Cushing’s syndrome is associated with a spectrum of systemic complications, including under-recognised effects on the musculoskeletal system. We present a case of a 37-year-old male with recurrent Cushing’s Disease who developed progressive lumbar radiculopathy secondary to severe Degenerative Disc Disease. Despite bilateral adrenalectomy, the patient exhibited persistent hypercortisolaemia and classical Cushingoid features. Imaging confirmed L4 disc herniation with nerve root compression. A multidisciplinary team initiated endocrine therapy and performed a successful minimally invasive lumbar discectomy, resulting in clinically documented neurological improvement during the immediate postoperative period. Chronic cortisol excess may disrupt spinal biomechanics and accelerate spinal degeneration through presumed bone demineralisation, muscle atrophy, altered fat distribution, and direct degradation of disc tissue. This case highlights the importance of early endocrine evaluation in patients with atypical or rapidly progressive spinal degeneration. Recognition and management of hypercortisolaemia are essential for surgical planning, optimising outcomes, and preventing recurrent spinal compromise.

Neuropathic pain is a complex chronic pain state caused by the dysfunction of somatosensory nervous system, and it affects the millions of people worldwide. At present, there are very few medical treatments available for neuropathic pain management and the intolerable side effects of medications may further worsen the symptoms. Despite the presence of profound knowledge that delineates the pathophysiology and mechanisms leading to neuropathic pain, the unmet clinical needs demand more research in this field that would ultimately assist to ameliorate the pain conditions. Efforts are being made globally to explore and understand the basic molecular mechanisms responsible for somatosensory dysfunction in preclinical pain models. The present review highlights some of the novel molecular targets like D-amino acid oxidase, endoplasmic reticulum stress receptors, sigma receptors, hyperpolarization-activated cyclic nucleotide-gated cation channels, histone deacetylase, Wnt/β-catenin and Wnt/Ryk, ephrins and Eph receptor tyrosine kinase, Cdh-1 and mitochondrial ATPase that are implicated in the induction of neuropathic pain. Studies conducted on the different animal models and observed results have been summarized with an aim to facilitate the efforts made in the drug discovery. The diligent analysis and exploitation of these targets may help in the identification of some promising therapies that can better manage neuropathic pain and improve the health of patients.
Adenosine Triphosphatases ; Chronic Pain ; Cyclic Nucleotide-Gated Cation Channels ; Drug Discovery ; Endoplasmic Reticulum Stress ; Ephrins ; Histone Deacetylases ; Humans ; Models, Animal ; Nervous System ; Neuralgia* ; Oxidoreductases ; Receptors, Eph Family ; Receptors, sigma