Abstract
Background and Objectives
In clinical practice, we have observed that patients with Parkinson disease (PD) often have blepharoclonus, but its prevalence is not well described in the literature. Understanding the relative frequencies of blepharoclonus in PD and atypical parkinsonian syndromes may shed light on the diagnostic utility of this clinical sign. We aimed to assess (1) the frequency of blepharoclonus in patients with PD in a single-center cohort; (2) the association of blepharoclonus with disease stage, tremor severity, and non-motor symptoms; and (3) the frequency of blepharoclonus in synucleinopathy vs non-synucleinopathy–associated parkinsonism.
Methods
We prospectively enrolled 85 patients, 75 with PD and 10 with atypical parkinsonism. Blepharoclonus was considered present if eyelid fluttering was sustained for >5 seconds after gentle eye closure. For each patient, demographics were collected, and we completed selected questions from the MDS-UPDRS (Unified Parkinson's Disease Rating Scale) part 2, REM Sleep Behavior Disorder Questionnaire, and MDS-UPDRS part 3 tremor assessments and recorded the presence/absence of dyskinesia.
Results
63 of 75 patients with PD (84%) had blepharoclonus. Among the 10 patients with atypical parkinsonism, 5 had synucleinopathy syndromes. Blepharoclonus was present in 3 of 5 patients with synucleinopathy and 0 of 5 patients with non-synucleinopathy–associated parkinsonian syndromes.
Discussion
Blepharoclonus is prevalent in our PD cohort, suggesting possible utility as a clinical marker for PD. The absence of blepharoclonus in a patient with parkinsonism may suggest a non-synucleinopathy (e.g., tauopathy). Analysis of a larger cohort of both PD and atypical parkinsonism would be needed to establish whether blepharoclonus distinguishes PD from atypical parkinsonism, or synucleinopathy from non-synucleinopathy.
Introduction
Blepharoclonus has been defined as brief repetitive contractions of the orbicularis oculi muscles bilaterally that are provoked by the action of closing the eyes, visualized as fluttering of the eyelids. Blepharoclonus should be distinguished from the tonic contraction that is characteristic of blepharospasm.1 Blepharoclonus has been likened to eyelid tremor or an exaggerated stretch response of the levator palpebrae and orbicularis oculi. It has been associated with head injury, Arnold-Chiari malformation, juvenile Huntington disease, brainstem lesions including multiple lacunar infarcts, and congenital hydrocephalus with associated parkinsonism.1-5 Some authors have noted a similar rhythm and frequency as palatal myoclonus.2 Others have noted that this eyelid “tremor” can vary in rate and frequency in an individual.1 In Marsden's Book of Movement Disorders, blepharoclonus is noted to be common in Parkinson disease, but this statement is without a citation.6 It may be a pathologic version of physiologic eyelid fluttering and may be due to alterations in the substantia nigra pars reticulata-superior colliculus pathway.7 The phenomenon of blepharoclonus in PD is not well studied and its prevalence in PD is not known. We have found a case report of a patient with PARK9 (ATP13A2 variant),8 which is not a synucleinopathy, but with pathology consistent with neuronal ceroid lipofuscinosis,9 who was noted to have “blepharoclonus” on examination, but the phenomenology of this clinical sign was not described.
In this study, we aimed to determine the prevalence and clinical associations of blepharoclonus in a cohort of patients with Parkinson disease as well as with atypical parkinsonism, including those with dementia with Lewy bodies (DLB), progressive supranuclear palsy (PSP), multiple system atrophy (MSA), and drug-induced parkinsonism (DIP).
Methods
Consecutive patients presenting with a diagnosis of parkinsonism were asked to participate in this study. We enrolled 85 adult (older than 18 years) patients with parkinsonism from the Movement Disorder Clinic at the University of Miami between July 2020 and July 2022. We aimed to include patients with PD, DLB, MSA, PSP, and DIP. Consecutive enrollment of patients with established parkinsonism diagnoses, before blepharoclonus assessment, was intended to mitigate ascertainment bias. Patients were excluded if they had concurrent disorders affecting eyelid mobility including eyelid-opening apraxia, blepharospasm, or known structural brainstem pathology (ischemic, hemorrhagic, neoplastic, demyelinating, etc) or if they had a history of orbicularis oculi, levator palpebrae, or Mueller muscle weakness due to facial nerve or oculomotor nerve palsies, Horner syndrome, prior blepharoplasty, or recent (within 4 months) botulinum toxin injection. All patients agreed to enroll, but 3 patients with PD were excluded because of prior blepharoplasty, recent botulinum toxin injection, and eyelid-opening apraxia.
All patients with parkinsonism were enrolled in parallel. We stopped enrolling patients with PD after attaining our goal of 75, but continued to enroll patients with atypical parkinsonism. PD, DLB, MSA, and PSP were defined as meeting clinically probably diagnostic certainty per the most recent MDS diagnostic criteria.10-13 DIP was defined by the Diagnostic and Statistical Manual of Mental Disorders 5th Edition (DSM-V) diagnostic criteria.14 In the PD group, we included patients with Hoehn and Yahr stages 1–5 and patients with or without deep brain stimulation and did not standardize dopaminergic medication status at the time of examination.
We standardized the examination for the presence of blepharoclonus as follows. Patients were first asked to close their eyes tightly followed by opening to assess for orbicularis oculi weakness, ptosis, or eyelid-opening apraxia. Then, we asked patients to gently close their eyes and keep them closed for 10 seconds and looked for eyelid fluttering (this could be repeated up to 2 more times for reproducibility and to correct for too forcible closure). We defined blepharoclonus as eyelid fluttering on gentle closure that persisted for at least 5 seconds and resolved with eye opening or more forceful closure. The examination was videotaped and presented to 2 independent raters for corroboration of results. Blepharoclonus had to be present on the video assessment to be considered present; if it was previously noted on examination but absent during taping, this was counted as absent. Video 1 provides examples of blepharoclonus in Segment 1 and examples of patients without blepharoclonus in Segment 2.
Segment 1 shows examples of patients with parkinsonism and blepharoclonus, and segment 2 provides examples of patients with parkinsonism without blepharoclonus.Download Supplementary Video 1 (35.1MB, mp4) via http://dx.doi.org/10.1212/200240_Video_1
Demographic and disease data were collected. The REM Sleep Behavior Disorder Questionnaire (RBDQ) was completed for each patient, and a diagnosis of RBD was made based on RBDQ score ≥5. This cutoff has been reported to have a sensitivity of 96% and specificity of 56% among patients with polysomnography-proven RBD.15 Selected MDS-UPDRS questions were used to assess motor and non-motor clinical features.
T-statistic was used to calculate significance (p value) for data presented as means (e.g., MDS-UPDRS subscores). Summated tremor score significance was calculated by Wilcoxon rank-sum test. Chi-square statistic was used to calculate p value for data presented as a proportion of the data set (e.g., presence of dyskinesia and RBDQ score ≥5).
Standard Protocol Approvals, Registrations, and Patient Consents
This study was approved by our institutional ethical standards committee, the University of Miami IRB. Written informed consent was obtained from all participants in the study. Authorization was obtained for disclosure of videos obtained during the study.
Data Availability
Anonymized data not published within this article will be made available by request from any qualified investigator.
Results
Eighty-five patients with parkinsonism were enrolled (Table 1). Of these, 75 had PD. Ten patients had atypical parkinsonism or DIP distributed as follows: 4 DLB, 3 DIP, 2 PSP, and 1 MSA. Our cohort was predominantly Hispanic (83.5%) and 36.5% female, with mean age of 66.1 years and mean disease duration of 4 years (excluding 2 patients with unknown disease duration).
Table 1.
Demographics and Prevalence of Blepharoclonus in Patients With PD
| Blepharoclonus | Parkinson disease (N = 75) | Atypical parkinsonism synuclein (N = 5) | Atypical parkinsonism non-synuclein (N = 5) | |||
| Present | Absent | Present | Absent | Present | Absent | |
| Diagnosis | ||||||
| PD | 63 | 12 | — | — | — | — |
| DLB | 2 | 2 | 2 | 2 | — | — |
| MSA | 1 | 0 | 1 | 0 | — | — |
| PSP | 0 | 2 | — | — | 0 | 2 |
| DIP | 0 | 3 | — | — | 0 | 3 |
| Age, y | ||||||
| Mean ± SD (range) | 66.0 ± 10.7 (39–93) | 66.8 ± 10.8 (51–83) | 61.7 ± 5.4 (54–66) | 66.6 ± 9.2 (56–82) | — | 69 ± 9.9 (56–82) |
| Sex, female | ||||||
| N (%) | 21 (32%) | 3 (25%) | 2 (67%) | 3 (43%) | — | 2 (60%) |
| Ethnicity | ||||||
| Hispanic | 50 | 10 | 2 | 0 | — | 4 |
| Non-Hispanic | 13 | 2 | 1 | 2 | 1 | |
| Disease duration, y | ||||||
| Median (range) | 4 (1–14) | 5 (2–18) | 3 (2–5) | 3 (3) | — | 4.5a |
| Hoehn and Yahr (stage) | ||||||
| 1 | 5 | 2 | 0 | 0 | — | 0 |
| 2 | 52 | 9 | 2 | 2 | 1 | |
| 3 | 2 | 1 | 0 | 0 | 1 | |
| 4 | 2 | 0 | 1 | 0 | 2 | |
| 5 | 0 | 0 | 0 | 0 | 1 | |
Abbreviation: DIP = drug-induced parkinsonism; DLB = dementia with Lewy bodies; MSA = multiple system atrophy; PD = Parkinson disease; PSP = progressive supranuclear palsy.
Patients with PSP had a disease duration of 4 and 5 y; disease duration is unknown for 2 of 3 patients with DIP.
Of the 75 patients with PD, 63 (84%) had blepharoclonus. There was 100% concordance among independent raters in determining the presence of blepharoclonus on video review. Blepharoclonus was present across the spectrum of disease severity, including patients with HY stages 1 through 4 (although the majority, 81%, were HY stage 2). Average disease duration was similar among PD patients with blepharoclonus (5.35 years) compared with PD patients without blepharoclonus (5.75 years). There was no sex differential in the PD group with or without blepharoclonus, with 33% and 25% female representation, respectively (χ2 statistic is 0.32; p = 0.57).
There were no significant differences between tremor, anxiety, depression, constipation, sleep disorder, excessive daytime sleepiness, hallucinations/delusions, or speech difficulty scores (as assessed by MDS-UPDRS subscores) or between RBDQ scores in PD patients with or without blepharoclonus (Table 2). The presence of dyskinesia trended toward an association with the absence of blepharoclonus, present in 50% of patients without blepharoclonus compared with 24.8% of patients with blepharoclonus, but this did not reach statistical significance (χ2 statistic is 3.43; p = 0.06).
Table 2.
Motor and Non-motor Features Among PD Patients With and Without Blepharoclonus
| Clinical characteristic | Assessment instrument (range of possible values) | Metric | Blepharoclonus present (N = 63) | Blepharoclonus absent (N = 12) | p Value |
| RBD | RBDQ (range 0–10) | N (%) with score ≥5 | 41 (65%) | 4 (33%) | 0.4 |
| Tremor | MDS-UPDRS 3.15–3.17 (range 0–12) | Mean | 4.9 | 3.3 | 0.19 |
| Concurrent dyskinesia | MDS-UPDRS part 3 | N (%) present | 15 (24.8%) | 6 (50%) | 0.06 |
| Depression | MDS-UDPRS 1.3 (range 0–4) | Mean | 0.84 | 1.1 | 0.44 |
| Anxiety | MDS-UDPRS 1.4 (range 0–4) | Mean | 2.1 | 1.5 | 0.11 |
| Constipation | MDS-UDPRS 1.11 (range 0–4) | Mean | 1.1 | 1.2 | 0.76 |
| Speech | MDS-UDPRS 2.1 (range 0–4) | Mean | 0.8 | 0.9 | 0.55 |
| Hallucinations/Delusions | MDS-UDPRS 1.2 (range 0–4) | Mean | 0.3 | 0.2 | 0.58 |
| Sleep problems | MDS-UDPRS 1.7 (range 0–4) | Mean | 1.3 | 1.1 | 0.48 |
| Daytime sleepiness | MDS-UDPRS 1.8 (range 0–4) | Mean | 1 | 1.2 | 0.31 |
Abbreviations: MDS-UPDRS = Movement Disorder Society Unified PD Rating Scale; RBD = REM sleep behavior disorder; RBDQ = RBD Questionnaire.
Of the 10 patients with atypical parkinsonism or DIP, 3 (30%) had blepharoclonus. All 3 had a form of atypical parkinsonism that is associated with an underlying synucleinopathy (2 with DLB and 1 with MSA). No patients with atypical parkinsonism unrelated to synuclein (PSP or DIP) had blepharoclonus.
Discussion
Because the clinical phenomenology of blepharoclonus has previously not been well characterized, any operational definition must consider the heterogeneity of normal eyelid movements on gentle eye closure. Under physiologic circumstances, the frequency and amplitude of eyelid movements may vary, and these movements may be inconsistently present or perhaps fatigable. The eyelids may demonstrate motor impersistence, with an initial phase during which the eyelids slowly rise on attempted maintenance of closure, followed by a quicker corrective movement toward the eyelid-closed position without oscillation or fluttering. By contrast, we defined blepharoclonus as eyelid fluttering on gentle closure that persisted for at least 5 seconds and resolved with eye opening or more forceful closure and found a high degree of concordance between raters in designating the presence or absence of blepharoclonus based on this definition. Moreover, we required that the movement had to be present on the videoed assessment to be counted, even if blepharoclonus had been present on assessment before video. Patients with slower and more irregular “fluttering” were considered not to have blepharoclonus. Our exclusion of patients with inconsistently present blepharoclonus may underestimate the prevalence because we do not know whether consistent vs inconsistent blepharoclonus has a different clinical relevance. Examples of eyelid closure followed by fatigable and irregular fluttering as well as motor impersistence are shown in Video 2. Objective, electrophysiologic assessment might better define and standardize the definition of blepharoclonus in patients with parkinsonism.
Examples of eyelid movements that occur with eyelid closure that were not consistent with our definition of blepharoclonus due to irregularity in frequency and impersistence.Download Supplementary Video 2 (31.9MB, mp4) via http://dx.doi.org/10.1212/200240_Video_2
Using the foregoing definition, blepharoclonus was a frequent clinical finding in our cohort; it was present in 84% of patients with PD and across a range of disease severity and duration. This prevalence rate is consistent with our previously reported rates from smaller non-overlapping cohorts. In a series of 30 randomly selected patients with PD, 86.6% had blepharoclonus16; and in a series of consecutively collected new PD patient encounters, 17 of 20 (85%) had blepharoclonus.17 Our cohort, although relatively small and recruited from a single center, included a predominantly Hispanic population (over 80% of the participants) and more than one-third were female.
The number of patients with atypical parkinsonism or DIP was too limited to draw firm conclusions, but the prevalence of blepharoclonus was substantially lower in this group of patients. Notably, blepharoclonus was not detected in any of the 5 patients with PSP or DIP, the 2 entities included in this cohort that are not characterized by synuclein pathology. A larger cohort of atypical parkinsonism and DIP will be needed to determine whether the difference in prevalence of blepharoclonus we have observed compared with PD is real and to evaluate the utility of blepharoclonus in differentiating synuclein from non-synuclein pathologies in patients with parkinsonism.
Other limitations of our study include the unknown prevalence of blepharoclonus in the “healthy/normal” population or in conditions with brainstem pathology; these are frequencies that will affect the diagnostic utility of this clinical marker. In addition, RBDQ was used as a surrogate for the gold standard of polysomnography to diagnose RBD. A further limitation is that patients often have multiple coexisting pathologies on autopsy, complicating analyses that assign clinical diagnoses/signs to a single pathologic category.
With these limitations in mind, blepharoclonus might, nevertheless, have value as a diagnostic clinical marker given its presence in early PD, but this would require determining the discriminative value of blepharoclonus in an unselected population of patients referred for evaluation of suspected PD. If blepharoclonus proves to be a discriminating clinical marker, and is present in early PD, then detecting the presence of this phenomenology might have clinical utility in detecting or confirming disease diagnosis. Assessing its prevalence in parkinsonian syndromes will clarify whether the presence or absence of this sign correlates with underlying pathology, i.e., whether blepharoclonus is more likely to be present in synucleinopathies more generally. Future studies should also include an assessment for blepharoclonus in patients with idiopathic REM sleep behavior disorder, and/or in pathogenic LRRK2 or GBA variant carriers, to determine whether blepharoclonus might be a prodromal feature of PD. With therapeutic research shifting toward interventions in earlier disease stages, an easily and inexpensively captured clinical marker such as blepharoclonus that could help with the diagnosis of PD would facilitate the refinement of cohorts for such trials.
In conclusion, blepharoclonus is prevalent in PD, and perhaps in other synucleinopathies, and may prove to be a useful clinical marker in early disease. Clinicians, when faced with a diagnostic conundrum, may take the absence of blepharoclonus in a patient to favor a diagnosis other than PD, DLB, or MSA. In the appropriate clinical context, the presence or absence of blepharoclonus might help discriminate “synucleinopathies” from “tauopathies” like PSP, or perhaps from secondary parkinsonism such as drug-induced or vascular etiologies. However, analysis of a larger cohort of both PD and atypical parkinsonism would be needed to establish whether blepharoclonus distinguishes PD from atypical parkinsonism, or synucleinopathy from non-synucleinopathy. Future studies should help to elucidate the role of blepharoclonus in the diagnosis of parkinsonism and in the study of presymptomatic disease.
Appendix. Authors
| Name | Location | Contribution |
| Jason Margolesky, MD | Neurology, University of Miami Miller School of Medicine, FL | Drafting/revision of the manuscript for content, including medical writing for content; major role in the acquisition of data; study concept or design; analysis or interpretation of data |
| Matthew Feldman, MD | Neurology, University of Miami Miller School of Medicine, FL | Drafting/revision of the manuscript for content, including medical writing for content; major role in the acquisition of data; analysis or interpretation of data |
| Sarah Marmol, MD | Neurology, University of Miami Miller School of Medicine, FL | Drafting/revision of the manuscript for content, including medical writing for content; major role in the acquisition of data; analysis or interpretation of data |
| Danielle S. Shpiner, MD | Neurology, University of Miami Miller School of Medicine, FL | Drafting/revision of the manuscript for content, including medical writing for content; analysis or interpretation of data |
| Corneliu Luca, MD, PhD | Neurology, University of Miami Miller School of Medicine, FL | Drafting/revision of the manuscript for content, including medical writing for content; analysis or interpretation of data |
| Henry P. Moore, MD | Neurology, University of Miami Miller School of Medicine, FL | Drafting/revision of the manuscript for content, including medical writing for content; study concept or design; analysis or interpretation of data |
| Carlos Singer, MD | Neurology, University of Miami Miller School of Medicine, FL | Drafting/revision of the manuscript for content, including medical writing for content; analysis or interpretation of data |
| Joanne Wuu, ScM | Neurology, University of Miami Miller School of Medicine, FL | Drafting/revision of the manuscript for content, including medical writing for content; analysis or interpretation of data |
| Ihtsham U. Haq, MD | Neurology, University of Miami Miller School of Medicine, FL | Drafting/revision of the manuscript for content, including medical writing for content; study concept or design; analysis or interpretation of data |
| Michael Benatar, MBChB, DPhil | Neurology, University of Miami Miller School of Medicine, FL | Drafting/revision of the manuscript for content, including medical writing for content; study concept or design; analysis or interpretation of data |
Study Funding
NINDS; NINDSU10 NS 077423Parkinson Foundation.
Disclosure
J. Margolesky reports research funding/salary support from NIH/NINDS. D.Shpiner reports support from the Parkinson Foundation. C. Luca received educational grants and consulting fees from Medtronic, Boston Scientific, and Abbott. H. Moore received compensation due to participation in Advisory Boards from Ipsen Pharma. He has received research funding/salary support from MODUS Outcomes LLC, TEVA Pharmaceuticals, Sage Therapeutics, Bukwang Pharmaceutical, Neurocrine Biosciences, CHDI Foundation, and Impax Laboratories LLC. He has received foundation grants from the American Parkinson's Disease Association (APDA) and the Huntington's Disease Society of America (HDSA). C. Singer received honoraria form the Movement Disorders Society and research support from the Parkinson's Foundation. J. Wuu reports research support from the NIH, ALSA, and MDA. I. Haq has consulted for compensation for Medtronics, Boston Scientific, and Abbott DBS. He has received research funding and/or salary support from the NINDS, NIA, NIMH, Parkinson's Foundation, American Parkinson's Foundation of America, Parkinson's Study Group, and the Michael J Fox Foundation. M. Benatar reports grants from the NIH, the Muscular Dystrophy Association, and the ALS Association; as well as consulting fees for Alector, Alexion, Annexon, Arrowhead, Biogen, Cartesian, Denali, Eli Lilly, Horizon, Immunovant, Novartis, Roche, Sanofi, Takeda, UCB, and UniQure. The University of Miami has licensed intellectual property to Biogen to support design of the ATLAS study. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Segment 1 shows examples of patients with parkinsonism and blepharoclonus, and segment 2 provides examples of patients with parkinsonism without blepharoclonus.Download Supplementary Video 1 (35.1MB, mp4) via http://dx.doi.org/10.1212/200240_Video_1
Examples of eyelid movements that occur with eyelid closure that were not consistent with our definition of blepharoclonus due to irregularity in frequency and impersistence.Download Supplementary Video 2 (31.9MB, mp4) via http://dx.doi.org/10.1212/200240_Video_2
Data Availability Statement
Anonymized data not published within this article will be made available by request from any qualified investigator.