What are the differential diagnoses, recommended investigations, and management strategies for isolated bilateral triceps denervation?

Isolated Bilateral Triceps Denervation

Isolated bilateral triceps denervation is an extremely rare presentation that demands urgent investigation for central spinal cord pathology, bilateral radial nerve injury at the spiral groove level, or atypical neuralgic amyotrophy, with MRI of the cervical spine and bilateral upper extremity nerve conduction studies being the essential first-line investigations.

Differential Diagnoses

Central Causes (Highest Priority)

• Cervical spinal cord lesions affecting the C6-C7 anterior horn cells or corticospinal tracts bilaterally, including demyelinating disease, transverse myelitis, or vascular malformations 1
• Bilateral longitudinally extensive transverse myelitis (LETM) can present with isolated motor findings and should be excluded, particularly if MOG-IgG or AQP4-IgG positive 2
• Acute inflammatory demyelinating polyneuropathy (AIDP) can rarely begin with isolated limb weakness before progressing to typical ascending pattern 1

Peripheral Nerve Causes

• Bilateral radial neuropathy at the spiral groove level, though bilateral simultaneous involvement is exceptionally rare outside of trauma or compression (e.g., "Saturday night palsy" bilaterally) 3
• Neuralgic amyotrophy (Parsonage-Turner syndrome) can present with isolated triceps weakness and may be bilateral, representing a variant presentation 3
• Bilateral axillary nerve injury with involvement of the long head of triceps, as the long head receives innervation from the axillary nerve or posterior cord in up to 90% of cases, not exclusively from the radial nerve as classically taught 4, 5

Anatomical Considerations

• The triceps has three heads with complex innervation: the long head frequently receives axillary nerve contribution (71% of specimens show non-classic patterns), while lateral and medial heads are radially innervated 4
• Isolated long head involvement suggests axillary pathology, while all three heads suggest radial nerve or C7 root/cord pathology 6, 5

Recommended Investigations

First-Line Imaging

• MRI cervical spine with and without contrast to exclude central cord lesions, demyelinating disease, vascular malformations, or compressive myelopathy 1
• MRI bilateral upper extremities focusing on the radial nerve course from axilla through spiral groove and axillary nerve in quadrilateral space 2

Electrodiagnostic Studies

• Bilateral nerve conduction studies (NCS) and electromyography (EMG) to localize the lesion level, distinguish demyelination from axonal loss, and assess for conduction block 1, 3
• EMG should specifically examine all three triceps heads separately, plus radial-innervated forearm extensors and axillary-innervated deltoid to map the lesion distribution 3, 6

Laboratory Workup

• MOG-IgG and AQP4-IgG serology using cell-based assays if central demyelinating disease suspected 2
• CSF analysis if myelitis or inflammatory neuropathy suspected: look for lymphocytic pleocytosis, elevated protein, and absence of oligoclonal bands (OCBs) which favors MOG-EM over MS 2
• Vasculitis workup including ESR, CRP, ANA, ANCA, cryoglobulins if mononeuritis multiplex suspected 1

Additional Studies When Indicated

• MR neurography with dedicated nerve sequences if peripheral nerve pathology suspected but standard MRI non-diagnostic 2
• Ultrasound of bilateral radial and axillary nerves can identify focal nerve enlargement, compression, or structural abnormalities when performed by experienced operators 1

Management Strategies

Acute Phase Treatment

For inflammatory/demyelinating causes:

• Pulse methylprednisolone 1g IV daily for 3-5 days PLUS IVIG 2g/kg over 5 days for suspected acute inflammatory demyelinating neuropathy with severe or progressing symptoms 1
• Do not delay corticosteroids if inflammatory etiology suspected, as delay leads to irreversible neurological damage 1

For MOG-EM or transverse myelitis:

• High-dose IV methylprednisolone as first-line, with plasma exchange if inadequate response 2
• Consider rituximab for relapsing cases or steroid-dependent disease 2

Supportive Care

• Physical therapy to prevent contractures and maintain range of motion during recovery
• Occupational therapy for adaptive strategies given bilateral upper extremity involvement
• Neuropathic pain management with gabapentin, pregabalin, duloxetine, or tricyclic antidepressants if pain present 1

Surgical Considerations

• Nerve decompression or repair only if focal compressive lesion identified on imaging and no recovery after 3 months 5
• Tendon transfers may be considered for permanent deficits after 12-18 months if no recovery

Critical Pitfalls to Avoid

• Do not assume pure radial nerve pathology without considering axillary nerve contribution to the long head of triceps, as this is present in the majority of individuals 4, 5
• Do not delay imaging in bilateral presentations, as this suggests central pathology requiring urgent diagnosis 1
• Do not taper corticosteroids too rapidly in inflammatory cases, as this causes symptom recurrence requiring restart at higher doses 1
• Do not miss neuralgic amyotrophy as a cause of isolated triceps weakness, which can present after exercise or vaccination and has excellent prognosis with conservative management 3
• Do not rely solely on clinical examination to distinguish long head from lateral/medial head involvement, as EMG is required for precise localization 6