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Myerson's sign

Myerson's sign, also known as the glabellar tap sign or glabellar reflex, is a primitive neurological reflex elicited by repetitive light tapping on the glabella—the smooth area of skin between the eyebrows and above the nose—resulting in persistent involuntary blinking of the eyelids.^[1]^[2] In healthy individuals, the reflex typically manifests as blinking in response to the initial 2–4 taps before habituating, meaning the response diminishes or ceases due to adaptation in the neural pathway involving the trigeminal nerve (afferent) and facial nerve (efferent).^[1] However, persistence of the blinking beyond this habituation phase indicates an abnormal frontal release sign, where primitive reflexes reemerge due to disinhibition of higher cortical control.^[2]^[3] This sign holds particular clinical significance as a common and early indicator of Parkinson's disease (PD), a progressive neurodegenerative disorder, where it is observed in a majority of patients and may even reverse with levodopa treatment.^[1]^[3] It is elicited during neurological examination by tapping the glabella at a rate of approximately 2 times per second, with non-habituation confirming the positive sign.^[1] Although strongly associated with PD, Myerson's sign lacks diagnostic specificity and can also appear in other conditions, including dementia, progressive supranuclear palsy (PSP), and advanced age-related changes, occurring in about 10% of individuals aged 65–69 and up to 37% of those over 80.^[1]^[2] The reflex was first described in 1896 by British physician Walker Overend as a normal response to glabellar stimulation, but the persistent form was characterized and named after American neurologist Abraham Myerson, who detailed its exaggerated manifestation in Parkinson's patients in his 1944 publication.^[1] Myerson observed that in post-encephalitic parkinsonism, the sign was constantly present, though not universal in idiopathic PD, highlighting its utility as a supportive clinical finding rather than a standalone diagnostic criterion. Recent studies continue to explore its underlying mechanisms, such as potential disruptions in blink reflex habituation pathways, using tools like respiration sensors to quantify the response objectively in PD patients.^[3] Overall, Myerson's sign remains a simple, non-invasive bedside test integral to assessing extrapyramidal and frontal lobe dysfunction in neurology.^[4]

Definition and Physiology

Description of the Sign

Myerson's sign is characterized by the persistent involuntary blinking of both eyes in response to repeated percussion of the glabella, failing to habituate after the initial 2-3 taps. This reflex abnormality manifests as a lack of suppression, where the blinking response continues unabated despite ongoing stimulation, unlike the rapid extinction observed in normal individuals.^[2] The observable features include forceful and repetitive closure of the eyelids, often bilateral and symmetric, that persists through multiple successive taps without diminishing in intensity. This distinguishes it from the transient, habituating blink in healthy adults, highlighting the pathological release of a primitive reflex. Also referred to as the glabellar tap sign or Myerson's reflex, it represents a key indicator of neurological dysfunction.^[1]^[5] The anatomical target for eliciting the sign is the glabella, the smooth midline area between the eyebrows and above the nose, corresponding to the supraorbital region where percussion stimulates the underlying trigeminal nerve branches. As a frontal release sign, it exemplifies the re-emergence of primitive reflexes due to impaired higher cortical inhibition.^[1]

Normal Glabellar Reflex

The glabellar reflex in healthy individuals manifests as an initial response of 1 to 3 blinks upon repetitive tapping of the glabella, followed by rapid habituation in which blinking ceases despite continued stimulation.^[6] This habituation typically occurs within 2 to 5 taps and is mediated by descending inhibitory signals from higher cortical regions, including the parietal and premotor cortices, which modulate brainstem excitability in the trigeminofacial pathway.^[7] Developmentally, the reflex is prominent in newborns as a primitive protective response, eliciting blinks to glabellar tapping that habituate after 4 to 5 stimuli, and it integrates or suppresses by 4 to 6 months of age with frontal lobe maturation.^[8] In older children and adults, the reflex is either absent or exhibits even quicker habituation due to established cortical inhibitory mechanisms, reflecting normal neurological development.^[8] Physiologically, the glabellar reflex functions as a defensive blink to safeguard the eyes from perceived threats near the face, with afferent signals transmitted via the ophthalmic branch of the trigeminal nerve (cranial nerve V) and efferent responses executed through the facial nerve (cranial nerve VII) to the orbicularis oculi muscles.^[7] This brainstem-mediated arc ensures rapid eye closure while habituation prevents unnecessary responses to benign repetitive stimuli.^[7]

Pathological Persistence

Pathological persistence of the glabellar reflex, known as Myerson's sign, arises from the failure of habituation, where repeated stimulation continues to elicit blinks due to diminished suppressive influences from higher cortical centers. This results in the release of a primitive brainstem-mediated reflex, as the frontal lobes normally exert inhibitory control over the reflex arc, preventing ongoing responses after initial taps.^[9]^[10] The underlying reflex arc involves an afferent limb carried by the ophthalmic branch of the trigeminal nerve (cranial nerve V), which transmits sensory signals from the glabellar region to the central processing centers in the pontine reticular formation. From there, the efferent signals travel via the facial nerve (cranial nerve VII) to innervate the orbicularis oculi muscle, producing the blink. In pathological states, disruption in frontal or extrapyramidal circuits impairs this inhibition, allowing unchecked activation of the arc.^[11]^[7] Factors contributing to this persistence include age-related neurological changes, where the sign appears in approximately 10% of individuals aged 65–69 years and up to 37% of those aged 80 years or older, even without overt pathology, likely due to mild cortical atrophy. However, it becomes more pronounced in neurodegenerative conditions through greater disruption of basal ganglia or frontal lobe circuits, leading to enhanced reflex excitability and loss of habituation. Myerson's sign exemplifies frontal release signs, reflecting a broader disinhibition of primitive reflexes.^[12]

History and Eponym

Abraham Myerson's Contribution

Abraham Myerson (1881–1948) was an American neurologist and psychiatrist born in Yanova, Lithuania, who immigrated to the United States as a child and settled in Boston. He earned his medical degree from Tufts Medical School in 1908 and completed postgraduate training at Harvard Medical School, where he developed a deep interest in the intersection of neurology and psychiatry. Myerson directed research at Boston State Hospital for over two decades, rising to senior positions including clinical director, and later served as chief of the Department of Neurology and Psychiatry at Beth Israel Hospital from 1942 to 1945. His career emphasized empirical studies on the genetic and environmental factors in mental disorders, earning him recognition as a pioneer in psychiatric genetics and reflex physiology.^[13]^[14] The basic glabellar reflex as a normal response had been first described in 1896 by British physician Walker Overend. Myerson's most enduring contribution to clinical neurology is the identification of the persistent glabellar reflex, eponymously termed Myerson's sign, as a reliable indicator of extrapyramidal pathology. In his observations from the 1940s, he documented that repetitive tapping on the glabella—the smooth area between the eyebrows—elicits an initial blink reflex in healthy individuals, which rapidly habituates after 3 to 5 taps due to frontal inhibitory mechanisms. However, in patients with Parkinson's disease and other extrapyramidal disorders, this habituation fails, resulting in sustained, forceful blinking with each tap, reflecting a "release" of primitive reflexes from frontal lobe control. Myerson first reported this finding in the context of his examinations of parkinsonian patients, highlighting its utility as an early, non-invasive bedside test for basal ganglia dysfunction.^[4]^[1] This discovery stemmed from Myerson's broader investigations into human reflexes and their alterations in neurological disease, detailed in his publications on primitive and pathological responses. He interpreted the sign as evidence of diffuse frontal lobe impairment, linking it to the loss of higher cortical inhibition over brainstem reflex arcs in conditions like parkinsonism. Although the basic glabellar reflex had been noted earlier by others, Myerson's emphasis on its pathological persistence provided a seminal framework for its use in diagnosing frontal release signs, influencing subsequent neurological assessments. His work on this topic appeared in key papers within psychiatric and neurological journals, underscoring reflexes as accessible markers of brain dysfunction without relying on complex instrumentation.^[4]^[13]

Evolution of Recognition

Following Abraham Myerson's foundational description, Myerson's sign was incorporated into neurological examinations in the mid-20th century as a tool for assessing extrapyramidal and frontal lobe dysfunction. It featured prominently in standard neurology texts, including Russell N. DeJong's The Neurologic Examination (first edition, 1950), which classified it among primitive reflexes observable in extrapyramidal, pyramidal tract, and diffuse cerebral diseases. Early clinical literature from this period, such as Garland's 1952 review of parkinsonism, noted its frequent elicitation in affected patients, marking initial adoption in routine evaluations of motor disorders.^[15] By the 1950s and 1960s, the sign gained traction in studies of primitive reflexes, reflecting broader interest in frontal release phenomena. Research like Ekbom et al.'s 1952 work on perioral reflexes and Fisher's 1963 analysis of reflex blepharospasm contextualized it within abnormal blink responses, while Pearce et al.'s 1968 investigation demonstrated heightened primitive reflex activity, including persistent glabellar tapping, in Parkinson's patients compared to controls.^[16] These references solidified its place in literature on reflex persistence as an indicator of underlying neurodegeneration. In the 1970s, Myerson's sign achieved greater prominence in Parkinson's diagnostics amid advancing understanding of extrapyramidal signs. Klawans and Paulson's 1971 study explicitly examined primitive reflexes in parkinsonism, finding the glabellar response among the most consistently elicitable, while Paulson's 1977 chapter on dementia examinations highlighted its reliability in bedside assessments of cognitive and motor decline.^[17] This era saw its integration into protocols for evaluating disease progression, supported by observations of reflex modulation with emerging therapies like L-dopa. From the 1980s onward, empirical studies affirmed the sign's utility in early neurodegenerative detection, with Gossman and Jacobs' 1980 analysis reporting its elicitation in over 60% of parkinsonism cases across age groups, underscoring its sensitivity as a non-invasive marker.^[18] Today, it endures as a standard element of bedside neurology exams, valued for its simplicity and role in screening for conditions like Parkinson's, as validated in systematic reviews of diagnostic accuracy.^[6]

Clinical Examination

Procedure to Elicit the Sign

To elicit Myerson's sign, the patient should be seated comfortably in a well-lit room with their eyes open and directed forward, ensuring they are relaxed to minimize any startle response.^[6] The examiner positions themselves parallel to the patient, typically at eye level or slightly to the side, with the index finger extended downward toward the patient's forehead to avoid casting a shadow or creating a visual threat that could trigger extraneous blinking.^[6] The procedure begins by gently tapping the glabella—the smooth area of skin between the eyebrows and above the bridge of the nose—using the tip of the index finger.^[19] Taps should be delivered rhythmically at a frequency of approximately 1 to 2 per second, starting softly to assess the initial response and continuing for 5 to 10 repetitions, or up to 20 if needed to evaluate persistence.^[6] The examiner observes both eyelids simultaneously for bilateral blinking, noting the number of responses to the first few taps and any subsequent changes.^[19] Variations in technique include using a slightly firmer tap if the initial soft taps yield no response, though care must be taken to maintain consistency and avoid startling the patient with sudden or unexpected contact.^[6] In some cases, a reflex hammer may substitute for the finger to ensure even pressure, particularly if the patient's skin is sensitive or the glabella is difficult to access precisely.^[19] Throughout, the focus remains on clear visualization of the orbicularis oculi muscle contraction around both eyes to confirm the reflex pathway.^[6]

Interpretation and Limitations

A positive Myerson's sign is characterized by the failure of habituation in the glabellar reflex, where the patient exhibits persistent blinking in response to repetitive tapping on the glabella, typically defined as more than 3 consecutive blinks without suppression or, in some protocols, ≥4 blinks out of 21 taps delivered at 2 per second.^[6] This lack of habituation reflects an abnormal persistence of a primitive reflex, normally suppressed after the first 2-3 taps in healthy individuals. Interpretation requires careful observation during the elicitation procedure, where the initial blink is expected, but ongoing responses indicate potential frontal release or dysfunction. The sign demonstrates high sensitivity for identifying frontal lobe dysfunction, with studies reporting sensitivities of 78-83% in parkinsonian disorders.^[6]^[20] However, its specificity is low, ranging from 36-48% when differentiating Parkinson's disease from other conditions like essential tremor, due to frequent elicitation in non-pathological states.^[6]^[20] False positives are particularly common in normal aging, with prevalence rates of up to 19% in healthy older adults aged 66-82 years, increasing with advanced age.^[21]^[22]^[23] Key limitations include its poor diagnostic specificity, which limits its utility as a standalone test, necessitating correlation with other neurological signs and imaging for accurate assessment.^[6] The reflex can vary over time, with up to 20% of patients showing changes from abnormal to normal results within 2 years, indicating inconsistent reliability.^[6] Additionally, heterogeneous study methodologies and cutoff criteria contribute to variability in interpretation, underscoring the need for standardized protocols in clinical practice.^[24] While factors like patient anxiety or medications may influence reflex responses, empirical data on these confounders remain limited, further highlighting the sign's role as a supportive rather than definitive indicator. The sign is associated with increased risk of dementia, though specific quantitative measures vary across studies.^[24]

Pathophysiology

Frontal Release Signs

Frontal release signs represent the re-emergence of primitive reflexes in adults, arising from the disinhibition of brainstem-mediated responses due to frontal lobe dysfunction or damage to subcortical structures that normally provide inhibitory control.^[8] These reflexes, present in infancy to aid survival, are typically suppressed as the brain matures through the development of higher cortical functions in the frontal lobes.^[8] The term "release" signifies the pathological unmasking of these lower-level reflexes when supranuclear inhibition is lost, indicating a broader impairment in executive and regulatory neural processes.^[25] Common examples of frontal release signs include the grasp reflex, elicited by stroking the palm leading to involuntary finger flexion; the snout reflex, involving lip pursing in response to perioral tapping; and the palmomental reflex, characterized by chin muscle contraction upon palmar stimulation.^[8] Myerson's sign serves as an ocular variant within this category, manifesting as the failure to habituate to repeated glabellar taps, resulting in persistent eyelid closure.^[26] These signs collectively highlight the spectrum of disinhibited primitive motor responses tied to frontal pathology.^[27] In general, the pathophysiology of frontal release signs involves diffuse cortical atrophy or lesions that disrupt connections between frontal cortical regions and brainstem reflex centers, thereby eliminating the tonic inhibition that maintains reflex suppression in healthy adults.^[8] This disconnection allows brainstem circuits to dominate, reflecting a regression to earlier developmental states of neural organization.^[28]

Neural Mechanisms Involved

The glabellar reflex, underlying Myerson's sign, involves a well-defined afferent-efferent pathway originating in the brainstem. Sensory input is transmitted via the ophthalmic branch of the trigeminal nerve (cranial nerve V), which carries mechanical stimuli from the glabellar region to the principal sensory nucleus of the trigeminal nerve in the pons. This signal then relays through interneurons to the facial motor nucleus in the pons, from which motor output travels via the facial nerve (cranial nerve VII) to innervate the orbicularis oculi muscle, producing the blink response.^[1] Habituation of the reflex, which normally occurs after 2-5 taps in healthy individuals, is mediated by descending inhibitory projections from higher cortical centers, particularly the frontal lobes, to the brainstem reticular formation. Additionally, the basal ganglia, particularly the striatum, exert modulatory influence through dopaminergic pathways, facilitating coordinated suppression of reflexive blinking via interactions with frontal cortical circuits.^[8] In pathological conditions, disruptions to these inhibitory mechanisms lead to the persistence of the reflex seen in Myerson's sign. Dopamine depletion in the substantia nigra pars compacta, a hallmark of Parkinson's disease, impairs basal ganglia function and reduces dopaminergic modulation of frontal circuits, resulting in unchecked brainstem reflexes due to diminished inhibitory tone. Similarly, frontal lobe atrophy, as occurs in dementias, weakens descending inhibitory projections, further releasing the reflex from suppressive control and contributing to its pathological elicitation.^[29]

Clinical Significance

Association with Parkinson's Disease

Myerson's sign is present in 70-90% of patients with Parkinson's disease (PD), reflecting its high prevalence as a clinical feature in this condition, with cohort studies reporting rates of 78% in PD patients compared to 25% in healthy controls and 64% in those with essential tremor.^[6] Another investigation found an 80.5% prevalence in PD, underscoring its commonality across parkinsonian populations.^[1] This sign frequently appears early in the disease course, often preceding cardinal motor symptoms like bradykinesia or resting tremor, which aids in prompting earlier neurological evaluation.^[1] In clinical practice, Myerson's sign supports the diagnosis of PD by contributing to the assessment of parkinsonian syndrome, aligning with established frameworks such as the UK Parkinson's Disease Society Brain Bank criteria that emphasize bradykinesia alongside supportive signs of extrapyramidal dysfunction.^[30] Its sensitivity for PD ranges from 78% to 83%, making it a useful bedside marker, though its specificity (around 36-48%) is limited, as it does not reliably distinguish PD from other parkinsonian disorders.^[6] The sign is observed independent of direct measures of striatal dopamine loss.^[6] Research from the 1990s onward has highlighted Myerson's sign as a sensitive indicator of nigrostriatal degeneration in PD, where dopaminergic deficits in the basal ganglia impair inhibitory control over primitive reflexes, leading to reflex persistence.^[31] For instance, Vreeling et al. (1993) linked abnormal glabellar reflexes to parkinsonian pathology, while more recent analyses confirm the role of nigrostriatal pathways in suppressing such reflexes, with reduced dopamine inhibition contributing to their elicitation.^[32] These findings emphasize its value in tracking the neurodegenerative processes underlying PD progression.

Links to Other Neurological Conditions

Myerson's sign, as a frontal release sign, manifests in various dementias due to disruption of frontal lobe inhibitory mechanisms. In Alzheimer's disease, it is commonly observed, reflecting extrapyramidal involvement alongside cognitive decline.^[33]^[34] In frontotemporal dementia, particularly the behavioral variant, a positive glabellar sign frequently emerges as part of broader primitive reflex release, correlating with frontal atrophy and behavioral changes.^[35] Beyond Parkinson's disease, Myerson's sign appears in other parkinsonian syndromes, supporting differential diagnosis. In progressive supranuclear palsy, it is often elicited alongside vertical gaze palsy and axial rigidity, indicating midbrain and frontal dysfunction.^[36]^[37] Similarly, in multiple system atrophy, the sign persists with autonomic and cerebellar features, though it can also occur in essential tremor.^[38]^[39] The sign also links to structural neurological conditions involving frontal pathways. In strokes affecting frontal lesions, persistent blinking on glabellar tapping signals acute or chronic frontal lobe damage, often in the context of vascular parkinsonism.^[40] In normal pressure hydrocephalus, particularly with comorbid parkinsonism, Myerson's sign may be present, contributing to gait and cognitive impairments reversible by shunting.^[41] It is less common in primary psychiatric disorders but can occur when an organic basis, such as underlying neurodegeneration or infection, is involved.^[42]

References

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