scholarly journals Evidence of Direct Toxicological Effects of Scorpion Venom on Central Nervous System in Tunisian Children

2018 ◽  
Vol 2018 ◽  
pp. 1-3 ◽  
Author(s):  
Mabrouk Bahloul ◽  
Basma Souissi ◽  
Olfa Turki ◽  
Mariem Dlela ◽  
Khaireddine Ben Mahfoudh ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Direct Action ◽  
Scorpion Venom ◽  
Neurological Manifestations ◽  
Scorpion Sting ◽  
Scorpion Envenomation ◽  
Toxicological Effects ◽  
Cerebral Mri ◽  
The Central Nervous System

Background. Severe scorpion envenomation can lead to severe neurological manifestations, which are an indicator of the severity of the scorpion sting. The direct action of scorpion venom on the central nervous system can explain partly these neurological disorders. Methods and Findings. We report a case of severe scorpion envenomation in 16-month-old boy with no pathological history admitted in ICU for severe scorpion envenomation. The result of cerebral MRI agrees with the hypothesis of direct action of scorpion venom on the central nervous system. Patient had improved; however, he has kept as neurological sequelae language disorders and blindness. The boy was discharged 21 days after ICU admission. Conclusion. Our observation confirms that severe scorpion envenomation can be complicated by severe neurological manifestations. Although one case report is not enough to conclude such important hypothesis regarding the direct effect of scorpion venom on central nervous system (especially that the age of patient is more than one year), our case agrees with this hypothesis.

Assessment of the relationship between the amount of scorpion venom in the central nervous system and the severity of scorpion envenomation in rats

Toxin Reviews ◽  
2019 ◽  
pp. 1-10
Author(s):  
Mehdi Ait Laaradia ◽  
Sara Oufquir ◽  
Moulay Abdelmonaim El Hidan ◽  
Fatimazahra Marhoume ◽  
Jawad Laadraoui ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Scorpion Venom ◽  
Scorpion Envenomation ◽  
The Central Nervous System ◽  
The Relationship

scholarly journals Infection of the central nervous system with dengue virus 3 genotype I causing neurological manifestations in Brazil

2016 ◽  
Vol 49 (1) ◽  
pp. 125-129 ◽  
Author(s):  
Danilo Bretas de Oliveira ◽  
Guilherme Machado ◽  
Gabriel Magno de Freitas Almeida ◽  
Paulo César Peregrino Ferreira ◽  
Cláudio Antônio Bonjardim ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Dengue Virus ◽  
Neurological Manifestations ◽  
Genotype I ◽  
The Central Nervous System

scholarly journals Elucidating the Neuropathologic Mechanisms of SARS-CoV-2 Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Mar Pacheco-Herrero ◽  
Luis O. Soto-Rojas ◽  
Charles R. Harrington ◽  
Yazmin M. Flores-Martinez ◽  
Marcos M. Villegas-Rojas ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Public Health Emergency ◽  
Converting Enzyme ◽  
Neurological Manifestations ◽  
Brain Areas ◽  
Angiotensin Converting Enzyme 2 ◽  
The Central Nervous System

The current pandemic caused by the new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a public health emergency. To date, March 1, 2021, coronavirus disease 2019 (COVID-19) has caused about 114 million accumulated cases and 2.53 million deaths worldwide. Previous pieces of evidence suggest that SARS-CoV-2 may affect the central nervous system (CNS) and cause neurological symptoms in COVID-19 patients. It is also known that angiotensin-converting enzyme-2 (ACE2), the primary receptor for SARS-CoV-2 infection, is expressed in different brain areas and cell types. Thus, it is hypothesized that infection by this virus could generate or exacerbate neuropathological alterations. However, the molecular mechanisms that link COVID-19 disease and nerve damage are unclear. In this review, we describe the routes of SARS-CoV-2 invasion into the central nervous system. We also analyze the neuropathologic mechanisms underlying this viral infection, and their potential relationship with the neurological manifestations described in patients with COVID-19, and the appearance or exacerbation of some neurodegenerative diseases.

Brain Respiration and Glycolysis in Cardiazol Convulsions

1940 ◽  
Vol 86 (361) ◽  
pp. 276-280 ◽  
Author(s):  
Leslie Dundonald MacLeod ◽  
Max Reiss
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Direct Action ◽  
Reducing Power ◽  
Liver Glycogen ◽  
Potassium Ions ◽  
Blood Picture ◽  
The Central Nervous System ◽  
Respiratory Centre ◽  
Convulsant Effect

Since Hildebrandt (1926) described the convulsant effect of cardiazol injection, several studies have been carried out on the mechanism of such convulsions. Zung and Tremonti (1931) suggested a direct action on the respiratory centre when cardiazol is used as a stimulant; Kerr and Antaki (1937) found no effect on brain glycogen or phosphocreatine in cardiazol-induced convulsions; Hashimoto (1937) found differences in distribution of calcium and potassium ions in the central nervous system after cardiazol. Goodwin and Lloyd (1938) recorded a direct effect on brain potential changes as shown on oscillographic records. Leibel and Hall (1938) found a large (75 per cent.) diminution of cerebral blood-flow at the onset of cardiazol convulsions. Weigand (1938) found no effect on liver glycogen or vitamin A content, reducing power of suprarenal cortex or blood picture. Denyssen and Watterson (1938) and Watterson and Macdonald (1939) attribute the convulsions to action on the vasomotor centre and note the action of vasodilator drugs in inhibiting convulsions. Wortis (1938) quoted by Quastel (1939) found no effect on brain respiration.

Interleukin-8 modulates feeding by direct action in the central nervous system

1993 ◽  
Vol 265 (4) ◽  
pp. R877-R882 ◽  
Author(s):  
C. R. Plata-Salaman ◽  
J. P. Borkoski
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Food Intake ◽  
Direct Action ◽  
Intraperitoneal Administration ◽  
Interleukin 8 ◽  
Short Term ◽  
Lipopolysaccharide Endotoxin ◽  
The Central Nervous System ◽  
Necrosis Factor

Interleukin-8 (IL-8) is released in response to infection, inflammation, and trauma. The most important stimuli for IL-8 release during these pathological processes are IL-1, tumor necrosis factor, and bacterial lipopolysaccharide (endotoxin), factors that have been shown to suppress feeding. In the present study, the participation of IL-8 on the central regulation of feeding was investigated. Intracerebroventricular (icv) microinfusion of recombinant human IL-8 (rhIL-8, 1.0-100 ng/rat) suppressed the short-term (2-h) food intake. The most effective dose of rhIL-8, 20 ng, decreased 2-h food intake by 25% and nighttime food intake by 23%. Intracerebroventricular microinfusion of anti-rhIL-8 antibody (200 and 500 ng) blocked the effect of 20 ng rhIL-8 on 2-h and nighttime food intakes. Computerized analysis of behavioral patterns for the 2-h period demonstrated a specific reduction of meal size (by 33%), whereas meal frequency and meal duration were not affected after the icv microinfusion of 20 ng rhIL-8. This short-term food intake suppression by icv rhIL-8 was accompanied by a small, but significant, increase in cerebrospinal fluid-brain and rectal temperatures. Intraperitoneal administration of rhIL-8 in doses equivalent to those administered centrally had no effect on food intake. The results suggest that IL-8 acts directly in the central nervous system to decrease feeding. This effect of IL-8 may contribute to the food intake suppression frequently accompanying pathological processes.

scholarly journals Signs and Symptoms of Central Nervous System Involvement and Their Pathogenesis in COVID-19 According to The Clinical Data (Review)

2021 ◽  
Vol 17 (3) ◽  
pp. 65-77
Author(s):  
N. V. Tsygan ◽  
A. P. Trashkov ◽  
A. V. Ryabtsev ◽  
V. A. Yakovleva ◽  
A. L. Konevega ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Data ◽  
Nervous Tissue ◽  
Central Nervous System Involvement ◽  
Signs And Symptoms ◽  
Neurological Manifestations ◽  
Altered Level ◽  
System Involvement ◽  
The Central Nervous System

Detailed clinical assessment of the central nervous system involvement in SARS-CoV-2 infection is relevant due to the low specificity of neurological manifestations, the complexity of evaluation of patient complaints, reduced awareness of the existing spectrum of neurological manifestations of COVID-19, as well as low yield of the neurological imaging.The aim. To reveal the patterns of central nervous system involvement in COVID-19 and its pathogenesis based on clinical data.Among more than 200 primary literature sources from various databases (Scopus, Web of Science, RSCI, etc.), 80 sources were selected for evaluation, of them 72 were published in the recent years (2016-2020). The criteria for exclusion of sources were low relevance and outdated information.The clinical manifestations of central nervous system involvement in COVID-19 include smell (5-98% of cases) and taste disorders (6-89%), dysphonia (28%), dysphagia (19%), consciousness disorders (3-53%), headache (0-70%), dizziness (0-20%), and, in less than 3% of cases, visual impairment, hearing impairment, ataxia, seizures, stroke. Analysis of the literature data revealed the following significant mechanisms of the effects of highly contagious coronaviruses (including SARS-CoV-2) on the central nervous system: neurodegeneration (including cytokine- induced); cerebral thrombosis and thromboembolism; damage to the neurovascular unit; immune-mediated damage of nervous tissue, resulting in infection and allergy-induced demyelination.The neurological signs and symptoms seen in COVID-19 such as headache, dizziness, impaired smell and taste, altered level of consciousness, bulbar disorders (dysphagia, dysphonia) have been examined. Accordingly, we discussed the possible routes of SARS-CoV-2 entry into the central nervous system and the mechanisms of nervous tissue damage.Based on the literature analysis, a high frequency and variability of central nervous system manifestations of COVID-19 were revealed, and an important role of vascular brain damage and neurodegeneration in the pathogenesis of COVID-19 was highlighted.

scholarly journals SARS-CoV-2 Impact on the Central Nervous System: Are Astrocytes and Microglia Main Players or Merely Bystanders?

2020 ◽  
Author(s):  
Veronica Murta ◽  
Alejandro Villarreal ◽  
Alberto Javier Ramos
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Manifestations ◽  
Signs And Symptoms ◽  
Experimental Models ◽  
Circumventricular Organs ◽  
Target Cells ◽  
Neurological Manifestations ◽  
Cns Inflammation ◽  
The Central Nervous System

With confirmed COVID-19 cases surpassing the 8.5 million mark around the globe, there is an imperative need to deepen the efforts from the international scientific community to gain comprehensive understanding of SARS-CoV-2. Although the main clinical manifestations are associated with respiratory or intestinal symptoms, reports of specific and non-specific neurological signs and symptoms, both at presentation or during the course of the acute phase, are increasing. Approximately 25-40% of the patients present neurological symptoms. The etiology of these neurological manifestations remains obscure, and probably involves several direct pathways, not excluding the direct entry of the virus to the Central Nervous System (CNS) through the olfactory epithelium, circumventricular organs, or disrupted blood-brain barrier (BBB). Furthermore, neuroinflammation might occur in response to the strong systemic cytokine storm described for COVID-19, or due to dysregulation of the CNS angiotensin system. Descriptions of neurological manifestations in patients in the previous coronavirus (CoV) outbreaks have been numerous for the SARS-CoV and lesser for MERS-CoV. Strong evidence from patients and experimental models suggests that some human variants of CoV have the ability to reach the CNS and that neurons, astrocytes and/or microglia can be target cells for CoV. A growing body of evidence shows that astrocytes and microglia have a major role in neuroinflammation, responding to local CNS inflammation and/or to dysbalanced peripheral inflammation. This is another potential mechanism for SARS-CoV-2 damage to the CNS. In this work we will summarize the known neurological manifestations of SARS-CoV-2, SARS-CoV and MERS-CoV, explore the potential role for astrocytes and microglia in the infection and neuroinflammation, and compare them with the previously described human and animal CoV that showed neurotropism. We also propose possible underlying mechanisms by focusing on our knowledge of glia, neurons, and their dynamic intricate communication with the immune system.

Pharmacological Induction of Plasticization in the Abdominal Cuticle of Rhodnius

1974 ◽  
Vol 61 (3) ◽  
pp. 705-718
Author(s):  
STUART E. REYNOLDS
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Hormone Receptor ◽  
Body Wall ◽  
Direct Action ◽  
The Body ◽  
Malpighian Tubules ◽  
Diuretic Hormone ◽  
The Central Nervous System ◽  
The Relationship

Injections of 5-hydroxytryptamine (5-HT, serotonin) are found to cause plasticization of the abdominal cuticle of Rhodnius larvae. This plasticization is a direct action of 5-HT on some element in the body wall; the central nervous system is not required. It is probable that 5-HT acts directly at a receptor on the epidermal cells. The relationship between structure and plasticizing activity for a number of 5-HT analogues has been investigated. The receptor resembles other ‘classical’ 5-HT receptors in its requirements, but is unlike the 5-HT/diuretic hormone receptor of Rhodnius Malpighian tubules.

Sign in / Sign up

Export Citation Format

Share Document