR4/MyD88/NF-κB pathway. In conclusion, overexpression of FGF10 could ameliorate neurological deficit, neuronal apoptosis, and neuroinflammation through inhibition of the TLR4/MyD88/NF-κB pathway, providing a potential therapeutic strategy for brain injury in the future.

scholarly journals Resuscitation from hemorrhagic shock after traumatic brain injury with polymerized hemoglobin

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Cynthia R. Muller ◽  
Vasiliki Courelli ◽  
Alfredo Lucas ◽  
Alexander T. Williams ◽  
Joyce B. Li ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Hemorrhagic Shock ◽  
Ischemia Reperfusion Injury ◽  
Diastolic Pressure ◽  
Ischemia Reperfusion ◽  
Treatment Strategies ◽  
Secondary Bleeding ◽  
Additional Testing ◽  
Systolic Blood Pressure Variability

AbstractTraumatic brain injury (TBI) is often accompanied by hemorrhage, and treatment of hemorrhagic shock (HS) after TBI is particularly challenging because the two therapeutic treatment strategies for TBI and HS often conflict. Ischemia/reperfusion injury from HS resuscitation can be exaggerated by TBI-induced loss of autoregulation. In HS resuscitation, the goal is to restore lost blood volume, while in the treatment of TBI the priority is focused on maintenance of adequate cerebral perfusion pressure and avoidance of secondary bleeding. In this study, we investigate the responses to resuscitation from severe HS after TBI in rats, using fresh blood, polymerized human hemoglobin (PolyhHb), and lactated Ringer’s (LR). Rats were subjected to TBI by pneumatic controlled cortical impact. Shortly after TBI, HS was induced by blood withdrawal to reduce mean arterial pressure (MAP) to 35–40 mmHg for 90 min before resuscitation. Resuscitation fluids were delivered to restore MAP to ~ 65 mmHg and animals were monitored for 120 min. Increased systolic blood pressure variability (SBPV) confirmed TBI-induced loss of autoregulation. MAP after resuscitation was significantly higher in the blood and PolyhHb groups compared to the LR group. Furthermore, blood and PolyhHb restored diastolic pressure, while this remained depressed for the LR group, indicating a loss of vascular tone. Lactate increased in all groups during HS, and only returned to baseline level in the blood reperfused group. The PolyhHb group possessed lower SBPV compared to LR and blood groups. Finally, sympathetic nervous system (SNS) modulation was higher for the LR group and lower for the PolyhHb group compared to the blood group after reperfusion. In conclusion, our results suggest that PolyhHb could be an alternative to blood for resuscitation from HS after TBI when blood is not available, assuming additional testing demonstrate similar favorable results. PolyhHb restored hemodynamics and oxygen delivery, without the logistical constraints of refrigerated blood.

scholarly journals Efficacy Of Robot-assisted Physiotherapy For Pain Management In Neurological Disorders-A Systematic Review

2021 ◽  
Vol 29 (03) ◽  
pp. 126-131
Author(s):  
Okasha Anjum ◽  
Hajra Ameer Shaikh ◽  
Nida Waheed ◽  
Syeda Wajeeha Raza Zaidi
Keyword(s):  
Systematic Review ◽  
Pain Management ◽  
Neurological Disorders ◽  
Spinal Cord Injuries ◽  
Large Body ◽  
Treatment Strategies ◽  
Gait Training ◽  
Training System ◽  
Robot Assisted ◽  
Randomized Controlled

Efficacy Of Robot-assisted Physiotherapy For Pain Management In Neurological Disorders-A Systematic Review Abstract Background: Neurological disorders (ND) are ranked as the leading cause of death and disability around the globe and the escalating burden summons the advancements in the treatment strategies hence this systematic review aimed to fill the knowledge gap regarding the efficacy of robot-assisted physiotherapy (RAPT) for pain management in ND. Methodology: Scientific trials were sought by an extensive search via electronic databases mainly PubMed, PEDro, and Scopus. Randomized controlled trials published from the year 2014 to April 2021, evaluating the potential effects of RAPT for pain management in ND were included in the review. The quality appraisal of the RCTs was analyzed via Cochrane tool for assessing risk of bias. Results: The Majority of the trials reported the effectiveness of RAPT using PARO robot, Armeo spring, Gloreha robot, and robotic Lokomat gait training system in significantly improving pain of ND such as stroke, dementia, phantom syndrome, and spinal cord injuries. Conclusions: Large body of evidence suggested RAPT as a potential solution in improving pain of various ND however further rigorous trials are necessary to draw conclusive recommendations. Keywords: Neurological disorders, pain, physiotherapy management, rehabilitation, robot-assisted physiotherapy, robotics

scholarly journals Exosomal MicroRNA Differential Expression in Plasma of Young Adults with Chronic Mild Traumatic Brain Injury and Healthy Control

Biomedicines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 36
Author(s):  
Rany Vorn ◽  
Maiko Suarez ◽  
Jacob C. White ◽  
Carina A. Martin ◽  
Hyung-Suk Kim ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Young Adults ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Pathophysiological Mechanism ◽  
Post Injury ◽  
Persistent Symptoms ◽  
Healthy Control ◽  
Underlying Mechanisms

Chronic mild traumatic brain injury (mTBI) has long-term consequences, such as neurological disability, but its pathophysiological mechanism is unknown. Exosomal microRNAs (exomiRNAs) may be important mediators of molecular and cellular changes involved in persistent symptoms after mTBI. We profiled exosomal microRNAs (exomiRNAs) in plasma from young adults with or without a chronic mTBI to decipher the underlying mechanisms of its long-lasting symptoms after mTBI. We identified 25 significantly dysregulated exomiRNAs in the chronic mTBI group (n = 29, with 4.48 mean years since the last injury) compared to controls (n = 11). These miRNAs are associated with pathways of neurological disease, organismal injury and abnormalities, and psychological disease. Dysregulation of these plasma exomiRNAs in chronic mTBI may indicate that neuronal inflammation can last long after the injury and result in enduring and persistent post-injury symptoms. These findings are useful for diagnosing and treating chronic mTBIs.

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