scholarly journals Idiopathic inflammatory demyelinating disease of the central nervous system in patients with inflammatory bowel disease: retrospective analysis of 9095 patients

2014 ◽  
Vol 41 (1) ◽  
pp. 99-107 ◽  
Author(s):  
K. M. De Felice ◽  
M. Novotna ◽  
F. T. Enders ◽  
W. A. Faubion ◽  
W. J. Tremaine ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Retrospective Analysis ◽  
Bowel Disease ◽  
Demyelinating Disease ◽  
The Central Nervous System ◽  
Inflammatory Bowel

scholarly journals Neuroinflammation as an etiological trigger for depression comorbid with inflammatory bowel disease

2022 ◽  
Vol 19 (1) ◽  
Author(s):  
Colin F. Craig ◽  
Rhiannon T. Filippone ◽  
Rhian Stavely ◽  
Joel C. Bornstein ◽  
Vasso Apostolopoulos ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Bowel Disease ◽  
Structural Changes ◽  
Intestinal Inflammation ◽  
In Vivo Models ◽  
The Central Nervous System ◽  
Inflammatory Bowel

AbstractPatients with inflammatory bowel disease (IBD) suffer from depression at higher rates than the general population. An etiological trigger of depressive symptoms is theorised to be inflammation within the central nervous system. It is believed that heightened intestinal inflammation and dysfunction of the enteric nervous system (ENS) contribute to impaired intestinal permeability, which facilitates the translocation of intestinal enterotoxins into the blood circulation. Consequently, these may compromise the immunological and physiological functioning of distant non-intestinal tissues such as the brain. In vivo models of colitis provide evidence of increased blood–brain barrier permeability and enhanced central nervous system (CNS) immune activity triggered by intestinal enterotoxins and blood-borne inflammatory mediators. Understanding the immunological, physiological, and structural changes associated with IBD and neuroinflammation may aid in the development of more tailored and suitable pharmaceutical treatment for IBD-associated depression.

scholarly journals Putative Metronidazole Neurotoxicosis in a Cat

2005 ◽  
Vol 42 (5) ◽  
pp. 665-669 ◽  
Author(s):  
E. J. Olson ◽  
S. C. Morales ◽  
A. S. McVey ◽  
D. W. Hayden
Keyword(s):  
Inflammatory Bowel Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Supportive Care ◽  
Bowel Disease ◽  
Clinical Signs ◽  
Histologic Evaluation ◽  
The Central Nervous System ◽  
Inflammatory Bowel ◽  
Adult Cat

A presumptive case of metronidazole toxicity in a 3.4-kg adult cat is described. The cat had been treated for suspected inflammatory bowel disease with an anti-inflammatory dose of prednisone and metronidazole (73.5-147 mg/kg PO q24h) for approximately 40 days prior to presentation. Clinical signs were primarily related to the central nervous system, including acute tetraparesis, unresponsiveness, tremors, and vocalization. The patient was euthanatized after 12 days of supportive care. Necropsy revealed no significant macroscopic lesions. Histologic evaluation revealed multifocal, fairly well-demarcated foci of necrosis in the brainstem, extending from the diencephalon to the medulla oblongata. To our knowledge, this is the first report to document histologic lesions associated with metronidazole administration in a cat.

Inflammatory Bowel Disease and Risk of Birth Defects in Offspring

2020 ◽  
Vol 14 (5) ◽  
pp. 588-594
Author(s):  
Nathalie Auger ◽  
Justin Côté-Daigneault ◽  
Marianne Bilodeau-Bertrand ◽  
Laura Arbour
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Birth Defects ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Central Nervous System Defects

Abstract Background and Aims The relationship between inflammatory bowel disease in pregnancy and birth defects is not understood. We evaluated whether Crohn’s disease and ulcerative colitis in pregnant women were associated with the risk of birth defects in the offspring. Methods We undertook a retrospective cohort study of 2 184 888 pregnancies in Quebec, Canada, between 1989 and 2016. We calculated risk ratios [RR] and 95% confidence intervals [CI] for the association between inflammatory bowel disease and the risk of birth defects, using generalised estimating equations adjusted for maternal characteristics. We assessed associations in the period before 2000, when immunosuppressive biologic therapy and folic acid food fortification were not yet available, compared with the period after 2000 when these interventions were more widespread. Results This study included 13 099 women with Crohn’s disease and 7798 with ulcerative colitis. Crohn’s disease was associated with 1.90 times [95% CI 1.10–3.28] the risk of abdominal wall defects [gastroschisis, omphalocoele, and diaphragmatic hernia] and ulcerative colitis was associated with 1.53 times [95% CI 1.02–2.30] the risk of central nervous system defects. The association of Crohn’s disease with abdominal wall defects was stronger before 2000 [RR 3.62, 95% CI 1.71–7.67] than after 2000 [RR 1.23, 95% CI 0.55–2.75]. Ulcerative colitis was associated with central nervous system defects regardless of time period. Conclusions These findings suggest that inflammatory bowel disease is associated with the risk of abdominal wall and central nervous system defects, and that introduction of immunobiologic medications is unlikely to be associated with added risk. Podcast This article has an associated podcast which can be accessed at https://academic.oup.com/ecco-jcc/pages/podcast

scholarly journals Brain-Gut Interactions in Inflammatory Bowel Disease: Mechanisms of Anorexia in Animal Models of Experimental Colitis

1996 ◽  
Vol 10 (5) ◽  
pp. 329-334
Author(s):  
Harvey P Weingarten
Keyword(s):  
Inflammatory Bowel Disease ◽  
Central Nervous System ◽  
Bowel Disease ◽  
Cytokine Production ◽  
Experimental Colitis ◽  
Physiological Processes ◽  
Disease Mechanisms ◽  
The Central Nervous System ◽  
Inflammatory Bowel ◽  
The Brain

Physiological processes within the bowel are influenced constantly by signals from other organs, primarily the brain. The mechanisms by which inflammation of the gastrointestinal tract results in anorexia are unknown. Understanding how the inflammation-related signals in the periphery are communicated to the central nervous system and activate cytokine production in the brain remains an enormous challenge. Elucidation of these gut-brain communication mechanisms is essential to the development of appropriate and efficacious treatments for the eating and weight disturbances associated with inflammatory bowel disease.

scholarly journals Molecular Communication Between Neuronal Networks and Intestinal Epithelial Cells in Gut Inflammation and Parkinson's Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Alice Drobny ◽  
Phuong A. Ngo ◽  
Markus F. Neurath ◽  
Friederike Zunke ◽  
Rocío López-Posadas
Keyword(s):  
Parkinson’S Disease ◽  
Inflammatory Bowel Disease ◽  
Central Nervous System ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Intestinal Epithelial Cells ◽  
Alpha Synuclein ◽  
Intestinal Epithelial ◽  
The Central Nervous System ◽  
Inflammatory Bowel

Intestinal symptoms, such as nausea, vomiting, and constipation, are common in Parkinson's disease patients. These clinical signs normally appear years before the diagnosis of the neurodegenerative disease, preceding the occurrence of motor manifestations. Moreover, it is postulated that Parkinson's disease might originate in the gut, due to a response against the intestinal microbiota leading to alterations in alpha-synuclein in the intestinal autonomic nervous system. Transmission of this protein to the central nervous system is mediated potentially via the vagus nerve. Thus, deposition of aggregated alpha-synuclein in the gastrointestinal tract has been suggested as a potential prodromal diagnostic marker for Parkinson's disease. Interestingly, hallmarks of chronic intestinal inflammation in inflammatory bowel disease, such as dysbiosis and increased intestinal permeability, are also observed in Parkinson's disease patients. Additionally, alpha-synuclein accumulations were detected in the gut of Crohn's disease patients. Despite a solid association between neurodegenerative diseases and gut inflammation, it is not clear whether intestinal alterations represent cause or consequence of neuroinflammation in the central nervous system. In this review, we summarize the bidirectional communication between the brain and the gut in the context of Parkinson's disease and intestinal dysfunction/inflammation as present in inflammatory bowel disease. Further, we focus on the contribution of intestinal epithelium, the communication between intestinal epithelial cells, microbiota, immune and neuronal cells, as well as mechanisms causing alterations of epithelial integrity.

scholarly journals Acute Disseminated Encephalomyelitis (ADEM): A Demyelinating Disease with Specific Morphological Features

2021 ◽  
pp. 106689692199356
Author(s):  
Fleur Cordier ◽  
Lars Velthof ◽  
David Creytens ◽  
Jo Van Dorpe
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Differential Diagnosis ◽  
Clinical Case ◽  
Demyelinating Disease ◽  
Acute Disseminated Encephalomyelitis ◽  
Demyelinating Diseases ◽  
Demyelinating Disorder ◽  
Immune Mediated ◽  
The Central Nervous System

Acute disseminated encephalomyelitis (ADEM) is a rare immune-mediated inflammatory and demyelinating disorder of the central nervous system. Its characteristic perivenular demyelination and inflammation aid in the differential diagnosis with other inflammatory demyelinating diseases. Here, we present a clinical case of ADEM, summarize its histological hallmarks, and discuss pitfalls concerning the most important neuropathological differential diagnoses.

scholarly journals Biology of the repair of central nervous system demyelinated lesions: an appraisal

1996 ◽  
Vol 54 (2) ◽  
pp. 331-334 ◽  
Author(s):  
L. A. V Peireira ◽  
M. A. Cruz-Höfling ◽  
M. S. J. Dertkigil ◽  
D. L. Graça
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Schwann Cells ◽  
Demyelinating Disease ◽  
Experimental Models ◽  
Primitive Cell ◽  
Marked Influence ◽  
Myelin Sheaths ◽  
Human Material ◽  
The Central Nervous System

The integrity of myelin sheaths is maintained by oligodendrocytes and Schwann cells respectively in the central nervous system (CNS) and in the peripheral nervous system. The process of demyelination consisting of the withdrawal of myelin sheaths from their axons is a characteristic feature of multiple sclerosis, the most common human demyelinating disease. Many experimental models have been designed to study the biology of demyelination and remyelination (repair of the lost myelin) in the CNS, due to the difficulties in studying human material. In the ethidium bromide (an intercalating gliotoxic drug) model of demyelination, CNS remyelination may be carried out by surviving oligodendrocytes and/or by cells differentiated from the primitive cell lines or either by Schwann cells that invade the CNS. However, some factors such as the age of the experimental animals, intensity and time of exposure to the intercalating chemical and the topography of the lesions have marked influence on the repair of the tissue.

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