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Abstract Indirect traumatic optic neuropathy (ITON) refers to optic nerve injury resulting from impact remote to the optic nerve. The mechanism of injury is not understood, and there are no confirmed protocols for prevention, mitigation or treatment. Most data concerning this condition comes from case series of civilian patients suffering blunt injury, such as from sports- or motor vehicle-related concussion, rather than military-related ballistic or blast damage. Research in this field will likely require the development of robust databases to identify patients with ITON and follow related outcomes, in addition to both in-vivo animal and virtual human models to study the mechanisms of damage and potential therapies.

Si-Wei You,1 Ming-Mei Wu,2 Fang Kuang,2 Kin-Sang Cho,3 Kwok-Fai So4,5 1Department of Ophthalmology, Xijing Hospital, 2Institute of Neurosciences, The Fourth Military Medical University, Xi'an, China; 3Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; 4GHM Institute of CNS Regeneration, Key Laboratory of Brain Function and Diseases, Jinan University, Guangzhou, 5Department of Ophthalmology, The State Key laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Hong Kong SAR, China Abstract: Optic neuropathy refers to disorders involving the optic nerve (ON). Any damage to ON or ON-deriving neurons, the retinal ganglion cells (RGCs), may lead to the breakdown of the optical signal transmission from the eye to the brain, thus resulting in a partial or complete vision loss. The causes of optic neuropathy include trauma, ischemia, inflammation, compression, infiltration, and mitochondrial damages. ON injuries include primary and secondary injuries. During these injury phases, various factors orchestrate injured axons to die back and become unable to regenerate, and these factors could be divided into two categories: extrinsic and intrinsic. Extrinsic inhibitory factors refer to the environmental conditions that influence the regeneration of injured axons. The presence of myelin inhibitors and glial scar, lack of neurotrophic factors, and inflammation mediated by injury are regarded as these extrinsic factors. Extrinsic factors need to trigger the intracellular signals to exert inhibitory effect. Proper regulation of these intracellular signals has been shown to be beneficial to ON regeneration. Intrinsic factors of RGCs are the pivotal reasons that inhibit ON regeneration and are closely linked with extrinsic factors. Intracellular cyclic adenosine monophosphate (cAMP) and calcium levels affect axon guidance and growth cone response to guidance molecules. Many genes, such as Bcl-2, PTEN, and mTOR, are crucial in cell proliferation, axon guidance, and growth during development, and play important roles in the regeneration and extension of RGC axons. With transgenic mice and related gene regulations, robust regeneration of RGC axons has been observed after ON injury in laboratories. Although various means of experimental treatments such as cell transplantation and gene therapy have achieved significant progress in neuronal survival, axonal regeneration, and restoration of the visual function after ON injury, many unresolved scientific problems still exist for their clinical applications. Therefore, we still need to overcome hurdles before developing effective therapy to treat optic neuropathy diseases in patients. Keywords: retinal ganglion cells, optic nerve injury, neuronal survival, axonal regeneration, vision restoration

Diabetes polyneuropathy is an important complication of diabetes polyneuropathy, and its notable sequelae of foot ulceration, autonomic dysfunction, and neuropathic pain are associated with significant morbidity and mortality. Despite the major impact on quality of life and health economic costs, it remains underdiagnosed until late in its natural history, and there is lack of any intervention that can reverse its clinical progress. Assessment of small fiber neuropathy (SFN) in diabetes offers an opportunity to detect abnormalities at an early stage so that both interventional studies and preventative measures can be enacted to prevent progression to the devastating complications of foot ulceration and cardiac dysautonomic death. Over the last two decades, significant advances have been made in understanding the pathophysiology of diabetes neuropathy and its assessment. In this review, we discuss limitations of the screening methods recommended in current clinical guidelines which are based on large nerve fiber assessments. Thereafter, we discuss in detail the various methods currently available to assess small fiber structure and function and examine their individual strength and limitations. Finally, we discuss the reasons why despite the considerable body of evidence available, legislators and global experts have yet to incorporate the assessment of SFN as routine clinical surveillance in diabetes management. We hope that these insights will stimulate further discussion and be instrumental in the early adoption of these methods so as to reduce the burden of complications arising due to diabetes polyneuropathy.

Introduction: Compression of the lateral antebrachial cutaneous nerve (LACN) is a rarely recognized but clearly definable syndrome. It should be taken into account in the differential diagnosis in the context of soldiers who are suspected of avoiding military duties by assuming the sick role. In this report, we describe a 23-year-old soldier who presented with avoidance of elbow extension due to a burning pain in the right forearm induced by extension. LACN neuropathy, which occurred after physical training including palm-away pull ups in the military camp and was initially suspected to be malingering, was later diagnosed according to the clinical and electrodiagnostic findings. People who are accused of malingering in military settings should be examined carefully also concerning the training-related injuries of the peripheral nervous and musculoskeletal systems. Especially for patients complaining of forearm pain that leads to inability to extend the elbow, LACN neuropathy should be considered in the differential diagnosis and confirmed by electrophysiological examination. Turk J Phys Med Rehab 2010;56:145-7.

Introduction: Compression of the lateral antebrachial cutaneous nerve (LACN) is a rarely recognized but clearly definable syndrome. It should be taken into account in the differential diagnosis in the context of soldiers who are suspected of avoiding military duties by assuming the sick role. In this report, we describe a 23-year-old soldier who presented with avoidance of elbow extension due to a burning pain in the right forearm induced by extension. LACN neuropathy, which occurred after physical training including palm-away pull ups in the military camp and was initially suspected to be malingering, was later diagnosed according to the clinical and electrodiagnostic findings. People who are accused of malingering in military settings should be examined carefully also concerning the training-related injuries of the peripheral nervous and musculoskeletal systems. Especially for patients complaining of forearm pain that leads to inability to extend the elbow, LACN neuropathy should be considered in the differential diagnosis and confirmed by electrophysiological examination. Turk J Phys Med Rehab 2010;56:145-7.

This article presents the results of a noncontrolled clinical study of 20 persons with Leber's hereditary optic neuropathy who were treated from 1976 to 1990 at the Low Vision Centre, Finnish Federation of the Visually Handicapped. It emphasizes the importance of early functional visual rehabilitation and the use of low vision aids to help patients perform their daily activities.

Leber's hereditary optic neuropathy (LHON) is a rare, maternally-inherited optic neuropathy caused by mitochondrial DNA point mutations and which can cause blindness. Currently, Raxone (idebenone) is the only available medicinal product authorised to treat LHON within the European Union and LHON remains an unmet medical need. The aim of this article was to summarise interventional clinical trials published over the past 5 years (between 2014 and 2019) with the primary purpose of treating LHON. Therapeutic approaches discussed include modulating agents of the mitochondrial electron transport chain such as Raxone, cysteamine bitartrate and KH176, inhibitors of apoptosis such as elamipretide, gene therapy medicinal products such as GS010 and scAAV2P1ND4 and retinal tissue regeneration medicinal products such as bone marrow-derived stem cells. ; peer-reviewed

A poster presentation regarding emerging treatments for Leber hereditary optic neuropathy and retinitis pigmentosa. Introduction: Leber Hereditary Optic Neuropathy (LHON) and Retinitis Pigmentos (RP) are rare-inherited diseases causing blindness with few treatments available within the European Union (EU). Raxon (idebenone) is the only approved medicinal product (MP) to treat LHON. Luxturna (voretigene neparvovec) is the only approved MP to treat RP. Aims: To understand emerging patterns pursued by pharmaceutical companies when developing medicinal products to treat LHON and RP. ; N/A

Complex early and late neuropathies resulting from direct and conductive electrical patterns of injury are disabling and extremely challenging to manage. We report a patient who suffered acute onset of right-hand weakness and decreased sensation following a radar equipment-related electrical injury. He received a carpal and Guyon tunnel release, regaining sensation and strength to his right hand by the first postoperative day.