Injury/Recovery
Here, I’ll give updates about my long-term injury that I had since a major car accident.
Availability
Firstly, I am still fully available for wrestling sessions, as always. The only permanent change since September 2025 is that I no longer offer lift & carry. Carrying around grown men simply places unnecessary risk on my spine. Judo throws remain part of my repertoire with no weight limit. I might still take you onto my shoulders for a brief moment, but I explicitly do not offer L&C anymore.
Abstract
After a car accident I was left with cervical damage and multiple degenerated discs. Chronic pain, nerve symptoms, and muscle loss led specialists to diagnose multi-level spinal compression, and spinal fusion was advised. In reality, the true cause was large-scale neuromuscular inhibition on my left side. The operations that were planned proved unnecessary once I identified the mechanism myself, restored activation, and for the first time achieved stable, measurable recovery.
Case Summary
Symptoms and Misdiagnosis
The first warning signs were progressive neurological symptoms:
- Loss of strength in my fingers
- Numb skin in my left arm
- Severe shoulder pain after activity
Because MRI scans also showed disc protrusions and osteophytes, specialists concluded these symptoms — including weakness in my back — were caused by multi-level nerve compression. Based on these findings, spinal fusion was seriously considered in both the lumbar and cervical spine.
Hidden Deficits
Outwardly I looked functional. My posture was maintained and I continued wrestling, which concealed the deficits. In reality I face(d):
- Chronic pain
- Recurrent shoulder instability
- Episodes of functional collapse
- Inabilities, such as being unable to sit up from lying without arm support (due to an inactive lumbar erector spinae), pinch something and hold on to it with my left hand, lean on my elbow and even sit in a chair for more than 10 minutes.
Medical Consultations
I consulted orthopedic surgeons, spinal specialists, musculoskeletal physicians, and neurosurgeons in several countries. Imaging confirmed structural changes, but the large-scale muscle inhibition itself was not identified. Because compensation allowed me to appear functional, the underlying deficit was overlooked.
Breakthrough and Reactivation
The turning point came when I managed to restore activation in my left ESL. On MRI the muscle showed severe atrophy with minimal residual contractile tissue. Conventional prognosis would consider reactivation after such duration highly unlikely. Through targeted neuromuscular input I was able to elicit contraction within 24 hours and subsequently maintain activity.
Integration and Progress
Reintegration was demanding, but unlike earlier overload collapses, the discomfort now reflected recalibration rather than failure.
At present the ESL is consistently active, with significant reduction of pain and stiffness in the lumbar region. Reactivation of other inhibited muscles is ongoing and more complex, but the trajectory is clearly progressive. Even during years of deficit I could wrestle at a high level; with each reactivated muscle, maximal output continues to increase.