What is the recommended diagnostic work‑up and management for a patient with suspected polyradiculopathy?

Polyradiculopathy: Diagnostic Work-Up and Management

Initial Diagnostic Approach

For suspected polyradiculopathy, obtain MRI of the affected spinal region (cervical, thoracic, or lumbosacral) without IV contrast as the primary imaging modality, combined with electrodiagnostic testing (EMG/NCS) and CSF analysis to differentiate between inflammatory, infectious, compressive, and neoplastic etiologies. 1, 2

Clinical Localization

The anatomic location of root involvement guides the diagnostic pathway:

• Extradural lesions (degenerative, neoplastic): Pain is the predominant initial complaint in 91% of cases 3
• Intradural-extraaxial lesions (inflammatory, infectious): Earlier disease onset, shorter symptom duration, higher disability scores, and pain in 87% of cases 3
• Intraaxial lesions (spinal cord pathology): Pain is uncommon (29% of cases), with prominent motor deficits 3

Key Clinical Features to Assess

Look specifically for:

• Distribution of weakness: Symmetric vs. asymmetric, proximal vs. distal involvement 2
• Reflex pattern: Reduction or loss of reflexes in affected segments 2
• Sensory loss: Dermatomal distribution and severity 2
• Sphincter dysfunction: Bladder/bowel involvement suggests cauda equina or conus involvement 4, 5
• Cranial nerve involvement: Suggests more extensive inflammatory process 6
• Temporal profile: Acute (cresting <6 months) vs. chronic (>6 months) 6

Imaging Strategy

MRI Without IV Contrast (First-Line)

MRI of the appropriate spinal region without IV contrast is the imaging modality of choice because it:

• Directly visualizes nerve roots and surrounding structures 1
• Detects disc herniations, spinal stenosis, and compressive lesions 1
• Identifies inflammatory changes in nerve roots 1
• Assesses for neoplastic involvement 1

Specific MRI protocols by region:

• Lumbosacral plexus MRI: Superior to lumbar spine MRI alone when clinical localization is uncertain between radiculopathy and plexopathy, with 71% of patients showing management changes based on findings 1
• Cervical spine MRI: Preferred for upper extremity polyradiculopathy 7
• Thoracic spine MRI: Essential when myelopathy or thoracic radiculopathy is suspected 1

When to Add IV Contrast

MRI with and without IV contrast is appropriate when:

• Initial noncontrast MRI is nondiagnostic or indeterminate 1
• Infectious etiology (e.g., CMV polyradiculopathy, sarcoidosis) is suspected 4, 5
• Neoplastic involvement requires characterization 1
• Inflammatory conditions need better delineation 1

CT Myelography (Alternative)

Consider CT myelography when:

• Patient has MRI-incompatible implanted devices 1
• Significant metallic artifact degrades MRI quality 1
• High-resolution assessment of thecal sac patency is needed 1

Caveat: Requires lumbar puncture for intrathecal contrast injection 1

Essential Laboratory Evaluation

CSF Analysis

Perform lumbar puncture with CSF analysis in all cases where inflammatory or infectious polyradiculopathy is suspected 2, 3:

• Cell count and differential: Elevated neutrophils suggest CMV polyradiculopathy in HIV patients 4; mononuclear pleocytosis suggests inflammatory causes 6
• Glucose: Hypoglycorrhachia is common in CMV polyradiculopathy 4
• Protein: Elevated in chronic inflammatory demyelinating polyradiculopathy (CIDP) and acute inflammatory demyelinating polyradiculopathy (AIDP) 2, 6
• Cytology: Essential when neoplastic involvement is suspected 3

CSF abnormalities are more common in intradural-extraaxial disease (inflammatory/infectious) compared to extradural or intraaxial causes 3

Electrodiagnostic Testing

EMG and nerve conduction studies (NCS) are mandatory to:

• Confirm polyradiculopathy and exclude polyneuropathy 2, 3
• Differentiate demyelinating from axonal patterns 2
• Identify subclinical involvement of additional nerve roots 3
• Correlate with MRI findings for anatomic localization 1

Key electrodiagnostic findings:

• Reduced compound muscle action potential (CMAP) amplitudes are more common in intradural-extraaxial disease 3
• Diffusely slow conduction velocity with proximal slowing suggests CIDP 6
• Multifocal involvement supports inflammatory etiology 2

Serologic Studies

Obtain targeted serologic testing based on clinical context:

• Autoimmune markers: When systemic lupus erythematosus (SLE) or other connective tissue disease is suspected 1
• Paraprotein screening: Serum protein electrophoresis and immunofixation for chronic polyradiculopathy 2
• Infectious serologies: CMV PCR in HIV patients, Lyme serology in endemic areas 4

Management Framework

Acute Polyradiculopathy

For acute inflammatory demyelinating polyradiculopathy (Guillain-Barré syndrome):

• Initiate treatment promptly; delay >2 weeks worsens outcomes 1
• Use intravenous immunoglobulin (IVIG) or plasma exchange as first-line therapy 2
• Monitor respiratory function closely 2

For infectious causes (e.g., CMV polyradiculopathy in HIV):

• Start ganciclovir immediately and continue indefinitely 4
• Improvement may be rapid but can take months; maintain therapy throughout 4
• Screen for concomitant CMV retinitis (often subclinical) 4

Chronic Polyradiculopathy

For chronic inflammatory demyelinating polyradiculopathy (CIDP):

• Corticosteroids are effective in approximately 60% of patients 6
• IVIG, plasma exchange, or rituximab for severe or refractory cases 1, 2
• Long-term immunosuppression may be necessary 6

Expected outcomes: Complete recovery is infrequent; approximately 60% achieve ambulatory status and return to work, 25% become wheelchair-dependent or bedridden, and 10% mortality 6

Compressive Etiologies

For extradural compression (disc herniation, spinal stenosis, neoplasm):

• Surgical decompression when there is progressive neurological deficit despite 6 weeks of conservative management 1, 7
• Laminectomy combined with corticosteroids for sarcoid polyradiculopathy 5

Systemic Disease-Related Polyradiculopathy

For SLE-related polyradiculopathy:

• Glucocorticoids alone or with immunosuppressive therapy achieve 60-75% response rate 1
• Consider IVIG, plasma exchange, or rituximab for severe cases 1

For sarcoid polyradiculopathy:

• Corticosteroids are first-line; 64% of treated patients improve 5
• Surgical decompression if compressive component is present 5

Red Flags Requiring Urgent Evaluation

Obtain immediate MRI and neurosurgical consultation for:

• Cauda equina syndrome: New-onset urinary retention, saddle anesthesia, bilateral leg weakness 1
• Progressive neurological deficits: Rapidly worsening weakness or sensory loss 7
• Sphincter dysfunction: New bladder or bowel dysfunction 4, 5
• Bilateral symptoms with myelopathy signs: Hyperreflexia, positive Babinski, spasticity 1, 7

Common Pitfalls

• Assuming single-level pathology: Multiple sites of nerve root involvement are common; image the entire relevant spinal region 7, 3
• Delaying CSF analysis: CSF findings are critical for differentiating inflammatory from compressive etiologies 3
• Stopping treatment prematurely: Infectious polyradiculopathy (especially CMV) requires prolonged therapy even after initial improvement 4
• Overlooking systemic disease: Screen for underlying conditions (HIV, sarcoidosis, SLE, paraproteinemia) in all cases 1, 2, 5
• Misinterpreting clinical localization: Plexopathy can mimic polyradiculopathy; electrodiagnostic testing is essential for differentiation 1, 2