Structure and function of retinal ganglion cells in subjects with a history of repeated traumatic brain injury

Klimo, Kelly R.; Stern-Green, Elizabeth A.; Shelton, Erica; Day, Elizabeth; Jordan, Lisa; Robich, Matthew; Racine, Julie; McDaniel, Catherine; VanNasdale, Dean A.; Yuhas, Phillip T.

doi:10.3389/fneur.2022.963587

Cited by 5 publications

(9 citation statements)

References 64 publications

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“…The work reported here is part of a larger project that sought to characterize retinal structure and function in participants with a history of multiple traumatic brain injuries. Some of the results of this larger study already have been reported ( 16 ).…”

Section: Methodssupporting

confidence: 57%

“…Details about the study participants, including comprehensive TBIs histories, are reported in a companion study ( 16 ). Briefly, twenty-five ( n = 25) case participants [mean ± standard deviation (SD) age = 32.2 ± 11.8 years; 52% female; 100% White] enrolled in the study.…”

Section: Resultsmentioning

confidence: 99%

“…The objective function of the human retina after multiple TBIs is also poorly characterized. Tzekov and colleagues used electroretinography (ERG) to demonstrate a reduced photopic negative response amplitude, a marker of RGC function ( 14 ), in a mouse model of repeated TBI ( 15 ), but this finding was not replicated in a human population with a history of multiple TBIs ( 16 ). Moreover, Freed and Hellerstein did not find abnormalities in the aspects of the full-field flash ERG (fERG) waveform driven by photoreceptors and bipolar cells in participants with a “documented mild TBI” ( 17 ).…”

Section: Introductionmentioning

confidence: 99%

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Henle fiber layer thickening and deficits in objective retinal function in participants with a history of multiple traumatic brain injuries

Stern-Green,

Klimo,

Day

et al. 2024

Front. Neurol.

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IntroductionThis study tested whether multiple traumatic brain injuries (TBIs) alter the structure of the Henle fiber layer (HFL) and degrade cell-specific function in the retinas of human participants.MethodsA cohort of case participants with multiple TBIs and a cohort of pair-matched control participants were prospectively recruited. Directional optical coherence tomography and scanning laser polarimetry measured HFL thickness and phase retardation, respectively. Full-field flash electroretinography (fERG) assessed retinal function under light-adapted (LA) 3.0, LA 30 Hz, dark-adapted (DA) 0.01, DA 3.0, and DA 10 conditions. Retinal imaging and fERG outcomes were averaged between both eyes, and paired t-tests or Wilcoxon signed-rank tests analyzed inter-cohort differences.ResultsGlobal HFL thickness was significantly (p = 0.02) greater in cases (8.4 ± 0.9 pixels) than in controls (7.7 ± 1.1 pixels). There was no statistically significant difference (p = 0.91) between the cohorts for global HFL phase retardation. For fERG, LA 3.0 a-wave amplitude was significantly reduced (p = 0.02) in cases (23.5 ± 4.2 μV) compared to controls (29.0 ± 8.0 μV). There were no other statistically significant fERG outcomes between the cohorts.DiscussionIn summary, the HFL thickens after multiple TBIs, but phase retardation remains unaltered in the macula. Multiple TBIs may also impair retinal function, indicated by a reduction in a-wave amplitude. These results support the potential of the retina as a site to detect TBI-associated pathology.

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Section: Methodssupporting

confidence: 57%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Henle fiber layer thickening and deficits in objective retinal function in participants with a history of multiple traumatic brain injuries

Stern-Green,

Klimo,

Day

et al. 2024

Front. Neurol.

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“…This type of injury first arises in the axonal head and by disorganization of the cytoskeleton and transport mechanisms, this in turn deteriorates the axon and the soma of the affected cell through a Ca2+ and calpain-induced process [53]. Even now, it is still a matter of debate if the surviving GCs will be able to maintain normal visual function in a long term [52, 54, 55], thus further studies are required in the future in this subject.…”

Section: Discussionmentioning

confidence: 99%

Traumatic brain injury induced microglial and Caspase3 activation in the retina

Kovács-Öller

Zempléni

Balogh

et al. 2022

Preprint

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Traumatic brain injury (TBI) is among the main causes of sudden death after head trauma. These injuries can result in severe degeneration and neuronal cell death in the CNS, including the retina which is a crucial part of the brain responsible for perceiving and transmitting visual information. The long-term effects of mild-repetitive TBI (rmTBI) are far less studied thus far, even though damages induced by repetitive injuries occurring in the brain are more common, especially amongst athletes. rmTBI can also have a detrimental effect on the retina and the pathophysiology of these injuries are likely to differ from the severe TBI (sTBI) retinal injury. Here we showed how rmTBI and sTBI can dissimilarly affect the retina. Our results indicate an increase in the number of activated microglial cells and Caspase3-positive cells in the retina in both traumatic models, suggesting a rise in the level of inflammation and cell death after TBI. The pattern of microglial activation appears evenly distributed and widespread but differs amongst the various retinal layers. sTBI induced microgial activation in both the superficial and deep retinal layers. In contrast to sTBI, no significant change occurred following the repetitive mild injury in the superficial layer, only the deep layer (spanning from the inner nuclear layer to the outer plexiform layer) shows microglial activation. This difference suggests that alternate response mechanisms play a role in the case of the different TBI incidents. The Caspase3 activation pattern showed a uniform increase in both the superficial and deep layers of the retina. This suggests a different action in the course of the disease in sTBI and rmTBI models and points to the need for new diagnostic procedures. Our present results suggest that the retina might serve as such a model of head injuries since the retinal tissue reacts to both forms of TBI and is the most accessible part of the human brain.

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“…This type of injury first arises in the axonal head and by disorganization of the cytoskeleton and transport mechanisms, this in turn deteriorates the axon and the soma of the affected cell through a Ca2 + and calpain-induced process [44]. Even now, it is still a matter of debate if the surviving GCs will be able to maintain normal visual function in a long term [44,46,47], thus further studies are required in the future in this subject.…”

Section: Caspase3 Activation Cell Death Markermentioning

confidence: 99%

Traumatic Brain Injury Induced Microglial and Caspase3 Activation in the Retina

Kovács-Öller¹,

Zempléni²,

Balogh³

et al. 2023

Preprint

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A Traumatic brain injury (TBI) is among the main causes of sudden death after head trauma. These injuries can result in severe degeneration and neuronal cell death in the CNS, including the retina which is a crucial part of the brain responsible for perceiving and transmitting visual information. The long-term effects of mild-repetitive TBI (rmTBI) are far less studied thus far, even though damages induced by repetitive injuries occurring in the brain are more common, especially amongst athletes. rmTBI can also have a detrimental effect on the retina and the pathophysiology of these injuries are likely to differ from the severe TBI (sTBI) retinal injury.Here we showed how rmTBI and sTBI can dissimilarly affect the retina. Our results indicate an increase in the number of activated microglial cells and Caspase3-positive cells in the retina in both traumatic models, suggesting a rise in the level of inflammation and cell death after TBI. The pattern of microglial activation appears evenly distributed and widespread but differs amongst the various retinal layers. sTBI induced microgial activation in both the superficial and deep retinal layers. In contrast to sTBI, no significant change occurred following the repetitive mild injury in the superficial layer, only the deep layer (spanning from the inner nuclear layer to the outer plexiform layer) shows microglial activation. This difference suggests that alternate response mechanisms play a role in the case of the different TBI incidents. The Caspase3 activation pattern showed a uniform increase in both the superficial and deep layers of the retina. This suggests a different action in the course of the disease in sTBI and rmTBI models and points to the need for new diagnostic procedures.Our present results suggest that the retina might serve as such a model of head injuries since the retinal tissue reacts to both forms of TBI and is the most accessible part of the human brain.

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Structure and function of retinal ganglion cells in subjects with a history of repeated traumatic brain injury

Cited by 5 publications

References 64 publications

Henle fiber layer thickening and deficits in objective retinal function in participants with a history of multiple traumatic brain injuries

Henle fiber layer thickening and deficits in objective retinal function in participants with a history of multiple traumatic brain injuries

Traumatic brain injury induced microglial and Caspase3 activation in the retina

Traumatic Brain Injury Induced Microglial and Caspase3 Activation in the Retina

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