Prolonged orbicularis oculi activity

Tozlovanu, Viorika; Forget, Robert; Iancu, Andreea; Boghen, Dan

doi:10.1212/wnl.57.6.1013

Cited by 42 publications

(12 citation statements)

References 17 publications

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“…The third EMG pattern, (involuntary levator inhibition [ILPI]) is the rarest type (n = 15/94 [15.9%]) and is hallmarked by a normal reciprocal relation between the OO and the LPS, along with episodes of involuntary LPS inhibition during periods of complete OO inactivity that involves the entire muscle including the pretarsal OO. 8,17,23,34,36,80 This electromyographic silence of the LPS along with a quiescent and normal OO is consistent with the classic description of AEO and has been referred to as “involuntary levator palpebrae inhibition” (ILPI), or the true type of eyelid apraxia. 22,41 According to some authors, ILPI is not compatible with a dystonia, but may more properly conform to the definition of a true apraxia, 22,27,37 a notion which has already been discredited in the previous section about clinical evidence.…”

Section: Resultssupporting

confidence: 61%

Debunking the Puzzle of Eyelid Apraxia: The Muscle of Riolan Hypothesis

Tawfik

Dutton

2022

Ophthalmic Plastic &Amp; Reconstructive Surgery

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Apraxia of eyelid opening (AEO) has been defined by the presence of an intermittent nonparalytic bilateral loss of the volitional ability to open the eyes or to maintain the eyelids in a sustained elevated position. It is not known whether the condition represents an apraxia, a dystonia, or a freezing phenomenon, and several different nomenclatorial terms have been suggested for this condition including the so-called AEO (scAEO), blepahrocolysis, focal eyelid dystonia, and so on. The primary goal of this review is to attempt to clarify the pathogenetic mechanisms underlying scAEO as a clinical phenomenon. This review also addresses the issue of whether scAEO is part of the spectrum of blepharospasm (BSP) which includes BSP, dystonic blinks and other dystonic eyelid conditions, or whether it is a separate phenomenologically heterogeneous disease with clinical features that merely overlap with BSP.Methods: A literature review was conducted in PubMed, MEDLINE, PubMed Central (PMC), NCBI Bookshelf, and Embase for several related keywords including the terms "apraxia of eyelid opening," "pretarsal blepharospasm," "blepharocolysis," "eyelid freezing," "eyelid akinesia," "levator inhibition," "blepharospasm-plus," as well as "blepharospasm." The clinical findings in patients with scAEO who fulfilled the classic diagnostic criteria of the disease that were originally set by Lepore and Duvoisin were included, while patients with isolated blepharospasm or dystonic blinks (DB) were excluded. In addition, electromyographic (EMG) studies in patients with scAEO were reviewed in detail with special emphasis on studies that performed synchronous EMG recordings both from the levator muscle (LPS) and the pretarsal orbicularis oculi muscle (OO).Results: The apraxia designation is clearly a misnomer. Although scAEO behaves clinically as a hypotonic freezing phenomenon, it also shares several cardinal features with focal dystonias. The authors broadly categorized the EMG data into 3 different patterns. The first pattern (n = 26/94 [27.6%]) was predominantly associated with involuntary discharges in the OO muscle and has been termed pretarsal blepharospasm (ptBSP). The commonest pattern was pattern no. 2 (n = 53/94 [56.38%]), which was characterized by involuntary discharges in the OO muscle, together with a disturbed reciprocal innervation of the antagonist levator muscle and is dubbed disturbed reciprocal innervation (DRI). This EMG pattern is difficult to discern from the first pattern. Pattern no. 3 (n = 15/94 [15.9%]) is characterized by an isolated levator palpebrae inhibition (ILPI). This levator silence was observed alone without EMG evidence of contractions in the pretarsal orbicularis or a disturbed reciprocal relation of both muscles.Conclusion: EMG evidence shows that the great majority (84%) of patients show a dystonic pattern, whereas ILPI (16%) does not fit the dystonic spectrum. The authors propose that a spasmodic contraction of the muscle of Riolan may be the etiological basis for levator inhibition in patients with ...

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Section: Resultssupporting

confidence: 61%

Debunking the Puzzle of Eyelid Apraxia: The Muscle of Riolan Hypothesis

Tawfik

Dutton

2022

Ophthalmic Plastic &Amp; Reconstructive Surgery

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“…Blepharospasm may co-exist, and AEO is occasionally unmasked by chemodenervation of the OO to treat blepharospasm, mistaken as treatment failure or ptosis due to the spread of botulinum toxin and treated with the addition of botulinum toxin to the pretarsal OO (122–124). While the OO is by definition clinically and electrophysiologically silent in AEO, selective electromyographic recordings of the pretarsal portion of the OO have revealed the presence of abnormal activity in some patients (125). Because of its technical challenges, this finding has been difficult to replicate on a larger scale, and it is unclear if these patients truly have AEO, a subtle variant of blepharospasm, or a distinct entity altogether that some have termed “OO motor persistence.”…”

Section: Apraxia Of Eyelid Opening and Closurementioning

confidence: 99%

Eyelid Dysfunction in Neurodegenerative, Neurogenetic, and Neurometabolic Disease

Hamedani

Gold

2017

Front. Neurol.

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Eye movement abnormalities are among the earliest clinical manifestations of inherited and acquired neurodegenerative diseases and play an integral role in their diagnosis. Eyelid movement is neuroanatomically linked to eye movement, and thus eyelid dysfunction can also be a distinguishing feature of neurodegenerative disease and complements eye movement abnormalities in helping us to understand their pathophysiology. In this review, we summarize the various eyelid abnormalities that can occur in neurodegenerative, neurogenetic, and neurometabolic diseases. We discuss eyelid disorders, such as ptosis, eyelid retraction, abnormal spontaneous and reflexive blinking, blepharospasm, and eyelid apraxia in the context of the neuroanatomic pathways that are affected. We also review the literature regarding the prevalence of eyelid abnormalities in different neurologic diseases as well as treatment strategies (Table 1).

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“…[13][14][15] Involuntary spasms of the pretarsal orbicularis oculi hindering lid elevation has been implicated; demonstration of abnormal persistence of electromyographic activity in the orbicularis oculi muscle during attempted lid elevation and the response to botulinum toxin injections in some of the patients support this theory. [15][16][17] Thus, ALO may share the pathophysiology of blepharospasm in which blink reflex abnormalities including decreased inhibition of the R2 response by electrical stimulation of supra-orbital nerve, and abnormal plasticity of the blink reflex circuit have been shown. [18][19][20][21] Inhibition of the levator palpebrae superioris (LPS) may be the mechanism in some cases of ALO.…”

Section: Discussionmentioning

confidence: 99%

Apraxia of Lid Opening in Subthalamic Nucleus Deep Brain Stimulation for Parkinson's Disease—Frequency, Risk Factors and Response to Treatment

Krishnan

Shetty

Puthanveedu

et al. 2021

Movement Disord Clin Pract

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BackgroundBackground: New-onset apraxia of lid opening (ALO) is reported to occur in Parkinson's disease (PD) patients following Deep Brain Stimulation (DBS). There are only few systematic studies on this uncommon disorder of eyelid movements. Objectives Objectives: We aimed to examine the frequency, temporal evolution, predisposing factors and response to treatment, of new-onset ALO in PD patients who underwent bilateral subthalamic nucleus (STN) DBS. Methods Methods: We retrospectively reviewed the data of patients who underwent STN DBS at our centre between 1999 and 2017, with a minimum of 2 years of follow up after surgery. Results Results: New-onset ALO was seen in 17 (9.1%) of the 187 patients after an average of 16.9 months (Range -6-36 months). Comparison of the groups with and without ALO revealed that ALO occurred more often in older patients, both at the onset of PD symptoms and at surgery and in those with non-tremor dominant subtypes of PD and freezing of gait at baseline. The extent of levodopa dose reduction after surgery and the pre-operative severity of motor symptoms were not risk factors. Response to adjustments of dopaminergic medications and stimulation parameters was ill-sustained or nil. Botulinum toxin therapy resulted in satisfactory improvement in the majority. Conclusions Conclusions: New-onset ALO is an uncommon phenomenon that manifests months after STN DBS. Development of ALO is likely to be due to the effects of chronic stimulation of basal ganglia-thalamo-cortical or brain stem circuits controlling lid movements in susceptible patients. Botulinum toxin therapy offers relatively better relief of symptoms than other strategies.Deep Brain Stimulation (DBS) is an effective treatment option for Parkinson's disease (PD) patients with motor complications of treatment. Subthalamic nucleus (STN) is the preferred target for DBS in PD in most centers. STN DBS improves the cardinal motor signs and the motor complications of levodopa treatment and enables reduction in dopaminergic drug doses. DBS is not free of adverse effects which are related to the neurosurgical procedure or effects of electrical stimulation. The long-term effects of chronic stimulation are not well characterized. New-onset dyskinesia, gait disturbances and apraxia of lid opening (ALO) are known to occur following DBS in PD at variable intervals from surgery. 1 ALO is an intermittent, non-paralytic inability to open the eye lids or keep the lids elevated. 2-4 ALO has been reported as an adverse effect of STN stimulation [5][6][7][8] and can be a source of significant visual disability in some patients. As the literature on ALO following STN DBS is limited, we examined its frequency, temporal evolution, predisposing factors and outcome of treatment.

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Prolonged orbicularis oculi activity

Abstract: Patients with ALO show significant delays in eye opening. An abnormal persistence of OOc activity, detectable electromyographically but not clinically, could be the main factor contributing to the delay in lid opening in these patients.

Cited by 42 publications

References 17 publications

Debunking the Puzzle of Eyelid Apraxia: The Muscle of Riolan Hypothesis

Debunking the Puzzle of Eyelid Apraxia: The Muscle of Riolan Hypothesis

Eyelid Dysfunction in Neurodegenerative, Neurogenetic, and Neurometabolic Disease

Apraxia of Lid Opening in Subthalamic Nucleus Deep Brain Stimulation for Parkinson's Disease—Frequency, Risk Factors and Response to Treatment

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