Blast-induced brain injury in rats leads to transient vestibulomotor deficits and persistent orofacial pain

Studlack, Paige; Keledjian, Kaspar; Farooq, Tayyiaba; Akintola, Titilola; Gerzanich, Volodymyr; Simard, J. Marc; Keller, Asaf

doi:10.1080/02699052.2018.1536282

Cited by 18 publications

(21 citation statements)

References 105 publications

(111 reference statements)

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“…Studlack et al previously used beam walk, accelerating rotarod, rearing, open field, elevated plus maze, and light-dark box task tests in bTBI injury model rats to evaluate their motor function and anxiety-related behavior. They observed that the accelerating rotarod test exhibited significant differences between the bTBI and control groups from day 1 to day 14 post injury [45]. We considered that the prolonged symptoms were suitable for evaluating the efficacy of AA2G and confirmed that the accelerating rotarod test exhibited significant differences between the LISW and control groups in the present study.…”

Section: Discussionsupporting

confidence: 85%

Oral ascorbic acid 2-glucoside prevents coordination disorder induced via laser-induced shock waves in rat brain

et al. 2020

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Oxidative stress is considered to be involved in the pathogenesis of primary blast-related traumatic brain injury (bTBI). We evaluated the effects of ascorbic acid 2-glucoside (AA2G), a well-known antioxidant, to control oxidative stress in rat brain exposed to laser-induced shock waves (LISWs). The design consisted of a controlled animal study using male 10week-old Sprague-Dawley rats. The study was conducted at the University research laboratory. Low-impulse (54 Pa•s) LISWs were transcranially applied to rat brain. Rats were randomized to control group (anesthesia and head shaving, n = 10), LISW group (anesthesia, head shaving and LISW application, n = 10) or LISW + post AA2G group (AA2G administration after LISW application, n = 10) in the first study. In another study, rats were randomized to control group (n = 10), LISW group (n = 10) or LISW + pre and post AA2G group (AA2G administration before and after LISW application, n = 10). The measured outcomes were as follows: (i) motor function assessed by accelerating rotarod test; (ii) levels of 8-hydroxy-2'deoxyguanosine (8-OHdG), an oxidative stress marker; (iii) ascorbic acid in each group of rats. Ascorbic acid levels were significantly decreased and 8-OHdG levels were significantly increased in the cerebellum of the LISW group. Motor coordination disorder was also observed in the group. Prophylactic AA2G administration significantly increased the ascorbic acid levels, reduced oxidative stress and mitigated the motor dysfunction. In contrast, the effects of therapeutic AA2G administration alone were limited. The results suggest that the prophylactic administration of ascorbic acid can reduce shock wave-related oxidative stress and prevented motor dysfunction in rats.

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Section: Discussionsupporting

confidence: 85%

Oral ascorbic acid 2-glucoside prevents coordination disorder induced via laser-induced shock waves in rat brain

et al. 2020

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“…We found that multifactorial brain injury induced persistent periorbital and plantar tactile hypersensitivity in mice. This result is consistent with a previous study showing persistent (8 weeks) whisker-pad tactile hypersensitivity after a single direct bullet-less gun-induced TBI in rats estimated at >70 PSI [49]. Interestingly, in a subsequent study, this phenotype was not produced when the TBI was performed in awake animals [50], despite the known protective effect of anesthetics [30].…”

Section: Long-term Vs Transient Hypersensitivity Induced By Tbisupporting

confidence: 92%

Multifactorial and closed head impact traumatic brain injuries cause distinct tactile hypersensitivity profiles

Wattiez

Castonguay

Gaul

et al. 2020

Preprint

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Chronic complications of traumatic brain injury (TBI) represent one of the greatest financial burdens and sources of suffering in society today. A substantial number of these patients suffer from post-traumatic headache (PTH), which is typically associated with tactile allodynia.Unfortunately, this phenomenon has been under-studied, in large part due to the lack of wellcharacterized laboratory animal models. We have addressed this gap in the field by characterizing the tactile sensory profile of two non-penetrating models of PTH. We show that multifactorial TBI, consisting of aspects of impact, acceleration/deceleration, and blast wave exposure, produces long term tactile hypersensitivity and central sensitization, phenotypes reminiscent of PTH in patients, in both cephalic and extracephalic regions. By contrast, closed head injury induces only transient cephalic tactile hypersensitivity, with no extracephalic consequences. Both models show more severe phenotype with repetitive daily injury for three days, compared to either one or three successive injuries in a single day, providing new insight into patterns of injury that may place patients at greater risk of developing PTH. Importantly, even after recovery from transient cephalic tactile hypersensitivity, mice subjected to closed head injury had persistent hypersensitivity to established migraine triggers, including calcitonin gene-related peptide (CGRP) and sodium nitroprusside, a nitric oxide donor. Our results offer new tools for studying PTH, as well as preclinical support for a pathophysiologic role of CGRP in this condition. SummaryTwo models of post-traumatic headache after traumatic brain injury provide novel laboratory tools and insights in relative risks of injury and therapeutic opportunities.

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“…Limited studies on glial pathology within the thalamus following blast injury have been reported. A study by Studlack et al focused on linking thalamic sensitization to headache and pain following blast injury ( 8 ). Their investigation included characterizing the astrocytic response within the VPM and the posterior thalamus (PO) which are associated with pain transmission.…”

Section: Discussionmentioning

confidence: 99%

“…These neurosensory conditions have become increasingly prevalent in military personnel exposed to blast events and are a common comorbidity of bTBI. Acute vestibulomotor deficits have been noted in 98% of patients diagnosed with bTBI and 72% of these patients report long-term vestibular impairment ( 8 , 9 ). Clinical manifestations of vestibular damage includes motor impairments leading to imbalance, motion intolerance, postural instability and dizziness ( 1 , 10 ).…”

Section: Introductionmentioning

confidence: 99%

Glial Activation in the Thalamus Contributes to Vestibulomotor Deficits Following Blast-Induced Neurotrauma

et al. 2020

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Vestibular impairment has become a frequent consequence following blast-related traumatic brain injury (bTBI) in military personnel and Veterans. Behavioral outcomes such as depression, fear and anxiety are also common comorbidities of bTBI. To accelerate pre-clinical research and therapy developments, there is a need to study the link between behavioral patterns and neuropathology. The transmission of neurosensory information often involves a pathway from the cerebral cortex to the thalamus, and the thalamus serves crucial integrative functions within vestibular processing. Pathways from the thalamus also connect with the amygdala, suggesting thalamic and amygdalar contributions to anxiolytic behavior. Here we used behavioral assays and immunohistochemistry to determine the sub-acute and early chronic effects of repeated blast exposure on the thalamic and amygdala nuclei. Behavioral results indicated vestibulomotor deficits at 1 and 3 weeks following repeated blast events. Anxiety-like behavior assessments depicted trending increases in the blast group. Astrogliosis and microglia activation were observed upon post-mortem pathological examination in the thalamic region, along with a limited glia response in the amygdala at 4 weeks. These findings are consistent with a diffuse glia response associated with bTBI and support the premise that dysfunction within the thalamic nuclei following repeated blast exposures contribute to vestibulomotor impairment.

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Blast-induced brain injury in rats leads to transient vestibulomotor deficits and persistent orofacial pain

Cited by 18 publications

References 105 publications

Oral ascorbic acid 2-glucoside prevents coordination disorder induced via laser-induced shock waves in rat brain

Oral ascorbic acid 2-glucoside prevents coordination disorder induced via laser-induced shock waves in rat brain

Multifactorial and closed head impact traumatic brain injuries cause distinct tactile hypersensitivity profiles

Glial Activation in the Thalamus Contributes to Vestibulomotor Deficits Following Blast-Induced Neurotrauma

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