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Contusional brain injury and intracerebral haemorrhage
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
These occur as a result of very severe head injury with short survival. The pattern is seen macroscopically and more readily microscopically with small haemorrhages occurring around blood vessels (see Chapter 11). These are particularly prominent in the frontal and temporal lobes, adjacent to midline structures and in the stem adjacent to the aqueduct and floor of the fourth ventricle. They are often associated with ‘tissue tear’ haemorrhages (see below). The precise aetiology is unclear but is probably related to vascular damage at the time of injury in association with primary axotomy. The majority of cases occur after road traffic incidents. Macroscopic differential diagnosis includes rare conditions such as acute haemorrhagic leukoencephalopathy (see Chapter 18).
The Pathophysiology of Traumatic Brain Injury
Published in Mark R. Lovell, Ruben J. Echemendia, Jeffrey T. Barth, Michael W. Collins, Traumatic Brain Injury in Sports, 2020
Christopher C. Giza, David A. Hovda
Even in the absence of significant degenerative change, concussive brain injury induces a complex pathophysiological cascade that begins with immediate disturbances of ionic flux, neurotransmitter release, glucose metabolism and cerebral blood flow. In an animal experimental model, acute increases in glucose utilization give way to diminished glycolysis and oxidative metabolism which may persist a week or longer. Calcium influx occurs early and recovers more rapidly, usually over several days. Axonal injury may be immediate, but delayed secondary axotomy has been reported weeks after injury in humans. Persistent dysfunction in excitatory and inhibitory neurotransmission is a potential mechanism for chronic cognitive and neurobehavioral symptoms following brain concussion. Current guidelines for return to play only upon resolution of all neurocognitive deficits are a good starting point, but more precise time-windows may be elucidated with increasing understanding of and improved ability to monitor specific derangements such as cerebral glucose metabolism, regional brain activation, and neurotransmitter levels.
Neurotrophic Factors
Published in Martin Berry, Ann Logan, CNS Injuries: Cellular Responses and Pharmacological Strategies, 2019
The extensive use of the septohippocampal axotomy model, at a time when NGF was the only neurotrophic factor available in sufficiently large quantities for experimentation in adult animals, has enabled the formulation of many fundamental concepts about neurotrophic factors. Advances in the understanding about degeneration and regeneration of the cholinergic basal forebrain neurons have been reviewed extensively elsewhere.67 Over a 2-week period following transection of the fimbriafornix, which interrupts the septohippocampal axons, ∼70% of the axotomized cholinergic neurons disappear. Over this period, these neurons atrophy and lose their markers ChAT, TrkA, and p75NGFR by which they can be identified among other more numerous septohippocampal and septal neurons.55,68–70 As is the case with other types of neurons, axotomy closer to the cell body causes greater apparent cell loss.71 Whether this is due to an increased severity of the lesion or to decreased support by cells around the removed portions of the axons remains to be resolved.
Thymoquinone protects DRG neurons from axotomy-induced cell death
Published in Neurological Research, 2018
Ramazan Üstün, Elif Kaval Oğuz, Ayşe Şeker, Hasan Korkaya
In contrast control group, the axons in the axotomy and experimental groups were divided into two parts: distal parts and proximal parts, following the axotomization with the laser beam (Figure 2d, f, h). Both proximal and distal sections suddenly retracted back a few to tens of micrometers (Figure 2d, f, h). In the distal segments, axons lost their integrity and neuronal attachment (Figure 2d, f, h) and that resulted in their degeneration followed by beading, fragmentation, and disappearance (Figure 2d, h). The proximal section was either fragmented or retracted to cell body (Figure 2d, h). Neuronal cell deaths have rapidly followed the fragmentation (it was not shown). In retraction, the axon initially began to withdraw back to perikaryon, and the proximal section retained its integrity with the cell body (Figure 2d). In axotomy group, after the injured neuron has overcome cut stress and briefly continued axon outgrowth. The outgrowing axons were weak and thin (Figure 3e, g, h) (video 2, red arrowhead).
Peripheral nerve injury and axonotmesis: State of the art and recent advances
Published in Cogent Medicine, 2018
Rui Alvites, Ana Rita Caseiro, Sílvia Santos Pedrosa, Mariana Vieira Branquinho, Giulia Ronchi, Stefano Geuna, Artur S.P. Varejão, Ana Colette Maurício
It is known that the peripheral nervous system (PNS) presents a better reparative and regenerative capacity than the central nervous system (CNS), and this difference is based essentially on the characteristics of the functional environments in each one of the systems (Lutz & Barres, 2014), the age of the injured individual, the type of injury observed and the integrity of the neural cell body of the injured nerve (Faroni, Mobasseri, Kingham, & Reid, 2015). Nevertheless, ineffective functional recovery is common in the injured peripheral nerve, particularly due to phenomena of chronic axotomy, chronic Schwann cell denervation (Sulaiman & Gordon, 2013) or severe disruption of endoneurial tubes that prevent normal progression of the regenerative process (Burnett & Zager, 2004). Muscular denervation is most often secondary to the injury of the corresponding peripheral nerve and manifests mainly by neurogenic atrophy and structural fibrosis (Sulaiman & Gordon, 2013). The muscle tends to atrophy as the bare fibers shrink and lose their ability to expand (Krarup, Boeckstyns, Ibsen, Moldovan, & Archibald, 2016).
Advances in molecular therapies for targeting pathophysiology in spinal cord injury
Published in Expert Opinion on Therapeutic Targets, 2023
Ha Neui Kim, Madeline R. McCrea, Shuxin Li
It will be interesting to study regeneration-associated genes recently identified from other cell types. A single-cell transcriptomic study from different RGC types has identified multiple genes to regulate RGC survival and regeneration after ONC, including CRH, GAL, WT1, galanin, and UCN [122]. Upregulating these proteins or neuropeptides promoted significant axon regeneration of RGCs after axotomy. Upregulating protrudin, a scaffold protein, could boost the accumulation of integrins, RAB11 endosomes, and ERs in axons and promote RGC axon regeneration [123]. PTPN2 inhibition combined with low-dose IFNγ enhanced regeneration of CNS axons through the cGAS-STING downstream pathway by amplifying IFNγ-STAT1 signaling [124]. Local treatment with M1, a small molecule that potentially promotes mitochondrial fusion and transport, enhanced in vivo axon regeneration of peripheral neurons, injured RGCs, and visual function in mice with ONC [125]. This group also reported that treatments with the small-molecule glycopyrrolate, an FDA-approved drug used to treat excessive sweating, promoted peripheral nerve regeneration, RGC survival, and sustained functional RGC regeneration in mice with ONC [126]. In C. Elegans, DLK-mediated injury signaling might activate autophagy, which suppressed axon regeneration by reducing the level of LIN-12 and NOTCH proteins [127]. A transcriptome profiling study in fly sensory neurons suggested the expression of ringer, a microtubule-associated protein, in sensory neurons before and after injury and its requirement for axon regeneration following the deletion of Rtca, a protein that regulates RNA metabolism [128].