File:11916 2023 1209 Fig1 HTML.webp
Size of this PNG preview of this WEBP file: 418 × 599 pixels. Other resolutions: 167 × 240 pixels | 335 × 480 pixels | 685 × 981 pixels.
Original file (685 × 981 pixels, file size: 116 KB, MIME type: image/webp)
File information
Structured data
Captions
Summary edit
Description11916 2023 1209 Fig1 HTML.webp |
English: Comprehensive overview of pathophysiology of trigeminal postherpetic neuralgia (TG-PHN). A VZV reactivation predominately occurs from V1 distribution of the trigeminal ganglia. B Representation of cellular response at the site of reactivation highlighting the (1) inflammatory response involving macrophages, T cells, mast cells, and blood vessels; (2) changes in trigeminal afferents, particularly alterations in nociceptors influencing pain signaling such as TRVP1/TRPA1, CGRP, NK-1R, and purinergic receptors P2XR, along with associated ligands like substance P (SubP) and CGRP, ultimately resulting in (3) loss of nerve fibers and sensory innervation. C Representation of VZV reactivation and (4) viral replication of VZV and associated inflammation in the trigeminal ganglia. This leads to (5) cell death and can cause (6) hypersensitivity in the ganglionic neurons, increasing pain signals to the brainstem. Hypersensitivity can also be attributed to increases in neurotransmitters CGRP, SubP, and ATP. D Trigeminal ganglionic neurons transmit signals to the spinal trigeminal ganglia, specifically the caudal subunit (SNVc), which transmits nociception and thermal sensation. Neuroinflammation, including (8) astrogliosis and microglia activation, can cause disruption in the microenvironment within the brainstem. The increase of neurotransmitters, shown in C, is also released onto second-order neurons. Along with a decrease in inhibitory GABAergic signaling, together leads to (9) an increase in pain signaling. E Represents the pain signaling pathway from SNVc to the ventral posteromedial nucleus (VPM), where it has been shown to decrease GABAergic signaling in the thalamus, increasing pain signaling relayed to cortical structures. F These pathophysiological changes ultimately lead to the wide array of pain qualities associated with TG-PHN as represented in this artistic depiction reprinted with permission from Ref. [26]. Figure 1 was created with BioRender.com |
Date | |
Source | https://link.springer.com/article/10.1007/s11916-023-01209-z |
Author | Christy S. Niemeyer, Michael Harlander-Locke, Andrew N. Bubak, Rachael Rzasa-Lynn & Marius Birlea |
Licensing edit
This file is licensed under the Creative Commons Attribution 4.0 International license.
- You are free:
- to share – to copy, distribute and transmit the work
- to remix – to adapt the work
- Under the following conditions:
- attribution – You must give appropriate credit, provide a link to the license, and indicate if changes were made. You may do so in any reasonable manner, but not in any way that suggests the licensor endorses you or your use.
This media file is uncategorized.
Please help improve this media file by adding it to one or more categories, so it may be associated with related media files (how?), and so that it can be more easily found.
Please notify the uploader with {{subst:Please link images|File:11916 2023 1209 Fig1 HTML.webp}} ~~~~ |
File history
Click on a date/time to view the file as it appeared at that time.
Date/Time | Thumbnail | Dimensions | User | Comment | |
---|---|---|---|---|---|
current | 21:34, 31 March 2024 | 685 × 981 (116 KB) | Ozzie10aaaa (talk | contribs) | Uploaded a work by Christy S. Niemeyer, Michael Harlander-Locke, Andrew N. Bubak, Rachael Rzasa-Lynn & Marius Birlea from https://link.springer.com/article/10.1007/s11916-023-01209-z with UploadWizard |
You cannot overwrite this file.
File usage on Commons
There are no pages that use this file.