scholarly journals Study of Haemodynamic Status after Anticholinergic Premedication During Electroconvulsive Therapy — A Comparative Study Between Atropine and Glycopyrolate

2009 ◽  
pp. 31-37
Author(s):  
Md Shahjahan ◽  
Md Shahidul Islam ◽  
AKM Akhtaruzzaman ◽  
KM Iqbal
Keyword(s):  
Airway Obstruction ◽  
Blood Brain Barrier ◽  
Electroconvulsive Therapy ◽  
Pharmacological Therapy ◽  
The Other ◽  
Brain Barrier ◽  
Antipsychotic Therapy ◽  
Blood Brain ◽  
Other Hand ◽  
Group I

Electroconvulsive therapy (ECT) is a highly successful treatment for severe depression and some other psychiatric disorder. 70%-80% patients respond to pharmacological therapy and at least 50% who do not respond to antidepressants do respond favourably to ECT. ECT is quicker, safer and more effective and has fewer side effects than drug therapy. ECT needs general anaesthesia; therefore interactions between psychotropic drugs, ECT and anaesthetic agents can occur. ECT is often associated with acute hyperdynamic response. CNS stimulants on the other hand may prolong seizure, also dysrrhythmias and elevate haemodynamic responses. Initial vagal responses immediately after application of current may lead to bradycardia and salivation, which may cause laryngospasm, bronchospasm and airway obstruction. There may be even asystole and hypoxic episodes. To prevent possible asystole, bradycardia and airway obstruction during ECT, atropine as premedication can be considered. Atropine premedications produces anticholinergic mediated tachycardia, which is in addition to intense sympathetic response after ECT stimulus that contributes to greater myocardial workload. On the other hand, glycopyrolate is a long acting muscarinic antagonist five to six times as potent as atropine. It does not cross blood brain barrier, placenta and eye. It controls secretions with doses that don't cause marked changes in heart rate. Its effect on blood pressure is less than atropine. Atropine crosses blood brain barrier and thus affecting CNS. Our present study was performed to compare haemodynamic status after anticholinergic premedication with atropine and glycopyrolate during ECT. This study was randomized, prospective study. 90 patients for ECT, age 15-50 years, ASA grading I&II, and receiving antipsychotic therapy with major depressive illness were randomly selected by blind envelop method and divided into three groups of 30 patients each. Group-I received atropine, group-II received glycopyrolate and group-III received no premedication. Results of the study showed that anticholinergic premedication is not essential for safe and effective ECT therapy, if at all needed glycopyrolate is the therapy of choice. Key words: ECT; Atropine premedication; glycopyrolate Journal of BSA, Vol. 18, No. 1 & 2, 2005 p.31-37

scholarly journals Disturbance of Intracerebral Fluid Clearance and Blood–Brain Barrier in Vascular Cognitive Impairment

2019 ◽  
Vol 20 (10) ◽  
pp. 2600 ◽  
Author(s):  
Masaki Ueno ◽  
Yoichi Chiba ◽  
Ryuta Murakami ◽  
Koichi Matsumoto ◽  
Ryuji Fujihara ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Blood Brain Barrier ◽  
Brain Function ◽  
Vascular Cognitive Impairment ◽  
Brain Dysfunction ◽  
Brain Parenchyma ◽  
The Other ◽  
Brain Barrier ◽  
Blood Brain ◽  
The Brain

The entry of blood-borne macromolecular substances into the brain parenchyma from cerebral vessels is blocked by the blood–brain barrier (BBB) function. Accordingly, increased permeability of the vessels induced by insult noted in patients suffering from vascular dementia likely contributes to the cognitive impairment. On the other hand, blood-borne substances can enter extracellular spaces of the brain via endothelial cells at specific sites without the BBB, and can move to brain parenchyma, such as the hippocampus and periventricular areas, adjacent to specific sites, indicating the contribution of increased permeability of vessels in the specific sites to brain function. It is necessary to consider influx and efflux of interstitial fluid (ISF) and cerebrospinal fluid (CSF) in considering effects of brain transfer of intravascular substances on brain function. Two pathways of ISF and CSF are recently being established. One is the intramural peri-arterial drainage (IPAD) pathway of ISF. The other is the glymphatic system of CSF. Dysfunction of the two pathways could also contribute to brain dysfunction. We review the effects of several kinds of insult on vascular permeability and the failure of fluid clearance on the brain function.

Analysis of the expression of nine secreted matrix metalloproteinases and their endogenous inhibitors in the brain of mice subjected to ischaemic stroke

2014 ◽  
Vol 112 (08) ◽  
pp. 363-378 ◽  
Author(s):  
Sébastien Lenglet ◽  
Fabrizio Montecucco ◽  
François Mach ◽  
Karl Schaller ◽  
Yvan Gasche ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Blood Brain Barrier ◽  
Cerebral Ischaemia ◽  
Recombinant Tissue Plasminogen Activator ◽  
Acute Stage ◽  
The Other ◽  
Brain Barrier ◽  
Global Changes ◽  
Endogenous Inhibitors ◽  
Blood Brain

SummaryMatrix metalloproteinases (MMPs) are a family of more than twenty secreted and cell-surface endopeptidases. Among them, MMP2, MMP3 and MMP9 are involved in blood-brain barrier injury and neuronal death after cerebral ischaemia. On the other hand, very little is known about the expression of the other secreted MMPs. Herein, we compared the global changes in MMP1, MMP2, MMP3, MMP7, MMP8, MMP9, MMP10, MMP12 and MMP13, and their endogenous inhibitors TIMP1 and TIMP2, both at the mRNA and protein levels, during the hyperacute (6 h), acute (24 h) and subacute (72 h) stages following transient focal cerebral ischaemia and treatment with recombinant tissue plasminogen activator (rtPA). We observed a significant increase in MMP1, MMP2, MMP9, MMP10, MMP13 and TIMP1 levels during the acute stage of reperfusion, which was further amplified during the subacute stage for MMP1, MMP2, MMP10 and TIMP1. In general, no change of MMP3, MMP7, MMP8, MMP12 and TIMP2 was observed. However, rtPA treatment induced a rapid increase in MMP1/TIMP2, MMP2/TIMP2, MMP8/TIMP2 and MMP9/TIMP2 ratios during the hyperacute stage of reperfusion compared to saline treatment, which may have potential implications in the early disruption of the blood-brain barrier after rtPA treatment.

scholarly journals Permeability of the blood-brain barrier for sodium iodide in some organic diseases of the nervous system

1937 ◽  
Vol 33 (11) ◽  
pp. 1319-1331
Author(s):  
N. I. Popov
Keyword(s):  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Blood Brain Barrier ◽  
Sodium Iodide ◽  
The Other ◽  
Brain Barrier ◽  
Theoretical Interest ◽  
Blood Brain ◽  
Medicinal Substances ◽  
The One

In the physiology and pathology of the nervous system, much attention is paid to the issue of the permeability of the blood-brain barrier. Along with the theoretical interest, this question is important for the practicing physician. If, on the one hand, a violation of the barrier leads to a disease of the nervous system, then, on the other hand, in diseases of the nervous system, it is often necessary to force the permeability of the barrier in one way or another in order to enable various medicinal substances (arsenic, mercury) to enter the cerebrospinal fluid

On the transfer of visdout to the cerebrospinal fluid in the treatment of syphilis in connection with the doctrine of the blood-brain barrier

1930 ◽  
Vol 26 (7) ◽  
pp. 114-118
Author(s):  
G. G. Kondratyev
Keyword(s):  
Cerebrospinal Fluid ◽  
Blood Brain Barrier ◽  
Nervous Tissue ◽  
Joint Venture ◽  
The Other ◽  
Brain Barrier ◽  
Special Mechanism ◽  
Blood Brain ◽  
Harmful Substances ◽  
The One

On the basis of numerous studies, it has been established that some substances introduced into the blood are easily detected in the cerebrospinal fluid and nervous tissue, while others circulating in the blood, even in very significant quantities, do not appear in them under normal conditions. On the contrary, all substances introduced into the joint venture. m., very quickly appear in the blood. This circumstance indicates that between the blood on the one hand, cn. m. f. and nervous tissue on the other hand, apparently, there is a special mechanism of a protective nature, which is able to make a choice between the substances circulating in the blood, selectively passing some and delaying others, and also quickly removing all harmful substances from the joint venture. m f., the so-called. blood-brain barrier (Stern, Gautier).

scholarly journals Time to test antibacterial therapy in Alzheimer’s disease

Brain ◽  
2019 ◽  
Author(s):  
Francesco Panza ◽  
Madia Lozupone ◽  
Vincenzo Solfrizzi ◽  
Mark Watling ◽  
Bruno P Imbimbo
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gut Microbiota ◽  
Blood Brain Barrier ◽  
Amyloid Β ◽  
The Other ◽  
Brain Barrier ◽  
The Past ◽  
Blood Brain ◽  
The Brain

Abstract Alzheimer’s disease is associated with cerebral accumulation of amyloid-β peptide and hyperphosphorylated tau. In the past 28 years, huge efforts have been made in attempting to treat the disease by reducing brain accumulation of amyloid-β in patients with Alzheimer’s disease, with no success. While anti-amyloid-β therapies continue to be tested in prodromal patients with Alzheimer’s disease and in subjects at risk of developing Alzheimer’s disease, there is an urgent need to provide therapeutic support to patients with established Alzheimer’s disease for whom current symptomatic treatment (acetylcholinesterase inhibitors and N-methyl d-aspartate antagonist) provide limited help. The possibility of an infectious aetiology for Alzheimer’s disease has been repeatedly postulated over the past three decades. Infiltration of the brain by pathogens may act as a trigger or co-factor for Alzheimer’s disease, with Herpes simplex virus type 1, Chlamydia pneumoniae, and Porphyromonas gingivalis being most frequently implicated. These pathogens may directly cross a weakened blood–brain barrier, reach the CNS and cause neurological damage by eliciting neuroinflammation. Alternatively, pathogens may cross a weakened intestinal barrier, reach vascular circulation and then cross blood–brain barrier or cause low grade chronic inflammation and subsequent neuroinflammation from the periphery. The gut microbiota comprises a complex community of microorganisms. Increased permeability of the gut and blood–brain barrier induced by microbiota dysbiosis may impact Alzheimer’s disease pathogenesis. Inflammatory microorganisms in gut microbiota are associated with peripheral inflammation and brain amyloid-β deposition in subjects with cognitive impairment. Oral microbiota may also influence Alzheimer’s disease risk through circulatory or neural access to the brain. At least two possibilities can be envisaged to explain the association of suspected pathogens and Alzheimer’s disease. One is that patients with Alzheimer’s disease are particularly prone to microbial infections. The other is that microbial infection is a contributing cause of Alzheimer’s disease. Therapeutic trials with antivirals and/or antibacterials could resolve this dilemma. Indeed, antiviral agents are being tested in patients with Alzheimer’s disease in double-blind placebo-controlled studies. Although combined antibiotic therapy was found to be effective in animal models of Alzheimer’s disease, antibacterial drugs are not being widely investigated in patients with Alzheimer’s disease. This is because it is not clear which bacterial populations in the gut of patients with Alzheimer’s disease are overexpressed and if safe, selective antibacterials are available for them. On the other hand, a bacterial protease inhibitor targeting P. gingivalis toxins is now being tested in patients with Alzheimer’s disease. Clinical studies are needed to test if countering bacterial infection may be beneficial in patients with established Alzheimer’s disease.

scholarly journals Safety and maximum tolerated dose of superselective intraarterial cerebral infusion of bevacizumab after osmotic blood-brain barrier disruption for recurrent malignant glioma

2011 ◽  
Vol 114 (3) ◽  
pp. 624-632 ◽  
Author(s):  
John A. Boockvar ◽  
Apostolos J. Tsiouris ◽  
Christoph P. Hofstetter ◽  
Ilhami Kovanlikaya ◽  
Sherese Fralin ◽  
...  
Keyword(s):  
Mr Imaging ◽  
Malignant Glioma ◽  
Blood Brain Barrier ◽  
Maximum Tolerated Dose ◽  
Brain Barrier ◽  
Recurrent Malignant Glioma ◽  
Median Reduction ◽  
Blood Brain ◽  
Group I ◽  
Group Ii

Object The authors assessed the safety and maximum tolerated dose of superselective intraarterial cerebral infusion (SIACI) of bevacizumab after osmotic disruption of the blood-brain barrier (BBB) with mannitol in patients with recurrent malignant glioma. Methods A total of 30 patients with recurrent malignant glioma were included in the current study. Results The authors report no dose-limiting toxicity from a single dose of SIACI of bevacizumab up to 15 mg/kg after osmotic BBB disruption with mannitol. Two groups of patients were studied; those without prior bevacizumab exposure (naïve patients; Group I) and those who had received previous intravenous bevacizumab (exposed patients; Group II). Radiographic changes demonstrated on MR imaging were assessed at 1 month postprocedure. In Group I patients, MR imaging at 1 month showed a median reduction in the area of tumor enhancement of 34.7%, a median reduction in the volume of tumor enhancement of 46.9%, a median MR perfusion (MRP) reduction of 32.14%, and a T2-weighted/FLAIR signal decrease in 9 (47.4%) of 19 patients. In Group II patients, MR imaging at 1 month showed a median reduction in the area of tumor enhancement of 15.2%, a median volume reduction of 8.3%, a median MRP reduction of 25.5%, and a T2-weighted FLAIR decrease in 0 (0%) of 11 patients. Conclusions The authors conclude that SIACI of mannitol followed by bevacizumab (up to 15 mg/kg) for recurrent malignant glioma is safe and well tolerated. Magnetic resonance imaging shows that SIACI treatment with bevacizumab can lead to reduction in tumor area, volume, perfusion, and T2-weighted/FLAIR signal.

scholarly journals The Roles of the Microbiome in Alzheimer’s Disease

2021 ◽  
Vol 2 (1) ◽  
pp. 159-167
Author(s):  
Zahin Hafiz ◽  
Moina Malek ◽  
William Ju
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Blood Brain Barrier ◽  
Metabolic Diseases ◽  
The Other ◽  
Therapeutic Interventions ◽  
Brain Barrier ◽  
Therapeutic Implications ◽  
Blood Brain ◽  
The Brain

The gut and the brain are in constant communication in a complex network known as the brain-gut axis. A growing body of research has found links between the brain-gut axis and Alzheimer’s Disease (AD). In this review, we will explore how the mammalian microbiome affects neuroinflammation and increases the permeability of the blood brain barrier in the context of AD. Research shows that the microbiome is associated with neuroinflammation in AD, which is presumably caused by the secretion of cytokines from specialized cells of the brain - microglia and astrocytes. On the other hand, metabolic diseases, caused by microbiota dysbiosis, can increase the permeability of the blood brain barrier. In addition, its higher permeability can allow blood plasma components to enter brain tissue and further develop AD pathology. Findings of the current research have tremendous therapeutic implications. Researchers have speculated whether the therapeutic modification of gut microbiota, through the use of antibiotics and probiotics, may show improvement in AD patients. Our understanding of the pathways and mechanisms involved in the brain-gut axis and AD is still very limited and requires further research before clinical and therapeutic interventions can occur.

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