Mechanisms of cancer-induced neurophysiological dysfunction and therapeutic strategies

Cancer is a multifaceted disease that affects the primary organ and induces widespread systemic effects, particularly the nervous system. Neurophysiological alterations in cancer patients have emerged as an important area of concern due to the impact on cognition, sensory and motor functions, and autonomic regulation. These alterations can arise from various mechanisms, including direct tumor invasion of neural tissues, paraneoplastic immune responses, metabolic dysregulation, and systemic inflammation [ 45 ]. Other causes can arise as a result of the adverse effects of cancer therapies such as chemotherapy, radiotherapy, and immunotherapy. Recent advancement in early detection offers improved therapeutic innovations, with global cancer survivorship increasing with over 43 million individuals [ 50 ]. However, this positive trajectory is accompanied by a growing incidence of treatment-associated neurotoxic effects. Notably, cognitive impairment, often referred to as “chemo brain,” affects up to 75% of patients during or following chemotherapy, while an estimated 30–40% develop persistent or late-onset neurological dysfunctions [ 4 ]. These complications include cognitive dysfunction, chemotherapy-induced peripheral neuropathy (CIPN), encephalopathy, seizures, and chronic neuropathic pain. Such deficits compromise functional independence and can lead to reduced adherence to treatment protocols, early discontinuation of potentially curative therapies, increased healthcare costs, and a significant psychosocial burden. These trends require an urgent need for integrated neuro-oncological care into standard cancer management frameworks [ 62 ]. Neurophysiological changes in cancer can affect nerve conduction velocity or EEG patterns, and may also present as more severe conditions such as focal deficits or global encephalopathy [ 29 ]. The interaction between tumors and the nervous system is bidirectional and complex. Tumors can alter neuronal function through mechanical compression, infiltration, or by releasing neuroactive substances and inflammatory mediators [ 44 ]. Concurrently, the nervous system may influence tumor growth through neural signaling pathways, immune modulation, and hormonal responses. This further emphasised the deeper role of the neuroimmune and neuroendocrine interface in cancer biology [ 30 ]. Despite a growing body of evidence highlighting the impact of cancer and its treatment on the nervous system, neurological assessment remains insufficiently integrated into routine oncology practice. The research landscape is similarly fragmented, with persistent gaps in understanding of the underlying mechanisms. The development of robust diagnostic tools and the validation of effective neuroprotective and rehabilitative interventions. Therefore, this review aims to synthesize the current understanding of cancer-related neurophysiological alterations, highlight emerging diagnostic and therapeutic strategies, and identify critical knowledge gaps to guide future clinical and translational research.