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Compressive myelopathy

Summary

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  • Compressive myelopathy is a neurological condition characterised by spinal cord compression
  • Causes include degenerative changes, tumours, trauma, and congenital abnormalities
  • Imaging plays a crucial role in diagnosis and treatment planning

Pathophysiology

  • Compression of the spinal cord leads to:
    • Mechanical disruption of neural tissue
    • Vascular compromise and ischaemia
    • Inflammatory responses
    • Demyelination and axonal degeneration
  • Chronic compression may result in:
    • Gliosis
    • Cystic cavitation
    • Atrophy of the spinal cord

Demographics

  • Incidence varies depending on the underlying cause
  • Cervical spondylotic myelopathy:
    • Most common cause in adults over 55 years
    • Male predominance (2.7:1)
  • Traumatic spinal cord injury:
    • Higher incidence in young adults and males
    • Bimodal distribution: peaks at 15-29 years and >65 years

Diagnosis

  • Clinical presentation:
    • Gait disturbances
    • Sensory changes
    • Motor weakness
    • Bowel and bladder dysfunction
  • Physical examination:
    • Hyperreflexia
    • Positive Hoffman's sign
    • Babinski sign
    • Decreased proprioception
  • Diagnostic tests:
    • Electromyography (EMG)
    • Nerve conduction studies
    • Somatosensory evoked potentials (SSEPs)

Imaging

  • Magnetic Resonance Imaging (MRI):
    • Gold standard for diagnosis
    • T2-weighted images: hyperintense signal within the cord
    • T1-weighted images: assess for cord atrophy
    • Gadolinium-enhanced T1: evaluate for tumours or infection
    • Diffusion Tensor Imaging (DTI): assess white matter tract integrity
  • Computed Tomography (CT):
    • Useful for assessing bony abnormalities
    • CT myelography: alternative when MRI is contraindicated
  • Plain radiographs:
    • Limited utility but may show:
    • Degenerative changes
    • Fractures
    • Congenital anomalies

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  • 70-year-old patient with rheumatoid arthritis presented with tingling in lower limbs and worsening gait.
  • There was no significant vertebral canal stenosis but the T2-hyperintense foci in both sides of the cord at C4-5 suggested a chronic compressive myelopathy.

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  • Patient with prior compression of the cord due to spondylosis.
  • The myelopathic segment is T2-hyperintense (particularly the grey matter) and small volume.

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  • 60-year-old patient with chronic myelopathic symptoms and severe bilateral upper limb radiculopathies.
  • MRI showed posterior-osteophyte disc complexes causing moderately severe vertebral canal narrowing.
  • The cord was atrophic and there was myelopathic signal change in the central and lateral cord.

Treatment

  • Conservative management:
    • Physical therapy
    • Pain management
    • Cervical collar or bracing
  • Surgical interventions:
    • Anterior cervical discectomy and fusion (ACDF)
    • Laminectomy with or without fusion
    • Corpectomy
    • Tumour resection
  • Emerging therapies:
    • Stem cell transplantation
    • Neuroprotective agents
    • Neurotrophic factors

Differential diagnosis

Differential Diagnosis Differentiating Feature
Multiple sclerosis Short (<3 vertebral segments) eccentric cord lesion on MRI; periventricular ovoid brain lesions; no structural compression
Transverse myelitis Intramedullary T2 signal without structural compressive cause; cord expansion; no disc or bony pathology
Spinal cord infarction Restricted diffusion on DWI; pencil-like anterior cord T2 signal; no compressive mass
Vitamin B12 deficiency Posterior column T2 hyperintensity ("inverted V" sign); no structural compression; symmetric dorsal involvement
Syringomyelia Central fluid-filled cavity on T2; follows CSF signal; may be associated with compressive cause
Spinal cord tumour Intramedullary enhancing mass with cord expansion; no disc or bony compressive pathology
Radiation myelopathy Located within prior radiation field; cord atrophy and T2 signal without compressive cause
Neuromyelitis optica spectrum disorder Often associated with optic neuritis; NMO-IgG antibody positive