Apraxia of Eyelid Opening After Brain Injury: A Case Report

Apraxia of eyelid opening (AEO) is a syndrome characterized by the patient's difficulty in initiating eyelid elevation spontaneously. Most of the reported cases were associated with extrapyramidal diseases. We report a case of AEO presented after traumatic brain injury, not with extrapyramidal diseases, and improved by dopaminergic treatment. A 49-year-old man underwent a traffic accident and was transferred to the emergency room in an unconscious state. Brain computed tomography (CT) revealed a subdural and epidural hemorrhage at right temporal and bilateral frontal lobes, and he received burr-hole trephination. After receiving comprehensive treatment including occupational therapy, cognition and mobility gradually improved, but he could not open his eyes voluntarily. With dopaminergic treatment (levodopa/benserazide 200/50 mg), he started to open his eyes spontaneously, especially when eating and undergoing physical training. This case showed that AEO may occur after brain injury and that dopaminergic treatment is beneficial also in AEO patients without extrapyramidal diseases.

Apraxia of Eyelid Opening Caused by Lithium

No abstract available.

Clinical and EMG Characteristics of Pretarsal Motor Persistence

Pretarsal motor persistence (PMP), a subtype of apraxia of the eyelid opening, is characterized by the inability to open the eyelids at will due to persistent activity of orbicularis oculi muscles following voluntary closure. Here, we describe clinical characteristic and the synchronous EMG recording from the levator palpebrae and orbicularis oculi muscles of PMP in patient with essential blepharospasm, idiopathic Parkinson's disease, and progressive supranuclear palsy.

Clinical Analysis of Blepharospasm and Apraxia of Eyelid Opening in Patients with Parkinsonism

BACKGROUND AND PURPOSE: Blepharospasm (BSP) and apraxia of eyelid opening (AEO) have been reported as dystonia related with parkinsonism. However, systematic analysis of clinical characteristics of BSP and AEO in parkinsonism has been seldom reported. To investigate the clinical characteristics of BSP and AEO in parkinsonism and to find out the clinical significance to differentiate parkinsonism. METHODS: We enrolled 35 patients who had BSP with or without AEO out of 1113 patients with parkinsonism (913 IPD, idiopathic Parkinson's disease; 190 MSA, multiple system atrophy, 134 MSA-p, 56 MSA-c and 10 PSP, progressive supranuclear palsy). We subdivided MSA into MSA-p (predominantly parkinsonism) and MSA-c (predominantly cerebellar) according to the diagnostic criteria proposed by Quinn. We analyzed the clinical features of BSP and parkinsonism including onset age, onset interval to BSP, characteristics of BSP, presence of AEO, coexisted dystonias on the other body parts, severity of parkinsonism and relationship with levodopa treatment. RESULTS: BSP with or without AEO were more frequently observed in atypical parkinsonism (PSP, 70%; MSA-p, 11.2%; MSA-c, 8.9%) than in IPD (0.9%). Reflex BSP was observed only in atypical parkinsonism (4 MSA-p, 1 MSA-c and 2 PSP). BSP preceding parkinsonism (Pre-BSP) was observed mainly in atypical parkinsonism (2 MSA-p, 1 MSA-c, 1 PSP and 1 IPD). The presence of AEO was more frequent in atypical parkinsonism than in IPD, but isolated AEO was not detected. BSP related to levodopa ('off' symptom or 'peak-dose' effect) were observed only in IPD. CONCLUSIONS: Reflex BSP, Pre-BSP and the presence of AEO may be a unique feature of atypical parkinsonism. BSP related to levodopa might be representative of IPD. No differences were found in the clinical features of BSP between MSA-p and MSA-c.

Apraxia of Eyelid Opening Secondary to Right Thalamic Infarction

Apraxia of eyelid opening is nonparalytic inability to open the eyes at will in the absence of visible contraction of the orbicularis oculi muscle. It is known that apraxia of eyelid opening is a feature of extrapyramidal diseases. We experienced a case with apraxia of eyelid opening after right thalamic infaction. We suggest that dysfunction of supranuclear control of the levator palpebrae superioris may be a pathophysiologic mechanism in apraxia of eyelid opening.