Video Report - June 2002
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Thixotropy: a novel explanation for the cause of lagophthalmos after peripheral facial nerve palsy
M Aramideh, JHTM Koelman, PP Devriese, F VanderWerf, JD Speelman
Department of Neurology (M Aramideh, JD Speelman), Clinical Neurophysiology Unit (M Aramideh, JHTM Koelman), Department of Otolaryngology, Facial Research Unit (PP Devriese), Department of Visual System Analysis (VanderWerf), Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.
Correspondence to: Dr. M. Aramideh, Department of Neurology, Academic Medical Centre, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. E-mail:
Accepted for publication: 1 March 2002
This video shows two patients with a peripheral facial nerve palsy. The degree of lagophthalmos can be observed following gentle closure of the eyelids before and after stretch of the upper eyelid on the affected side.
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One of the major complications of a peripheral facial nerve palsy (PFP) is the occurrence of corneal ulceration due to lagophthalmos, i.e., incomplete closure of the affected eyelid.
It is widely accepted that lagophthalmos after PFP is directly caused by paresis of the orbicularis oculi muscle (eyelid closure muscle). Yet, some of the signs and symptoms, which may be observed in patients with PFP cannot be explained by paresis of the orbicularis oculi muscle alone. First of all, gentle closure of the eyelid , as for example occurs when a person falls into sleep, is completely brought about by inhibition of the tonic activity of the levator palpebrae muscle (eyelid opener muscle)1. Secondly, upward and downward saccadic lid movements, accompanying saccadic eye movements, are mainly due to modification of the tonic activity of the levator palpebrae muscle. Finally, the downward and upward smooth pursuit movements of the lids are again secondary to alterations in the level of activity of the levator palpebrae muscle. If these above mentioned movements of the lids are not caused by the orbicularis oculi muscle activity, what is then the reason that patients with PFP are unable to perform these movements properly. Furthermore, gold implantation in the affected upper eyelid or injection of the botulinum toxin into the levator palpebrae muscle is helpful in closing the affected lid, while no modification of the orbicularis oculi activity occurs with these treatment modalities.
As the orbicularis oculi and the levator palpebrae muscles have a reciprocal antagonistic activity1, we hypothesized that stiffness of the levator palpebrae is the cause of lagophthalmos. In a recent paper, we reported on the positive effect of stretch of the levator palpebrae muscle on lagophthalmos in a group of patients with PFP 2. Here, we present the video of two patients showing the effect of our intervention on lagophthalmos.
The first patient is a 35 years old man with a right-sided peripheral facial nerve palsy due to herpes zoster infection. He had a minor lagophthalmos. The second patient is 32 years old, who had Bell�s palsy and lagophthalmos on the left side. Both patients were examined within one week after the onset of their palsy.
The patients were asked to close the lids gently, as though they were attempting to sleep. The width of the palpebral fissure and, thereby, the degree of lagophthalmos could be measured immediately.
Our intervention consisted of complete passive closure of the affected eyelid, followed by manual stretch of the upper eyelid, and hence of the levator palpebrae, with a downward motion as far as possible. The levator was stretched for a period of approximately 15 seconds. The patients were then asked to open the lids and, subsequently, to close them gently again, so that the amount of lagophthalmos could be measured again (see video fragments).
In striated muscles, the term thixotropy has been applied to describe the dry friction-like behaviour of passive muscle to movement, as distinction from its elastic (length dependent) or viscous (velocity dependent) behaviour3.
Contraction of striated muscle fibres is caused by formation of sliding cross-bridges between the actin and myosin, the so-called contractile elements within the muscle fibers. These are recycling cross-bridges with a high turn-over. When a muscle is at rest, i.e., muscle is neither contracting nor being stretched, more stable, passive cross-bridges are formed between the actin and myosin filaments. The formation of this cross-bridges causes a certain tonus, stiffness of the muscle fibres, which is also referred to as thixotropy3. If muscle fibres are not stretched, the muscle stays shortened due to formation of these cross-bridges. As soon as the muscle is passively stretched, the cross-bridges detach and the muscle fibres become more slack.
However, if a muscle remains passive and its length unchanged, the stable cross-bridges remain intact for long periods. A consequence of the cross-bridges formation is that it leads to excessive stiffening of muscle fibres3.
Under physiological conditions, during each periodic blink, the levator palpebrae muscle relaxes, followed by contraction of the orbicularis oculi muscle which causes the levator palpebrae muscle to be stretched and the cross-bridges to be detached. However, this physiological mechanism is disturbed in patients with PFP. Due to disturbed blinking on the side of the orbicularis oculi paresis, the levator palpebrae muscle is not being stretched sufficiently and so the levator cross-bridges remain intact. This would result in excessive stiffness of the levator muscle after peripheral facial nerve palsy causing lagophthalmos on the affected side.
Many patients with PFP and lagophthalmos also exhibit two additional signs and symptoms that are in accordance with our hypothesis. Firstly, patients may show further widening of the palpebral fissure on the affected side compared to the unaffected side which indicated that the levator palpebrae muscle is shortened on the affected side. Secondly, after requesting these patients to close gently their eyelids, one sees clearly the site of attachment of the levator palpebrae muscle fibres aponeurosis on the affected side which is, in addition, also displaced more proximally. This sign is also in favour of the assumption that patients with PFP are unable to relax their levator palpebrae muscle.
In a group of patients with a PFP who had lagophthalmos, we manually stretched the levator palpebrae muscle, thereby, detaching the cross-bridges within the levator palpebrae muscle fibres, as can also be seen in the video fragments of two patients. The effect of this upper eyelid stretch manoeuvre, in terms of reduction of lagophthalmos was clinically significant and relevant.
Lagophthalmos following peripheral facial nerve palsy is caused by thixotrophic stiffening of the levator palpebrae muscle. Whether early intervention in term of manual stretch of the affected eyelid would prevent the occurrence of lagophthalmos, synkinesia, or other complications of PFP requires further investigations. Until such studies are undertaken, we instruct our patients to passively close their affected lids and to manually stretch the levator muscle repeatedly during the daytime.
1. Aramideh M, Koelman JHTM, Devriese PP, Speelman JD, Ongerboer de Visser BW. Thixotropy of levator palpebrae as the cause of lagophthalmos after peripheral facial nerve palsy. J Neurol Neurosurg and Psychiatry 2002; 72: 665-667.
2. Evinger C, Manning KA, Sibony PA. Eyelid movements. Mechanisms and normal data. Invest Ophthalmol Vis Sci 1991;32:387�400.
3. Proske U, Morgan DL, Gregory JE. Thixotropy in skeletal muscle and in muscle spindles: A review. Progress in Neurobiology 1993;41:705-721.