scholarly journals Hypoxic-ischemic brain injuries after cardiosurgical interventions: clinical options of somatogenic asthenic symptom complex in patients in the preoperative period

2021 ◽  
Vol 25 (3) ◽  
pp. 404-408
Author(s):  
D. S. Mankovsky
Keyword(s):  
Cardiac Surgery ◽  
Brain Injuries ◽  
Clinical Signs ◽  
Preoperative Period ◽  
Ischemic Brain ◽  
Thematic Map ◽  
Probabilistic Distribution ◽  
Preoperative Stage ◽  
Clinical Variants ◽  
Symptom Complex

Annotation. The article presents the results of studying the symptomatology of different clinical variants of somatogenous asthenic symptom complex (SASC). The primary material of the study was a specially developed thematic map, the completion of which involved the implementation of clinical and anamnestic study and taking into account about 30 symptoms. Clinical and statistical methods were used: anamnestic quantitative analysis, variation statistics, probabilistic distribution of clinical signs with assessment of the reliability of the obtained results. It was found that in the structure of SASC the largest share belongs to the asthenic variant: is – 40.7%, while astheno-anxiety – 26.3%, astheno-subdepressive – 20.3%, and the smallest – dissomnic (12.7%). The symptomatic structure of SASC variants is characterized by the prevalence of the phenomena of physical and mental asthenia with symptoms of bodily synthesis, which allows to determine the most characteristic symptomatic complexes for cardiac surgery patients. The symptom complexes defined in research on each of variants of SASC allow to objectify at a preoperative stage a psychosomatic condition for maintenance of the integrated neurologic support of cardiosurgical patients.

Relevant Modulation by Ferrous Ions of N-Methyl-D-Aspartate Receptors in Ischemic Brain Injuries

2004 ◽  
Vol 1 (5) ◽  
pp. 429-440 ◽  
Author(s):  
Noritaka Nakamichi ◽  
Hirotaka Oikawa ◽  
Yuki Kambe ◽  
Yukio Yoneda
Keyword(s):  
Brain Injuries ◽  
Ferrous Ions ◽  
Ischemic Brain

scholarly journals Receptor for Advanced Glycation End Products Is Involved in LPA5-Mediated Brain Damage after a Transient Ischemic Stroke

Life ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 80
Author(s):  
Arjun Sapkota ◽  
Sung Jean Park ◽  
Ji Woong Choi
Keyword(s):  
Ischemic Stroke ◽  
Advanced Glycation End Products ◽  
Brain Injuries ◽  
Artery Occlusion ◽  
Advanced Glycation ◽  
Ischemic Brain ◽  
Blood Brain Barrier Disruption ◽  
Glycation End Products ◽  
End Products ◽  
Ischemic Core

Lysophosphatidic acid receptor 5 (LPA5) has been recently identified as a novel pathogenic factor for brain ischemic stroke. However, its underlying mechanisms remain unclear. Here, we determined whether the receptor for advanced glycation end products (RAGE) could be involved in LPA5-mediated brain injuries after ischemic challenge using a mouse model of transient middle cerebral artery occlusion (tMCAO). RAGE was upregulated in the penumbra and ischemic core regions after tMCAO challenge. RAGE upregulation was greater at 3 days than that at 1 day after tMCAO challenge. It was mostly observed in Iba1-immunopositive cells of a post-ischemic brain. Suppressing LPA5 activity with its antagonist, TCLPA5, attenuated RAGE upregulation in the penumbra and ischemic core regions, particularly on Iba1-immunopositive cells, of injured brains after tMCAO challenge. It also attenuated blood–brain barrier disruption, one of the core pathogenesis upon RAGE activation, after tMCAO challenge. As an underlying signaling pathways, LPA5 could contribute to the activation of ERK1/2 and NF-κB in injured brains after tMCAO challenge. Collectively, the current study suggests that RAGE is a possible mediator for LPA5-dependent ischemic brain injury.

Delayed-Onset Neuropathological Complications From a Foramen Magnum and Occipital Crest Focused Traumatic Brain Injury of the Vietnam War and Other Conflicts: Part I, Case Report

2021 ◽  
Author(s):  
Frederick M Burkle ◽  
Kevin S Hadley ◽  
Leah L Ridge ◽  
Jan K Herman ◽  
Firas H Kobeissy
Keyword(s):  
Case Report ◽  
Vietnam War ◽  
Brain Injuries ◽  
Right Hemisphere ◽  
Clinical Signs ◽  
Vitreous Hemorrhage ◽  
Signs And Symptoms ◽  
Foramen Magnum ◽  
Delayed Onset ◽  
Clinical Signs And Symptoms

ABSTRACT Introduction The diagnosis of traumatic brain injuries is typically based on hemispheric blasts resulting in degrees of unconsciousness and associated cerebral injuries. This case report describes a Vietnam War era setting in which a traumatic blast wave struck the posterior cranium in the region of the foramen magnum, occipital crest, and other skull openings (orbit, oronasal, and ear) and the unique secondary clinical signs and symptoms experienced over time. Materials and Methods This case report describes secondary delayed-onset clinical signs and symptoms consistent with progressive decades-long physical and functional complications. The traumatic blast resulted in brief unconsciousness, decreased vision in left eye, confusion, right sided hemotympanum, deafness, severe tinnitus, severe nasopharynx pain and difficulty swallowing, pain in right posterior and occipital area of the head, and loss of dental amalgams. Subsequent exams revealed progressive hyperacusis, sea sickness, dysdiadochokinesis, diagnosis of 9th and 10th cranial nerve traumatic schwannomas, hyperdense changes to the frontal lobe white matter, progressive tinnitus, chronic vertigo, right-sided high-frequency hearing loss, progressive oculo-gyric crisis of Tumarkin-like seizures, left-sided chronic vitreous hemorrhage, and diminished right hemisphere performance of the brain based on neurophysiological assessment. No post-traumatic stress, depression, or other emotional or psychiatric difficulties were claimed. Conclusion This case report, unique to the English language scientific literature, discusses in detail the secondary signs and symptoms of a foramen magnum and occipital crest focused-associated blast injury.

scholarly journals Evidence-Based Psychiatry: Paraclinical Diagnostics of Asthenic Syndrome in Schizophrenia Based on the Determination of Leukocyte-Inhibitory Index

Psychiatry ◽  
2020 ◽  
Vol 18 (2) ◽  
pp. 6-12
Author(s):  
A. N. Simonov ◽  
T. P. Klyushnik ◽  
S. A. Zozulya
Keyword(s):  
Confidence Intervals ◽  
Bootstrap Method ◽  
Clinical Signs ◽  
Total Sample ◽  
Delta Method ◽  
Proteolytic System ◽  
Leukocyte Elastase ◽  
Objective Criterion ◽  
Regression Methods ◽  
Symptom Complex

A leukocyte-inhibitory index (LII) is the ratio of the proteolytic enzyme leukocyte elastase (LE) to its inhibitor, an α1- proteinase inhibitor (α1-PI). LII characterizes the activity of the proteolytic system and can be considered as a potential objective criterion that determines both the course and the outcome of the disease. The changes of LII in schizophrenia patients with clinically diagnosed asthenia (schizoasthenia) and patients with schizophrenia without clinical signs of this syndrome were revealed. The objective: to study the possibility of the 95% confidence intervals for a comparative assessment of LII in patients with schizoasthenia and patients with schizophrenia without clinical signs of asthenic syndrome to obtain correct statistical conclusions. Patients and methods: Overall, 95 patients aged 20–55 years with paroxysmal-progressive (F20.x1) and paranoid (F20.00) schizophrenia were examined: 61 patients in the total sample were clinically diagnosed with asthenic symptom-complex. The enzymatic activity of LE and the functional activity of α1-PI were determined in blood serum. LII was calculated according to the formula. The confidence intervals were built using 4 different methods: Fieller’s theorem, delta method, regression methods and bootstrap method. Results: the statistical analysis indicates that the 95% confidence intervals of these indicators for the examined patient groups do not overlap. Therefore, these indicators relate to different populations, which mean the examined groups are characterized by different variants of the ratio of the proteolytic system components. Conclusion: the assessment of LII can serve as an objective statistically correct criterion for presence or absence of asthenic disorder in patients with schizophrenia in addition to clinical examination.

scholarly journals New cerebrovascular agent with hypotensive activity

2019 ◽  
Vol 5 (2) ◽  
pp. 71-77
Author(s):  
Galina A. Kim ◽  
Tamara S. Gan’shina ◽  
Elena V. Kurza ◽  
Ilya N. Kurdyumov ◽  
Denis V. Maslennikov ◽  
...  
Keyword(s):  
Blood Flow ◽  
Antihypertensive Agent ◽  
Brain Injuries ◽  
Cerebrovascular Disorders ◽  
Male Rats ◽  
Hypotensive Activity ◽  
Duration Of Action ◽  
Ischemic Brain ◽  
Cerebrovascular Activity ◽  
The Brain

Introduction: In cerebrovascular disorders, special attention is paid to a hypertensive cerebrovascular crisis, which combines a vascular injury of the brain and hypertension. The paper studies the cerebrovascular properties of the calcium channel blocker of S-Amlodipine nicotinate antihypertensive agent. Materials and methods: Tests were performed on 96 nonlinear male rats, measuring local blood flow in the cerebral cortex in 36 awake animals, using a laser Doppler flowmeter. Cerebral circulation was recorded in the animals when modeling ischemic and hemorrhagic brain injuries. Results and discussion: S-Amlodipine nicotinate (0.1 mg/kg i/v) shows a pronounced cerebrovascular activity in the models of ischemic and hemorrhagic injuries of the brain. In terms of the vasodilating effect in ischemic brain injury, the drug is comparable to mexidol, nimodipine, picamilon, but is superior to nimodipine and picamilon in terms of duration of action, and in the model of hemorrhagic stroke, S-Amlodipine nicotinate is superior to nimodipine and is comparable to picamilon and mexidol. The analysis of the mechanism of action of the agent revealed the participation of GABA A-receptors in the implementation of cerebrovascular properties of the agent. Conclusion: Significant cerebrovascular activity of S-Amlodipine nicotinate (0.1 mg/kg i/v) antihypertensive agent was revealed. The presence of GABAergic mechanism on cerebral blood flow in the agent action along with blockade of slow calcium channels ensures its high efficacy in treatment of both ischemic and hemorrhagic brain injuries.

scholarly journals Endogenous calcitonin gene-related peptide suppresses ischemic brain injuries and progression of cognitive decline

2018 ◽  
Vol 36 (4) ◽  
pp. 876-891 ◽  
Author(s):  
Liuyu Zhai ◽  
Takayuki Sakurai ◽  
Akiko Kamiyoshi ◽  
Yuka Ichikawa-Shindo ◽  
Hisaka Kawate ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Brain Injuries ◽  
Calcitonin Gene Related Peptide ◽  
Ischemic Brain ◽  
Related Peptide ◽  
Calcitonin Gene

Thyrotoxic hepatitis

2017 ◽  
Vol 63 (1) ◽  
pp. 46-50
Author(s):  
Dmitrij V. Pikulev ◽  
Aleksej V. Klemenov
Keyword(s):  
Liver Injury ◽  
Clinical Symptoms ◽  
Correct Diagnosis ◽  
Clinical Signs ◽  
Rare Condition ◽  
Liver Function Tests ◽  
Biliary Cirrhosis ◽  
Liver Pathology ◽  
Drug Induced ◽  
Clinical Variants

In most cases, liver pathology in hyperthyroidism is confined to asymptomatic changes in laboratory indices, while clinical signs are much rarer. Three clinical variants of liver pathology in patients with hyperthyroidism can be differentiated: drug-induced hepatitis that develop in response to administration of thyrostatic agents (mainly propylthiouracil); concomitant autoimmune liver diseases (autoimmune hepatitis, primary biliary cirrhosis), and hepatopathies as a direct manifestation of thyrotoxicosis (thyrotoxic hepatitis). Thyrotoxic hepatitis is a rare condition difficult to diagnose. The variety of etiological factor of liver pathology in hyperthyroidism, universal clinical symptoms, and the lack of specific histological markers make it difficult to make a correct diagnosis. A clinical case of Graves’ disease complicated with severe thyrotoxic hepatitis, the edema-ascites syndrome and hyperbilirubinemia is reported. The patient was diagnosed with thyrotoxic hepatitis after all other reasons for liver pathology have been ruled out. The concomitant thyrogenic myocardiodystrophy, cardiomegaly and atrial fibrillation required ruling out the diagnosis of cardiogenic liver injury and made diagnosing more difficult. Normalization of the thyroid status in patients receiving mercazolyl therapy was accompanied by alleviation of clinical symptoms of hepatitis and the positive dynamics of the indices of liver function tests. A brief review of the data on clinical variants and mechanisms of liver injury in patients with thyrotoxicosis is presented.

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