Brain radiation is a crucial tool in neuro-oncology for enhancing local tumor control, but it can lead to mild-to-profound and progressive impairments in cognitive function. Radiation-induced brain injury is a significant adverse effect of radiotherapy for cranioencephalic tumors, primarily caused by indirect cellular damage through the formation of free radicals. This results in late neurotoxicity manifesting as cognitive impairment due to free radical production. The aim of this review is to highlight the role of different substances, such as drugs used in the clinical setting and antioxidants such as ascorbate, in reducing the neurotoxicity associated with radiation-induced brain injury. Currently, there is mainly preclinical and clinical evidence supporting the benefit of these interventions, representing a cost-effective and straightforward neuroprotective strategy.

Lumbar disc herniation (LDH) is a primary cause of radiculopathy, a prevalent and debilitating neurological condition characterized by nucleus pulposus (NP) extrusion from the intervertebral disc (IVD), leading to the compression of nearby neural structures and causing neuropathic pain and neurological deficits. The pathophysiology of LDH involves progressive IVD degeneration, triggered by the accumulation of mechanical stress, inflammatory processes, and oxidative stress, leading to cellular damage, disc cell apoptosis, and extracellular matrix degradation. Clinically, LDH patients typically present with radicular pain, neurological deficits, and symptoms of sciatica, which may vary in intensity depending on the level and extent of the herniation. Diagnosis relies on clinical correlation and imaging studies, with magnetic resonance imaging as the gold standard. Treatment for a herniated NP depends on the symptoms and severity of nerve compression. Without severe or progressive neurological deficits, first-line treatment includes conservative management. Surgery is indicated when there is significant nerve compression, refractory pain, or progressive neurological deficits. This comprehensive review focuses on LDH, aiming to provide a neurologically oriented appraisal. First, it delves into the pathomechanism of LDH, offering updated insights into the biological and biomechanical processes that lead to disc herniation and subsequent nerve involvement. Second, it examines current diagnostic approaches, including advanced imaging techniques and neurological assessment methods, used to accurately identify and characterize LDH. Finally, it explores the evolving spectrum of management strategies, encompassing conservative treatments and various interventional and surgical options, with a particular emphasis on the neurological outcomes and considerations associated with each approach.