Various Causes of Paraparesis
Paraparesis results from spinal cord lesions caudal to the second thoracic segment, with the most common causes being spinal tuberculosis (30%), acute transverse myelitis (20%), primary spinal cord tumors (10%), vascular disorders including spinal cord ischemia, and less commonly, inborn errors of metabolism and demyelinating diseases. 1, 2
Etiological Categories
Compressive Causes
- Spinal tuberculosis is the leading cause of non-traumatic paraparesis, particularly in endemic regions, presenting with backache (75% of cases) and progressive weakness 2
- Primary spinal cord tumors account for 10% of cases and require surgical decompression, with combined surgery and radiotherapy showing superior outcomes to radiotherapy alone for malignant compression 3, 2
- Extradural, intradural/extramedullary, and intramedullary lesions can be differentiated by MRI patterns to guide specific management 4
Vascular Causes
- Spinal cord ischemia following thoracic aortic surgery occurs in 2-6% of descending thoracic repairs and 3-10% of thoracoabdominal repairs 1, 3
- Risk factors include emergency surgery, dissection, prolonged aortic cross-clamp time, aortic rupture, advanced age, prior abdominal surgery, and renal dysfunction 3
- Cerebral venous thrombosis involving the sagittal sinus can cause bilateral motor signs including paraparesis and requires screening for prothrombotic conditions 1, 3
Inflammatory and Demyelinating Causes
- Acute transverse myelitis represents 20% of non-traumatic paraparesis cases and may require CSF examination showing elevated protein and cells 2, 3
- Multiple sclerosis can present with spastic paraparesis, with MRI showing periventricular plaques and CSF demonstrating oligoclonal bands and elevated myelin basic protein 5
Metabolic Causes
- Inborn errors of metabolism can present as isolated spastic paraparesis in adults for years before other systemic manifestations appear, making them critical to identify as they are often treatable 1, 6
Diagnostic Approach
Initial Clinical Assessment
- Document the rate of symptom onset: acute onset suggests vascular or inflammatory causes, while gradual progression suggests neoplastic or metabolic etiologies 7
- Identify accompanying symptoms: backache (75%), paresthesias (62.5%), bladder/bowel dysfunction, and sensory level help localize the lesion 2
- Assess for spasticity (present in 57.5%), hyperreflexia, clonus, and Babinski signs to confirm upper motor neuron involvement 2, 8
- Screen for exacerbating factors: constipation, urinary tract infections, and pressure ulcers can worsen existing spasticity 8
Laboratory Evaluation
- Complete blood count, chemistry panel, PT/aPTT for suspected vascular causes 3
- CSF examination when inflammatory or infectious causes are suspected, looking for elevated protein, cells, oligoclonal bands, and myelin basic protein 3, 5
- Prothrombotic screening if cerebral venous thrombosis is suspected 1, 3
Imaging Strategy
- MRI of the spine without and with contrast is the primary imaging modality, classifying findings into six patterns: extradural, intradural/extramedullary, intramedullary, intramedullary-tract specific, spinal cord atrophy, or normal-appearing cord 4
- CT myelography can delineate primary spinal cord tumors and confirm diagnosis in spinal TB, showing block in 58.5% of compressive cases 2
- Brain MRI should be obtained if multiple sclerosis is suspected, looking for periventricular plaques 5
Management Strategies
Vascular Causes (Post-Aortic Surgery)
- Cerebrospinal fluid drainage is the primary spinal cord protective strategy in high-risk patients (Class I recommendation) 3
- Maintain spinal cord perfusion pressure through proximal aortic pressure maintenance and distal aortic perfusion (Class IIa) 3
- Prevent postoperative hypotension aggressively in the ICU, and continue CSF drainage for >40 hours to reduce paraparesis incidence 1, 3
- Moderate systemic hypothermia during open repairs provides additional protection (Class IIa) 3
- Neurophysiological monitoring with somatosensory or motor evoked potentials can detect spinal cord ischemia and guide treatment (Class IIb) 3
Compressive Causes
- Surgical decompression for spinal cord compression from tumors or mass lesions, with combined surgery and radiotherapy superior to radiotherapy alone for malignant compression 3
- Anti-tuberculous therapy for spinal tuberculosis, often combined with surgical decompression in cases with neurological deficit 2
Inflammatory Causes
- Pulse steroid therapy for acute transverse myelitis and multiple sclerosis exacerbations improves outcomes 5
Spasticity Management
- Eliminate triggers first: treat constipation, urinary tract infections, and pressure ulcers 8
- Neurophysiotherapy as the foundation of spasticity management 8
- Oral medications: baclofen, tizanidine, or dantrolene for generalized spasticity 8
- Focal botulinum toxin injections for localized spasticity 8
- Intrathecal baclofen pump for severe, refractory spasticity 8
Rehabilitation and Complications Prevention
- Early mobilization to prevent deconditioning 3
- Neurogenic bladder and bowel management to prevent secondary complications 3
- Pain management as pain is frequently reported 3
- Referral to specialists: physical therapy, ophthalmology if visual symptoms, and psychological support for incomplete recovery 1
Prognosis
- Two-thirds of patients with paraparesis following spinal cord ischemia recover some function, and approximately half with complete paraplegia recover to the point of walking 1, 3
Critical Pitfalls to Avoid
- Do not miss treatable metabolic causes by limiting workup to structural and inflammatory etiologies only 6
- Do not delay CSF drainage in post-aortic surgery patients, as continued drainage >40 hours significantly reduces paraparesis incidence 1, 3
- Do not overlook cerebral venous thrombosis in patients with bilateral motor signs, as this requires anticoagulation rather than spinal-directed therapy 1, 3