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HOME > J Mov Disord > Volume 15(2); 2022 > Article
Letter to the editor
Hand Movement-Induced Eyeblink Bursts in a Patient With Parkinson’s Disease
Gohei Yamada1orcid, Mitsuya Horiba2orcid, Takanari Toyoda1orcid, Eiichi Katada1orcid, Noriyuki Matsukawa3orcid
Journal of Movement Disorders 2022;15(2):190-192.
DOI: https://doi.org/10.14802/jmd.21161
Published online: May 10, 2022
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1Department of Neurology, Nagoya City University West Medical Center, Aichi, Japan

2Department of Rehabilitation Medicine, Nagoya City University Graduate School of Medical Sciences, Aichi, Japan

3Department of Neurology, Nagoya City University Graduate School of Medical Sciences, Aichi, Japan

Corresponding author: Gohei Yamada, MD, PhD Department of Neurology, Nagoya City University West Medical Center, 1-1 Hirate-cho, Kita-ku Nagoya, Aichi 462-8508, Japan / Tel: +81-52-991-8121 / Fax: +81-52-991-8161 / E-mail: gohyamada@yahoo.co.jp
• Received: November 1, 2021   • Revised: December 20, 2021   • Accepted: January 14, 2022

Copyright © 2022 The Korean Movement Disorder Society

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Dear Editor,
Blink reflex hyperexcitability is a characteristic manifestation in Parkinson’s disease (PD) [1]. The blink reflex is a brainstem reflex evoked by mechanical stimulation of the cornea, electrical stimulation of the supraorbital nerve, auditory stimulation, visual stimulation, and mechanical or electrical stimulation of the limbs. Here, we present the first case of eyeblink bursts that were induced while the patient performed hand movement.
A 70-year-old male patient presented with a 3-year history of freezing of gait, walking with short steps, festination, frequent falls, and a 2-year history of toe tremor. An initial neurological examination in the off-medication condition revealed mild rigidity in both legs, freezing of gait when starting to walk, short stride length, shuffling gait, bilateral reduced arm swing during walking, postural instability, and hyperreflexia in both legs (Supplementary Video 1 in the online-only Data Supplement). Freezing of gait was not obvious when the patient had a large space to walk in. Rest tremors at rest were observed in the left big and second toes. The patient was then instructed to perform movements including hand opening and closing, finger tapping with the thumb and index finger, and hand pronation and supination. When the patient gazed at his finger tapping movement, eyeblink bursts immediately occurred. This unusual eyeblink burst was induced by the movement of both the right and the left hand. Before evaluating the finger tapping movement, the examiner demonstrated finger tapping while the patient looked on. During this short time (1–2 seconds), no eyeblink burst occurred. When the patient gazed at his hand opening and closing, eyeblink bursts occurred twice per 4 trials. When the patient gazed at his hand performing pronation and supination, eyeblink bursts occurred. The amplitude of finger tapping movement and hand pronation and supination appeared to decrease on the left side. Postural or action tremor, oculomotor dysfunction, cognitive dysfunction, olfactory dysfunction, alien limb syndrome, apraxia, and gait and limb ataxias were absent. Myerson’s sign was negative. Neurological examinations were performed again under the on-medication condition (400 mg/day of levodopa). Gait speed and stride length appeared to be slightly increased (Supplementary Video 2 in the online-only Data Supplement). While the amplitude of finger tapping and hand pronation and supination was consistently large on the left side compared with that in the off-medication condition, gazing at the finger tapping movement induced eye blink bursts as in the off-medication condition. When the patient avoided eye contact with the hand movements by gazing straight forward, during left hand pronation and supination, or left hand opening and closing, eyeblink bursts occurred. In 123I-metaiodobenzylguanidine myocardial scintigraphy, the heart/mediastinum uptake ratios were 3.67 and 3.62 (> 2.2) at the two sample times of 15 min and 3 h, respectively (Figure 1A and B). Brain magnetic resonance imaging revealed no abnormalities, including no predominant midbrain atrophy (Figure 1C). 123I-FP-CIT single-photon emission computed tomography demonstrated a decrease in 123I-FP-CIT uptake in the bilateral striatum (Figure 1D). The patient had bradykinesia in both legs and the left hand, resting tremor in the left toes, mild rigidity in both legs, experienced mild benefits from levodopa treatment, and showed no red flag signs. According to the clinical diagnostic criteria for PD from the Movement Disorder Society, the patient was diagnosed with clinically probable PD [2].
Here, eyeblink burst was frequently induced by visual perception of various hand movements. To the best of our knowledge, this unusual phenomenon has not been described in the previous literature. We thus named the phenomenon “hand-movement-induced eye blink bursts.” In our case, the visual perception of hand movement could have played a crucial role in developing eye blink bursts. Eye blinks are observed in voluntary blinks, spontaneous blinks, blink reflexes, or glabellar reflexes. The blink reflex can be induced by visual stimulations (such as bright light), auditory stimulation, and mechanical or electrical stimulation of the limbs [3-5]. Considering that hand movement was presumed to always be included in the patient’s visual field (central or peripheral), eyeblink bursts might occur as a protective response from repetitive hand movements. However, visual perception of hand movement is also less stimulating than bright light, direct stimulation of the cornea, or objects rapidly nearing the face. Eye blink bursts did not occur during gazing at the examiner’s hand movement. The short distance between the face and the patient’s hand movement or the proprioception of the hand may be associated with eyeblink bursts. Some hand movements with or without gazing at the hand movement did not induce eyeblink bursts. This may be attributable to the difference in hand movement performance or attention to the patient’s hand movement. Gazing at hand movements might strengthen attention to hand movements and lead to eyeblink bursts. As we did not evaluate eyeblink during hand movement in the closed-eye condition, the extent of contribution of proprioception to eyeblink bursts remains uncertain.
The underlying mechanism of hand-movement-induced eye blink bursts is unclear. However, enhanced excitability of the blink reflex is a characteristic manifestation in patients with PD [1,6]. The basal ganglia have an inhibitory effect on the excitability of brainstem interneurons that are associated with the blink reflex through the colliculus superior, nucleus raphe magnus, and spinal trigeminal complex [1]. In patients with PD, neuronal loss of dopaminergic neurons in the substantia nigra is a core neuropathological change that may decrease the inhibitory output of the basal ganglia and the disinhibition of excitatory brainstem interneurons [1]. Thus, visual perception of the patient’s own hand movement under the enhanced excitability of the blink reflex may represent a potential mechanism of hand-movement-induced eye blink bursts. Since hand movement-induced eye blink bursts occurred in both on- and off-medication conditions, they may be attributable to nondopaminergic dysfunction.
In conclusion, this is the first study to reveal that eyeblink bursts can be induced by visual perception of repetitive hand movement. Although further studies are needed, hand movement-induced eyeblink bursts may be a potential hallmark of PD.
The online-only Data Supplement is available with this article at https://doi.org/10.14802/jmd.21161.

Video 1.

The video was initially recorded in the off-medication condition. Freezing of gait, short stride length, bilateral reduced arm swing during walking, slow gait speed in a narrow space, resting tremors in the left big and second toes, hand-movement-induced eyeblink bursts, and bradykinesia in the left hand are shown. During finger tapping, the patient was instructed to perform the task as largely and quickly as possible.

Video 2.

Within 1 week, the video was recorded again in the off-medication condition. Hand-movement-induced eyeblink bursts, bradykinesia in the left hand, and bilateral reduced arm swing (a stick in the right hand might be involved) are shown. During finger tapping, the patient was instructed to perform the task as largely as possible. The patient underwent hand openingclosing and hand pronation-supination without special instructions. Four days later, videos were recorded in the on-medication condition. The gait speed and stride length appeared to be mildly increased, and the arm swing was visibly increased. A hand-movement-induced eyeblink burst is shown. During finger tapping, the patient was instructed to perform the task as largely as possible. The patient underwent hand opening-closing and hand pronation-supination without special instructions.

Ethics Statement

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional research committee and with the 1975 Helsinki declaration and its later amendments or comparable ethical standards. Informed consent was obtained from the patient included in the study.

Conflicts of Interest

The authors have no financial conflicts of interest.

Funding Statement

None

Author Contributions

Conceptualization: Gohei Yamada. Data curation: Gohei Yamada, Mitsuya Horiba. Investigation: Gohei Yamada. Writing—original draft: Gohei Yamada. Writing—review & editing: all authors.

Figure 1.
123I-metaiodobenzylguanidine myocardial scintigraphy shows normal heart (H)/mediastinum (M) ratios in the early (15 min) (A) and delayed images (3 h) (B). Sagittal T1 magnetization prepared rapid acquisition with gradient echo imaging does not show atrophy of the midbrain and pons (C). 123I-FP-CIT single-photon emission computed tomography shows a decrease in 123I-FP-CIT uptake in the bilateral striatum (D).
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