Editing Diffuse axonal injury (section)

===Cytoskeleton disruption===
[[File:APP immunostaining in a mouse brain after traumatic brain injury.png|thumb| Immunoreactive axonal profiles are observed as either granular (B, G, H) or more elongated, fusiform (F) swellings in the [[corpus callosum]] and the [[brain stem]] (H) at 24h post [[traumatic brain injury]]. Example of APP immunoreactive neurons (arrow heads) observed in the [[Cerebral cortex|cortex]] underneath the impact site (E, G). No APP staining was observed in healthy control animals (D).<ref name="Mouzon2012"/>
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Axons are normally elastic, but when rapidly stretched they become brittle, and the axonal [[cytoskeleton]] can be broken. Misalignment of cytoskeletal elements after stretch injury can lead to tearing of the axon and death of the neuron. [[Axonal transport]] continues up to the point of the break in the cytoskeleton, but no further, leading to a buildup of transport products and local swelling at that point.<ref name="Staal">{{cite journal | vauthors = Staal JA, Dickson TC, Chung RS, Vickers JC | year = 2007 | title = Cyclosporin-A treatment attenuates delayed cytoskeletal alterations and secondary axotomy following mild axonal stretch injury | journal = Developmental Neurobiology | volume = 67 | issue = 14| pages = 1831–1842 | pmid = 17702000 | doi = 10.1002/dneu.20552 | s2cid = 19415197 | url = https://figshare.com/articles/journal_contribution/22860839 }}</ref> When this swelling becomes large enough, it can tear the axon at the site of the cytoskeleton break, causing it to draw back toward the cell body and form a bulb.<ref name="Smith"/> This bulb is called a "retraction ball", the [[histology|histological]] hallmark of diffuse axonal injury.<ref name="Wasserman"/>

When the axon is torn, [[Wallerian degeneration]], in which the part of the axon distal to the break degrades, takes place within one to two days after injury.<ref name="Lopachin">{{cite journal | author = LoPachin RM, Lehning EJ | year = 1997 | title = Mechanism of calcium entry during axon injury and degeneration | journal = [[Toxicology and Applied Pharmacology]] | volume = 143 | issue = 2| pages = 233–244 | pmid = 9144441 | doi = 10.1006/taap.1997.8106 | bibcode = 1997ToxAP.143..233L }}</ref> The axolemma disintegrates,<ref name="Lopachin"/> myelin breaks down and begins to detach from the cell in an anterograde direction (from the body of the cell toward the end of the axon),<ref name="Cowie">{{cite web |vauthors=Cowie RJ, Stanton GB |year=2005 |url=http://www.med.howard.edu/anatomy/gas/wk12/Lect.%2037_Axoplasmic%20Flow,%20injury.htm |title=Axoplasmic transport and neuronal responses to injury |archive-url=https://web.archive.org/web/20051029215534/http://www.med.howard.edu/anatomy/gas/wk12/Lect.%2037_Axoplasmic%20Flow%2C%20injury.htm |archive-date=2005-10-29 |publisher=Howard University College of Medicine |access-date=2008-01-17}}<!--♦♦♦web♦♦♦--></ref> and nearby cells begin [[phagocytosis|phagocytic]] activity, engulfing the cellular debris.<ref>{{cite journal | vauthors = Hughes PM, Wells GM, Perry VH, Brown MC, Miller KM | year = 2002 | title = Comparison of matrix metalloproteinase expression during wallerian degeneration in the central and peripheral nervous systems | journal = Neuroscience | volume = 113 | issue = 2| pages = 273–287 | pmid = 12127085 | doi = 10.1016/s0306-4522(02)00183-5 | s2cid = 37213275 }}</ref>