What are the possible etiologies and recommended work‑up for a patient presenting with loss of vibratory sensation over the chest wall?

Vibratory Sensation Loss Over the Chest Wall: Etiologies and Work-Up

Primary Etiologic Consideration

Loss of vibratory sensation over the chest wall most commonly indicates posterior column dysfunction in the spinal cord, specifically affecting the dorsal column-medial lemniscus pathway, though peripheral neuropathy affecting large-diameter sensory fibers must also be considered. 1, 2

Neuroanatomic Localization

Spinal Cord Pathology (Most Common)

• Vibratory sensation is carried primarily through the dorsal columns (fasciculus gracilis and cuniculus) and potentially the dorsal spinocerebellar tracts, making posterior column lesions the most likely etiology for isolated vibratory loss 2, 3
• The dorsal spinocerebellar tract may also contribute to conscious proprioception and vibration sense, as demonstrated in patients with Brown-Séquard syndrome who had spared dorsal columns but lost vibratory sensation 2
• Vibratory sense can be lost independently of joint position sense and discriminatory touch, indicating separate fiber pathways within the posterior columns 3

Key Spinal Cord Etiologies to Consider

• Subacute combined degeneration (vitamin B12 deficiency): causes selective posterior column degeneration with early vibratory loss in lower extremities that can progress rostrally 1
• Multiple sclerosis: can cause demyelination of posterior columns with dissociated sensory loss 3
• Spinal cord infarction: particularly affecting the posterior spinal artery distribution 2
• Tabes dorsalis (neurosyphilis): classic cause of posterior column degeneration
• Cervical spondylotic myelopathy: compression affecting posterior columns

Peripheral Neuropathy Considerations

Large-Fiber Neuropathies

• Late-stage Lyme disease peripheral neuropathy presents as mild, diffuse "stocking-glove" process with reduced vibratory sensation of distal lower extremities as the most frequent examination finding 1
• Patients typically have intermittent limb paresthesias and radicular pain, with electrophysiologic studies showing confluent mononeuritis multiplex 1
• Two-tier IgG seropositivity for Borrelia burgdorferi is expected in Lyme peripheral neuropathy; absence of antibody should prompt alternative diagnosis 1

Drug-Induced Neuropathies

• Thalidomide-induced peripheral neuropathy (TIPN) causes bilateral symmetrical sensory disorders with distal paresthesia affecting toes initially, with deep vibratory sensitivity affected later 1
• TIPN occurs in 70% of patients treated for 12 months, showing selective loss of large-diameter fibers on sural nerve biopsy 1
• Bortezomib-induced peripheral neuropathy (BIPN) predominantly affects sensory nerves with proprioception changes and reduced deep tendon reflexes, though vibratory sensitivity changes are documented 1

Metabolic Causes

• Vitamin B1 (thiamine) deficiency is increasingly associated with loss of vibratory sensation in lower extremities, even with suboptimal rather than frank deficiency 1
• Early signs include cognitive decline, abnormal gait, and muscle weakness preceding overt neurologic deficits 1

Recommended Diagnostic Work-Up

Initial Clinical Assessment

1. Perform systematic sensory examination testing vibratory sense at multiple levels (toes, ankles, knees, iliac crests, sternum, fingers) using 128-Hz tuning fork to map the rostral extent of deficit 1
2. Test joint position sense and discriminatory touch separately, as these may be preserved despite vibratory loss, helping localize the lesion 3
3. Assess deep tendon reflexes bilaterally, as reduced or absent reflexes suggest peripheral neuropathy rather than central lesion 1
4. Examine for associated neurologic signs: weakness, ataxia, Romberg sign, Lhermitte sign (suggests cervical cord pathology) 1

Laboratory Evaluation

• Vitamin B12 level with methylmalonic acid and homocysteine if B12 is low-normal (subacute combined degeneration) 1
• Thiamine (vitamin B1) level, particularly in elderly or those with poor nutrition 1
• Lyme serology (two-tier testing with ELISA and IgG immunoblot) if endemic area exposure or compatible history 1
• Complete blood count, comprehensive metabolic panel, thyroid function
• Syphilis serology (RPR/VDRL with confirmatory testing)
• Hemoglobin A1c (diabetic neuropathy, though typically affects small fibers first)

Neuroimaging

• MRI of cervical and thoracic spine with and without gadolinium is the primary imaging study to evaluate for:
  • Demyelinating lesions (multiple sclerosis) 3
  • Compressive myelopathy (spondylosis, tumor, epidural abscess)
  • Spinal cord infarction 2
  • Posterior column signal abnormality (subacute combined degeneration shows T2 hyperintensity)

Electrodiagnostic Studies

• Nerve conduction studies and electromyography to differentiate peripheral neuropathy from central lesions 1
• In peripheral neuropathy, expect low amplitude sensory action potentials with length-dependent, sensory, axonal polyneuropathy pattern 1
• Normal nerve conduction studies with vibratory loss strongly suggest central (spinal cord) pathology 1

Specialized Testing When Indicated

• Lumbar puncture with CSF analysis if Lyme disease, multiple sclerosis, or neurosyphilis suspected 1
  • For Lyme: CSF lymphocytic pleocytosis, elevated protein, evidence of intrathecal antibody production 1
• Sural nerve biopsy rarely needed but shows perivascular lymphocytes in Lyme neuropathy and selective large-fiber loss in TIPN 1

Critical Clinical Pitfalls

• Do not assume peripheral neuropathy based solely on "stocking-glove" distribution—posterior column lesions can present similarly but require entirely different management 1, 3
• Vibratory sense loss alone does not localize the lesion; you must test joint position sense and discriminatory touch to determine if other posterior column functions are affected 3
• Normal CSF does not exclude Lyme peripheral neuropathy, as the pathophysiology occurs outside the subarachnoid space 1
• Intrathecal antibody production to Borrelia burgdorferi may persist for years after successful treatment, so this parameter does not indicate active disease 1
• Chest wall vibratory sensation during phonation or external vibration is a normal phenomenon mediated by Pacinian receptors and should not be confused with pathologic vibratory sense loss 4, 5