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Section of midbrain of a case of chronic traumatic encephalopathy (CTE) showing tau-immunoreactive pathology (brown immunolabelling) in various nuclei and fibre tracts (CA: cerebral aqueduct, Csp: cortico-spinal tract, FPon: fronto-pontine fibres, ML: medial lemniscus, MLF: medial longitudinal fasciculus, PAG: periqueductal gray, SC: superior colliculus, SCP: superior cerebellar peduncle, SN: substantia nigra, TrN: trochlear nucleus). Pathology is particularly evident in the SC, SN, and TrN. Tau immunohistochemistry (AT8, haematoxylin).

Section of midbrain of a case of chronic traumatic encephalopathy (CTE) showing tau-immunoreactive pathology (brown immunolabelling) in various nuclei and fibre tracts (CA: cerebral aqueduct, Csp: cortico-spinal tract, FPon: fronto-pontine fibres, ML: medial lemniscus, MLF: medial longitudinal fasciculus, PAG: periqueductal gray, SC: superior colliculus, SCP: superior cerebellar peduncle, SN: substantia nigra, TrN: trochlear nucleus). Pathology is particularly evident in the SC, SN, and TrN. Tau immunohistochemistry (AT8, haematoxylin).

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Traumatic brain injury (TBI) and its associated concussion are major causes of disability and death. All ages can be affected but children, young adults and the elderly are particularly susceptible. A decline in mortality has resulted in many more individuals living with a disability caused by TBI including those affecting vision. This review descr...

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... Hence, functional magnetic resonance imaging (fMRI) studies of oculomotor control nuclei during vergence and saccadic eye movement have revealed bilateral signals in control patients originating in the superior colliculus and oculomotor and abducens nuclei, such signals being significantly reduced in chronic TBI. 68 Various pathological changes have also been observed in the midbrain in some cases of CTE affecting the superior colliculus and associated nuclei and in fibre tracts controlling eye movement 125 (Figure 1). In addition, examination of eye movement enables higher cortical functioning and the involvement of many diffuse brain pathways to be assessed. ...
Context 2
... Hence, func- tional magnetic resonance imaging (fMRI) studies of oculomotor control nuclei during vergence and saccadic eye movement have revealed bilateral signals in control patients originating in the superior colliculus and oculomotor and abducens nuclei, such sig- nals being significantly reduced in chronic TBI. 68 Various pathological changes have also been observed in the midbrain in some cases of CTE affecting the superior colliculus and associated nuclei and in fibre tracts controlling eye movement 125 (Figure 1). In addition, examination of eye movement enables higher cortical functioning and the involvement of many diffuse brain pathways to be assessed. ...

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... For example, both traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) create profound effects on the structure and function of the brain, influencing how individuals process and respond to visual stimuli. TBI, often resulting from sudden impacts to the head, can lead to defects in primary vision, eye movement, saccadic and smooth pursuit movements, motion vision, and visuo-spatial function (Armstrong, 2018). The visual reaction time of patients with head injuries is slower than that of healthy control individuals (Levin, 1998). ...
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... It has been suggested that axonal damage at the brainstem can elicit eye movement abnormalities resulting in delayed response to stimuli and during pursuit tasks (18). The neuro-ophthalmological function is a pivotal marker for brain damage as it seems sensitive to traumatic and mild traumatic brain injuries (1,7,30). The impairment of neuro-ophthalmological function in patients following a concussion correlates with the severity of concussion symptoms (5,12,19,29). ...
... V isual problems following acquired brain injury (ABI) are a complex and multifaceted condition (1) that poses significant challenges to individuals (2), healthcare professionals, and society (3)(4)(5)(6). Various aspects of visual processing lead to a wide range of visual impairments (7), including reduced visual acuity, visual field defects, oculomotor dysfunction, binocular vision abnormalities, and higher-level visual processing deficits (8). The prevalence of overall visual problems after ABI has been estimated to range from 54% to 73% (9,10), depending on the type of problem, time of assessment, and assessment methods used. ...
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... The prevalence of vision impairment in neurodegenerative conditions such as multiple sclerosis, Alzheimer's disease, and Parkinson's disease, has been reported between 1.7-58% [5][6][7]. However, studies often consist of small numbers, with some authors considering visual acuity decline as the only measure of vision impairment [3,5], without considering other visual impairments that may occur following neurological impairment such as, difficulties with visual field loss, ocular motility disorders, and visual perceptual deficits [8,9]. ...
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... Several studies have reported prolonged visual symptoms in PCS. 34,36,41 It has been hypothesized that with the heavy burden of the visual sensory system, some other common persistent symptoms, such as headache and dizziness, may result from mismatched perceptions between central and peripheral visual processing, highlighting potential oculomotor and neuro-visual dysfunction. 42 Standard vision training therapy conducted by an optometrist is usually indicated for strabismus, phorias, and binocular vision deficiencies, and more often, it uses established oculomotor methods. ...
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... Another study reported ongoing decline in retinal nerve fiber layer thickness in a longitudinal cohort following patients over several years [41]. Visual problems associated with TBI are heterogeneous and can vary depending on the type of injury and its severity [46], but vision impairment represents an important functional outcome that should be included in preclinical and clinical studies. In this study we used a moderate to severe model of TBI consisting of a right-sided controlled cortical impact to the dura mater. ...
... It is unclear how delayed administration of a complement inhibitor would impact visual outcomes. However, the rate of disability, and particularly visual disability is quite high after TBI [46], which means that many individuals will have missed the window for acute complement inhibitor treatment. We have previously reported on inflammatory outcomes with delayed treatment paradigms in which a complement inhibitor was administered beginning either at 7, 28 or 56 days after CCI [10,11]. ...
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... Given that approximately half of the brain's neural pathways are dedicated to vision, the visual system is particularly vulnerable to shearing injury following mTBI 11 . As a result, considerable attention has been drawn to a variety of visual impairments associated with mild traumatic brain injury (mTBI) [12][13][14] , including defects in visual acuity 15 , blurred vision 12 , deficits in accommodation 16 and binocular disparity 17 . However, little attention has been given to the perception of visual stimuli or the integration of visual information following mTBI. ...
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... Traumatic brain injury (TBI) is a leading cause of morbidity and disability across multiple domains (1), including psychiatric health, pain, cognition, and somatic complications involving cardiovascular, respiratory, endocrine, urinary, visual, and gastrointestinal systems (1)(2)(3)(4)(5)(6)(7)(8). Consequently, individuals who sustained a TBI are reported to have high rates of medication use, and studies show that 45-85% of TBI patients are prescribed psychotropic and pain medications (9)(10)(11)(12)(13)(14)(15)(16)(17). ...
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Introduction Traumatic brain injury (TBI) is associated with health problems across multiple domains and TBI patients are reported to have high rates of medication use. However, prior evidence is thin due to methodological limitations. Our aim was thus to examine the use of a wide spectrum of medications prescribed to address pain and somatic conditions in a population-based cohort of TBI patients, and to compare this to a sex- and age-matched cohort. We also examined how patient factors such as sex, age, and TBI severity were associated with medication use. Methods We assessed Swedish nationwide registers to include all individuals treated for TBI in hospitals or specialist outpatient care between 2006 and 2012. We examined dispensed prescriptions for eight different non-psychotropic medication classes for the 12 months before, and 12 months after, the TBI. We applied a fixed-effects model to compare TBI patients with the matched population cohort. We also stratified TBI patients by sex, age, TBI severity and carried out comparisons using a generalized linear model. Results We identified 239,425 individuals with an incident TBI and 239,425 matched individuals. TBI patients were more likely to use any medication [Odds ratio (OR) = 2.03, 95% Confidence Interval (CI) = 2.00–2.05], to present with polypharmacy (OR = 1.96, 95% CI = 1.90–2.02), and to use each of the eight medication classes before their TBI, as compared to the matched population cohort. Following the TBI, TBI patients were more likely to use any medication (OR = 1.83, 95% CI = 1.80–1.86), to present with polypharmacy (OR = 1.74, 95% CI = 1.67–1.80), and to use all medication classes, although differences were attenuated. However, differences increased for antibiotics/antivirals (OR = 2.02, 95% CI = 1.99–2.05) and NSAIDs/antirheumatics (OR = 1.62, 95% CI = 1.59–1.65) post-TBI. We also found that females and older patients were more likely to use medications after their TBI than males and younger patients, respectively. Patients with more severe TBIs demonstrated increased use of antibiotics/ antivirals and NSAIDs/antirheumatics than those with less severe TBIs. Discussion Taken together, our results point to poor overall health in TBI patients, suggesting that medical follow-up should be routine, particularly in females with TBI, and include a review of medication use to address potential polypharmacy.
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