Benign essential blepharospasm (BEB) is a neurologic

178 The American Journal of Cosmetic Surgery Vol. 32, No. 3, 2015 ORIGINAL SCIENTIFIC PRESENTATION Minimal Orbicularis Myectomy: Does It Relieve Sp...
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The American Journal of Cosmetic Surgery Vol. 32, No. 3, 2015

ORIGINAL SCIENTIFIC PRESENTATION

Minimal Orbicularis Myectomy: Does It Relieve Spasms in Benign Essential Blepharospasm? Sameera Irfan, FRCS

Introduction: A new technique of minimally invasive orbicularis myectomy is described. A study is presented to show its efficacy in relieving spasms in benign essential blepharospasm and to note any complications resulting from it. Materials and Methods: In a prospective clinical, interventional study conducted at oculoplastics department of a tertiary care center, 25 consecutive cases (50 eyes) of benign essential blepharospasm were included, from January 2012 to December 2014. The patients consisted of 19 women and 6 men between the ages 28 and 66 years (mean age, 52 years). After a thorough history, a complete ophthalmological examination, and assessment of functional disability, they received appropriate therapy for triggering factors such as dry eyes, meibomitis, blepharitis, and trachoma for 1 month, after which a minimal orbicularis myectomy of both the upper and lower lids was performed simultaneously under local anesthesia by a single surgeon. The cases were followed up after 1 week, 1 month, 3 months, 6 months, and 1 year. Results: Six cases (24%) needed simultaneous brow suspension; 4 cases (16%) had blepharoplasty for dermatochalasis. Postoperatively, ecchymosis of lids was noted in 13 cases (52%) and lid swelling in 3 cases (12%). No lad lag, lid asymmetry, or corneal exposure was seen in any case. Three cases needed frontalis suspension for apraxia of upper lids, which was done 1 month postoperatively. Patient satisfaction was 100%, with improved functional disability.

Received for publication February 18, 2015. From Mughal Eye Trust Hospital Lahore, Punjab, Pakistan. Disclosure: The author has no financial interest in any of the products, devices, or drugs mentioned in this article. Corresponding author: Sameera Irfan, FRCS, Mughal Eye Trust Hospital, 301-H Johar Town, Lahore, Punjab 54600, Pakistan (e-mail: sam. [email protected]). DOI: 10.5992/AJCS-D-15-00009.1

Conclusion: Minimal orbicularis myectomy was found to be effective in providing a long-term relief of spasms and was not associated with any complications. However, proper patient selection is mandatory.

B

enign essential blepharospasm (BEB) is a neurologic disorder characterized by excessive, involuntary blinking that may progress to spasms of the eyelid muscles. It is a type of dystonia1 (movement disorder) in which prolonged muscle contractions result in sustained eyelid closure, repetitive eyelid movements, or twitching. It is seen in both men and women although more frequently in the middle-aged and elderly women.2 The symptoms appear in adulthood and gradually worsen, starting with increased frequency of blinking associated with ocular irritation. In the early stages, an analysis of the blink rate might be helpful for the diagnosis of BEB.3 In later stages, BEB results in increasing difficulty in keeping the eyes open and excessive light sensitivity (oculophotodynia).4 Spasms mostly occur during the day and disappear during sleep, only to reappear after waking. As the condition progresses, the patient is forced to keep the eyelids closed for prolonged periods of time and is unable to carry out normal activities such as reading, watching television, driving, or even walking; this results in substantial visual disturbance or functional blindness, anxiety, and depression.5 It is important to note that the blindness is caused solely by the sustained, uncontrollable eyelid closure and not by a dysfunction of the eyes per se. These spasms may progressively spread to other facial muscles, including the brow, jaw, and tongue (oromandibular dystonia).6 In the general population, the prevalence of BEB is 5 in 100,000.7 It is speculated to occur in genetically predisposed individuals in the presence of triggering

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Figure 1.

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Neural control of eyelid opening and closing.

factors8 that cause ocular irritation, although no genes have yet been isolated. A positive family history may not always be present, and sporadic cases are seen as well.9 Triggering factors such as dry eyes, blepharitis, and meibomitis must be identified and treated prior to any specific therapy to relieve the spasms. An instance of BEB must be differentiated from apraxia of the eyelids,10 in which there is a spasmodic closure of the eyelids; once the spasm is over, the patient is unable to open the eyes spontaneously but has to manually lift the upper lids with fingers and stay open until the next spasm occurs. Brows are seen to be elevated in such a patient in an attempt to forcibly open the lids. According to muscle physiology, there is a balance between the agonist-antagonist muscles in every part of the body; for the agonist muscle to carry out a specific action, the antagonist muscle must relax. The contraction of the orbicularis oculi (OO) muscle results in periodic, reflex blinking and firm eyelid closure, while the contraction of its antagonist, levator palpebrae superioris, results in elevation of the upper lid.11 The frontalis muscle helps the levator by retracting the lid in an extreme upward gaze. Hence, to blink, the levator muscle is inhibited abruptly so as to allow the palpebral portion of the OO to close the lids momentarily; it then resumes its prior level of activity once the contraction of OO is over.

This tonic activity of the levator and voluntary eye opening/closing is controlled by the cerebral cortex (R>L); during sleep or on gentle eye closure, the activity of the levator ceases completely through the inhibitory influence of the cerebral cortex. The execution of blinks and blink frequency is mediated through the basal ganglia (extrapyramidal dopaminergic circuit), which inhibits the levator while at the same time allows the OO to contract and close the lids, as demonstrated in Figure 1. The late age of onset of blepharospasm and its association with progressive neurodegenerative diseases (Parkinsonism) strongly suggests a central disturbance of 1 or more neurotransmitters and/or synaptic transmission in genetically predisposed patients. To explain the pathogenesis of BEB, Anderson et al12 proposed the theory of a defective circuit composed of an afferent arm with impulses traveling via the ophthalmic division of the trigeminal nerve to the control center in the basal ganglia and/or midbrain. From the center (cerebral cortex), efferent impulses exerting a positive feedback control are sent via the facial nerve to the eyelid protactor muscles (orbicularis, corrugatorsuperciliaris, and procerus), which are inhibited; as these muscles relax, the levator muscle, supplied by the oculomotor nerve, is free to elevate the upper lids. In BEB, the sensory limb of the circuit responds to multiple stimuli such as ocular or eyelid

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Table 1. Presenting Symptoms in 25 Cases and Their Improvement After 6 Months Postoperatively Symptom Irritation Photophobia Watery eyes Heaviness of eyes Burning sensation Anxiety/depression Visual disability

Preoperatively, n (%) 22 (88) 15 (28) 7 (28) 9 (36) 16 (64) 25 (100) 25 (100)

irritation, pain, stress, anxiety, or excess light. This excess of stimuli is transmitted to a genetically predisposed center, which may also be weakened by injury or an aging process, and it fails to send inhibitory impulses to the eyelid protractors, which then continue to be stimulated and keep the lids closed. Hence, the levator muscle cannot contract and carry out its action of elevating the upper lids. Long-standing blepharospasm results in anatomic changes of brow droop, dermatochalasis, entropion, and laxity of canthal tendons. A multidirectional approach has been suggested to manage such patients starting with educating them regarding their disease, its triggering factors, and how to avoid them as well as the role of support groups, pharmacotherapy, hypnosis, acupuncture, botulinum toxin, and surgical interventions that have been tried. The first line of therapy is aimed at the sensory limb of the vicious circle to reduce the flow of triggering impulses to the center. This can be achieved by tinted sunglasses to reduce light sensitivity (photo-oculodynia).13 Treatment of dry eyes and blepharitis should be instituted as well, as this has been shown to reduce the frequency and severity of spasms. Associated anxiety can be relieved by tricyclic antidepressants (lorazepam). Pharmacotherapy directed to relieve spasms is aimed at 3 levels: cholinergic excess (in which anticholinergic drugs will act at the neuromuscular junction and relieve the spasm), dopamine excess,14 and GABA hypofunctioning. However, pharmacotherapy has shown to be less effective than Botox injections and is reserved for patients not responding to Botox. The botulinum toxin15 interferes with the release of acetylcholine at the motor nerve endings and causes temporary muscle paralysis, with the effect lasting about 3 to 5 months. Repeated injections are required for a long-term relief of symptoms. Botox injections can result in complications16,17 such as ptosis, lagophthalmos, corneal exposure,

6 Months Postoperatively, n (%) 0 0 3 (12) 2 (8) 0 9 (36) 0

Improvement (%) 100 100 88 98 100 64 100

photophobia, and diplopia. The incidence of ptosis has been reported to be 50% if injections are not given carefully. Botox has been reported to be effective in only 86% of patients. Surgical intervention has been reserved as the last option in the form of myectomy18 involving the orbicularis (pretarsal, preseptal, and orbital portions) in both the upper and lower lids. It may be combined with the excision of procerus and corrugator muscles. Such an extensive procedure often results in chronic lymphedema of the eyelids. Alcohol injection to paralyze the facial nerve has been tried but results in complications such as loss of facial expressions and movement and eyelid malpositioning. We describe here a surgical procedure that involves minimal excision of a muscle strip including all parts of the OO muscle, with the idea being to create a break in the continuity of circularly running fibers. This is a minimally invasive technique. A study was conducted to see how effective this new surgical technique is in offering permanent relief of spasms in BEB and to note any complications resulting from it. Materials and Methods This is a prospective clinical trial conducted at the oculoplastics department of a tertiary care center. A total of 25 consecutive cases (50 eyes) were included in the study, conducted over a 3-year period, from January 2012 to December 2014. Patients consisted of 19 women and 6 men between the ages 28 and 66 years (mean age, 52 years). They were referred to the oculoplastics clinic because of their inability to keep their eyes open and frequent blinking. Patients were specifically asked regarding the onset of symptoms of blepharospasm, as shown in Table 1, and the aggravating or relieving factors, outlined in Table 2. Any positive family history for blepharospasm was noted. A thorough history was taken regarding the extent of

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Table 2. Triggering Factors at First Clinical Presentation Sign Dry eyes Meibomitis Blepharitis Trachoma Concretions upper lid Trichiasis Tear film break-up time Schirmer’s test Brow droop Dermatochalasis

Preoperatively, n (%) 19 (76) 25 (100) 8 (32) 9 (76) 17 (68) 3 (12) 21 (84) 7 (28) 6 (24) 4 (16)

their symptoms, how it was affecting their lives, the presence of depression and anxiety, ocular irritation, grittiness, burning sensation, watering, photophobia, any previous surgery, injection of Botox in the eyelids, or any systemic illness. During the examination, the frequency of blinking was noted as well as the severity and extent of spasms and whether they involved only the eyelids or the eyebrows, facial muscles, and neck muscles. A special note was made if fewer spasms were observed during talking and eye movement. A complete ophthalmological examination was conducted to determine best corrected visual acuity, presence of blepharitis, meibomitis, trachoma, corneal sensitivity, dry eye assessment with fluorescein staining of the cornea and conjunctiva, tear film break-up time. Schirmer’s 2 test was performed. Functional disability (Table 3) was assessed by inquiring about the patients’ 4 major daily life activities and then grading each at 3 levels ranging from 1 (minimal disability) to 3 (activity impossible). Study exclusion criteria were the presence of systemic illness such as multiple sclerosis, focal brain Table 3.

6 Months Postoperatively, n (%) 2 (8) 3 (12) 0 0 0 0 3 (12) 0 0 0

tumor, Parkinson disease, cerebral palsy, Meig syndrome (BEB plus involuntary movements of the lower facial and/or jaw muscles), Tourette syndrome, and ocular myasthenia. Patients with blepharospasm secondary to ocular conditions such as conjunctivitis, keratitis, uveitis, ocular trauma, ptosis, apraxia of the upper eyelids, facial palsy, and ocular myokymia were also excluded from the study. Patients were given treatment of their associated condition aggravating the spasms including dry eyes, blepharitis, meibomitis, or trachoma. Once the condition of the eyelids and ocular surface had improved, the new surgical technique was fully explained, and a verbal consent was taken from the patients and the guardians. Any patient taking blood-thinning medications was asked to stop them 10 days prior to surgery. Photographs the patients’ faces were taken preoperatively in all cases after taking their consent. Surgical Technique

All 4 eyelids were operated simultaneously. The cases with a brow droop or dermatochalasis had a

Functional Disability Grading*

Grading Preoperatively, n 1 Month Postoperatively, n Function 1 2 3 1 2 3 Reading 25 25 Watching TV 2 23 25 Walking 2 23 25 Going downstairs 18 18 Driving 16 16 Shopping 25 25 Color matching 9 16 25 *Grade 1, minimal disability; grade 2, moderate; grade 3, severe.

6 Months Postoperatively, n 1 2 3 16 3 6 19 6 19 6 11 1 6 14 18 1 6 19 6

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Figure 2. Principle of minimal orbicularis myectomy: a block of muscle including pretarsal, preseptal, and orbital parts from both upper and lower lids simultaneously to create a break in the ring.

simultaneous brow lift/blepharoplasty. Local anesthesia was prepared as a mixture of 2% lignocaine 2.5 mL + 2% bupivacaine 2.5 mL + 0.1 mL of 1:1000 adrenaline injected subcutaneously with a 27-gauge needle at the lateral canthal angle, raising a wheal superotemporally and another one inferotemporally. It was allowed to infiltrate deeper tissues using a firm pressure with an eye pad held over the wheals for 5 minutes. An eyelid traction suture (4/0 silk) was passed through the gray line of the superior and inferior eyelids laterally, and a lid guard was inserted under the eyelid to be operated to protect the eyeball. To expose the orbicularis muscle, a lid-crease skin incision was made in the lateral half of the upper lid with a No. 11 Bard-Parker knife. The skin was undermined superolaterally as far as the superior orbital rim and inferiorly, until the edge of the tarsal plate, to expose the underlying orbicularis muscle. The muscle was lifted upward with a pair of fine-tooth forceps above the tarsus, about half an inch from the lateral canthal angle, and a muscle strip, 8- to 10-mm wide was excised with a Fugo plasma blade starting from the tarsus until the superior orbital rim, in a diagonal direction upward and laterally, as shown in Figure 2. This strip included the orbital, septal, and distal part of the pretarsal orbicularis muscle. Care was taken to leave the proximal half of the pretarsal muscle intact. The underlying levator aponeurosis and the orbital septum were left intact. The Fugo plasma blade was

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used because it cuts precisely and coagulates tissue at the same time, achieving hemostasis; hence, surgery was performed in a bloodless field. The skin was closed with a running 7/0 Vicryl suture. The lower lid orbicularis muscle was exposed with a subciliary skin incision at the lateral half of the lower lid while the eyelid was retracted upward with the traction suture. The skin was undermined and the orbicularis muscle was exposed to the inferior orbital margin. The muscle was grasped 5 mm below the incision, leaving the Horner’s muscle intact; an 8- to 10-mm-wide strip was excised with the Fugo plasma blade in a diagonal direction downward and laterally to the orbital rim (Figure 2). The cut ends of the muscle were allowed to retract from each other. The subciliary skin incision was closed with a running 7/0 Vicryl suture. A similar procedure was performed on the other 2 lids. A pressure dressing was applied for 24 hours. All patients were prescribed oral antibiotic twice a day for 3 days. After removing the dressing the following morning, they were instructed to apply cold fomentation with ice packs twice a day and an antibiotic-steroid skin cream twice a day and to continue with their topical medication for dry eyes or blepharitis. The patients were reviewed after 5 days postoperatively and then after 2 weeks, 1 month, 3 months, 6 months, and 1 year. A note was made of their subjective symptoms, and the presence and extent of blepharospasm was noted. The condition of the ocular surface was also noted. Final postoperative pictures were taken at 6 months. Results Of the 25 consecutive cases included in the study, a positive family history was present in only 3 cases (12%); the rest were all sporadic. Eighteen cases (72%) had received repeated Botox injections in the past, with no sustained improvement in symptoms. None of the cases had any kind of surgery for the spasms. The symptoms as demonstrated in Table 1 show excessive blinking and visual disability as the most common symptoms present in all 25 cases (100%). Irritation of eyes or a foreign-body feeling was present in 22 cases (88%), burning sensation was found in 16 cases (64%), photophobia in 15 cases (60%), heaviness of eyes in 9 cases (36%), and watery eyes in 7 cases (28%). Anxiety regarding disease and functional disability was present in all cases (100%); on specific interrogation,

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it was also found to be a major triggering factor (Table 2) since it was present to a milder degree prior to the onset of blepharospasm in 23 of 25 cases (92%), which worsened as the disease progressed. Other triggering factors detected on ocular examination include meibomitis in all 25 cases (100%), tear film instability as detected by reduced (