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Spread of muscle spasms in hemifacial spasm

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Authors: Antonella Conte MD, PhD, Marika Falla MD, Maria Concetta Diana MD, Matteo Bologna MD, PhD, Antonio Suppa MD, PhD, Andrea Fabbrini MD, Carlo Colosimo MD, Alfredo Berardelli MD and Giovanni Fabbrini MD

Article first published online:  4 NOV 2014 | DOI: 10.1002/mdc3.12106

Hemifacial spasm (HFS) is a common clinical condition characterized by involuntary contractions in facial muscles.[1] Muscle spasms usually start in the periocular muscles and, only in a few cases (ranging from 1.3% to 17% of the patients), in the lower part of the face.[2-5] From the site of origin, HFS may spread to other facial muscles.[4] No studies have investigated systematically in HFS the frequency of spread from the site of origin to other facial muscles or whether the clinical features differ in patients with and without spread. Knowing more about spread is important because this feature may negatively impact patients' quality of life and worsen HFS severity. To clarify these issues, we studied, in a large sample of patients with primary HFS, the frequency and types of spread and whether spread correlates with disease severity or with specific patients' clinical demographic features.


We initially recruited 193 consecutive patients with diagnosis of primary HFS attending the movement disorder outpatient clinic of the Department of Neurology and Psychiatry, “Sapienza” University of Rome (from January to October 2013). Fifteen patients unable to provide detailed information were excluded from the study, and the study comprised 178 patients (76 females; mean age at examination: 65.8 ± 12.5 years; Table 1). The diagnosis of primary HFS, made by neurologists who are experts in movement disorders, was based on the presence of unilateral involuntary facial muscle contractions affecting one or more muscle groups innervated by the facial nerve.[1, 3, 4] All patients were chronically treated with botulinum toxin. None of the patients had cognitive abnormalities. Patients with bilateral HFS were included if the facial spasm had a nonsimultaneous onset and if the contractions were asynchronous. Diagnosis of secondary HFS was based on history of injury or trauma on the same side of the face, history of previous facial palsy, signs of facial palsy on clinical neurological examination, and absence of brain MRI lesions. We excluded patients with other facial dyskinesias (such as blepharospasm, oromandibular dystonia, facial tics, myokymia, focal seizures, hemimasticatory spasm, or psychogenic conditions) and patients with signs of synkinesis with history and signs of peripheral nerve lesions.

Table 1. Demographics and clinical features of 178 patients with hemifacial spasm
Demographics and Clinical Features Total No. (%)
Gender, M/F 76 (42.7)/102 (57.3)
Age at examination, years 65.8 ± 12.5
Age at onset, years 55.1 ± 13
Family history 4 (2.2)
Disease duration, years 10.8 ± 7.4
Unilateral 176 (98.9)
Right side 74 (42)
Left side 102 (58)
Bilateral 2 (1.1)
Severity Mild: 78 (43.8)
Moderate: 89 (50.0)
Severe: 11 (6.2)
Botulinum toxin dosages Mild: 15.4 ± 5 UI
Moderate: 24.5 ± 7 UI
Severe: 41.5 ± 18 UI

We collected, with a face-to-face questionnaire, data about gender, age, family history for HFS, age at HFS onset, symptom duration, muscles involved by the spasm at the time of onset, and spread of spasm to other facial muscles. Spread of the spasm to other facial muscles was considered to be present in those patients whose spasms onset in a single site and involved both upper and lower facial muscles at the time of examination. Latency of spread was measured by asking the patient the time interval between the onset of muscle spasm (upper or lower part of the face) and the subsequent involvement of other part of the face. All patients underwent a complete neurological examination to assess the distribution of the muscle spasm at the time of examination. Severity of spasm was graded as mild, moderate, and severe on the basis of clinical examination performed by a neurologist expert in movement disorders. Differences in clinical severity were also confirmed by the dosages of botulinum toxin used for the injection.

To evaluate reliability of patients' recall, 45 of the 178 patients originally enrolled were retested using the same face-to-face questionnaire approximately 1 year after the first assessment. To further confirm the spread of muscle spasm, we also reviewed all medical records and verified whether the site of botulinum toxin injections changed over time.

The experimental procedures were carried out in accord with the Declaration of Helsinki and approved by the institutional review board of the University of Rome Sapienza. All participants gave their informed written consent.

All data were evaluated for significance with SPSS software (version 19.0; SPSS, Inc., Chicago, IL). Comparisons between groups were assessed by Student's t test or chi-square (χ2) test. Pearson's correlation coefficient was also used to disclose relations between demographic and clinical variables. Intraclass correlation coefficient was used to evaluate reproducibility of patients' recall at the retest. The significance level was set to P < 0.05. Variables are given as mean ± standard deviation (SD).


Muscle spasms began in 143 (80.3%) patients in the periocular muscles, in 9 (5.1%) in the orbicularis oris muscle, and in 26 (14.6%) patients simultaneously in the upper and lower facial muscles. The onset in the orbicularis oculi muscle alone predominated in women (63.6%), whereas the onset in the lower facial muscles alone or in the orbicularis oculi and lower facial muscles simultaneously was more frequent in males (77.8% vs. 22.2% and 53.8% vs. 46.2%, respectively; χ2 = 6.896; P = 0.032).

No statistical differences were found in the other demographic and clinical variables between patients whose HFS onset sites differed. Age at examination was 64.1 ± 15.8 years in patients with onset in the upper facial muscles, 64.3 ± 13.6 years in patients with onset in the lower facial muscles, and 64.4 ± 14.4 years in patients with onset in the upper and lower facial muscles. Age at onset was 55.9 ± 16.1 years in patients with onset in the upper facial muscles, 53.0 ± 13.5 years in patients with onset in the lower facial muscles, and 54.4 ± 14.6 years in patients with onset in the upper and lower facial muscles. Disease duration was 10.8 ± 7.5 years in patients with onset in the upper facial muscles, 11.2 ± 6.6 years in patients with onset in the lower facial muscles, and 10.2 ± 7.4 years in patients with onset in the upper and lower facial muscles.

In all the patients who reported spread, spread in a different part of the face was confirmed by neurological examination. Muscle spasm spread to other muscles in the same side of the face in 143 of the 152 (94.1%) patients who had spasm onset in the upper or in the lower part alone. Muscle spasms spread in 134 (94%) of the 143 patients with HFS onset in the orbicularis oculi muscle and in all the 9 patients with onset in the lower facial muscles. Only 9 patients with upper facial muscle involvement at onset did not have spread at the time of the enrollment. We did not find significant differences in gender proportions between patients with and without spread (patients with spread were 59 males [41.2%] and 84 females [58.8%]; patients without spread were 4 males [44.4%] and 5 females [55.6%]). The mean ± SD age of the 9 patients without spread was 62.7 ± 21.3 years, and symptoms duration in these patients was 5.3 ± 3.7 years. Latency of spread was 26.9 ± 38.8 months. Latency of spread significantly correlated with disease duration (r = 0.42; P < 0.00001) and inversely correlated with age at disease onset (r = −0.34; P < 0.00001).

Intraclass correlation coefficient in the 45 patients who were retested approximately 1 year after the first assessment was very good for recall of the site of onset and spread to other facial muscle (0.87; 95% confidence interval [CI]: 0.78–0.92) and moderate for recall of latency of spread (0.62; 95% CI: 0.37–0.79). Reviewing medical records, we found that in 112 of the 143 patients, botulinum toxin injection was performed initially in the upper or lower part of the face and, subsequently, in both sites of the face. In the remaining 31 patients, muscle spasms involved both the upper and lower facial muscles, and botulinum toxin was injected from the beginning in the upper and lower part of the face.


In this study, we found that muscle spasm begun in the orbicularis oculi muscle in the majority of the patients. Spread of the muscle spasms to the other facial muscles of the same side of the face was present in the large part of patients studied, and latency of spread was related to disease duration and age at onset. Spread of muscle spasms to the other ipsilateral facial muscles is therefore a typical feature of HFS.

A limitation of our study is that we assessed the spread of HFS with a retrospective evaluation, and therefore the results depend on patients' subjective report. HFS patients might not be aware of mild twitches, and patient's recall might reflect severity of spasm. Notwithstanding these limitations, we believe that the data reported in this article are consistent. The retest of a subgroup of 45 patients showed a very good consistency of spread recall and a moderate consistency for latency recall. Furthermore, on reviewing clinical records, the presence of spread was also confirmed by changes in botulinum toxin injection sites during the course of the disease.

The negative correlation we found between age at onset and spread latency implies that age negatively impacts the course of the disease and that aged facial nerve fibers are more prone to develop spread. Our observation is in line with MRI anatomical evidence showing that the facial nerve is significantly shorter in older than in young people.[6] Given that facial nerve length in the most intracranial portion of the facial nerve[6, 7] also plays a pathophysiological role in the HFS and that latency of spread is related to disease duration, we conclude that development of spread represents the natural course of HFS. Hence we conjecture that in the ~10% of patients who had no spread, this would probably appear with a longer observation time.

Although our study design did not specifically address pathophysiological mechanisms of spread, we can raise some hypothesis. Spread may be a result of lateral excitation of facial axons caused by ephaptic transmission[8-11] or facial nucleus hyperexcitability (chronic facial nerve irritation makes the facial nucleus hyperexcitable and opens dormant synapses, causing cross-transmission in the facial nucleus).[10-13] In a study by Ishikawa et al.,[14] the researchers demonstrated that botulinum toxin injection reduced facial nucleus hyperexcitability. If spread is the result of facial nucleus hyperexcitability, in our patients who had been chronically treated for years with botulinum toxin, we should have expected a lower spread rate. We might speculate therefore that spread in HFS possibly arises through an ephaptic mechanism on the facial nerve trunk.

In conclusion, in this article, we showed that, in patients with HFS, spread of muscle spasms likely represents the natural history of HFS.


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