scholarly journals К ВОПРОСУ ПРЕВЕНЦИИ И РАННЕЙ ИДЕНТИФИКАЦИИ ХАРАКТЕРА И ПРИЧИН ПОСЛЕОПЕРАЦИОННЫХ ОСЛОЖНЕНИЙ ПРИ ВМЕШАТЕЛЬСТВАХ ПО ПОВОДУ РАЗЛИЧНЫХ КЛИНИКО-АНАТОМИЧЕСКИХ ФОРМ ТЯЖЕЛОЙ ЧЕРЕПНО-МОЗГОВОЙ ТРАВМЫ

World Science ◽  
2021 ◽  
Author(s):  
Napoleon Meskhia
Keyword(s):  
Blood Pressure ◽  
Postoperative Complications ◽  
Clinical Signs ◽  
Diagnostic Errors ◽  
Postoperative Management ◽  
Postoperative Hemorrhage ◽  
Neurological Symptoms ◽  
Brain Swelling ◽  
Lethal Outcome ◽  
The Brain

The analysis of the causes of postoperative complications was carried out, as well as of the failures and errors or the same omissions in postoperative management. The total number of cases was 177 (5%) among more than 3500 patients, being operated on various clinical and anatomical forms of craniocerebral trauma.In 63.8% (in 113 patients), worsening of condition was associated with the postoperative hemorrhage, which in 54% of cases was shell- recurrent. In 36.6% of observations (in 64 patients), deteriorated states of the brain swelling or edema were associated with an increase of cerebral edema.The main causes of the postoperative volume hemorrhages were the inadequacy of homeostasis and fluctuations in blood pressure during the first hours and days after surgery, with a tendency of significant increase of that latter. Diagnostic errors were the result of underestimation or incorrect evaluation of neurological symptoms and clinical signs of repeated volumetric hemorrhages.Late diagnosis of postoperative complications resulted in a lethal outcome in 79 (44.6%) cases among 177 patients with the complications in the postoperative process. Neurological and clinical signs and their combinations characteristic for postoperative volumetric hemorrhages are given in the article, as well as are offered the ways of their prevention.

scholarly journals Risk factors and clinical and neurological consequences of intraoperative rupture of brain aneurysms in microsurgical operations

2020 ◽  
pp. 66-76
Author(s):  
Bindu A. V. ◽  
Orlov M. Yu. ◽  
Litvak S. O. ◽  
M. V. Yeleynik
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
High Blood Pressure ◽  
Cerebral Edema ◽  
Neurological Symptoms ◽  
Arterial Aneurysm ◽  
Duration Of Surgery ◽  
Intraoperative Rupture ◽  
Atherosclerotic Changes ◽  
The Brain

Objective. to assess the frequency, risk factors and clinical and neurological consequences of intraoperative rupture of arterial aneurysm (AA) of the brain (B) in clipping operations of the B AA . Materials and approaches. A retrospective analysis of microsurgical operations clipping of cerebral aneurysms in 1449 (100%) patients for the period from 2011 to 2018 was performed, of which 141 (9.73%) cases had intraoperative rupture of the aneurysm (IORA). Preoperative examination: clinical and neurological examination, CT of the brain, cerebral angiography( CAG), duplex scanning of the main vessels of the head and neck. The analyzed criteria are risk factors of IORA: AA size, localization, shape, duration of surgery after the primary rupture of AA, the presence of hypertension and the patient's condition before surgery. Results. The frequency of IORA in clipping operations of B AA was 9.73% (141 patients) in a series of observations 1441 (100%). Most often IORA-141 (100%) was registered in clipping operations of AA of complex ACA-AcomA (86 (61%) cases out of 141 (100%)). IORA is possible at all stages of the operation with the maximum frequency of contact breaks – 135 (95.74%); the rarest-6 ( 4.26%)  -  non - contact IORA (at the stage of craniotomy)  was recorded. At the preoperative stage, the vast majority of patients with subsequent IORA were diagnosed with cerebral edema, AA of large size, atherosclerotic changes in the aneurysm-affected segment of the artery and cervical areas of the aneurysm, high blood pressure during surgery, adhesive arachnoid changes. At the time of discharge from the hospital, according to the Glasgow results scale: 69 (48.94%) full or partial restoration of labor activity, 18 (12.77%) had limited daily activities without the need for outside assistance, 37 (26 24%) deep disability ) Deaths were in the group of "contact" IORA -  17 (12.06%). At 6 ( 4.26%) of "non-contact" IORA,  a deepening of initial neurological symptoms was recorded with a suppression of the level of consciousness, the addition of pyramidal insufficiency, speech impairment and psycho-organic syndrome, and a deepening of the phenomena of initial cerebral arterial vasospasm. Conclusions. IORA is predominantly in contact with a frequency of occurrence-9.73 %. The most common risk factors for IORA were: cerebral edema, large AA, atherosclerotic changes in the aneurysm-affected artery segment and cervical aneurysm sites, high blood pressure during surgery, adhesions arachnoid changes. IORA leads to deepening of initial neurological symptoms, phenomena of initial vasospasm of cerebral arteries with the level of total mortality-17 (12.06%).

RAS in the Central Nervous System: Potential Role in Neuropsychiatric Disorders

2018 ◽  
Vol 25 (28) ◽  
pp. 3333-3352 ◽  
Author(s):  
Natalia Pessoa Rocha ◽  
Ana Cristina Simoes e Silva ◽  
Thiago Ruiz Rodrigues Prestes ◽  
Victor Feracin ◽  
Caroline Amaral Machado ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Therapeutic Potential ◽  
Neuropsychiatric Disorders ◽  
Extensive Literature ◽  
Ang Ii ◽  
Mas Receptor ◽  
The Central Nervous System ◽  
The Brain

Background: The Renin-Angiotensin System (RAS) is a key regulator of cardiovascular and renal homeostasis, but also plays important roles in mediating physiological functions in the central nervous system (CNS). The effects of the RAS were classically described as mediated by angiotensin (Ang) II via angiotensin type 1 (AT1) receptors. However, another arm of the RAS formed by the angiotensin converting enzyme 2 (ACE2), Ang-(1-7) and the Mas receptor has been a matter of investigation due to its important physiological roles, usually counterbalancing the classical effects exerted by Ang II. Objective: We aim to provide an overview of effects elicited by the RAS, especially Ang-(1-7), in the brain. We also aim to discuss the therapeutic potential for neuropsychiatric disorders for the modulation of RAS. Method: We carried out an extensive literature search in PubMed central. Results: Within the brain, Ang-(1-7) contributes to the regulation of blood pressure by acting at regions that control cardiovascular functions. In contrast with Ang II, Ang-(1-7) improves baroreflex sensitivity and plays an inhibitory role in hypothalamic noradrenergic neurotransmission. Ang-(1-7) not only exerts effects related to blood pressure regulation, but also acts as a neuroprotective component of the RAS, for instance, by reducing cerebral infarct size, inflammation, oxidative stress and neuronal apoptosis. Conclusion: Pre-clinical evidence supports a relevant role for ACE2/Ang-(1-7)/Mas receptor axis in several neuropsychiatric conditions, including stress-related and mood disorders, cerebrovascular ischemic and hemorrhagic lesions and neurodegenerative diseases. However, very few data are available regarding the ACE2/Ang-(1-7)/Mas receptor axis in human CNS.

scholarly journals Efficacy of Intravenous Liposomal Amphotericin B (AmBisome) against Coccidioidal Meningitis in Rabbits

2002 ◽  
Vol 46 (8) ◽  
pp. 2420-2426 ◽  
Author(s):  
Karl V. Clemons ◽  
Raymond A. Sobel ◽  
Paul L. Williams ◽  
Demosthenes Pappagianis ◽  
David A. Stevens
Keyword(s):  
Spinal Cord ◽  
Amphotericin B ◽  
Liposomal Amphotericin ◽  
White Blood Cells ◽  
Clinical Signs ◽  
Liposomal Amphotericin B ◽  
Coccidioides Immitis ◽  
Lower Protein ◽  
Motor Abnormalities ◽  
The Brain

ABSTRACT The efficacy of intravenously administered liposomal amphotericin B (AmBisome [AmBi]) for the treatment of experimental coccidioidal meningitis was compared with those of oral fluconazole (FLC) and intravenously administered conventional amphotericin B (AMB). Male New Zealand White rabbits were infected by intracisternal inoculation of arthroconidia of Coccidioides immitis. Starting 5 days postinfection, animals received one of the following: 5% dextrose water diluent; AMB given at 1 mg/kg of body weight; AmBi given at 7.5, 15, or 22.5 mg/kg intravenously three times per week for 3 weeks; or oral FLC given at 80 mg/kg for 19 days. One week after the cessation of therapy, all survivors were euthanatized, the numbers of CFU remaining in the spinal cord and brain were determined, and histological analyses were performed. All AmBi-, FLC-, or AMB-treated animals survived and had prolonged lengths of survival compared with those for the controls (P < 0.0001). Treated groups had significantly lower numbers of white blood cells and significantly lower protein concentrations in the cerebrospinal fluid compared with those for the controls (P < 0.01 to 0.0005) and had fewer clinical signs of infection (e.g., weight loss, elevated temperature, and neurological abnormalities including motor abnormalities). The mean histological scores for AmBi-treated rabbits were lower than those for FLC-treated and control rabbits (P < 0.016 and 0.0005, respectively); the scores for AMB-treated animals were lower than those for the controls (P < 0.0005) but were similar to those for FLC-treated rabbits. All regimens reduced the numbers of CFU in the brain and spinal cord compared with those for the controls (P ≤0.0005). AmBi-treated animals had 3- to 11-fold lower numbers of CFU than FLC-treated rabbits and 6- to 35-fold lower numbers of CFU than AmB-treated rabbits. Three of eight animals given 15 mg of AmBi per kg had no detectable infection in either tissue, whereas other doses of AmBi or FLC cleared either the brain or the spinal cord of infection in fewer rabbits. In addition, clearance of the infection from both tissues was achieved in none of the rabbits, and neither tissue was cleared of infection in AMB-treated animals. Overall, these data indicate that intravenously administered AmBi is superior to oral FLC or intravenous AMB and that FLC is better than AMB against experimental coccidioidal meningitis. These data indicate that AmBi may offer an improvement in the treatment of coccidioidal meningitis. Additional studies are warranted.

scholarly journals L2HGDH Missense Variant in a Cat with L-2-Hydroxyglutaric Aciduria

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 682
Author(s):  
Matthias Christen ◽  
Nils Janzen ◽  
Anne Fraser ◽  
Adrian C. Sewell ◽  
Vidhya Jagannathan ◽  
...  
Keyword(s):  
Current Knowledge ◽  
Genetic Defect ◽  
Clinical Signs ◽  
Missense Variant ◽  
Microcytic Anemia ◽  
Abnormal Behavior ◽  
Functional Candidate Gene ◽  
History Of ◽  
The Brain ◽  
Hydroxyglutaric Acid

A 7-month-old, spayed female, domestic longhair cat with L-2-hydroxyglutaric aciduria (L-2-HGA) was investigated. The aim of this study was to investigate the clinical signs, metabolic changes and underlying genetic defect. The owner of the cat reported a 4-month history of multiple paroxysmal seizure-like episodes, characterized by running around the house, often in circles, with abnormal behavior, bumping into obstacles, salivating and often urinating. The episodes were followed by a period of disorientation and inappetence. Neurological examination revealed an absent bilateral menace response. Routine blood work revealed mild microcytic anemia but biochemistry, ammonia, lactate and pre- and post-prandial bile acids were unremarkable. MRI of the brain identified multifocal, bilaterally symmetrical and T2-weighted hyperintensities within the prosencephalon, mesencephalon and metencephalon, primarily affecting the grey matter. Urinary organic acids identified highly increased levels of L-2-hydroxyglutaric acid. The cat was treated with the anticonvulsants levetiracetam and phenobarbitone and has been seizure-free for 16 months. We sequenced the genome of the affected cat and compared the data to 48 control genomes. L2HGDH, coding for L-2-hydroxyglutarate dehydrogenase, was investigated as the top functional candidate gene. This search revealed a single private protein-changing variant in the affected cat. The identified homozygous variant, XM_023255678.1:c.1301A>G, is predicted to result in an amino acid change in the L2HGDH protein, XP_023111446.1:p.His434Arg. The available clinical and biochemical data together with current knowledge about L2HGDH variants and their functional impact in humans and dogs allow us to classify the p.His434Arg variant as a causative variant for the observed neurological signs in this cat.

Experimental delayed radiation necrosis of the brain

1979 ◽  
Vol 51 (5) ◽  
pp. 587-596 ◽  
Author(s):  
Albert N. Martins ◽  
Ralph E. Severance ◽  
James M. Henry ◽  
Thomas F. Doyle
Keyword(s):  
Rhesus Monkeys ◽  
Radiation Necrosis ◽  
Clinical Signs ◽  
Control Group ◽  
Content Type ◽  
Brain Irradiation ◽  
Primate Brain ◽  
High Doses ◽  
The Brain ◽  
Male Rhesus

✓ The authors have designed an experiment to detect a hitherto unrecognized interaction between high doses of the glucocorticoid, dexamethasone, and brain irradiation. Eighteen juvenile male rhesus monkeys received 1800 rads to the whole brain in 8.5 minutes. For 1½ days before and 10½ days after the irradiation, nine animals received approximately 2.9 mg/kg/day of dexamethasone intramuscularly in addition to irradiation, while the remaining nine animals served as the control group and received saline. All animals eventually developed a progressive neurological syndrome, and died of delayed radiation necrosis of the brain. The two groups were compared with regard to latency to onset of clinical signs, survival time, and number, distribution, and location of lesions of radionecrosis. Large doses of dexamethasone did not alter the susceptibility of the primate brain to delayed radiation necrosis. Detailed morphological study of the radionecrotic lesions supports the hypothesis that most, if not all, of the lesions develop as the consequence of injury to blood vessels.

scholarly journals Is High Blood Pressure Self-Protection for the Brain?

2016 ◽  
Vol 119 (12) ◽  
Author(s):  
Esther A.H. Warnert ◽  
Jonathan C.L. Rodrigues ◽  
Amy E. Burchell ◽  
Sandra Neumann ◽  
Laura E.K. Ratcliffe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Self Protection ◽  
The Brain

scholarly journals Autonomic dysfunction in post-COVID patients with and witfhout neurological symptoms: a prospective multidomain observational study

2021 ◽  
Author(s):  
Alex Buoite Stella ◽  
Giovanni Furlanis ◽  
Nicolò Arjuna Frezza ◽  
Romina Valentinotti ◽  
Milos Ajcevic ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Orthostatic Intolerance ◽  
Neurological Symptoms ◽  
Postural Tachycardia Syndrome ◽  
Symptom Scale ◽  
Autonomic Symptom ◽  
Postural Tachycardia ◽  
Ambulatory Services

AbstractThe autonomic nervous system (ANS) can be affected by COVID-19, and dysautonomia may be a possible complication in post-COVID individuals. Orthostatic hypotension (OH) and postural tachycardia syndrome (POTS) have been suggested to be common after SARS-CoV-2 infection, but other components of ANS function may be also impaired. The Composite Autonomic Symptom Scale 31 (COMPASS-31) questionnaire is a simple and validated tool to assess dysautonomic symptoms. The aim of the present study was to administer the COMPASS-31 questionnaire to a sample of post-COVID patients with and without neurological complaints. Participants were recruited among the post-COVID ambulatory services for follow-up evaluation between 4 weeks and 9 months from COVID-19 symptoms onset. Participants were asked to complete the COMPASS-31 questionnaire referring to the period after COVID-19 disease. Heart rate and blood pressure were manually taken during an active stand test for OH and POTS diagnosis. One-hundred and eighty participants were included in the analysis (70.6% females, 51 ± 13 years), and OH was found in 13.8% of the subjects. Median COMPASS-31 score was 17.6 (6.9–31.4), with the most affected domains being orthostatic intolerance, sudomotor, gastrointestinal and pupillomotor dysfunction. A higher COMPASS-31 score was found in those with neurological symptoms (p < 0.01), due to more severe orthostatic intolerance symptoms (p < 0.01), although gastrointestinal (p < 0.01), urinary (p < 0.01), and pupillomotor (p < 0.01) domains were more represented in the non-neurological symptoms group. This study confirms the importance of monitoring ANS symptoms as a possible complication of COVID-19 disease that may persist in the post-acute period.

scholarly journals Divergent mechanism regulating fluid intake and metabolism by the brain renin-angiotensin system

2012 ◽  
Vol 302 (3) ◽  
pp. R313-R320 ◽  
Author(s):  
Curt D. Sigmund
Keyword(s):  
Blood Pressure ◽  
Fluid Intake ◽  
Renin Angiotensin System ◽  
Metabolic Effects ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Intracellular Form ◽  
Efferent Pathways ◽  
The Brain ◽  
Pituitary Adrenal Axis

The purpose of this review is two-fold. First, I will highlight recent advances in our understanding of the mechanisms regulating angiotensin II (ANG II) synthesis in the brain, focusing on evidence that renin is expressed in the brain and is expressed in two forms: a secreted form, which may catalyze extracellular ANG I generation from glial or neuronal angiotensinogen (AGT), and an intracellular form, which may generate intracellular ANG in neurons that may act as a neurotransmitter. Second, I will discuss recent studies that advance the concept that the renin-angiotensin system (RAS) in the brain not only is a potent regulator of blood pressure and fluid intake but may also regulate metabolism. The efferent pathways regulating the blood pressure/dipsogenic effects and the metabolic effects of elevated central RAS activity appear different, with the former being dependent upon the hypothalamic-pituitary-adrenal axis, and the latter being dependent upon an interaction between the brain and the systemic (or adipose) RAS.

Control of Blood Pressure and the Distribution of Blood Flow

1991 ◽  
Vol 7 (S1) ◽  
pp. 79-84 ◽  
Author(s):  
Hans T. Versmold
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Adrenergic Innervation ◽  
Systemic Blood ◽  
Low Cardiac Output ◽  
Neurohumoral Control ◽  
The Brain

Systemic blood pressure (BP) is the product of cardiac output and total peripheral resistance. Cardiac output is controlled by the heart rate, myocardial contractility, preload, and afterload. Vascular resistance (vascular hindrance × viscosity) is under local autoregulation and general neurohumoral control through sympathetic adrenergic innervation and circulating catecholamines. Sympathetic innovation predominates in organs receivingflowin excess of their metabolic demands (skin, splanchnic organs, kidney), while innervation is poor and autoregulation predominates in the brain and heart. The distribution of blood flow depends on the relative resistances of the organ circulations. During stress (hypoxia, low cardiac output), a raise in adrenergic tone and in circulating catecholamines leads to preferential vasoconstriction in highly innervated organs, so that blood flow is directed to the brain and heart. Catecholamines also control the levels of the vasoconstrictors renin, angiotensin II, and vasopressin. These general principles also apply to the neonate.

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