Machine learning versus clinical scoring systems for predicting poor wound healing after posterior surgery for thoracolumbar tuberculosis.

Spinal cord injury (SCI) is one of the most complex medical conditions and remains a major social and economic burden worldwide []. The main causes of SCI are traffic accidents, falls from heights, and violent trauma []. The estimated lifetime cost of a single traumatic SCI case ranges from 500,000 to 2 million USD [, ]. Each year, 250,000 to 500,000 new cases occur globally according to the World Health Organization (WHO), with an incidence rate of about 40.1 cases per million people. The condition is more common in males than in females []. SCI usually leads to lifelong disability and is characterised by two stages of injury, namely the primary and secondary phases [, ]. The primary injury results from direct mechanical trauma to the spinal cord, leading to tissue contusion, compression, hemorrhage, or even transection. These events disrupt cell membrane integrity, cause ionic and neurotransmitter imbalances, and lead to demyelination and rupture of sensory and motor nerve fibers. As a result, neurons in the affected region undergo rapid death, causing an immediate loss of neurological function []. Initial mechanical damage also compromises the blood-spinal cord barrier. This results in haemorrhaging, ischaemia, microvascular loss, oedema, inflammation, oxidative stress, lipid peroxidation and the release of toxic compounds from injured neurons and glial cells []. These processes trigger neuroinflammation. Proinflammatory cytokines induce different types of programmed cell death, including apoptosis, pyroptosis, and necroptosis. Activated microglia and infiltrating immune cells such as lymphocytes, monocytes, and neutrophils amplify the inflammatory response. The release of cytokines and chemokines further promotes neural stem cell differentiation into astrocytes, leading to glial scar formation, demyelination, and excessive local fibrosis []. In the early stage, glial scars have protective functions. They restrict lesion expansion, contain inflammation, and prevent the spread of toxins to nearby tissues []. However, glial scars pose a significant barrier to regeneration at a later stage. In contrast to peripheral nerve injury, scars in the central nervous system persist and inhibit axonal regrowth through physical and chemical means. One example of this is the presence of chondroitin sulfate proteoglycans (CSPGs). They also alter the microenvironment by suppressing neurotrophic factors and limiting the repair of neurons, astrocytes, oligodendrocytes, and their precursor cells []. Although decades of medical progress have greatly improved the survival of patients with SCI, there is still no clinically effective treatment that can restore neural conductivity []. This highlights the urgent need for more effective therapeutic strategies.