 |
 |

Craniofacial, Temporal Bone, and Audiologic Abnormalities in the Spectrum of Hemifacial Microsomia
Reza Rahbar, DMD, MD;
Caroline D. Robson, MD;
John B. Mulliken, MD;
Lynn Schwartz, MS, CCC-S;
James Dicanzio, MS;
Margaret A. Kenna, MD;
Trevor J. McGill, MD;
Gerald B. Healy, MD
Arch Otolaryngol Head Neck Surg. 2001;127:265-271.
ABSTRACT
 |  |
Objectives To evaluate the clinical, audiologic, and temporal bone computed tomograpic
findings in patients with hemifacial microsomia and to use the OMENS (each
letter of the acronym indicates 1 of the following 5 dysmorphic manifestations:
O, orbital asymmetry; M, mandibular hypoplasia; E, auricular deformity; N,
nerve involvement; and S, soft tissue deficiency) grading system to assess
possible correlations between the severity of dysmorphic features with the
type of abnormalities in the temporal bone and with degree of hearing deficit.
Design Retrospective study.
Setting Tertiary care children's hospital.
Patient Forty patients with hemifacial microsomia.
Result Mandibular hypoplasia and auricular abnormalities were the most common
clinical manifestations, present in 39 patients (97%) and 38 patients (95%),
respectively. Conductive hearing loss was noted in 35 patients (86%) and sensorineural
hearing loss in 4 patients (10%). Facial nerve weakness was present in 20
patients (50%). Twenty patients had unilateral aural atresia, 12 patients
had unilateral aural stenosis, and 7 patients had bilateral anomalies. Moderate
hypoplasia or atresia of the middle ear was noted in 36 patients (90%) and
ossicles were malformed in 30 patients (75%). Hypoplasia of the oval window
was the most common inner ear abnormality.
Conclusions Severity of craniofacial features (total OMENS score) significantly
correlated with the degree of temporal bone abnormality, but no correlation
was noted with the degree or type of hearing loss. We recommend the following:
(1) use of the OMENS classification system for documentation and analysis
of dysmorphic finding in hemifacial microsomia; (2) complete audiologic evaluation
in all patients with hemifacial microsomia regardless of the type of craniofacial
abnormalities; and (3) temporal bone computed tomography for further evaluation
of hearing deficit.
INTRODUCTION
HEMIFACIAL microsomia (HFM) is a term coined by Gorlin and colleagues.1, 2 This disorder has also been called
"otomandibular dysostosis,"3 "first branchial
arch syndrome,"4 "second branchial arch syndrome,"5 "oculoauriculovertebral sequence,"6
"Goldenhar syndrome,"7 "lateral facial dysplasia,"8 and "craniofacial microsomia."9
Hemifacial microsomia manifests in a highly variable phenotype. It is the
second most common craniofacial malformation after cleft lip and cleft palate.
Any structures derived from the first and second pharyngeal arches can be
affected. Although unilateral presentation is preponderant, bilateral anomalies
are also seen in 30% of these patients.10
This study analyzed the severity of the craniofacial features, temporal
bone abnormalities, and audiologic findings in patients with HFM. We also
sought to assess a possible relationship between the clinical and dysmorphic
features of these patients with the abnormalities in the temporal bone computed
tomographic (CT) scans and the severity and type of hearing loss.
PATIENTS AND METHODS
PATIENTS
The medical records of 162 patients with the diagnosis of HFM seen in
the Craniofacial Center at The Children's Hospital, Boston, Mass, were reviewed.
Only those patients with complete medical records who had undergone temporal
bone CT scan and audiologic workup were included in the study. Forty patients
were eligible for this retrospective study.
Medical records were reviewed and data were recorded for the following:
the patient's sex, age, family history, facial nerve function, history of
otologic disease, and audiologic evaluation. Temporal bone CT scans were reviewed
for abnormalities of the external auditory canal (EAC), middle ear, ossicles,
inner ear, mastoid development, facial nerve canal, and mandibular condyle.
The OMENS classification system11 was
used to grade the abnormal components in patients with HFM. Each letter of
the acronym indicates 1 of the 5 major dysmorphic manifestations: O, orbital
asymmetry; M, mandibular hypoplasia; E, auricular deformity; N, nerve involvement;
and S, soft tissue deficiency. Each of these 5 anatomical features was graded
from 0 to 3 (ie, 0 indicates none; 3, worse) according to the severity using
physical examination findings, photographs, and radiographs, including posteroanterior,
lateral, and cephalometry. A total OMENS score was obtained by summing the
5 anatomical features (Table 1).
|
|
|
|
Table 1. OMENS Classification System*
|
|
|
A single neuroradiologist (C.D.R.) reviewed the temporal bone CT scans.
For analysis, radiographic findings of each anatomical category were assigned
an ordinal integer score. Data were recorded on the following: EAC (normal
[0], stenosis [1], or atresia [2]), middle ear (normal [0], hypoplastic [1],
or atretic [2]). ossicles (normal [0], malformed and fused [1], or unidentified
[2]), mastoid (normal [0], poor pneumatization [1], or absent pneumatization
[2]), facial nerve (normal [0], displaced [1], or could not be identified
[2]), condyle (normal [0], displaced [1], or hypoplastic [2]), and inner ear
abnormality (normal [0] or abnormal [1]). A total radiographic score was obtained
by summing the scores for each category.
STATISTICAL METHODS
Individual and total OMENS scores were compared with the total radiographic
score, type, and degree of hearing loss. Patients manifesting unilateral and
bilateral anomalies were analyzed separately. For patients with bilateral
involvement comparisons were performed on the basis of side rather than patient
since each side was evaluated separately. For analysis, the degree of hearing
loss was assigned an ordinal integer score, ie, 0 (normal), 1 (mild), 2 (moderate),
3 (moderate-severe), 4 (severe), or 5 (profound).
Since numerical results were ordinal scores rather than continuous variables,
nonparametric procedures were used for all analyses. Correlation between the
OMENS scores and both the hearing loss and the radiographic score was assessed
using the Spearman rank correlation coefficient ( ). Comparison of OMENS
scores on the basis of type of hearing loss was performed using the Kruskal-Wallis
procedure.5 Patient summaries were expressed
as medians, ranges, and frequency distributions. Owing to the nature of this
study, the conservative Bonferroni correction for multiple testing was not
applied. However, to provide a higher degree of protection to the experimentwise
type I error rate, we considered the results to be statistically significant
if P<.01. Statistical analysis was performed using
SAS version 6.12 (SAS Institute, Cary, NC).
RESULTS
CLINICAL FINDINGS
There were 17 male (43%) and 23 female patients (57%), ranging in age
from 2 to 37 years (mean age, 12 years). None of these patients had chromosomal
anomalies, a history of teratogenesis, or a family history of craniofacial
abnormalities. There were 17 (43%) left-sided, 16 (40%) right-sided, and 7
(17%) bilateral presentations (Table 2).
The 5 major OMENS features (ie, orbital, mandible, ear, nerve, and soft
tissue) are listed in Table 1.
Abnormal orbital size and position were noted in 4 patients (12%) with unilateral
HFM and 1 patient (14%) with bilateral HFM. Mandibular hypoplasia, ranging
from a small short ramus to complete absence of a ramus, was noted in 32 patients
(97%) with unilateral HFM and 7 patients (100%) with bilateral HFM. Unilateral
HFM as defined in Table 1 presented
as follows: E1 (n = 6 [18%]), E2 (n = 6 [18%]), and E3 (n = 19 [58%]). Bilateral
HFM presented as E1 (n = 2 [29%]), E2 (n = 2 [29%]), and E3 (n = 3 [42%]).
Six patients (15%) had preauricular tags.
Facial nerve weakness as defined in Table 1 was documented in 16 patients (48%) with unilateral HFM.
Four patients had weakness of N1 (frontal or zygomatic), 7 patients had weakness
of N2 (ie, buccal, marginal mandibular, or cervical), and 5 had weakness of
N3 (complete facial nerve). Two of these patients also had weakness of the
unilateral hypoglossal nerve (CN12). Four patients (57%) with bilateral HFM
had facial nerve paresis. Two of these patients had bilateral and 2 had unilateral
manifestations of facial nerve weakness (Table 2). Soft tissue or muscle deficiency was noted in 19 patients
(58%) with unilateral HFM and 2 patients (29%) with bilateral HFM.
A history of chronic otitis media was noted in 20 patients (60%) with
unilateral HFM and 3 patients (43%) with bilateral HFM. Fifteen patients (45%)
with unilateral HFM and 1 patient (14%) with bilateral HFM had undergone placement
of tympanostomy tubes. Five patients (15%) with unilateral HFM and 5 patients
(71%) with bilateral HFM were successfully using hearing aids.
AUDIOLOGIC FINDINGS
Patients with unilateral HFM (Table
2) initially had the following: normal hearing (n = 1 [3%]), mild
conductive hearing loss (CHL) (n = 2 [6%]), moderate CHL (n = 1 [3%]), moderate-severe
CHL (n = 5 [15%]), severe CHL (n = 14 [42%]), profound CHL (n = 3 [9%]), profound
sensorineural hearing loss (SNHL) (n = 2 [6%]), and bilateral moderate to
severe CHL (n = 2 [6%]). Three patients (9%) initially had bilateral hearing
loss (Table 2). Patients with
bilateral HFM (Table 2) initially
had the following: bilateral moderate to severe CHL (n = 3 [43%]), bilateral
severe CHL (n = 2 [29%]), bilateral moderate mixed hearing loss (n = 1 [14%]),
or unilateral severe CHL (n = 1 [14%]).
RADIOLOGICAL FINDINGS
Atresia of the EAC was noted in 20 patients (61%) with unilateral HFM
and in 4 patients (57%) with bilateral HFM. Canal stenosis was observed in
12 patients (36%) with unilateral HFM and in 2 patients (28%) with bilateral
HFM. Only 1 patient with unilateral HFM had a normal EAC. One patient with
bilateral HFM had atresia on one side and stenosis on the other (Figure 1 and Figure 2).
|
|
|
|
Figure 1. HFM indicates hemifacial microsomia;
EAC, external auditory canal; and ME, middle ear. All values are expressed
as percentages of patients.
|
|
|
|
|
|
|
Figure 2. A-B, A 3-dimensional image of
hemifacial microsomia. C, View of unilateral external auditory canal stenosis
(arrow). D, View of bilateral external auditory canal stenosis (arrows). E,
View of hypoplastic condyle (arrow). F, View of malformed and fused ossicles
(arrow). G, view of abnormal semicircular canal (arrow). H, View of hypoplastic
oval window (arrow). I, View of abnormal cochlea (arrows).
|
|
|
Patients with unilateral HFM had the following findings: normal middle
ear (ME) (n = 4 [12%]), hypoplastic ME (n = 23 [70%], and atretic ME (n =
6 [18%]). All patients with bilateral HFM had hypoplastic MEs. Ossicles were
malformed and fused in 24 patients (73%) with unilateral HFM and 6 patients
(86%) with bilateral HFM. Ossicles could not be identified in 8 patients (24%)
with unilateral HFM because of severe atresia of the ME.
Mastoid air cells were absent in 14 (42%) and poorly developed in 8
patients (24%) with unilateral HFM; and absent in 4 (57%) and poorly developed
in 2 (29%) patients with bilateral HFM. Thirty patients (90%) with unilateral
HFM and 7 patients (100%) with bilateral HFM had displacement and some degree
of condylar hypoplasia.
Abnormalities of the facial nerve canal were noted in 35 (88%) of the
40 patients. Anterior displacement of the facial nerve, most commonly in the
mastoid segment, was seen in 21 patients (64%) with unilateral HFM and in
4 patients (57%) with bilateral HFM. The facial nerve canal could not be identified
in 8 patients (24%) with unilateral HFM and in 2 patients 29% with bilateral
HFM.
Hypoplastic oval window was the most common inner ear abnormality and
was noted in 12 patients (36%) with unilateral HFM and in 2 patients (29%)
with bilateral HFM. An abnormal cochlea was noted in 1 patient with unilateral
HFM and in 1 patient with bilateral HFM; these 2 patients had profound SNHL
and bilateral moderate mixed hearing loss, respectively. Other inner ear abnormalities
noted in patients with unilateral HFM were as follows: hypoplastic vestibule
(n = 2), hypoplastic semicircular canals (n = 1), atretic facial nerve recess
(n = 1), and atretic round window (n = 2).
STATISTICAL RESULTS
Patients' demographics and summarized data are listed in Table 3 and Table 4.
Patients with unilateral HFM had a significant correlation between the "E"
score (auricular abnormality) and the radiographic score ( +0.57, P<.001). However, no significant correlation was found
for other individual scores (orbit, mandible, nerve, or soft tissue). Total
OMENS score (severity of craniofacial features) correlated significantly with
the total radiographic score for both unilateral ( = 0.47, P = .006) and bilateral
( = 0.83, P<.001)
presentations. All significant values were positive, indicating that
the high total OMENS scores are associated with high radiographic scores and
vice versa. No statistically significant correlation between the OMENS scores
and the degree or type of hearing loss was observed for either unilateral
or bilateral presentations. The P values for all
statistical tests are summarized in Table
3 and Table 4.
|
|
|
|
Table 3. Patient Demographics
|
|
|
|
|
|
|
Table 4. Tests of Association (P) Predictors*
|
|
|
COMMENT
The incidence of HFM has been estimated at 1 in 5600 births.11 It usually manifests with varying degrees of hypoplasia
and asymmetry of bony and soft tissue of the face that is usually unilateral
but not uncommonly bilateral7 patients in our series. It has been suggested
that there is a 3:2 predilection for males and the right side of the face.12 In our sample, no evidence of sex preference or dominance
of facial asymmetry to either side was noted; confirming our earlier study
of 121 patients.11
The cause of HFM is thought to be pathogenically heterogeneous. It is
as if the defective genes, teratogens, and vascular anomalies singly or collectively
can cause disruption of normal development leading to a wide spectrum of the
anomalies seen in these patients. Poswillo13
devised a chemically induced murine phenocopy and showed that focal hemorrhage
from the stapedial artery supplying the first and second pharyngeal arches
could be the primary cause. However, it is unlikely that embryonic hematoma
formation could account for the wide range of HFM features, particularly those
outside the craniofacial regions. Johnston and coworkers14, 15
showed that exposure to thalidomide and retinoic acid could lead to anomalies
similar to HFM. Accutane (13-cis retinoic acid) interferes
with proliferation and migration of neural crest cells, causing facial and
cardiac abnormalities similar to the HFM. Otani et al16
proposed a transgenic mouse model with an insertional mutation on chromosome
10. Hemifacial microsomia can also occur in patients with chromosomal disorders
such as trisomy 18, trisomy 7, 9 mosaicism, and terminal deletion of 22q.
There are also pedigrees with HFM, and in some affected families the history
is consistent with autosomal dominant or recessive inheritance.17, 18, 19, 20
Several classification systems have been proposed to document and analyze
the clinical manifestations of HFM. Mandibular hypoplasia seems to be the
element central to all these schemes. Pruzansky21
described the 3 types of mandibular abnormalities; however, he did not account
for other associated manifestations of HFM. Harvold et al22
described 5 types of mandibular anomalies, but did not include auricular,
neural, and orbital anomalies. David et al12
presented the skeletal, auricular, and soft tissue (SAT) system modeled after
the TMN classification of tumors. However, this system does not permit independent
evaluation of the orbital and cranial nerve abnormalities. The OMENS system,
proposed in 1991,11 is an expansion of Pruzansky's
classification. It includes 5 of the major craniofacial manifestations of
HFM and allows independent grading of the dysmorphic features. In this system,
each anatomical abnormality is graded from 0 (normal) to 3 (most severe).
Cousley23 compared the SAT with the OMENS system
and concluded that the OMENS system was more sensitive to the wide phenotypic
heterogeneity of HFM. The OMENS system was later expanded by Horgan et al24 to OMENS-Plus to include the extracraniofacial anomalies.
The association between HFM and anomalies of the other organs (ie, central
nervous system, cardiac, pulmonary, renal, gastrointestinal, and skeletal)
has been well documented. Sporadic malformations present in a frequency of
1 in 1000 births (ie, congenital lip and palate, tracheoesophageal fistula,
atrial septal defect, and tetralogy of Fallot). The term "associated anomaly"
is used when a defect occurs in 10% to 15% of the cases and is pathogenically
related to the primary abnormality. Associated anomalies in patients with
HFM are reported as: central nervous system, 5% to 15%24, 25;
cardiac, 45% to 55%26 and 26.4%3;
genitourinary, 5% to 6%25 or 10%24;
pulmonary and gastrointestinal, 10%24; and
skeletal, 41%.24
Patients with HFM can present with a wide range of anomalies; however,
facial nerve weakness and hearing loss are the most common functional deficits.
The prevalence of facial nerve palsy with HFM varies in range as seen from
the following sources: 10%, Grabb27; 19%, Converse
et al28; 25%, Murray et al29;
22%, Bassila and Goldberg30; 45%, Vento et
al11; and 22%, Carvalho et al.10
In our series 20 (50%) of the 40 patients showed some degree of facial nerve
weakness, and 2 patients also had unilateral hypoglossal nerve weakness. Facial
nerve weakness could be due to the deficiency of the mesoderm of the pharyngeal
arches, neural ectoderm, or a combination of both. Evaluations of the temporal
bones have shown the following: (1) abnormal course and exit point of the
facial nerve over the temporamandibular joint28;
(2) development of the nervous intermedius component of the facial nerve,
and no development of the mastoid component31;
(3) hypoplasia of the entire course of the facial nerve.32
The most common type of hearing deficit in HFM is conductive loss34
patients (86%) in our series. However, the presentation of SNHL in these patients
remains underappreciated. The overall incidence of congenital SNHL in the
general population is 0.001% to 0.004%, and 3% to 4% in patients with craniofacial
syndromes.30 The incidence of SNHL in our patients
was 10% (4 patients) consistent with other reports, 11% (Carvalho et al10) and 16% (Bassila and Goldberg30).
Hemifacial microsomia can manifest as a structural abnormality in any
tissue derived from the first and second pharyngeal arches. The mandibular
and auricular deformities are the main components of the dysmorphic features.
In our series, 39 patients (97%) had mandibular hypoplasia and 38 patients
(95%) showed auricular abnormalities. Our data showed a significant correlation
between the severity of the external auricular anomalies ("E" score) and the
extent of temporal bone abnormalities in patients with unilateral HFM. We
also found that the overall severity of craniofacial features (total OMENS
score) correlated significantly with the degree of the temporal bone abnormalities
(total radiographic score) for patients with unilateral and bilateral HFM.
Thus, in patients with abnormal hearing, temporal bone CT scan must be obtained
to further assess the degree of stenosis and atresia of EAC, status of the
ossicular chain and ME, and inner ear anomalies. The timing of the temporal
CT scan must be individualized based on the the age of the patient, severity
or worsening of the hearing status, and no otologic surgery. At our craniofacial
center, a 3-dimensional CT study is always done in preparation for mandibular
elongation in the age range of 5 to 7 years. Whenever possible, a combined
study for temporal bone abnormalities and type of mandibular hypoplasia should
be done concurrently.
Also, our data show that there is no correlation between the severity
of the dysmorphic features of HFM and the degree or type of hearing loss.
Patients with minimal dysmorphic features can present with a moderate-severe
degree of hearing loss. Failure to appreciate this finding could delay proper
and timely diagnosis, thereby prolonging sensory deprivation and delayed speech
and language acquisition. Thus, we strongly recommend a complete audiologic
evaluation of every child with a diagnosis of HFM, regardless of the type
or the severity of the clinical manifestations.
CONCLUSIONS
Our results confirmed that evaluation and interpretation of data using
the OMENS classification system provide a logical and comprehensive manner
to document, independently analyze, and compare the major dysmorphic features
of HFM. Furthermore, we agree with Cousley23
that an asterisk be added to the "E" component of the acronym (OME*NS) to
indicate the type and degree of hearing loss.
AUTHOR INFORMATION
Accepted for publication August 11, 2000.
Presented in part at the American Society of Pediatric Otolaryngology
Combined Otolaryngological Society Meeting, Orlando, Fla, May 2000.
From the Department of Otolaryngology and Communication Disorders (Drs
Rahbar, Kenna, McGill, and Healy), Department of Radiology (Dr Robson), Division
of Plastic Surgery (Dr Mulliken), Division of Audiology (Ms Schwartz), and
the Department of Clinical Research (Mr Dicanzio), The Children's Hospital;
and Harvard Medical School, (Drs Rahbar, Kenna, McGill, Healy, Robson, and
Mulliken), Boston, Mass.
Corresponding author: Reza Rahbar, DMD, MD, Department of Otolaryngology
and Communication Disorders, The Children's Hospital, 300 Longwood Ave, Boston,
MA 02115 (e-mail: rahbar{at}a1.tch.harvard.edu).
REFERENCES
 |  |
1. Gorlin RJ, Pindborg JJ, Cohen MM Jr. In: Syndromes of the Head and Neck. 2nd ed. New York, NY: McGraw-Hill Co; 1976.
2. Gorlin RJ, Cohen MM Jr, Levin LS. In: Syndromes of the Head and Neck. 3rd ed. New York, NY: Oxford University Press; 1990.
3. François JJ, Haustrate L. Anomalies colobamateuses du globe oculiare et syndrome du premier arc. Ann Ocul. 1954;26:340-368.
4. Stark RB, Saunders DE. The first branchial syndrome: the oral-mandibular-auricular syndrome. Plast Reconstr Surg. 1962;29:229-329.
5. Grabb WC. The first and second branchial arch syndrome. Plast Reconstr Surg. 1965;36:485-508.
PUBMED
6. Gorlin RJ, Jue KL, Jacobsen V, Goldschmidt E. Oculoauriculovertebral dysplasia. J Pediatr. 1963;63:991-999.
FULL TEXT
| PUBMED
7. Goldenhar M. Associations malformatives de l'oil et de l'oveille, en particulier
le syndrome dermoïde epibulbaire-appendices auricularies-fistula auris
congenita et ses relations avec la dysostose mandibulo-faciale. J Genet Hum. 1952;1:243-282.
8. Ross RB. Lateral facial dysplasia (first and second branchial arch syndrome:
hemifacial microsomia). Birth Defects Orig Artic Ser. 1975;11:51-59.
9. Converse JM, Coccaro PJ, Becker M, Wood-Smith D. Clinical aspects of craniofacial microsomia. In: Converse JS, McCarthy JG, Wood-Smith D, eds. Symposium on Diagnosis and Treatment of Crainofacial Anomalies. St
Louis, Mo: CV Mosby; 1979:461-475.
10. Carvalho GJ, Song CS, Vargervik K, Lalwani AK. Auditory and facial nerve dysfunction in patients with hemifacial microsomia. Arch Otolaryngol Head Neck Surg. 1999;125:209-212.
FREE FULL TEXT
11. Vento AR, LaBrie RA, Mulliken JB. The OMENS classification of hemifacial microsomia. Cleft Palate Craniofac J. 1991;28:68-77.
FULL TEXT
|
ISI
| PUBMED
12. David DJ, Mahammarat C, Cooter RD. Hemifacial microsomia: a multisystem classification. Plast Reconstr Surg. 1987;80:525-535.
PUBMED
13. Poswillo DE. The pathogenesis of first and second branchial arch syndrome. Oral Surg Oral Med Oral Pathol. 1973;35:302-328.
FULL TEXT
| PUBMED
14. Johnston MC, Bronsky PT, Millicovski G. Embryology of the head and neck. In: McCarthy JG, ed. Plastic Surgery. Vol
4. Philadelphia, Pa: WB Saunders Co; 1990:2410-2495.
15. Johnston MC, Bronsky PT. Animal models for human craniofacial malformations. J Craniofac Genet Dev Biol. 1991;11:227-291.
16. Otani H, Tanaka O, Naora H, et al. Microtia as an autosomal dominant mutation in a transgenic mouse line:
a possible animal model of branchial arch anomalies. Anat Anz. 1991;172:1-9.
PUBMED
17. Seltzer ES, Ruiz-Castaneda N, Stevern C, Ryden S, Frias JL. Etiologic heterogeneity in the oculoauriculovertebral syndrome. J Pediatr. 1981;98:88-90.
FULL TEXT
|
ISI
| PUBMED
18. Rollnick BR, Kaye CI. Hemifacial microsomia and variants: pedigree data. Am J Med Genet. 1983;15:233-253.
PUBMED
19. Regenbogen L, Godel V, Goya V, Goodman RM. Further evidence for an autosomal dominant form of oculoauriculovertebral
dysplasia. Clin Genet. 1982;21:161-167.
ISI
| PUBMED
20. Figueroa AA, Friede H. Craniovertebral malformations in hemifacial microsomia. J Craniofac Genet Dev Biol Suppl. 1985;1:167-78.
PUBMED
21. Pruzansky S. Not all dwarfed mandibles are alike. Birth Defects Orig Artic Ser. 1969;1:120-129.
22. Harvold EP, Vargeruik K, Chierici G. Treatment of Hemifacial Microsomia. New York, NY: Alan R Liss Inc; 1983.
23. Cousley RR. A comparison of two classification systems for hemifacial microsomia. Br J Oral Maxillofac Surg. 1993;31:78-82.
PUBMED
24. Horgan JE, Padwa BL, LaBrie RA, Mulliken JB. OMENS-Plus: analysis of craniofacial and extracraniofacial anomalies
in hemifacial microsomia. Cleft Palate Craniofac J. 1995;32:405-412.
PUBMED
25. Rolnick BR, Kaye CI, Nagatoshi K, Hauck W, Martin AO. Oculoauriculovertebral dysplasia and variants: phenotypic characteristics
of 294 patients. Am J Med Genet. 1987;26:361-375.
FULL TEXT
|
ISI
| PUBMED
26. Johnston MC. Embryology of the head and neck. In: McCarthy JG, ed. Plastic Surgery. Vol
4. Philadelphia, Pa: WB Saunders Co; 1990:2451-2459.
27. Grabb WC. The first and second branchial arch syndrome. Plast Reconstr Surg. 1965;36:485-508.
28. Converse JM, Coccaro PJ, Becker M, Wood-Smith D. On hemifacial microsomia: the first and second branchial arch syndrome. Plast Reconstr Surg. 1973;51:268-279.
PUBMED
29. Murray JE, Kaban LB, Mulliken JB. Analysis and treatment of hemifacial microsomia. Plast Reconstr Surg. 1984;74:186-199.
PUBMED
30. Bassila MK, Goldberg R. The association of facial palsy and/or sensorineural hearing loss in
patients with hemifacial microsomia. Cleft Palate J. 1989;26:287-291.
PUBMED
31. Sekhar HKC, Tokita N, Alexic S, Sachs M, Daly JF. Temporal bone findings in hemifacial microsomia. Ann Otol Rhinol Laryngol. 1978;87:399-403.
PUBMED
32. Sando I, Ikeda M. Temporal bone histopathologic findings in oculoauriculovertebral dysplasia:
Goldenhar's syndrome. Ann Otol Rhinol Laryngol. 1986;95:396-403.
PUBMED
RELATED ARTICLE
Archives of OtolaryngologyHead & Neck Surgery Reader's Choice: Continuing Medical Education
Arch Otolaryngol Head Neck Surg. 2001;127(3):342-343.
FULL TEXT
|