Mechanism of Spinal Cord Injury in Myelomalacia

Pathophysiological Mechanisms

The American College of Radiology suggests that degenerative disease is the most common cause of extrinsic compression leading to myelomalacia, particularly in the cervical spine 1, 2
Compression factors include spinal degenerative changes 3, disc herniations 3, spinal malalignment 4, and congenitally short pedicles that accentuate compression 2
Post-surgical complications such as seromas, pseudomeningoceles, hematomas, and epidural abscesses can cause extrinsic compression 2
Tumors in extradural and intradural extramedullary spaces can compress the spinal cord 2

Spinal cord ischemia is a significant cause of myelomalacia 3, 5
Vascular malformations can cause progressive myelopathy through venous hypertension 6 and spinal cord edema 6
Breakdown of the blood-cord barrier leads to patchy intramedullary enhancement 1
Ischemic damage can result from atheromatous disease 5, complications of aortic surgery 5, systemic hypotension 5, thoracoabdominal aneurysms or dissection 5, and sickle cell disease 5

Acute compression or trauma leads to central hemorrhage and spreading ischemia 6
Breakdown of the blood-cord barrier occurs 1
Progressive necrosis develops in the affected areas 6
Edema worsens compression and further compromises blood supply 1
Post-traumatic infarction and cavitation develop 6
Myelomalacia and gliosis become evident on MRI 1, 2
Intramedullary cord signal changes represent prognostic factors for neurosurgical outcomes 1

MRI is the gold standard for detecting myelomalacia and gliosis 1, 2
Characteristic findings include T2 hyperintensity within the spinal cord 6, possible enhancement at and below the level of stenosis 1, and cord atrophy in chronic cases 1
Diffusion-weighted imaging can show signal alteration earlier than T2-weighted images in acute ischemic injury 5
Contrast enhancement patterns can help differentiate between ischemic, inflammatory, and neoplastic causes 5

Intramedullary cord signal changes on MRI in patients with spondylotic myelopathy represent important prognostic factors 1, 2
The presence of myelomalacia does not necessarily correlate with poor neurological outcomes, as patients with preoperative myelomalacia can still show significant neurological improvement 4

Myelomalacia should not be confused with other causes of T2 hyperintensity such as demyelination, inflammation, or neoplasm 1
The presence of cord signal changes does not always correlate with clinical outcomes 4
Imaging must be interpreted in conjunction with clinical findings, as the degree of radiographic abnormality may not match symptom severity 4

The Nomenclature Committee on Cell Death (NCCD) classifies cell death into two broad categories: Accidental cell death (ACD) - caused by severe insults including physical trauma, and Regulated cell death (RCD) - involves genetically encoded molecular machinery 7, 8

Necrosis is the predominant form of cell death in myelomalacia, characterized by cytoplasmic swelling, mechanical rupture of the plasma membrane, dilation of cytoplasmic organelles, and moderate chromatin condensation 8, 9
Myelomalacia involves irreversible plasma membrane permeabilization, which the NCCD considers a definitive marker of cell death 7