Mechanism of Spinal Cord Injury in Myelomalacia
The primary mechanism of spinal cord injury in myelomalacia is ischemic damage leading to softening of the spinal cord tissue, which can result from various causes including extrinsic compression, vascular abnormalities, and trauma. 1
Pathophysiological Mechanisms
Extrinsic Compression
- Degenerative disease (spondylotic myelopathy) is the most common cause of extrinsic compression leading to myelomalacia, particularly in the cervical spine 1
- Compression factors include:
- Spinal degenerative changes
- Disc herniations
- Epidural lipomatosis
- Spinal malalignment
- Congenitally short pedicles that accentuate compression 1
- Post-surgical complications such as seromas, pseudomeningoceles, hematomas, and epidural abscesses can cause extrinsic compression 1
- Tumors (primary or metastatic) in extradural and intradural extramedullary spaces can compress the spinal cord 1
Vascular Mechanisms
- Spinal cord ischemia is a significant cause of myelomalacia 1
- Vascular malformations (e.g., spinal arteriovenous malformations) can cause progressive myelopathy through:
- Venous hypertension
- Spinal cord edema
- "Spinal steal" phenomenon where blood is diverted away from normal cord tissue 2
- Breakdown of the blood-cord barrier leads to patchy intramedullary enhancement 1
- Ischemic damage can result from:
- Atheromatous disease
- Complications of aortic surgery
- Systemic hypotension
- Thoracoabdominal aneurysms or dissection
- Sickle cell disease 1
Traumatic Mechanisms
- Trauma can cause direct injury to the spinal cord and vascular structures 3
- Traumatic injury can lead to:
- Subluxation of vertebrae
- Fractures
- Space-occupying subdural hematomas
- Lesions of the dorsal truncus arteriosus spinalis 3
- The initial trauma (primary injury) causes immediate damage, followed by secondary injury involving inflammatory responses 4
Pathological Progression
Initial Phase
- Acute compression or trauma leads to central hemorrhage and spreading ischemia 1
- Inflammatory responses are triggered as part of secondary injury 4
- Breakdown of the blood-cord barrier occurs 1
Intermediate Phase
- Progressive necrosis develops in the affected areas 1
- Inflammatory cells infiltrate the damaged tissue 4
- Edema worsens compression and further compromises blood supply 1
Late Phase
- Post-traumatic infarction and cavitation develop 1
- Myelomalacia (softening of the spinal cord) and gliosis become evident on MRI 1
- Intramedullary cord signal changes represent prognostic factors for neurosurgical outcomes 1
Imaging Findings
- MRI is the gold standard for detecting myelomalacia and gliosis 1
- Characteristic findings include:
- T2 hyperintensity within the spinal cord
- Possible enhancement at and below the level of stenosis
- Cord atrophy in chronic cases 1
- Diffusion-weighted imaging can show signal alteration earlier than T2-weighted images in acute ischemic injury 1
- Contrast enhancement patterns can help differentiate between ischemic, inflammatory, and neoplastic causes 1
Clinical Correlation
- Intramedullary cord signal changes on MRI in patients with spondylotic myelopathy represent important prognostic factors 1
- The presence of myelomalacia does not necessarily correlate with poor neurological outcomes, as patients with preoperative myelomalacia can still show significant neurological improvement 1
- Spinal cord involvement in multiple myeloma can lead to severe neurological deficits through compression mechanisms 5, 6
Common Pitfalls and Caveats
- 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 1
- Imaging must be interpreted in conjunction with clinical findings, as the degree of radiographic abnormality may not match symptom severity 1
- Delayed diagnosis and treatment can lead to irreversible neurological damage, making early identification crucial 6