Cosmetic Surgery Tips

How many units of botox for hemifacial spasm

Hemifacial spasm is a condition that affects the muscles on one side of the face. It can cause a person to have trouble closing their eye, or make it difficult for them to smile. In this guide, we review the aspects of How many units of botox for hemifacial spasm, hemifacial spasm botox injection technique, new treatment for hemifacial spasm, and hemifacial spasm life expectancy.

Botox is an FDA-approved treatment for hemifacial spasm, but not all patients will need the same amount of injections to get relief from their symptoms. The number of units needed depends on several factors, including how severe your condition is and where exactly you are having muscle activity problems.

We’ve put together some quick tips on what to look for when choosing the right dose of Botox for hemifacial spasm so you can feel confident about your treatment plan!

Introduction. Hemifacial spasm is a common indication for botulinum toxin use. Aim of this study was to find out the efficacy and safety of long-term use of botulinum toxin for hemifacial spasms in Sri Lanka.

Methods. A group of 28 patients with hemifacial spasms who had been given botulinum toxin for more than 7 years were included in the study. Botulinum toxin was given at multiple sites including over the eyelid, at the ipsilateral orbicularis oculi, nasalis, orbicularis oris, mentalis and contralateral orbicularis oris sites on a dilution of 2 ml/100 units. Patients were then followed up every 3 months. Degree of improvement, side effects if any, the total number of units used and the information regarding the last injection used were collected.

Results. There were 24 females with a female preponderance of 86%. Mean age (SD) at first injection of the patients was 58.7 (9.1) years. Mean (SD) duration of the repeated use was 10.5 (2.2) years. Range of the duration of treatment was from 7 to 15 years. During this duration, mean (SD) number of injections given was 25.2 (8). Average number of units given for each patient during these multiple injections was 20.3 (2.6). Improvement was seen in 96.5% of the times and side effects were seen only in 2.7% of the time and included heaviness of the eye, mild lower facial weakness and pain at the site of injection which did not last long. Patient compliance was good even after repeated long term use. There were no systemic side effects and drug resistance to botulinum toxin was not seen in these patients.

Conclusion. These findings show that the long-term use of botulinum toxin for more than 10 years seems to be safe and efficacious for hemifacial spasm.

Shear wave elastography for characterization of breast lesions: Shearlet transform and local binary pattern histogram techniques

Shear wave elastography (SWE) examination using ultrasound elastography (USE) is a popular imaging procedure for obtaining elasticity information of breast lesions. Elasticity parameters obtained through SWE can be used as biomarkers that can distinguish malignant breast lesions from benign ones. Furthermore, the elasticity parameters extracted from SWE can speed up the diagnosis and possibly reduce human errors. In this paper, Shearlet transform and local binary pattern histograms (LBPH) are proposed as an original algorithm to differentiate malignant and benign breast lesions. First, Shearlet transform is applied on the SWE images to acquire low frequency, horizontal and vertical cone coefficients. Next, LBPH features are extracted from the Shearlet transform coefficients and subjected to dimensionality reduction using locality sensitivity discriminating analysis (LSDA). The reduced LSDA components are ranked and then fed to several classifiers for the automated classification of breast lesions. A probabilistic neural network classifier trained only with seven top ranked features performed best, and achieved 98.08% accuracy, 98.63% sensitivity, and 97.59% specificity in distinguishing malignant from benign breast lesions. The high sensitivity and specificity of our system indicates that it can be employed as a primary screening tool for faster diagnosis of breast malignancies, thereby possibly reducing the mortality rate due to breast cancer.

We examined the relationship between hemifacial spasm (HFS; a form of cranio-cervical dystonia) and chronic primary headache, including tension-type headache (TTH). We also examined whether botulinum toxin A (BoNT/A) therapy for HFS ameliorates concomitant TTH.

Fifty-one HFS patients receiving BoNT/A therapy were recruited. Patients’ characteristics (including age, gender, chronic headache history, exercise habits, stiff neck, cervical spondylolysis history), stress factors, worsening/new onset of headache associated with HFS, and dose of BoNT/A were examined. We diagnosed headache types according to The International Classification of Headache Disorders, 3rd edition, beta. Numerical Rating Scale (NRS) and Headache Impact Test-6 (HIT-6) scores for headache severity were compared between the 6-week baseline before BoNT/A therapy and 6-week follow-up after BoNT/A therapy.

Of 51 patients with HFS, 17 (33.3%) reported worsening or new onset of headache (especially TTH) associated with HFS (Group-S), and 34 were not aware of headache (Group-N). Twelve patients (70.6%) in group-S reported improvement of headache after BoNT/A therapy. NRS (from 7 [5–9] to 0 [0–5], p < 0.01) and HIT-6 (from 55 [54–64] to 44 [36–52], p < 0.001) scores were significantly improved after BoNT/A therapy. Logistic regression analysis revealed significant interaction between TTH associated with HFS and the presence of stress factors (odds ratio 43.11: 2.95–629.39, p < 0.001) and history of chronic headache (odds ratio 28.53: 2.96–275.10, p < 0.001).

Primary headache, especially TTH, is associated with HFS. BoNT/A therapy for HFS may also be indirectly effective for treatment of TTH.

Type Ia endoleaks after fenestrated and branched endografts may lead to component instability and increased aortic mortality

Fenestrated and branched endografts allow for proximal sealing zone extension into or above the visceral aorta to optimize landing in healthy aorta. We describe the incidence, causes, and implications of proximal endoleak development in patients undergoing complex endovascular aortic aneurysm repair.

All patients undergoing a fenestrated/branched repair were entered onto a prospective database, and this analysis included all those with at least one postoperative contrast computed tomography scan. Preoperative and postoperative three-dimensional imaging was reanalyzed to characterize morphology and identify endoleak. A blinded assessor used the preoperative imaging to resize the repairs in the endoleak group and a matched cohort of patients without endoleak. The outcome measures were proximal endoleak development, mortality, and component stability, and a comparison was made with all patients undergoing complex aortic repair.

From 2001 to July 2013, 969 patients underwent repair in a physician-sponsored investigational device exemption trial. Excluded were 24 emergency patients and 21 patients without requisite imaging, leaving 924 available for analysis. A proximal type Ia endoleak developed in 26 patients (2.8%). Poor choice of landing zone was implicated in most cases, with an area of sealing in the visceral aorta, compared with the thoracic aorta, being significantly associated with endoleak development (P < .01). Aortic-related mortality was significantly higher in the endoleak group (26.9%) than in the group without endoleak (6.2%; P = .001). These patients also experienced a higher incidence of component instability of 30.8% compared with 9.6% in patients without type Ia endoleak (P < .01).

Fenestrated/branched endovascular repair has a low incidence of sealing zone failure despite the increased complexity. However, development of a proximal endoleak destabilizes the repair and leads to increased mortality. Increasing complexity of design seems to improve the long-term outcome for patients requiring complex aortic repair.

Use of parallel grafts to save failed prior endovascular aortic aneurysm repair and type Ia endoleaks

The aim of this study was the evaluation of the clinical and radiologic outcomes of parallel grafts in the treatment of patients with failed prior endovascular aneurysm repair and type Ia endoleak.

Prospectively collected clinical and radiologic data of consecutive patients with prior endovascular aneurysm repair and evidence of type Ia endoleak were analyzed. All patients were treated between January 2009 and November 2014 by use of parallel grafts, ie, chimney/snorkel or periscope grafts and abdominal endovascular devices. Primary outcome of the study was the technical success. Secondary outcomes were patency of the chimney grafts and shrinkage of aneurysm morphology.

Technical success was 94.4% (17 of 18). One patient showed evidence of persistent type Ia endoleak after triple chimney graft placement and treated by Onyx embolization (Covidien, Plymouth, Minn) successfully. The mean preoperative and postoperative aneurysm diameters were 7.1 ± 1.7 and 7.0 ± 2 cm. Primary patency of the chimney grafts was 96.7% and assisted patency was 100% after successful retrograde recanalization of an acute occlusion of the superior mesenteric artery from the celiac trunk and the gastroduodenal artery. One patient who had undergone the sandwich technique with transfemoral placement of the flexible Viabahn (W. L. Gore & Associates, Flagstaff, Ariz) due to impossible catheterization of the target vessel from the upper extremity presented with contained rupture caused by gutter-associated endoleak and underwent urgent embolization with Onyx successfully. No procedure-related death or open conversion was observed in the entire follow-up period.

Use of parallel grafts showed midterm safety and feasibility with low incidence of persistent endoleaks requiring intervention or progression of aneurysm diameter. Reproducible results from other vascular centers will establish the chimney technique in the treatment of type I endoleaks as a viable endovascular modality.

This study analyzed outcomes for patients with persistent intraoperative type Ia endoleaks after standard endovascular aneurysm repair (EVAR).

The study group was identified from a consecutive cohort of 209 patients undergoing EVAR in a tertiary center in the United Kingdom during a 2-year period. Data prospectively collected on departmental computerized databases were retrospectively analyzed. Primary outcome parameters were defined as freedom from type Ia endoleak, EVAR-related reintervention, aneurysm rupture, and aneurysm-related mortality.

A completion angiogram identified 44 patients (21%) as having a type Ia endoleak, and 33 (75%) had a persistent endoleak after intraoperative adjunctive procedures, including repeated balloon moulding, aortic cuff extension, and Palmaz stent (Cordis, Miami Lakes, Fla) deployment. In the 11 patients (25%) whose endoleak was successfully abolished intraoperatively, there was no recurrence of type Ia endoleak or secondary intervention to treat type 1a endoleak during a median follow-up period of 27 months. Of the 33 patients with persistent endoleak, 31 (94%) demonstrated resolution of the endoleak on first surveillance computed tomography angiography. One patient was lost to follow-up. Embolization of the endoleak in another patient was successful using Onyx (Micro Therapeutics, Inc, Irvine, Calif) 8 days after the initial procedure. No type Ia endoleak was identified after this on any surveillance imaging, and the patient was alive 28 months later with a stable aneurysm size. In the rest of the patients, no recurrence of the endoleak in any subsequent imaging was noticed, and no secondary intervention was required during follow-up. No aneurysm-related deaths occurred, and 91% of the patients had a stable or shrinking aneurysm.

Despite adjunctive intraoperative maneuvers, persistent type Ia endoleaks can be relatively common. Our study indicates that they may be observed in selected patients. Further research is required to investigate the natural course and management of type Ia endoleaks identified intraoperatively.

Genetic therapies, including transfected immune cells and viral vectors, continue to show clinical responses as systemically deliverable and targeted therapeutics, with the first such approaches having been approved for cancer treatment. The majority of these employ cytokine transgenes. However, expression of cytokines early after systemic delivery can result in increased toxicity and nonspecific induction of the immune response. In addition, premature immune-mediated clearance of the therapy may result, especially for viral-based approaches. Here, it was initially verified that cytokine (interleukin (IL)2) or chemokine (CCL5) expression from a systemically delivered oncolytic virus resulted in reduced oncolytic activity and suboptimal immune activation, while IL2 also resulted in increased toxicity. However, all these limitations could be overcome through incorporation of exogenous regulation of cytokine or chemokine transgene function through fusion of a small and externally controllable destabilizing domain to the protein of interest. Regulation allowed an initial phase without cytokine function, permitting enhanced delivery and oncolytic activity before activation of cytokine function and a subsequent phase of enhanced and tumor-targeted immunotherapeutic activity. As a result of this exogenous regulation of cytokine function, both oncolytic and immune-mediated mechanisms of action were optimized, greatly enhancing therapeutic activity, while toxicity was significantly reduced.

hemifacial spasm botox injection technique

The facial dystonias benign essential blepharospasm and hemifacial spasm are rare disorders,1 which usually start with an increase in frequency of blinking, are often associated with dry eye syndrome, and sometimes occur with precipitating factors. 2, 3 With time, the phenomenon becomes more frequent until it causes difficulty with carrying out daily activities, and impairs health-related quality of life, causing social embarrassment, anxiety, and depression.3, 4, 5 Rarely the spasm can cause functional blindness.5

A variety of treatments are available for facial dystonias: treatment of dry eye symptoms, referral to patient groups,3 treatment with drugs including antidepressants, anxiolytics, anticonvulsants, anti-Parkinson drugs, and muscle relaxants,6 and surgery including facial nerve avulsion,7 orbicularis oculi myectomy,8, 9, 10 and brow suspension.11, 12

Since the mid-1980s, the treatment of facial dystonias has been revolutionised following the introduction of botulinum toxin,13 which has been shown to be very effective in the treatment of benign essential blepharospasm and hemifacial spasm.14 However, difficulties remain; it is difficult to determine the appropriate dose for an individual patient, and also to manage refractory cases.

Dose regimes have been published for specific diagnoses, and botulinum toxin is known to have an effect that lasts about 3 months. Therefore, facial dystonias are often treated with a standard dose regime and then reviewed after 3 months. However, the standard doses do not fit all patients, and this creates a management dilemma when a patient returns at 3 months and reports that the treatment was not successful, or they ‘did not get on with the treatment’. At our institution, a dedicated clinic called the ‘blepharospasm clinic’ follows a structured protocol for the treatment of facial dystonias, and other diagnoses including aberrant regeneration of the seventh nerve, myokymia, and hyperlacrimation. The protocol aims to titrate the dose of toxin to the individual patient so as to optimise the control of symptoms, and aims to give a logical framework for the management of refractory cases that is easy to understand and to explain to the patient.

Patients and methods

A retrospective noncomparative review of the clinical records of all patients who had attended the ‘blepharospasm clinic’ at Moorfields Eye Hospital between January 2000 and January 2003 was performed. The ethics committee at Moorfields Eye Hospital approved the study protocol.

A computer search was used to identify all patients who had attended the clinic. In the early years of the clinic, not all patients were treated with the protocol to tailor the toxin dose, therefore a subset of patients who had less than 5 years follow-up was analysed separately, termed ‘new patients’. Although some of the ‘new patients’ were first seen in the clinic before the study period of 2000–2003, they were all managed using the protocol described below. This subset was analysed to determine the number of visits required to titrate the dose, the doses of toxin used, and the change in symptoms following treatment.

Management protocol

Patients in the clinic had undergone a structured protocol for the treatment of facial dystonias. Firstly, an attempt is made to tailor the dose of botulinum toxin to the individual patient. At their first clinical visit in week 1, the patient is given a standard dose of botulinum toxin. For blepharospasm and hemifacial spasm, the standard dose was 20 U of dysport in six locations around the palpebral structures of each eye, and 10 U of dysport in two locations on the upper lid for those patients with evidence of pretarsal spasm (Figure 1). The standard dose can be altered according to clinical judgement. Patients with aberrant facial nerve regeneration and myokymias are treated with lower initial doses according to clinical judgement. In week 1 treatment is also started for any signs or symptoms of dry eye or blepharitis. Patients with hemifacial spasm are referred to a neurologist for further assessment and neuroimaging (in parallel with treatment for the spasm). All patients are given a patient information leaflet that includes the details of the ‘Dystonia Society’. The patient is then reviewed 1 week later, that is, week 2. If the spasm is controlled the patient continues with the same injections every 3–4 months as required for the individual patient on a regular basis. If however the spasm is not fully controlled, further injections are given to any muscles that remain in spasm, and the patient is reviewed 1 week later, that is week 3. On review at week 3, if the spasm is now controlled, the patient is given an appointment for 3 months and at that appointment the sum of the previous two injections is given. If at the week 3 appointment the spasm is not controlled, then further injections are given to any muscles that remain in spasm and an appointment made for week 4. At week 4, if the spasm is now controlled an appointment is given for 3–4 months. This process continues until either the spasm is controlled, or side effects of the treatment become intolerable. The long-term dose of toxin is the sum of the doses given at each visit until control is achieved.

Patients who have severe spasm that cannot be controlled without producing side effects are offered surgery, that is, a protractor myectomy (orbicularis strip or extended blepharoplasty). The purpose is to reduce the bulk of the orbicularis muscle in the area that can be reached through a cosmetic blepharoplasty incision such that the patients can keep their eyes open spontaneously or the spasm can be controlled with toxin injections without producing intolerable side effects. Facial nerve avulsion is reserved for the elderly or infirm in whom a protractor myectomy is contraindicated on anaesthetic grounds; it has a shorter effect, and more complications than protractor myectomy, but is a shorter operation with a lower perioperative morbidity.15

Patients who return with a ptosis may have either been over-treated with toxin producing a paralysis of the levator palpebrae superioris, or they may have under-treated pretarsal blepharospasm (Figure 2). A history of intermittent ptosis suggests pretarsal spasm; however a constant ptosis may be due to either levator palpebrae superioris weakening due to spill-over of adjacent botulinum toxin, or spasm of the pretarsal orbicularis oculi,16, 17, 18, 19 which can be treated with pretarsal injections of botulinum toxin.19, 20 These patients are given a further injection of pretarsal toxin and reviewed 1 week later. The pretarsal injections are given as close to the lid margin as possible as recommended by Mackie19 for the control of Riolan’s muscle. If pretarsal spasm is controlled, and any ptosis resolved, the patient can be reviewed at 3–4 months and the pretarsal injections repeated in conjunction with any other periorbital injections.

Sometimes, pretarsal spasm cannot be controlled without weakening the levator palpebrae superioris and changing a ptosis due to orbicularis spasm for one due to levator paralysis. In these patients, our protocol is to control the spasm with as much botulinum toxin as is required, and to treat the resultant paralytic ptosis with a brow suspension after a trial of ptosis props (Figure 3). The trial of ptosis props is to identify those patients who will not be helped by a brow suspension due to either dry eyes or a spastic Bell’s phenomenon (Figure 4). There is a subgroup of patients with facial dytonias in whom the eyeballs roll up under the upper eyelids making them functionally blind even though the eyelids are open and the spasm of the orbicularis muscles has been reduced. These patients are offered systemic centrally acting medication such as clonazepam to try and control this spastic Bell’s phenomenon. If the patient does tolerate ptosis props, a brow suspension procedure is offered using a material that is easy to remove such as a supramid prolene suture, so that it can be easily reversed if the surgery is poorly tolerated.


A total of 332 patients attended the ‘blepharospasm clinic’ between January 2000 and January 2003: 210 women who had a median age at first visit of 63 years (range 28–92) and 122 men who had a median age at first visit of also 63 years (range 13–83). A total of 193 patients (58.4%) had a diagnosis of essential blepharospasm, 118 patients (35.6%) hemifacial spasm, 12 patients (3.6%) aberrant seventh nerve regeneration, and eight patients (2.4%) other diagnoses, including myokymia and hyperlacrimation.

Data on the duration of symptoms before first attendance at the ‘blepharospasm clinic’ were available for 94 patients; the median duration was 36 months (range 3–600).

In total, 74 patients (56 with benign essential blepharospasm and 18 with hemifacial spasm) reported a history of failed medical management of the spasm.

We identified 182 ‘new patients’; 113 women (62%) with a median age at first visit of 62 years (range 13–92) and 69 men (38%) with a meidan age at first visit of 61 years (range 18–80). In total, 106 patients (59%) had a diagnosis of benign essential blepharospasm, 60 (33%) hemifacial spasm, eight (4.5%) aberrant regeneration of the seventh nerve, and seven (3.5%) other diagnoses.

Dose titration

Analysis of the datasheets for the 182 ‘new patients’ revealed that 118 patients needed one visit to control the spasm (65%) (they required only one set of injections to control the symptoms), 41 patients needed two visits (23%) (after the first week the spasm was not under control, and they required a second set of injections to control the symptoms), and three visits were needed in 22 patients (12%) (these patients required three sets of injections to control the spasm). Maximum visits is three in this group of patients. One patient did not reattend after the first visit. Table 1 shows the number of visits until stable by diagnosis.

The preparation of botulinum toxin used was Dysport (Speywood Pharmaceuticals, Maidenhead, England) in 159 patients and Botox (Allergan Inc, Irvine, CA, USA) in 13 patients, six patients changed from Dysport to Botox, one patient changed from Botox to Dysport, in two patients the preparation was unknown. The median total dose of botulinum toxin to control symptoms was 190 U (10–700) Dysport for benign essential blepharospasm, 80 U (3.5–420) Dysport for hemifacial spasm, 48 U (12–80) Dysport for aberrant seventh nerve regeneration, and 60 U (20–360) Dysport for other diagnoses. As a unit of Botox is about three times as effective as a unit of Dysport, the dose of toxin used for those treated with Botox was multiplied by three to produce an equivalent Dysport dose.

This method of titrating the botulinum toxin dose resulted in an improvement in symptoms in 169 patients (92.8%), did not improve the symptoms in six patients (3.3%), and was unknown in seven patients (3.8%) due to poor documentation or because the patients did not reattend the clinic. Table 2 shows treatment outcome by diagnosis.


The data sets of all the 332 patients who attended the clinic between January 2000 and January 2003 were used to analyse the follow-up. The median follow-up was 49 months (range 0–216). In total, 56 patients (17%) did not attend one or more clinic appointments during their course of treatment and 34 patients (10%) were discharged from the clinic or lost to follow-up; 11 patients moved out of the region, eight were dissatisfied with their treatment, and the reasons were unknown in 15 patients.

The median interval between treatments was 3 months. The interval between clinical visits decreased in 32 patients (9.7%), increased in 168 patients (50.8%), stayed the same in 107 patients (32.3%), and could not be accurately determined in 24 patients (7.2%). Table 3 shows the change in interval between visit by diagnosis. In a subgroup of 88 patients who had more than 10 years follow up the results were similar; the interval had decreased in seven patients (7.9%), increased in 48 patients (54.8%), stayed the same in 27 patients (30.7%), and could not be accurately determined in six patients (6.8%).

Side effects

A total of 236 patients (71.3%) reported a complication or a side effect of treatment at some stage during the follow-up period (median follow-up 49 months) (Table 4). In most of the patients, the symptoms were mild; 175 patients (52.7%) had a mild ptosis, which did not affect the visual axis, 48% of patients had a mild lagophthalmos not requiring treatment for dry eye, and 137 patients (41.3%) had only a mild ptosis and/or a mild lagophthalmos and no other side effects. A total of 99 patients (29.8%) experienced one or more of the other side effects at some stage during their total length of follow-up, including 92 patients (27.7%) who had one or more episodes of diplopia and 16 patients (4.8%) who had a marked ptosis affecting vision.


In total, 47 patients (14%) had surgery at some stage during their management in the ‘blepharospasm clinic’; 41 patients with a diagnosis of blepharospasm (21.2% of patients with a diagnosis of blepharospasm) and five patients with hemifacial spasm (4.2% of patients with a diagnosis of hemifacial spasm). In all, 36 patients underwent protractor myectomy, 13 patients brow suspension/frontalis sling ptosis surgery (all these patients had a diagnosis of blepharospasm) and two patients underwent both procedures separately. No patient underwent facial nerve avulsion in this series. In total, 15 patients had a trial of ptosis props; 13 of these subsequently had a brow suspension, and two patients that declined surgery after the trial of props were treated with systemic medication, which helped control their spastic Bell’s phenomenon, although they were still unable to tolerate ptosis props.

Following myectomy, symptoms improved in 24/36 patients (67%), resolving in one patient (3%), and stayed the same in 13 patients (36%). Botulinum toxin injections were continued in 29/36 patients (81%); the dose of botulinum toxin fell from a preoperative median dose of 140 U (range 7.5–560) to a median dose of 100 U (range 12–600), and the interval between injections increased from a preoperative median of 2 months (range 0–5) to a mean of 3 months (range 0–6). The median follow-up was 21 months (range 1–168).

Following brow suspension, symptoms improved in 12 patients (92%), and stayed the same in the other patients. Nine patients (85%) required continued injections of botulinum toxin; the mean dose of botulinum toxin fell from 240 U (range 30–400) before surgery to 160 U (range 20–320) after surgery. The median follow-up period was 47 months (range 1–104).


In this study, more than 35% of new patients required two or more initial weekly sets of injections to control the spasm and to determine the future dose to be given every 3 months or so. This suggests that there are many patients for whom the standard dose does not provide optimal control of symptoms.

The results of treatment are difficult to assess accurately in a retrospective study; however, 95% of patients experienced an improvement in symptoms that allowed them to see well enough to manage their lives without assistance. These figures compare favourably to other retrospective studies that report improvements in symptoms in 85–95% of patients.2, 3, 5, 20 Only eight patients stated that they were dissatisfied with the treatment, and a further 15 were lost to follow-up for unknown reasons during the 3-year period. Although 236 of patients (71.3%) experienced side effects at some stage during their treatment, the follow-up period was long (median 49 months), and the majority of these patients (137 patients) had a mild ptosis that did not interfere with the vision, or a mild lagophthalmos that did not require treatment. Additionally, although it is not possible to accurately identify the duration of the side effects in this retrospective study, they generally lasted less than 6 weeks, and no patient was left with a permanent complication.

Diplopia was experienced by over a quarter of patients, and ‘severe ptosis’ by nearly 5% of patients. This is important to consider when counselling patients, especially as diplopia and ptosis may prevent the patient from driving.

Studies have shown the presence of antibodies to botulinum toxin in those patients on long-term treatment, although these antibodies may not have an effect on the patient’s clinical response to treatment.21 There is also an anxiety among patients that the treatment will become less effective with time,22 although the duration of benefit from toxin treatment has been shown to be stable over time.23 In this study, the interval between treatments decreased in only about 10% of patients and increased in about half of the patients. This suggests that the duration of benefit is stable over time for most patients, but in a small subgroup injections are required more frequently. This may be due to disease progression, or the production of antibodies. The explanation for the group requiring less frequent injections with time may be that if muscles remain inactive and partially paralysed for long enough they may partially atrophy.

For those patients with refractory blepharospasm there is an array of treatment options, all of which have their limitations. We have developed a simple and logical treatment protocol for those patients with refractory spasm. Since chemodenervation with botulinum toxin has been such a successful treatment, patients can become extremely distressed in the event of treatment failure. The treatment protocol outlined here is easy to explain to patients, and gives opportunities for the patient to be involved in planning the treatment strategy, thus enhancing the patient – doctor relationship.

In all, 36 patients had a protractor myectomy during the course of their treatment in the ‘blepharospasm clinic’. These were patients in whom botulinum toxin injections were not able to control the spasm without producing unacceptable side effects. Surgery alone improved symptoms in only 64% of patients, and 89% required continued injections of toxin. However, after surgery the dose of toxin required to control the spasm was reduced, and the interval between treatments increased.

The results of ptosis surgery with brow suspension were better; 92% of patients had an improvement in symptoms following surgery, and no cases required reversal of the surgery. This high success rate is due to careful patient selection and the use of a trial of ptosis props prior to surgery to identify those patients likely to suffer from symptoms of dry eye or an excessive Bell’s phenomenon. The patients most likely to benefit from brow suspension ptosis surgery were those with pretarsal spasm (apraxia) in whom pretarsal and Riolan’s muscle botulinum toxin injections controlled the spasm, but the apraxia inhibited the levator muscle action. Aponeurosis and levator muscle surgery in this group merely increases lagophthalmos and does not help lid opening. A brow suspension/frontalis sling does help the patient to see, provided the frontalis muscle functions normally and Bell’s phenomenon is not excessive. Most of these patients, not surprisingly, continued to require pretarsal botulinum toxin and some needed systemic medication to control their Bells phenomenon. Two patients declined a brow suspension after a trial of ptosis props, and were treated with medical management combined with botulinum toxin injections.

new treatment for hemifacial spasm

In most patients with hemifacial spasm, the treatment of choice is injection of botulinum toxin under electromyographic (EMG) guidance. Chemodenervation safely and effectively treats most patients, especially those with sustained contractions. Relief of spasms occurs 3-5 days after injection and lasts approximately 6 months.

Medications used in the treatment of hemifacial spasm include carbamazepine and benzodiazepines for noncompressive lesions. Carbamazepine, benzodiazepines, and baclofen also may be used in patients who refuse botulinum toxin injections. Compressive lesions need to be treated surgically. Microvascular decompression surgery may be effective for those patients who do not respond to botulinum toxin. A study of 246 patients who underwent microvascular decompression surgery found no significant difference in outcomes and complications between patients who had botulinum toxin injections prior to their first surgery and those who did not.

Botulinum Toxin Injection

The treatment of choice for hemifacial spasm is botulinum toxin injection of botulinum toxin under EMG guidance. Side effects of botulinum toxin injection (eg, facial asymmetry, ptosis, facial weakness) usually are transient. Most patients report a highly satisfactory response. Caution patients that although botulinum toxin ablates the muscular spasm, the sensation of spasm often persists. [9, 10]

Pharmacologic Therapy

Medications may be used in early hemifacial spasm (when spasms are mild and infrequent) or in patients who decline botulinum toxin injection. Use medications in patients with noncompressive lesions and early idiopathic hemifacial spasm. Response to medication varies but can be satisfactory in early or mild cases. The most helpful agents are carbamazepine and benzodiazepines (eg, clonazepam). Often, medication effects attenuate over time, necessitating more aggressive treatment.

Surgical Decompression

Treat compressive lesions surgically. Ectatic blood vessels cause hemifacial spasm by compressing the facial nerve as it exits the brainstem. Surgical decompression of these blood vessels can yield excellent results. [11, 12, 13, 14] A study evaluating the effect of microvascular decompression surgery on idiopathic hemifacial spasm with compression on different zones of facial nerve found that proper detection of offending vessels and complete decompression may increase cure rate.

hemifacial spasm life expectancy

If you’re living with hemifacial spasms, you may feel embarrassed or self-conscious when your facial muscles move involuntarily, and you’re likely frustrated that you can’t control it when a spasm happens. But don’t let a treatable condition diminish your quality of life.

At the AdventHealth Neuroscience Institute, we offer minimally invasive treatments for hemifacial spasm so you can regain control and confidence. And although we treat more neuroscience patients — and perform more neurosurgical procedures — than any other hospital in the nation, we still see each patient as a person with unique needs.

About Hemifacial Spasm

Hemifacial spasm, sometimes called a facial twitch, is an involuntary contraction of the facial muscles. As the prefix “hemi-” implies, spasms will almost always affect half or one side of the face.

Although the condition isn’t usually painful, hemifacial spasms can cause frustration and anxiety for people who live with the neurological disorder. The most common cause of hemifacial spasm is a compressed facial nerve. Usually, the nerve is compressed by an abnormal blood vessel or artery.

Hemifacial spasm symptoms can be slightly different for everyone. Twitches around the eye, cheek and corner of the mouth on one side of the face are the most common signs.

Severe spasms can pull the eyelid entirely closed and cause the eye to water, which can interfere with vision. Some people also experience spasms that cause ear pain and hearing loss. Unlike other facial nerve disorders like trigeminal neuralgia , hemifacial spasm symptoms can continue during sleep.

Facial nerve compression is the most common cause of hemifacial spasm. Vascular abnormalities are usually the source of the compression. Abnormal veins or arteries touch a facial nerve and trigger electrical impulses that cause involuntary muscle movements.

Vascular disorders that can cause facial nerve compression include:

In some cases, brain tumors or lesions can also press on facial nerves. Bell’s palsy, a condition that causes paralysis and drooping on one side of the face from facial nerve trauma, can contribute to hemifacial spasm.

See a doctor right away if you experience any signs of twitching, drooping or other involuntary movements on one side of your face. While a hemifacial spasm is not considered a medical emergency, it’s extremely important to rule out the possibility of a more serious condition like a transient ischemic attack (TIA), sometimes called a mini-stroke.

A doctor should also conduct diagnostic tests to determine the underlying cause of your facial nerve compression. Magnetic resonance imaging, or MRI, can rule out the possibility of a stroke or tumor. An angiogram, which is a type of X-ray that uses dye to create a map of your body’s blood vessels, can reveal vascular abnormalities in the brain.

A study of nerve conduction in the face can also be useful to confirm a hemifacial spasm diagnosis. An electromyogram (EMG) and a nerve conduction velocity (NCV) study can measure muscle and nerve activity.

Medications like anticonvulsants can help reduce the severity of facial twitches from hemifacial spasm. Muscle-relaxing injections such as Botox® may also be recommended as a nonsurgical approach to hemifacial spasm treatment.

Hemifacial Spasm Surgery: Microvascular Decompression

Microvascular decompression is a minimally invasive procedure that separates nerves from the veins or arteries that may be exerting pressure on them. During this procedure, a surgeon makes a small incision behind your ear and removes a very tiny piece of the skull. After gaining access to the compressed nerve, a special type of sponge is placed between the nerve and blood vessel to eliminate pressure.

A Team Approach for Exceptional Outcomes

Our multidisciplinary care team uses the most innovative technology available to provide you with the best possible care. From diagnosis to rehabilitation and everything in between, we deliver exceptional outcomes and compassionate care for you and the people you love.

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