The Central Nervous System and Carbon Monoxide Poisoning II. Anatomical Study of Brain Lesions following Intoxication with Carbon Monoxide (22 cases)

1967 ◽  
pp. 31-74 ◽  
Author(s):  
J. Lapresle ◽  
M. Fardeau
Keyword(s):  
Central Nervous System ◽  
Carbon Monoxide ◽  
Nervous System ◽  
Carbon Monoxide Poisoning ◽  
Anatomical Study ◽  
Brain Lesions ◽  
The Central Nervous System

PROSPECTIVE METHODS FOR CORRECTION OF NEUROTOXIC IMPAIRMENTS CAUSED BY SEVERE CARBON MONOXIDE POISONING (REVIEW)

2017 ◽  
pp. 27-34
Author(s):  
P. G. Tolkach ◽  
V. A. Basharin ◽  
S. Kh. Sarmanaev
Keyword(s):  
Central Nervous System ◽  
Carbon Monoxide ◽  
Nervous System ◽  
Carbon Monoxide Poisoning ◽  
Complete Recovery ◽  
Intercellular Signaling ◽  
The Central Nervous System ◽  
Colonystimulating Factor ◽  
Review Reports ◽  
Stress Activation

The review sets forth perspective directions of correction of neurotoxic disorders in case of carbon monoxide damage. It was shown that carbon monoxide intoxication, in addition to the development of hemic hypoxia, leads to indirect lesions in the structures of the central nervous system that develop both in the early and delayed periods of poisoning. Those lesions can be caused by the development of oxidative stress, activation of programmed cell death, impact on the intercellular signaling system etc. There is evidence that oxygen monotherapy does not lead to a complete recovery of cognitive functions in a delayed period of severe carbon monoxide poisoning. It was found out that to correct central nervous system functions disorders in case of acute damage by carbon monoxide, it is necessary to use agents possessing neuroprotective mechanisms of action. The review reports data on the effectiveness of hydrogenated solution, methane solution, allopurinol, erythropoietin, granulocyte colonystimulating factor, remifentanil, mesenchymal stem cells, cerebrolysin for correction of the central nervous system disorders in this type of pathology.

Use of rituximab in lymphomatoid granulomatosis with isolated central nervous system involvement

2020 ◽  
Vol 13 (9) ◽  
pp. e235412
Author(s):  
Jesse Mooneyham ◽  
Cesar Gentille ◽  
Andrea Barbieri ◽  
Shilpan Shah
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Single Agent ◽  
Central Nervous System Involvement ◽  
Brain Lesions ◽  
The Body ◽  
Lymphomatoid Granulomatosis ◽  
Vasogenic Oedema ◽  
The Central Nervous System

A 33-year-old woman presented to the emergency room with severe headaches. A CT scan of the head revealed two brain lesions with associated vasogenic oedema. Diagnostic resection of one of the lesions followed by pathological analysis revealed grade III lymphomatoid granulomatosis (LYG). Staging investigations elsewhere in the body were negative, isolating this case of LYG to the central nervous system, an atypical presentation. After the resection, she was treated with single-agent rituximab 375 mg/m2. The follow-up MRI demonstrated the resolution of brain lesions and no progression of the disease.

scholarly journals Regenerative Potential of Carbon Monoxide in Adult Neural Circuits of the Central Nervous System

2020 ◽  
Vol 21 (7) ◽  
pp. 2273
Author(s):  
Eunyoung Jung ◽  
Seong-Ho Koh ◽  
Myeongjong Yoo ◽  
Yoon Kyung Choi
Keyword(s):  
Central Nervous System ◽  
Carbon Monoxide ◽  
Nervous System ◽  
Neurotrophic Factors ◽  
Neural Circuits ◽  
Cns Injury ◽  
Cns Regeneration ◽  
The Central Nervous System ◽  
Endogenous Neural Stem Cells

Regeneration of adult neural circuits after an injury is limited in the central nervous system (CNS). Heme oxygenase (HO) is an enzyme that produces HO metabolites, such as carbon monoxide (CO), biliverdin and iron by heme degradation. CO may act as a biological signal transduction effector in CNS regeneration by stimulating neuronal intrinsic and extrinsic mechanisms as well as mitochondrial biogenesis. CO may give directions by which the injured neurovascular system switches into regeneration mode by stimulating endogenous neural stem cells and endothelial cells to produce neurons and vessels capable of replacing injured neurons and vessels in the CNS. The present review discusses the regenerative potential of CO in acute and chronic neuroinflammatory diseases of the CNS, such as stroke, traumatic brain injury, multiple sclerosis and Alzheimer’s disease and the role of signaling pathways and neurotrophic factors. CO-mediated facilitation of cellular communications may boost regeneration, consequently forming functional adult neural circuits in CNS injury.

scholarly journals Toxicity of Shiga Toxin 1 in the Central Nervous System of Rabbits

2001 ◽  
Vol 69 (10) ◽  
pp. 6545-6548 ◽  
Author(s):  
Jun Fujii ◽  
Yoshimasa Kinoshita ◽  
Takashi Yutsudo ◽  
Hatsumi Taniguchi ◽  
Tom Obrig ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Spinal Cord ◽  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Magnetic Resonance ◽  
Shiga Toxin ◽  
Brain Lesions ◽  
Resonance Imaging ◽  
The Central Nervous System

ABSTRACT The action of Shiga toxin (Stx) on the central nervous system was examined in rabbits. Intravenous Stx1 was 44 times more lethal than Stx2 and acted more rapidly than Stx2. However, Stx1 accumulated more slowly in the cerebrospinal fluid than did Stx2. Magnetic resonance imaging demonstrated a predominance of Stx1-dependent lesions in the spinal cord. Pretreatment of the animals with anti-Stx1 antiserum intravenously completely protected against both development of brain lesions and mortality.

scholarly journals Abnormal Reaction to Central Nervous System Injury in Mice Lacking Glial Fibrillary Acidic Protein and Vimentin

1999 ◽  
Vol 145 (3) ◽  
pp. 503-514 ◽  
Author(s):  
Milos Pekny ◽  
Clas B. Johansson ◽  
Camilla Eliasson ◽  
Josefina Stakeberg ◽  
Åsa Wallén ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Glial Fibrillary Acidic Protein ◽  
Intermediate Filament ◽  
Glial Scar ◽  
Scar Formation ◽  
Brain Lesions ◽  
Acidic Protein ◽  
The Central Nervous System

In response to injury of the central nervous system, astrocytes become reactive and express high levels of the intermediate filament (IF) proteins glial fibrillary acidic protein (GFAP), vimentin, and nestin. We have shown that astrocytes in mice deficient for both GFAP and vimentin (GFAP−/−vim−/−) cannot form IFs even when nestin is expressed and are thus devoid of IFs in their reactive state. Here, we have studied the reaction to injury in the central nervous system in GFAP−/−, vimentin−/−, or GFAP−/−vim−/− mice. Glial scar formation appeared normal after spinal cord or brain lesions in GFAP−/− or vimentin−/− mice, but was impaired in GFAP−/−vim−/− mice that developed less dense scars frequently accompanied by bleeding. These results show that GFAP and vimentin are required for proper glial scar formation in the injured central nervous system and that some degree of functional overlap exists between these IF proteins.

scholarly journals Aino Virus Antigen in Brain Lesions of a Naturally Aborted Bovine Fetus

1998 ◽  
Vol 35 (5) ◽  
pp. 409-411 ◽  
Author(s):  
Y. Noda ◽  
Y. Uchinuno ◽  
H. Shirakawa ◽  
S. Nagasue ◽  
N. Nagano ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Brain Lesion ◽  
Neutralizing Antibody ◽  
Virus Antigen ◽  
Brain Lesions ◽  
Significant Feature ◽  
The Central Nervous System ◽  
The Brain

A bovine fetus aborted at 187 days of gestation was serologically and immunohistopathologically examined. Serum and cerebrospinal fluid samples had high titers of virus-neutralizing antibody for Aino virus. A severe necrotizing encephalopathy was noted. Aino virus antigen was demonstrated in neuroglial cells within the brain lesion. The destruction of developing neuronal cells appeared to be a significant feature of the pathogenesis of lesions due to Aino virus infection in the central nervous system.

Degeneration and regeneration of axons in the lesioned spinal cord

1996 ◽  
Vol 76 (2) ◽  
pp. 319-370 ◽  
Author(s):  
M. E. Schwab ◽  
D. Bartholdi
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Current Knowledge ◽  
Inflammatory Cells ◽  
Brain Lesions ◽  
Rapid Expansion ◽  
Tissue Loss ◽  
Growth Guidance ◽  
The Central Nervous System

For many decades, the inability of lesioned central neurons to regrow was accepted almost as a "law of nature", and on the clinical level, spinal cord and brain lesions were seen as being irreversible. Today we are starting to understand the mechanisms of neuronal regeneration in the central nervous system and its presence in the periphery. There is now a rapid expansion in this field of neuroscience. Developmental neurobiology has produced tools and concepts that start to show their impact on regeneration research. This is particularly true for the availability of antibodies and factors and for the rapidly growing cellular and molecular understanding of crucial aspects of neurite growth, guidance, target finding, and synapse stabilization. New cell biological concepts on the mechanisms of neuron survival and death and on the interaction of inflammatory cells with the central nervous system also find their way into the field of spinal cord and brain lesions and have, indeed, led already to new therapeutic approaches. This review briefly summarizes the current knowledge on the mechanisms involved in degeneration and tissue loss and in axonal regeneration subsequent to spinal cord lesions, particularly in mammals and humans.

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