Functional epiphora is a clinical condition which is not due to an anatomic defect. Most studies agree that it involves the action of the orbicularis oculi muscle, particularly its deeper segment (Horner’s muscle), but the exact mechanism is not clear.

To evaluate the orbicularis oculi muscle in functional epiphora patients using electromyography (EMG).

A total of 8 Chinese patients (16 eyes) with functional epiphora were enrolled in this study, and ten volunteers (10 eyes) were included as normal controls. Five epiphora patients (five eyes) with facial palsy served as positive controls. Quantitative EMG was performed in the deeper segment of orbicularis oculi muscle. The average duration of each EMG waveform was measured.

The average duration of EMG waveforms in the normal control group, the functional epiphora group, and the facial palsy group were 6.39 ± 0.73 ms, 9.39 ± 1.32 ms and 11.2 ± 1.42 ms, respectively. The duration of EMG waveforms was significantly longer in the functional epiphora group than in the normal control group (P < 0.05), and shorter than that in the facial palsy group (P < 0.05).

These data indicate the presence of neurogenic orbicularis oculi muscle damage in epiphora patients, which may be the cause of functional epiphora. The etiology of neurogenic damage in the orbicularis oculi muscle requires further investigation.

Epiphora is a bothersome clinical condition, which may require extensive diagnostic efforts. The patient’s history and/or clinical signs, which may include lacrimal hypersecretion, canalicular (presac) obstruction or stenosis, nasolacrimal (postsac) obstruction or stenosis, or even a functional (nonanatomic) defect, which might be due to “lacrimal pump” failure, can provide critical information in identifying this disorder[1]. Functional epiphora is a clinical condition which is not due to an anatomic defect, and the cause of functional epiphora is not very clear[2,3]. Although some controversy exists concerning the exact mechanism of functional epiphora, most studies agree that it involves the action of the orbicularis oculi muscle, particularly its deeper segment (Horner’s muscle), which inserts on the lacrimal sac.

Electromyography (EMG) is a supplement to clinical examination, which can distinguish myopathic from neurogenic muscle wasting and weakness. To determine the etiology of muscle weakness in functional epiphora, we used EMG to evaluate the orbicularis oculi muscle, in order to provide an approach for the diagnosis of functional epiphora.

EMG waveforms in the normal control group, the functional epiphora group and the facial palsy group are shown in Figure 2. The average duration of each EMG waveform was measured. The average duration of each action potential was calculated from 7-10 different action potentials. Our data showed that the average duration of the EMG waveform was 6.39 ± 0.73 ms, 9.39 ± 1.32 ms and 11.2 ± 1.42 ms in the control group, the functional epiphora group and the facial palsy group, respectively. The duration of EMG waveforms in the functional epiphora group and facial palsy group were significantly longer than those in the normal control group (P < 0.05), indicating the presence of neurological damage in functional epiphora patients (Figure 3).

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Figure 2 The electromyography waveforms in the subjects. The time between the two vertical white bars is the duration of the electromyography waveform. 1: The normal control group; 2: The functional epiphora group; 3; The facial palsy group. The bar represents 10 ms.

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Figure 3 The duration of the electromyography waveform in the different groups. The durations in group 2 and group 3 were significantly longer than that in group 1 (P < 0.05). 1: The normal control group; 2: The functional epiphora group; 3: The facial palsy group.

Epiphora may present as a watery (usually due to punctual or canalicular causes) or mucous (the so called “sticky eye”) condition[8,9]. Watery epiphora can significantly affect the patient’s quality of life and may be more difficult to treat than mucopurulent discharge[2]. However, the exact reasons underlying epiphora remain unclear. According to Jone’s theory, contraction of Horner’s muscle may cause expansion of the sac and creation of a negative pressure resulting in tear suction[8-10]. Alternatively, the Rosengren Doane theory postulates that the elastic expansion of the lacrimal papillae that occurs upon eyelid opening aspirates tears into the sac and the subsequent contraction of the orbicularis oculi creates a positive pressure gradient that may drive tears along the nasolacrimal duct into the nose[8-10].

The causes of muscle wasting and weakness can be divided into myopathic and neurogenic mechanisms, which can be distinguished by EMG. EMG represents an obligatory tool for assessing myopathic from neurogenic muscle motor neuron disease to demonstrate the widespread denervation and fasciculation required for a comprehensive diagnosis. EMG can detect abnormalities such as chronic denervation or fasciculation, which may not be apparent in clinically normal muscle. Isolating the discharge of single motor units as achieved by triggering and delaying their display, enables parameters of the motor unit potential to be measured. Amplitude and duration were measured, and these motor unit parameters varied with the muscle examined. Chronic re-innervation was associated with long duration motor unit potentials with a normal number of phases. Generally, the amplitude of motor unit potentials was less than 2 mV, and the durations were 10–5 ms with 3–4 phases. Intramuscular sprouting and re-innervation can occur in chronic partial denervation, and the amplitudes might be 10–20 mV and durations might increase to 20–30 ms. In primary muscle disease, only slight motor unit amplitude potentials of short duration were observed; typical amplitude and duration values would be 0.5 mV and 5–10 ms, respectively[11].

A recent study revealed that EMG of the orbicularis oculi muscle is very sensitive in patients with ptosis[12]. In this study, we used EMG to evaluate Horner’s muscle and its relation to functional epiphora. Amplitude and duration were measured, and these motor unit parameters varied with the muscle examined. In general, high amplitude and long duration motor unit potentials with a normal number of phases in EMG suggest chronic re-innervation. Facial palsy is definitely a neurogenic muscle motor neuron disease; therefore, we included facial palsy patients as positive controls in this study. The results demonstrated that the duration of the EMG waveform in the facial palsy patients was significantly longer than that in the normal controls. Consistent with the data from the functional epiphora patients, the duration of the EMG waveform was significantly longer than that in the normal controls, which suggested that chronic denervation in the orbicularis oculi muscle, particularly in the lower segment (Horner’s muscle) may contribute to this condition. It is noteworthy that the extent of increase in the duration of the EMG waveform in the facial palsy patients was more significant as compared to that in the functional epiphora patients, and this may be due to a different degree of neurogenic muscle motor neuron disease.

Thus, longer duration might mean chronic partial denervation, which suggests neurogenic muscle motor neuron disease in the functional epiphora patients, which might help us to treat functional epiphora in another way.

According to previous studies, lacrimal scintigraphy, can identify treatment strategies for functionally acquired epiphora[13,14]. For example, a horizontal shortening of the lower eyelid may be present which can then augment the action of the lacrimal “pump” (as lower eyelid laxity has been associated with decreased lacrimal pump function[13]). However, if the cause of functional epiphora is chronic denervation in the orbicularis oculi muscle, lacrimal scintigraphy may not be good enough to identify treatment strategies for this disease.

In addition, the cross-sectional study method used should be taken into account, the small number of patients included in the study and the lack of a control group for analysis of treatment decision specificity, require further investigation. Our results revealed that EMG of the orbicularis oculi muscle is a valuable tool for identifying treatment approaches for functional epiphora. The etiology of neurogenic damage in the orbicularis oculi muscle requires further investigation.

The authors would like to thank the members of the Department of Ophthalmology, Zibo Central Hospital.