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Lhermitte's sign

Lhermitte's sign is a transient neurological symptom characterized by an electric shock-like sensation that radiates down the spine and into the limbs, typically triggered by flexion of the neck.^[1] This paroxysmal paresthesia, also known as the barber chair phenomenon, is non-painful in most cases but can be startling and is often indicative of underlying pathology in the cervical spinal cord.^[1]^[2] First described in 1917 by Pierre Marie and Chatelin as a symptom in patients with multiple sclerosis (MS), it was later elaborated upon by French neurologist Jean Jacques Lhermitte in 1924, who linked it specifically to demyelination in MS and from whom the sign derives its name.^[1]^[2] Historically, it has been recognized as a classic but non-specific indicator of spinal cord involvement, with early reports emphasizing its occurrence in inflammatory and traumatic conditions.^[2] The sign is most commonly associated with MS, where it affects approximately 9-41% of patients, though prevalence varies by study and disease stage.^[1] Other notable causes include cervical spondylotic myelopathy, spinal cord tumors, trauma, radiation myelopathy (particularly following intensity-modulated radiation therapy for head and neck cancers), transverse myelitis, Behçet's disease, and nutritional deficiencies such as vitamin B12 deficiency.^[1]^[2] In MS, it often emerges during relapses involving the cervical cord and may resolve spontaneously as inflammation subsides.^[3]^[2] Pathophysiologically, Lhermitte's sign arises from demyelination or irritation of the large-diameter sensory fibers in the dorsal (posterior) columns of the cervical spinal cord, leading to ectopic neuronal firing when these fibers are mechanically stretched during neck flexion.^[1]^[2] This hyperexcitability is exacerbated by microglial activation and ephaptic transmission between adjacent axons in the demyelinated areas.^[1] Clinically, the sensation is brief, lasting seconds, and may extend to the trunk or be elicited by other head movements like extension, though flexion is the most reliable trigger.^[1]^[2] Diagnosis relies on a detailed history and physical examination, with magnetic resonance imaging (MRI) of the cervical spine often revealing lesions or compression; somatosensory evoked potentials (SSEPs) can support findings of dorsal column dysfunction.^[1] Treatment focuses on addressing the underlying etiology, such as disease-modifying therapies for MS or surgical decompression for structural causes, while symptomatic relief may involve anticonvulsants like carbamazepine or gabapentin, neck braces, or physical therapy.^[1]^[2] In many cases, the sign is self-limiting and does not require intervention beyond monitoring.^[1]

Clinical Presentation

Description

Lhermitte's sign is defined as a transient, electric shock-like sensation that radiates from the neck down the spine and into the limbs, typically elicited by flexion of the neck.^[1] This paroxysmal phenomenon is characterized by its brief duration, usually lasting only a few seconds, and its non-persistent nature, occurring episodically without ongoing discomfort between episodes.^[4] The sensation is often described as dysesthetic or paresthetic rather than a true pain, resembling a sudden jolt or tingling that travels along the posterior column pathways.^[2] Historically, it has been referred to descriptively as the "barber chair phenomenon," evoking the image of a sharp, startling feeling akin to an electric current.^[4] While Lhermitte's sign can arise in various neurological contexts, it is most commonly associated with multiple sclerosis, where it serves as a notable clinical indicator.^[3]

Symptoms and Triggers

Lhermitte's sign manifests primarily as a sudden, transient electric shock-like sensation that originates at the occiput and radiates downward along the spine to the lower back, frequently extending into the arms, trunk, or legs.^[1] Patients often describe this as a sharp jolt or current-like feeling, akin to an electrical discharge traveling through the body.^[2] The sensation is typically brief, lasting only a few seconds, and resolves spontaneously upon returning the neck to a neutral position.^[1] Variations in presentation include differences in radiation patterns, which are usually bilateral.^[5] A related variation, known as reverse Lhermitte's sign, involves an upward-radiating sensation triggered by neck extension.^[1]^[2] Intensity ranges from mild tingling or paresthesia to severe, debilitating shocks that may cause patients to gasp or halt activities.^[1] While most episodes are intermittent and self-limiting, persistent symptoms are rare, with the sign generally recurring only upon provocation rather than occurring continuously.^[2] The primary trigger is forward flexion of the neck, such as when bending down to tie shoes or looking at one's feet, which stretches the cervical spinal cord and elicits the sensation.^[3] Secondary triggers encompass coughing, sneezing, or lateral head turns, which increase intrathecal pressure or alter cord tension, as well as non-mechanical factors like fatigue, stress, heat exposure, or yawning.^[6]^[1] These provoking factors highlight the sign's paroxysmal nature and its association with demyelination in the dorsal columns of the cervical spinal cord, particularly during acute inflammatory episodes.^[1]

History

Discovery

The initial observation of what would later become known as Lhermitte's sign occurred in 1917, when French neurologists Pierre Marie and Chatelin described an electric shock-like sensation triggered by neck flexion in patients with head and cervical spine trauma sustained during World War I.^[1] This phenomenon was noted in the context of wartime injuries, highlighting early insights into spinal cord irritation, though it was not yet linked to specific demyelinating processes.^[7] In 1918, Beriel and Devic first described the sign in the context of multiple sclerosis.^[2] At the time, multiple sclerosis (MS) had been formally identified by Jean-Martin Charcot in 1868, but detailed clinical examinations of sensory symptoms in MS were still developing, particularly as post-World War I neurology clinics in France grappled with a surge of neurological cases from combat-related injuries.^[8] Jean Lhermitte, a prominent French neurologist working in Paris clinics such as the Salpêtrière Hospital, built on these observations through his clinical practice in the post-World War I era, where he encountered numerous patients with demyelinating diseases amid the broader advancement of neurological diagnostics. In 1924, Lhermitte published a seminal article in Revue Neurologique titled "Un cas de forme sensitive de la sclérose en plaques," detailing the sign in MS patients as a transient electric discharge sensation elicited by cervical flexion, based on direct observations of affected individuals.^[9] These cases underscored the sign's utility as an early indicator of posterior column involvement in MS, marking a pivotal moment in its association with demyelination during a period when MS recognition was solidifying through refined clinical correlations.^[1]

Eponym and Terminology

Lhermitte's sign is an eponym honoring Jean Lhermitte (1877–1959), a prominent French neurologist known for his contributions to clinical neurology, particularly in multiple sclerosis research. Although the phenomenon was first described in 1917 by Pierre Marie and Chatelin in the context of spinal cord lesions following trauma, it was Lhermitte who systematically explored and characterized it in 1920, publishing a seminal article in 1924 that linked the symptom to demyelination in multiple sclerosis. This work elevated its recognition, leading to the eponym's adoption despite the earlier descriptions, as Lhermitte's detailed analysis established its clinical and etiological significance.^[1]^[10] The term "Lhermitte's sign" is widely used in neurological literature, but some sources prefer "Lhermitte's phenomenon" to reflect its subjective nature as a patient-reported symptom rather than an objective clinical sign elicited by examination. This distinction aligns with medical terminology conventions, where signs are observable by clinicians and phenomena are experiential. The eponym gained traction internationally around 1928 when introduced to American medical texts, solidifying its place despite debates over attribution priority to Marie or Chatelin.^[1]^[10] Common synonyms include the "barber chair sign" or "barber chair phenomenon," derived from the electric shock-like sensation patients might experience when their head is tilted backward during a haircut, mimicking neck flexion. These alternative names emphasize the trigger mechanism but do not alter the core eponymous reference in modern neurology, where Lhermitte's association persists due to his influential role in understanding its pathophysiology.^[1]

Pathophysiology

Mechanism

Lhermitte's sign is triggered by flexion of the neck, which mechanically stretches the dorsal columns of the cervical spinal cord, thereby irritating demyelinated sensory fibers within these posterior structures.^[2] This stretching occurs primarily at the level of the upper cervical cord, where the posterior aspect experiences increased tension during forward bending of the head.^[1] The mechanical tension imposed on the posterior spinal cord structures during neck flexion leads to ectopic neural firing in the affected axons, as the demyelinated segments become susceptible to mechanical deformation.^[2] In the presence of demyelinating lesions, this tension disrupts the normal insulation of nerve fibers, allowing abnormal impulse generation at sites of vulnerability.^[1] Electrophysiologically, the sign arises from transient depolarization in sensory afferents, driven by stretch-induced hyperexcitability of demyelinated neurons, which lowers the threshold for action potential initiation and promotes ephaptic transmission between adjacent fibers.^[2] This hyperexcitability results in paroxysmal bursts of activity that propagate along the sensory pathways, manifesting as the characteristic shock-like sensation.^[1]

Neurological Basis

Lhermitte's sign primarily arises from demyelination or damage in the posterior (dorsal) columns of the cervical spinal cord, particularly at levels C2 to C5.^[1]^[5] These columns, consisting of the fasciculus gracilis and fasciculus cuneatus, contain large-diameter myelinated sensory fibers that transmit proprioceptive and vibratory signals from the body to the brain.^[1]^[11] The pathological changes involve loss of myelin sheaths around these axons, which exposes them to mechanical stress during neck movements such as flexion. This demyelination leads to increased neuronal hyperexcitability and ephaptic transmission, where electrical impulses cross between adjacent demyelinated fibers, generating abnormal sensory signals.^[5]^[2] Supporting evidence comes from radiographic studies of multiple sclerosis patients, where lesions in the posterior columns of the cervical cord strongly correlate with the presence of Lhermitte's sign, confirming the anatomical basis. Although direct autopsy studies are limited, pathological examinations in MS cases have shown plaque formations in these regions aligning with symptom occurrence.^[1] The sign's elicitation involves brief stretching of these vulnerable structures during head flexion.^[2]

Associated Conditions

Demyelinating Diseases

Lhermitte's sign exhibits the strongest association with multiple sclerosis (MS), the most common primary demyelinating disease of the central nervous system, where it arises from demyelination and inflammation in the posterior columns of the cervical spinal cord.^[1] Prevalence among MS patients ranges from approximately 10% to 40%, with studies reporting figures such as 33% in a cohort of 114 patients and 16% in a larger reassessment of 694 cases, often manifesting early in relapsing-remitting MS during initial episodes or relapses.^[13]^[14] This symptom typically reflects irritation of demyelinated axons, exacerbated by neck flexion, and tends to be transient, resolving as inflammation subsides.^[1] The sign also occurs in neuromyelitis optica spectrum disorder (NMOSD), another immune-mediated demyelinating condition characterized by longitudinally extensive transverse myelitis and similar spinal cord lesions affecting the central nervous system.^[1] Prevalence in NMOSD is higher than in MS, with one study documenting 20.5% of patients experiencing it compared to 4.3% in MS, while other reports indicate rates up to 35-60%, underscoring the role of aquaporin-4 antibody-associated cord pathology.^[15]^[16] These lesions, often more extensive than those in MS, contribute to the electric shock-like sensations triggered by head movement.^[1] Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is another demyelinating disorder linked to Lhermitte's sign, particularly in cases involving transverse myelitis with dorsal column involvement. While prevalence data are limited due to fewer studies, it has been reported in MOGAD patients with spinal cord inflammation, often presenting similarly to NMOSD but with potentially better recovery outcomes.^[17] Subacute combined degeneration of the spinal cord, resulting from vitamin B12 deficiency, represents another demyelinating-like process where Lhermitte's sign can emerge, mimicking MS through vacuolar myelopathy and posterior column involvement.^[18] This nutritional deficiency leads to impaired myelin synthesis and axonal degeneration, particularly in the dorsal and lateral columns, with case reports highlighting the sign as an initial presentation reversible upon B12 supplementation.^[19]^[20] In MS, Lhermitte's sign carries prognostic implications by signaling active cervical cord inflammation, often correlating with gadolinium-enhancing lesions on MRI and potentially heralding impending exacerbations in relapsing-remitting disease.^[1] Its emergence underscores ongoing demyelinating activity, prompting evaluation for disease-modifying therapies to mitigate progression.^[13]

Other Causes

Lhermitte's sign can arise from mechanical compression of the cervical spinal cord due to degenerative conditions such as cervical spondylosis or stenosis, where osteoarthritic changes lead to narrowing of the spinal canal and irritation of dorsal column fibers upon neck flexion.^[1] In these cases, the sign results from stretch-induced dysfunction in the compressed cord segments, often presenting in older adults with chronic neck pain and myelopathy.^[21] Transverse myelitis, an inflammatory disorder of the spinal cord, can also cause Lhermitte's sign through acute inflammation and demyelination affecting the dorsal columns; it may occur idiopathically, post-infectious, or as part of other autoimmune processes.^[1] Post-traumatic etiologies include whiplash injuries or direct spinal cord trauma, where the sign may emerge delayed after the initial event, even without overt neurological deficits, due to subclinical demyelination or axonal stretch in the cervical region.^[22] Spinal cord injuries can similarly provoke the symptom as a sequela, reflecting ongoing sensitivity in the dorsal columns from the mechanical insult.^[1] Iatrogenic causes encompass radiation myelopathy following therapeutic irradiation of the neck or upper chest, typically manifesting weeks to months post-treatment as a transient electric shock sensation from temporary demyelination in the cervical cord.^[23] Chemotherapy agents, particularly platinum-based compounds like cisplatin or oxaliplatin, may induce the sign through neurotoxic effects on sensory pathways, often resolving after discontinuation but highlighting dose-dependent vulnerability.^[1]^[24] Rare non-demyelinating associations include intramedullary tumors such as ependymoma, which can present with Lhermitte's sign due to tumor-induced distortion and secondary demyelination of dorsal column axons, typically progressing with tumor growth.^[25] Arnold-Chiari malformation may elicit the symptom through caudal displacement of cerebellar tonsils causing cord traction, often chronic and worsening with posture changes.^[1] In Behçet's disease, an inflammatory vasculopathy, the sign arises from neuro-Behçet involvement of the spinal cord, potentially transient during acute flares but indicative of underlying meningoencephalitis.^[26] These rare causes underscore the importance of imaging to differentiate from demyelinating processes like multiple sclerosis.

Diagnosis

Clinical Evaluation

The clinical evaluation of Lhermitte's sign begins with a straightforward bedside test performed during the neurological examination. The patient is typically seated comfortably, and the clinician instructs them to slowly flex the neck forward, bringing the chin toward the chest, while observing for any reported sensations or visible reactions such as flinching. A positive response is indicated by the patient's report of a transient, electric shock-like sensation radiating down the spine and into the extremities, which typically lasts only a few seconds.^[1]^[27] This sign demonstrates variable sensitivity and specificity depending on the underlying condition. In patients with multiple sclerosis (MS), the prevalence ranges from 9% to 41%, with one study reporting an incidence of 16% among approximately 700 individuals, reflecting its elicitation in a subset of affected patients but not as a universal feature. Overall, it lacks high specificity for MS alone, though it shows 97% specificity for compressive myelopathy in broader neurological contexts.^[1]^[2] Within the broader neurological examination, Lhermitte's sign is integrated as part of sensory testing for suspected myelopathy, often alongside assessments of deep tendon reflexes, coordination, and proprioception to evaluate dorsal column function and overall spinal cord integrity. The test is particularly relevant when cervical cord involvement is suspected, helping to localize potential lesions without requiring additional equipment.^[1]^[2] Evaluation also incorporates patient history to contextualize the finding, with clinicians querying symptoms suggestive of MS such as prior optic neuritis, gait disturbances, or sensory changes like paresthesia, which may correlate with the sign's presence and guide further diagnostic considerations. Triggers like neck movements or fatigue reported in the history can enhance the test's interpretive value during elicitation.^[1]

Imaging and Tests

Magnetic resonance imaging (MRI) of the cervical spine serves as the gold standard for evaluating the underlying causes of Lhermitte's sign, revealing structural abnormalities such as demyelinating plaques or compressive lesions.^[6] In multiple sclerosis (MS), MRI typically demonstrates T2-hyperintense lesions in the dorsal columns of the cervical spinal cord, present in approximately 95% of patients exhibiting the sign compared to 52% without it.^[1] For cervical spondylosis, imaging may show spinal cord compression due to degenerative changes like disc herniation or osteophytes.^[28] Cerebrospinal fluid (CSF) analysis is often performed to support the diagnosis of associated demyelinating diseases, particularly MS, where oligoclonal bands are detected in the majority of cases, indicating intrathecal immunoglobulin production.^[29] Blood tests for vitamin B12 levels are essential when deficiency is suspected, as subacute combined degeneration can mimic demyelinating pathology and cause the sign, with low serum levels confirming the etiology.^[30] Somatosensory evoked potentials (SSEPs) assess central conduction delays, showing prolonged latencies in the median and tibial nerves that correlate with cervical demyelinating lesions in MS patients with Lhermitte's sign.^[1] If MRI is contraindicated, such as in patients with pacemakers, computed tomography (CT) myelography can visualize spinal cord compression or abnormalities as an alternative.^[31] Electromyography (EMG) may be used to exclude peripheral nerve involvement, particularly if symptoms suggest radiculopathy rather than central myelopathy.^[27] In differentiating demyelinating causes, MRI lesion characteristics are key: short-segment lesions (spanning 1-2 vertebral segments) in the cervical cord favor MS, whereas longitudinally extensive transverse myelitis lesions (≥3 segments) suggest neuromyelitis optica spectrum disorder (NMOSD).^[32]^[33] Emerging artificial intelligence tools are being developed to analyze MRI characteristics and predict Lhermitte's sign in MS patients, as of 2025.^[34]

Management

Treatment of Underlying Cause

The primary approach to managing Lhermitte's sign involves addressing the underlying etiology to prevent progression and promote resolution of the neurological dysfunction.^[1] In cases associated with multiple sclerosis (MS), disease-modifying therapies (DMTs) are employed to mitigate demyelination and reduce lesion activity in the cervical spinal cord, where plaques often correlate with the sign's presence in up to 95% of affected patients.^[1] Examples of DMTs used in MS, which may indirectly benefit symptoms like Lhermitte's sign by managing the disease, include injectable interferons such as interferon beta-1a, which decrease relapse rates and slow disability progression by modulating immune responses, and monoclonal antibodies like ocrelizumab, which target CD20-positive B cells to suppress inflammatory activity and lesion formation on MRI.^[35] For acute MS relapses that may exacerbate the sign, high-dose intravenous corticosteroids, such as methylprednisolone, are administered to accelerate recovery by reducing edema around active lesions.^[35] For Lhermitte's sign stemming from vitamin B12 deficiency, which can lead to subacute combined degeneration of the spinal cord, prompt supplementation is essential to halt demyelination and restore myelin integrity.^[1] Initial treatment typically involves intramuscular injections of hydroxocobalamin (1 mg daily for the first week, followed by weekly doses), which effectively replenishes stores and reverses neurological symptoms, including the sign, in responsive cases.^[36] Oral high-dose cyanocobalamin (1-2 mg daily) may be used for maintenance once levels normalize, particularly in pernicious anemia or dietary deficiency etiologies.^[36] In compressive etiologies, such as cervical spondylotic myelopathy or spinal tumors, surgical intervention targets the mechanical irritation of the dorsal columns to alleviate the sign and prevent irreversible damage.^[1] Procedures like laminectomy or anterior cervical discectomy with fusion decompress the spinal cord, often leading to rapid symptom resolution; for instance, in spondylosis cases, postoperative improvement of Lhermitte's sign has been observed within days.^[21] For radiation-induced myelopathy, adjusting radiation dosing protocols in ongoing or future treatments minimizes further cord injury, though established cases may require supportive measures alongside etiology-specific care.^[1] Across etiologies, serial MRI of the cervical spine is crucial for monitoring treatment efficacy, allowing visualization of lesion resolution, reduced gadolinium enhancement in MS plaques, or decompression outcomes, thereby guiding adjustments to therapy and correlating with clinical improvement in the sign.^[1] In refractory scenarios, brief reference to symptomatic options may complement these targeted interventions.^[1]

Symptomatic Relief

Symptomatic relief for Lhermitte's sign focuses on alleviating the transient electric shock-like sensations through medications that target neuropathic pain and neural hyperexcitability, particularly when the underlying condition is stable or treatment is ongoing. First-line pharmacological options include anticonvulsants such as carbamazepine and gabapentin, which help stabilize neuronal membranes and reduce paroxysmal symptoms.^[37]^[38] Carbamazepine is typically initiated at 200-400 mg twice daily, titrated up to 600-1200 mg per day based on response and tolerance, and has demonstrated rapid symptomatic improvement in small case series of multiple sclerosis patients experiencing Lhermitte's sign.^[39]^[40] Gabapentin, another sodium channel modulator, is commonly dosed at 300-1200 mg three times daily, providing relief by dampening aberrant nerve firing, though individual responses vary.^[41]^[38] Alternatives like oxcarbazepine may be considered for better tolerability.^[37] These agents are preferred due to their efficacy in paroxysmal neuropathic symptoms associated with demyelination.^[37] For patients with prominent neuropathic pain components or inadequate response to anticonvulsants, tricyclic antidepressants such as amitriptyline (starting at 10-25 mg at bedtime, up to 75-150 mg daily) may be considered to modulate pain pathways, though evidence is more general to multiple sclerosis-related dysesthesias rather than Lhermitte's sign specifically.^[42]^[43] Opioids are generally avoided due to their limited efficacy in neuropathic pain and risk of short-term relief followed by tolerance.^[37] Non-pharmacological strategies include physical therapy to strengthen neck muscles and improve posture, thereby stabilizing the cervical spine and minimizing symptom triggers like forward flexion. Patients are advised to avoid provocative movements, and acupuncture has shown anecdotal benefits for overall multiple sclerosis pain, though controlled evidence for Lhermitte's sign remains limited.^[44] Symptomatic treatments can integrate with disease-modifying therapies to enhance quality of life without addressing the root pathology.^[38] A systematic review of observational data from over 450 patients indicates variable symptomatic improvement with carbamazepine and gabapentin, often in small-scale studies lacking randomized controls.^[38] Common side effects include dizziness, somnolence, and gastrointestinal upset, necessitating monitoring and dose adjustments, particularly in older adults or those with comorbidities.^[39]^[40]

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