Background: The pathomechanism of blast TBI and blunt TBI is different. In blast injury, evidence indicate that a single blast exposure can often manifest long-term neurological impairments. However, its pathomechanism is still elusive and treatments were symptomatic. Poly ADP Ribose Polymerase-1 (PARP1) is being implicated in the parthanatos and secondary neuroinflammation. Animal studies indicate the over-activation of as a major downstream event underlying the neurological sequalae of several traumatic and neurodegenerative disorders irrespective of the mode of cell death. PARP over-activation forms ADP polymers on several nuclear proteins known as trans-PARylation by consuming NAD+ and ATP. As NAD+ is a substrate for sirtuins, it too has been implicated in the oxidative stress underlying TBI pathology. Hypothesis: We recently established the implication of PARP1 following blast overpressure (BOP) and its differential response on astrocytes and microglial cells. We found that the inhibition of PARP is proven to be beneficial by attenuating oxidative stress. In this study, we hypothesized the involvement of the PARP1-SIRT-NRF2 axis following Blast induced PARP over-activation in glial cells for the manifestation of oxidative stress in BOP insults. Objective: Our objective is to determine the downstream modulation of the PARP-Sirt-NRF2 axis and changes in ATP levels following blast exposure in astrocytes and microglia cell lines. Results: As a result of NAD+ being a common substrate for PARP1 and Sirtuins, we found the decreased expression of SIRT1, SIRT3 and NRF2, a major transcriptional regulator for the expression of antioxidant genes. We found that ATP levels were elevated post-BOP from both glycolysis and oxidative phosphorylation (OXPHOS), an increase of ATP by glycolysis more significant than OXPHOS source indicating the pro-inflammation post-BOP. Conclusion: This result shows that blast-induced PARP over-activation impacts the deacetylation activity of sirtuins and consequently impacts the regulation of antioxidant levels in astrocytes and microglia.

Bilateral Semicircular Canal Dehiscence Analyzed Using the International Classification of Functioning, Disability, and Health (ICF) Framework: Case report.Ignacio Novoa-Cornejo1 , Vijaya Prakash Krishnan Muthaiah1*, Victor Mercado-Martinez2,Gustavo Ulloa-Alvarado 2,3,Carlos Pino-Urrutia2 , Krishnamoorthy Gunasekaran1Department of Rehabilitation Sciences, School of Public Health and Health Professions, State University of New York at Buffalo, Buffalo, NY, United States.2 Instituto de Neurorrehabilitación y Balance, Viña del Mar, Valparaíso, Chile.3 Exercise and Rehabilitation Sciences Institute, School of Physical Therapy, Faculty of Rehabilitation Sciences, Universidad Andres Bello, Santiago 7591538, Chile.4Department of Medical Biochemistry, College of Health Sciences, Dambi Dollo University, Dambi Dollo Ethiopia.* Represents equal first authorship.Abstract A severe case of bilateral superior semicircular dehiscence was presented in Instituto de Neurorrehabilitación y Balance, Chile. The patient reports hearing and vestibular problems in certain situations; a complete analysis is carried out from the clinical history to neurological laboratory studies and imaging to diagnose bilateral semicircular canal dehiscence finally. Health condition management is under the ICF model, which will allow for determining and classifying the problems and possible interventions for this interesting clinical case.Keywords Bilateral semicircular canal dehiscence, ICF framework, vestibular disorder.

Introduction Spontaneous intracerebral hemorrhage (ICH) accounts for 10-20% of strokes worldwide, with hypertensive vasculopathy being the most common underlying cause [1]. Brainstem hemorrhages represent one-third of ICH and often arise in the pons [2]. Vital sensorimotor pathways and cranial nerve nuclei traverse this region. Thus, characteristic signs of pontine ICH include hemiparesis, cranial nerve palsies, and impaired consciousness [3].Oculomotor nerve involvement causes ipsilateral ptosis and pupillary dilation with preservation of extraocular movements due to sparing of the superior branch [4]. Abducens palsy and internuclear ophthalmoplegia reflect medial longitudinal fasciculus damage [2]. Beyond focal deficits, brainstem hemorrhages frequently precipitate headaches and tinnitus due to vascular irritation of pain and auditory pathways [5]. Persistent, troublesome tinnitus impairs concentration and quality of life [6].The International Classification of Functioning, Disability, and Health (ICF) codifies the multifactorial impacts of health conditions like stroke [7]. The ICF enhances rehabilitation by elucidating specific limitations in body structures/functions, activities, participation, and environmental interactions. ICF-based assessment informs goal setting and interventions to optimize functioning and societal participation.This report presents an ICF profile of a patient with tinnitus and oculomotor palsy following pontine hemorrhage. MRI confirmed the hemorrhagic lesion. ICF components were examined to capture the breadth of disability. Tinnitus management and multidisciplinary therapies were tailored accordingly to promote recovery.