Craniofacial Muscles

274 A.O. Grobbelaar and A.C.S. Woollard
Eighty fi ve percent of patients recovered some movement within 3 weeks and the
remaining within 3–5 months. Complete remission occurred in week 1 for 6%,
week 2 for 33%, and week 3 for 16%. Interestingly, no patients achieved remission
between 3 weeks and 3–5 months, indicating that in the latter group there was total
degeneration of the nerve. Ten percent reached remission at 3–5 months and 5% at
5–6 months.
Overall, 71% of patients achieved a full recovery with 58% occurring within the
fi rst 2 months, though there was signi fi cant difference between those who initially
had an incomplete or complete paralysis (94% vs. 61%, P < 0.001). No patient who
still had abnormal movement 6 months after onset of paralysis regained full function.
The speed of onset of recovery was a critical prognostic indicator as was the
age of the patient. Ninety percent of children under 14 years achieved a full recovery,
84% of those 15–29, 75% of those 30–44, and less than 33% of those over 60.
Whilst Bell’s palsy was no more common in pregnant women, it did result in a
poorer prognosis (61% vs. 80% complete recovery, P < 0.001) (Peitersen 2002 ) .
Eight hundred and sixty nine patients had facial palsies with identi fi able causes
(i.e., not idiopathic/Bell’s palsies). It is worth expanding on cases in the context of
diabetes mellitus, those caused by HZV, and pediatric cases. Approximately 3% of
cases occurred in patients with diabetes mellitus (diabetes has an estimated incidence
of 3–4% in the Danish population). Two-thirds of these were incomplete
paralyses but did poorly, with only 25% achieving full recovery, in contrast to the
normal picture with incomplete palsy. It is thought that this is explained by the
underling diabetic neuropathy. Herpes zoster (HZV) oticus, or Ramsay-Hunt syndrome,
is associated with a very poor prognosis (Hunt 1908 ) and tends to af fl ict an
older subset of patients. Most of the time, it caused a complete paralysis (88%) and
was often associated with vestibular disturbances and irreversible hearing loss typically
of the higher tones. The diagnosis of HZV is based on clinical observations of
vesicles, which may not locate around the ear, necessitating a thorough examination
of the head, neck, and mucosal surfaces. The vesicles may appear before, with, or
after the palsy. Diagnosis can be con fi rmed by the detection of antibodies in serum
and CSF. Prognosis was also poor in this group with 46% achieving a fair recovery
and 54% a bad one. In addition, Peitersen feels that treatment with acyclovir does
not affect outcomes markedly (Peitersen 2002 ) .
The pediatric cases (349 cases, 13.5% overall) were dominated by neonatal cases
(169 cases) and Bell’s palsy (138 cases). The remaining cases were congenital bilateral
palsies, trauma, or infectious causes (Peitersen 2002 ) . There has been considerable
discussion over whether neonatal paralysis is congenital or due to birth trauma.
Congenital causes can be as a result of teratogenesis, aplasia of the facial nerve
nucleus or as part of a syndrome such as Treacher-Collins or Moebius. Of the neonatal
cases, the majority (80%) are due to birth trauma (Smith et al. 1981 ) .
One of the most dif fi cult aspects of evaluating facial palsy is the lack of a
common tool for measuring recovery that allows comparison between groups. The
complexity of normal facial movement and the variety of homeostatic functions that
the muscles of expression also encompass makes a succinct scale of total de fi cit
impossible. There have been several attempts to classify facial palsies according to