Cervical spine injuries often present clinicians with complex diagnostic dilemmas. When a patient reports sudden paroxysmal sensations following blunt trauma, healthcare providers must methodically localize the lesion. Recently, clinicians evaluated a compelling case involving a 59-year-old man who developed a delayed Lhermitte sign three to four weeks after sustaining a workplace fall. Immediately following the impact, the patient experienced a transient global sensory loss that resolved within minutes. Subsequently, he developed a posterior neck ache and bilateral paresthesias extending along the C6 dermatomal distribution. Although these acute symptoms vanished after several hours, he later experienced severe electric shock-like sensations radiating down his spine upon neck flexion. Serial neuroimaging revealed completely normal spinal cord architecture. Consequently, this scenario underscores how transient mechanical concussive injuries can induce delayed neurophysiological phenomena without overt structural damage. Understanding this temporal evolution allows clinicians to avoid unnecessary invasive interventions while providing appropriate reassurances.

Clinical Presentation and the Delayed Lhermitte Sign Phenomenon

Clinicians historically associate Lhermitte phenomenon with demyelinating conditions like multiple sclerosis. However, post-traumatic presentations represent an equally critical clinical entity that emergency physicians and neurologists regularly encounter. In this patient, the clinical evolution followed a distinct triphasic pattern. Initially, the direct impact produced a brief spinal cord concussion, precipitating transient sensory extinction across all dermatomes. After several minutes, localized posterior neck discomfort emerged alongside tingling across the bilateral thumb and index fingers. These sensory symptoms mapped cleanly to bilateral C6 dermatomes, suggesting temporary mechanical irritation of cervical sensory pathways. Fortunately, the peripheral paresthesias completely resolved within hours without persistent motor deficits. Nevertheless, several weeks later, the patient noted lightning-like paroxysms traversing his trunk whenever he bent his chin toward his chest. This classic provocation confirmed the delayed Lhermitte sign. Importantly, serial neurological evaluations demonstrated preserved motor strength, intact deep tendon reflexes, and preserved proprioception. Physicians must recognize that such delayed paroxysmal manifestations often cause immense anxiety for recovering trauma patients. Therefore, prompt clinical recognition helps prevent diagnostic confusion, excessive testing, and unwarranted escalations.

Pathophysiology of Post-Traumatic Dorsal Column Concussion

To comprehend this clinical paradox, physicians must examine the unique biomechanical properties of the cervical spinal cord. During sudden hyperflexion or hyperextension trauma, the cervical canal narrows dynamically, imparting mechanical deformation forces onto the dorsal columns. In particular, the large-diameter myelinated sensory fibers in the fasciculus cuneatus and gracilis experience acute shearing stress. Consequently, this mechanical strain disrupts axonal membrane stability without necessarily rupturing structural cell boundaries. Experimental models reveal that mechanical concussive injury induces transient focal demyelination and microvascular alterations. Furthermore, regenerating axonal segments express aberrant voltage-gated sodium channels along their exposed axolemma. This molecular remodeling substantially lowers the threshold for action potential propagation. Because damaged myelin impairs saltatory conduction, gentle mechanical tension triggers spontaneous, synchronized ectopic firing. Specifically, when the patient flexes his neck, the spinal canal elongates, stretching these vulnerable dorsal column fibers. This sudden mechanical elongation ignites intense trains of action potentials that ascend to sensory cortical areas. Clinically, the brain perceives these abnormal afferent bursts as searing electric shocks radiating symmetrically into the limbs. Thus, transient demyelination and axonal hypersensitivity perfectly explain the delayed symptomatic latency.

Diagnostic Workup and Ruling Out Structural Cord Pathology

When evaluating post-traumatic sensory phenomena, clinicians must promptly distinguish functional concussions from surgical emergencies. For example, cervical spine fractures, traumatic disc herniations, and epidural hematomas can rapidly compromise spinal cord integrity. Therefore, clinicians must perform emergency neuroimaging without delay. In this case, initial computed tomography and comprehensive magnetic resonance imaging of the brain and spine demonstrated no acute fractures, dislocations, or parenchymal lesions. Furthermore, follow-up contrast-enhanced spinal MRI confirmed the absolute absence of intramedullary T2 hyperintensities, cord edema, or hematomyelia. Notably, magnetic resonance imaging of the brain ruled out preexisting intracranial demyelination, confirming that multiple sclerosis did not trigger the episode. In addition to high-resolution structural neuroimaging, clinicians often utilize electromyography and nerve conduction studies to evaluate peripheral root function. However, when paroxysms arise strictly from dorsal column stretching, peripheral studies characteristically yield normal findings. Somatosensory evoked potentials can occasionally reveal delayed central conduction velocities, validating subclinical posterior column involvement. Nevertheless, normal imaging reassuringly indicates that surgical decompression is completely unwarranted. Consequently, clinicians rely heavily on serial examinations to confirm the non-progressive nature of the injury.

Differential Diagnosis of Paroxysmal Spinal Paresthesias

A broad differential diagnosis must always accompany delayed electric sensations following physical injury. First, clinicians must thoroughly consider traumatic cervical radiculopathy. Although radiculopathy also causes radiating paroxysmal shocks, the symptoms classically follow discrete unilateral dermatomes, worsen with Spurling maneuver, and spare the torso. Second, primary inflammatory myelopathies, such as transverse myelitis and neuromyelitis optica spectrum disorder, represent urgent considerations. These autoimmune conditions provoke acute cord swelling, prominent hyperreflexia, and bowel or bladder incontinence, findings entirely absent in concussive trauma. Third, physicians must diligently screen for metabolic myelopathies, particularly subacute combined degeneration caused by vitamin B12 deficiency. In India and worldwide, nutritional inadequacies and nitrous oxide exposure frequently deplete cobalamin stores, inducing profound dorsal column demyelination. Furthermore, cervical spondylotic myelopathy warrants detailed consideration, especially in individuals over fifty years old. Degenerative osteophytes or thickened ligamentum flavum can chronically narrow the spinal canal, predisposing the spinal cord to concussion during minor falls. Finally, clinicians must exclude radiation myelopathy and toxic drug-induced neuropathies. Ultimately, careful chronological correlation between trauma, transient dermatomal symptoms, and normal serial neuroimaging helps clinicians secure the definitive diagnosis.

Clinical Management, Prognosis, and Monitoring Strategies

Reassurance forms the cornerstone of effective management for patients experiencing post-traumatic dorsal column symptoms. Because patients frequently interpret intense electric sensations as impending paralysis, clear physician communication alleviates debilitating psychological stress. In most individuals, traumatic dorsal column demyelination undergoes spontaneous remyelination over several months. Consequently, clinical symptoms gradually diminish in intensity and frequency without surgical intervention. However, when paroxysmal shocks disrupt daily activities or provoke distress, targeted pharmacotherapy provides substantial symptomatic relief. For instance, membrane-stabilizing anticonvulsants like carbamazepine, oxcarbazepine, and gabapentin effectively suppress aberrant sodium channel firing. Moreover, low-dose tricyclic antidepressants or pregabalin can modulate neuropathic sensory pathways. Physicians should advise patients to avoid extreme neck hyperflexion maneuvers during early recovery stages. In addition, temporary use of a soft cervical collar may prevent repetitive mechanical stretching of injured cord axons. Nevertheless, long-term immobilization remains unnecessary and counterproductive. Physical therapists should instead guide patients through gentle isometric strengthening exercises once acute soreness subsides. Fortunately, prospective studies show that post-traumatic sensory phenomena carry an excellent prognosis, with complete spontaneous resolution expected within six to twelve months.

Frequently Asked Questions

What causes delayed Lhermitte sign after trauma?

Blunt cervical trauma can cause a mild spinal cord concussion that shears dorsal column axons. Over several weeks, localized post-traumatic demyelination and aberrant sodium channel clustering develop along damaged nerve fibers. Consequently, neck flexion mechanically stretches these hyperactive posterior columns, triggering synchronized ectopic action potentials perceived as electric shocks.

How is post-traumatic Lhermitte sign differentiated from multiple sclerosis?

Clinicians differentiate traumatic Lhermitte sign from multiple sclerosis through meticulous clinical history and magnetic resonance imaging. Post-traumatic cases feature a clear inciting injury, monophasic illness, and normal spinal cord imaging. In contrast, multiple sclerosis typically reveals dissemination in time and space, brain white matter lesions, and intramedullary demyelinating plaques.

What is the typical prognosis and treatment for traumatic Lhermitte phenomenon?

Traumatic Lhermitte phenomenon carries an excellent prognosis, with spontaneous remyelination typically resolving symptoms within six to twelve months. Management emphasizes patient reassurance and temporary avoidance of extreme neck flexion. For severely disruptive symptoms, physicians may prescribe membrane-stabilizing medications, such as carbamazepine, gabapentin, or pregabalin, to suppress ectopic neural firing.

Disclaimer: This content is for informational and educational purposes only and does not constitute medical advice. Treatment decisions should always be made by a qualified healthcare provider based on individual clinical evaluation. Refer to the latest local and national guidelines for clinical practice.

References

1. Jafari Tadi M et al. Clinical Reasoning: A 59-Year-Old Man With Delayed Electric Shock-Like Sensations After a Fall. Neurology. 2026 Oct 13. doi: 10.1212/WNL.0000000000218525. PMID: 42727039.
2. Chan RC, Steinbok P. Delayed onset of Lhermitte's sign following head and/or neck injuries. Report of four cases. J Neurosurg. 1984;60(3):609-612.
3. Khare S, Seth D. Lhermitte Sign. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024.