It has been hypothesized that there are two mechanisms of acute traumatic spinal cord injury (SCI): the primary mechanical damage and the secondary injury due to additional pathological processes initiated by the primary injury. Neurological damage due to laceration, contusion, distraction or compression of the spinal cord is called ''primary injury''. This mechanical injury leads to a cascade of biochemical and pathological changes, described as ''secondary injury'', which occurs minutes to weeks after the initial trauma and causes further neurological deterioration. This secondary cascade involves vascular changes, an inflammatory response, neurotoxicity, apoptosis and glial scarring, and further compromises neurological impairment after traumatic spinal cord injury. Edema, ischemia and loss of autoregulation continue to spread bi-directionally from the initial lesion along the spinal cord for up to 72 hours after the trauma.
It has been postulated that the damage caused by the primary injury mechanism is irreversible and therapeutic approaches in recent years have focused on modulating the secondary injury cascade.
Researchers found significantly greater numbers of myelinated fibers in peripheral nerves after a single ESWT application in an experimental model on rats after a homotopic nerve autograft into the sciatic nerve.
In another study a spinal cord ischemia model in mice was performed. ESWT was applied immediately after surgery and the treated animals showed a significantly better motor function and decreased neuronal degeneration compared to the control group within the first 7 days after surgery.
Researchers investigated the effect of low-energy ESWT for the duration of three weeks on a thoracic spinal cord contusion injury model in rats. Animals in the ESWT group demonstrated significantly better locomotor improvement and reduced neuronal loss compared to the control animals at 7, 35, and 42 days after contusion.
It has been postulated previously, that ESWT improves the metabolic activity of various cell types and induces an improved rate of axonal regeneration.
ESWT might be a promising therapeutic strategy in the treatment of traumatic SCI.
The underlying study aims to investigate the effect of ESWT after acute traumatic spinal cord injury in humans within 48 hours of trauma in order to intervene in the secondary injury phase with the objective to reduce the extent of neuronal damage.
Patients with acute traumatic spinal injuries who are awake, responsive, and oriented at admission
Patients from the age of 18 years
Admission to hospital within 24 hours after injury
Written consent to participate in the study
Patients who cannot cooperate or are not capable to give consent to participate
Serious traumatic brain injuries that prevent accurate participation in study procedures and/or adequacy of informed consent Participation in other interventional clinical trials
Serious concomitant injuries that prevent the neurological initial assessment
Preexisting neurological conditions that affect the primary endpoint of the study and potentially mask or reduce the therapeutic effect of the ESWT application