Cosmetic Facial Surgery

583
A
B
FIGURE 12-133.  Patient underwent a
single pass of CO2 Lite laser skin resur-
facing, which heals in about a week.
Good improvement of fine wrinkles and
dyschromias is seen.
A
B
FIGURE 12-134.  Patient treated with a single pass of CO2 Lite
laser skin resurfacing at 3.5 J/cm2, which heals in about 1
week. The lower lids were treated with an additional pass. Good
improvement of fine wrinkles and smoothing of the skin texture
is seen.
A
B
FIGURE 12-135.  Patient treated with a
single pass of CO2 Lite laser skin
resurfacing at 3.5 J/cm2, which heals
in about 1 week. The lower lids were
treated with an additional pass. Good
improvement of fine wrinkles and
smoothing of the skin texture is seen.

584
Chapter 12  •  Skin Resurfacing
A
B
FIGURE 12-136.  Patient treated with a single pass of Active FX laser skin resurfacing with a setting of 100 mJ and a density of
2. Moderate improvement of dyschromias is seen, but the degree of improvement is less than the more aggressive cases.
A
B
FIGURE 12-137.  Patient treated with a single pass of ultrapulse fractional (Active FX) CO2 laser skin resurfacing at 100 mJ and
a density of 2. The lentigines on the left cheek were treated with additional passes of the same setting. This case was performed
with topical anesthesia only and is representative of newer laser technology.

Chapter 12  •  Skin Resurfacing
585
B
A
D
C
FIGURE 12-138.  African-American patient was treated for neurofibromatosis with three passes of 90 mJ and a density of 6. This
case shows the total removal of skin pigment and repigmentation over time. A, Patient pre-laser. B, Immediately post laser.
C, 2 weeks post laser. D, 8 weeks post laser. Aggressive treatment on this type of dark skin is a rare occurrence.

586
Chapter 12  •  Skin Resurfacing
B
A
FIGURE 12-139.  Submental platysmaplasty incisions can often produce unfavorable scars and respond quite well to multipass
laser skin resurfacing. Patient is shown before (A) and after (B) two passes of 80 mJ and a density of 6.
A
B
FIGURE 12-140.  Patient developed an unsightly raised scar after trichophytic brow and forehead lift. She was treated with two
nondébrided passes of CO2 laser skin resurfacing (LSR) at 80 mJ and a density of 6. Multipass, high-energy CO2 LSR is an
excellent means of improving these scars.
A
B
FIGURE 12-141.  Patient sustained hypertrophic scarring in a motorcycle accident. She was first treated with Z-plasty scar revi-
sion followed by several sessions of multipass, high-energy CO2 laser skin resurfacing.

Chapter 12  •  Skin Resurfacing
587
A
B
FIGURE 12-142.  Patient sustained a deep laceration from
a fall and was treated with two sessions of three-pass
CO2 laser skin resurfacing at 80 mJ and a density of 6.
Table 12-2  Complications From 500 CO2 Laser Skin Resurfacing
Treatments
Complication
Percentage of Occurrence
Erythema
100%
Hyperpigmentation
37%
Acne flare
15%
Milia
11%
Contact dermatitis
10%
Herpes simplex infection
7.4%
Hypopigmentation
1%
Hypertrophic scarring
0%
Ectropion
0%
Post–Laser Skin Resurfacing Edema
All burns cause fluid shifts in the surrounding tissues, and the
level of post-LSR edema can be impressive in some patients.
Although the edema in itself is not harmful, it is extremely
disconcerting for the patient and their family. Edema generally
appears in the early stages and resolves quickly with cold com-
presses. In significant cases, I place the patient on prednisone
60 mg once a day for 5 days, which has proven very safe and
effective for resolution (Figure 12-143).
Extended Post-Laser Erythema
Persistent erythema is always a concern with aggressive CO2
laser. It is related to the depth of injury, the postop care, and
most importantly to the patient’s skin type. My experience is
that 99% of aggressive CO2 LSR patients will reepithelialize in
about 10 to 12 days and begin using makeup. Their erythema
usually resolves between 3 weeks and 3 months but in the lighter
Fitzpatrick skin types can persist longer. In Fitzpatrick 1 and 2
skin types with ectatic vessels and/or rosacea, erythema can
persist for many months. Other patients with tendencies to
easily blush from vasodilatation (e.g., Valsalva, alcohol, caffeine
consumption or emotional stimuli) are prone to extended ery-
thema. Some practitioners favor treatment with vitamin C
preparations or azelaic acid 15%, others use LED diode light
systems in hopes of reducing erythema. The biggest step I have
taken in reducing post-LSR erythema is to not débride the char
between laser passes. The consent process must put the patient
on notice that post-laser erythema can persist for months but is
rarely permanent (Figure 12-144). Bacterial, yeast, or herpetic
infections can also extend erythema and sometimes go undiag-
nosed as causative agents. Contact allergy from antibiotic creams
or ointments must also be ruled out (Figure 12-145).
Post Laser Day 3
Post Laser Day 1
Postoperative Edema
B
A
FIGURE 12-143.  Patient post–laser skin resurfacing day 1 (A) and the same
patient 48 hours later after employing cold compresses and beginning an
oral steroid regimen (B).
Data from Nanni CA, Alster TS: Complications of carbon dioxide laser resurfacing. An evaluation
of 500 patients. Dermatol Surg 1998;24:315–320.

588
Chapter 12  •  Skin Resurfacing
1 month
3 months
5 months
A
B
C
FIGURE 12-144.  Patient was treated with aggressive periorbital CO2 laser skin resurfacing and it took almost 5 months for her
erythema to resolve. This is an unusually long time, but extended cases are a possibility.
FIGURE 12-145.  Patient exhibits an unusually extended and intense post–
laser skin resurfacing erythema at 4 weeks. She has been using triple
antibiotic ointment and the erythema quickly resolved upon cessation.
PIH
Postinflammatory Hyperpigmentation
A
B
FIGURE 12-146.  Patient was exposed to sun several weeks after aggres-
sive CO2 laser skin resurfacing and developed severe postinflammatory
hyperpigmentation. This resolved in several weeks with a regimen of
hydroquinone 4% and sunscreen.
Post-Resurfacing Hyperpigmentation
Postinflammatory hyperpigmentation (PIH) in my experience
is so common, it should be characterized as a sequela, not a
complication. Regardless of the use of pretreatment or the
modality, it appears that about a third of aggressive resurfacing
patients (laser or peel) will experience PIH. Obviously, darker
skin types have significantly increased incidence of hyperpig-
mentation. It is not only the inflammation secondary to the
resurfacing procedure but any source of inflammation including
sun, snow reflection, overhead lighting, forced air from car
defrost, or hair dryer causing irritation and inflammation from
post-laser or postpeel topical self-medicating. Postresurfacing
melanocytes are very reactive. The hyperpigmentation usually
manifests as a blotchy bronzing generalized over the treated area
(Figure 12-146). This classically occurs at about 30 days and
usually responds well to treatment with Retin-A and hydroqui-
none 4% (Figure 12-147). In stubborn cases, the pigmentation
can actually worsen from the irritation of the Retin-A or bleach-
ing agent. Patients may respond by using topical and systemic
antiinflammatory steroid treatment. I tell all deep laser or
medium-depth chemical peel patients that they are going to
hyperpigment. The 30% who do expect it, and the 70% who
don’t are very relieved. Pre-resurfacing skin conditioning, sun
avoidance, and judicious use of sunscreens are paramount in the
prevention of PIH.
Post–Laser Skin Resurfacing Infections
Bacterial, yeast, and viral infection can be seen with facial resur-
facing procedures. Although prophylactic treatment with anti-
biotics and antiherpetic medications is not evidence based, it is
undoubtedly the standard of care in most localities. Having
performed hundreds of full-face chemical peels and laser resur-
facing procedures since 1997, I have only seen a handful of
significant documented, culture-proven infections. Changing
from closed to open wound care has seemed to reduce the inci-
dence of post-LSR infection.
Although not always consistent, the temporal window of
infection occurrence after LSR can many times predict the type
of infection (Box 12-5). Infections seen at 1 or 2 days are fre-
quently staphylococcal, infections seen from 2 to 4 days are
gram negative in nature, infections seen at 5 to 7 days post-LSR
are candidal, and post-laser infections seen at 2 to 15 days are
viral.26

Chapter 12  •  Skin Resurfacing
589
One challenge was a late occurring Pityrosporum infection
that manifested about 8 weeks after aggressive CO2 facial resur-
facing (Figure 12-148). The patient complained of itching and
burning but had relatively few lesions. Pityrosporum was cul-
tured and responded well to ketoconazole therapy. Although
this was not technically an infection but rather an overgrowth,
post-laser emollients and systemic antibiotics empirically used
to treat the supposed bacterial infection probably facilitated the
Pityrosporum yeast. Although most infections represent common
organisms, dermatologic consultation may be necessary with
more unusual cases.
Candidal infections can often occur after LSR and in my
experience manifest as delayed-healing, erythematous regions
that itch and burn (Figure 12-149 and 12-150). A KOH prep
(potassium hydroxide) that demonstrates hyphae or a culture
should be performed for correct diagnosis, because many prac-
titioners will mistakenly diagnose and treat this as a bacterial
infection.
Some patients can develop vaginal yeast infections from the
original surgical antibiotic coverage and must be meticulous in
not spreading this to the healing face.
Staphylococcal infections arising from native skin microbes
are common post-laser infections, and if suspected, a Gram stain
and culture should be obtained. Patients often manifest the
“staph sign,” which is crusting around the nasal antrum and also
B
A
FIGURE 12-147.  A, Patient with significant post-laser hyperpigmentation at 30 days. B, Resolution 14 days later after treatment
with creams.
Box 12-5  Temporal Relationships With Common Post-LSR Infections
Day 1–2: Staphylococcus
Day 2–4: Gram-negative bacteria
Day 5–7: Candida infections
Day 2–15: Viral infections
Day 12–24: Scarring
frequently exhibit scleral injection from staph infection. Any
patient with any suspected infection must be on bland wound
care. Heavy ointments can worsen the condition. Washing with
Cetaphil Gentle cleanser and using Aquaphor or a very thin coat
of Biafine cream is helpful. All other skin products should be
discontinued until resolution. Occasionally a yeast infection can
coexist with a bacterial infection and complicate the diagnosis
and treatment, underlining the importance of culture and sen-
sitivity studies. Figure 12-151 shows two culture-proven
FIGURE 12-148.  Persistent erythema accompanied by itching and burning
tuned out to be a Pityrosporum infection.

B
A
FIGURE 12-149.  A, Patient 1 week after aggressive CO2 laser skin resurfacing (LSR). B, At 2 weeks post LSR she has unhealed,
erythematous regions bilaterally that were shown to be a Candida infection and responded quickly to antifungal antibiotics and
topical cream.
A
B
FIGURE 12-150.  Patient with a Candida infection that responded to antifungal therapy with ketoconazole.
B
A
FIGURE 12-151.  These patients developed post–laser skin resurfacing Staphylococcus aureus infection and were successfully
treated. The patient in A was treated with sulfamethoxazole and trimethoprim (Bactrim DS), and the patient in B was treated
with ciprofloxacin.
590

Chapter 12  •  Skin Resurfacing
591
post-LSR staph infections that were sensitive to ciprofloxacin
and responded well clinically.
Methicillin-Resistant Staphylococcus aureus
(MRSA) Post-LSR Infection
Since my entry into private practice in 1983, MRSA has pro-
gressed from a rare institutional infection in medically compro-
mised patients to a community-acquired disease with increased
clinical prevalence. Staphylococcal infection was actually des­
cribed in 1880 as a clinical entity and responded to penicillin
with its emergence in the 1940s. The staphylococcal bacterium
quickly developed enzymatic resistance to penicillin. By 1959,
95% of staphylococcal infections were resistant to penicillin, and
methicillin was developed to overcome enzymatic resistance.
Unfortunately, within 12 months, MRSA strains had mutated.
The 1970s and 1980s did not see much activity but community-
acquired MRSA (CA-MRSA) appeared in the 1990s in healthy
patients. The MRSA strain of Staphylococcus is spread from com-
munity surfaces, and a significant percentage of the population
is colonized in the nose or on the skin.27 Colonized individuals
are infected but not affected and can transfer the bacteria. A
colonized surgeon or staff member could transfer MRSA to
surgical patients, so many progressive offices routinely culture
the nares of all office personnel and treat carriers.
Compromised patients are susceptible to infection, and LSR
patients with exposed dermis or epidermis would be considered
compromised. Patients colonized with MRSA can be treated
with mupirocin (Bactroban) applied to the skin and/or intrana-
sally (Bactroban nasal), which helps eliminate the MRSA and
reduces the risk of the bacteria spreading to other sites on the
patient’s body or to other patients. Treatment to eliminate
MRSA carriage consists of Bactroban ointment every 8 hours
to the nares, axillae, and umbilicus in addition to a single tablet
of Bactrim DS for 30 days. Some surgeons place all peel or LSR
patients on nasal mupirocin ointment beginning several days
preoperatively as a prophylactic measure. Unfortunately, some
strains of MRSA are resistant to mupirocin.27
I began performing LSR in 1997 and performed hundreds
of full-face cases, but I never experienced a significant case of
MRSA infection until 2008 and saw two serious cases within
months of each other. The first case concerned a 52-year-old
white male patient who was treated with two-plus passes of
80 mJ at a density of 6 and simultaneous blepharoplasty. The
patient’s immediate post-laser course was unremarkable, and he
was seen 6 days later for routine follow-up (Figure 12-152, A).
Two days later, the patient called the office with complaints of
hard, painful nodules forming on his neck (which was not
lasered) but did not report facial lesions. He was seen in the
office on post-laser day 13 and presented with multiple painful,
indurated abscesses on his right and left neck and the lower
cheeks bilaterally, which was lasered skin (see Figure 12-152, B).
The lesions were biopsied and sent for pathology, Gram stain,
and culture and sensitivity. The patient returned to the office
on post-laser day 15, and the lesions had spread from the bilat-
eral neck to the bilateral face (see Figure 12-152, C). The pathol-
ogy report was returned as MRSA sensitive to sulfamethoxazole
and trimethoprim (Bactrim DS). The patient improved over the
next 3 weeks to an asymptomatic state and is shown at 60 days
post-LSR (see Figure 12-152, D).
Another case of post-laser MRSA infection is shown in
Figure 12-153. This healthy patient underwent full-face CO2
LSR and presented about a week later with her face very irri-
tated, itchy, and burning, and numerous abscesses had devel-
oped on her extremities and trunk. She gave a history of noticing
a small area on her forearm that appeared to have a “black seed”
that she attempted to remove by scratching with her fingernail.
Several days later, she noticed a “boil” on her forearm, which
then spread to her trunk and face.
This patient was initially treated with sulfamethoxazole and
trimethoprim (Bactrim DS) but due to her systemic infection
was hospitalized. Upon hospital admission, the treating infec-
tious disease physician placed the patient on intravenous van-
comycin because her cultures showed sensitivity to this drug.
She developed an allergic reaction and was subsequently
switched to intravenous linezolid and healed uneventfully over
the next week. The rapid spread of this MRSA infection under-
lines the seriousness of this type of infection; in a medically
compromised patient, it could have proven fatal. The patient is
shown 10 days post-LSR in Figure 12-153, D–F and 24 days
post-LSR in Figure 12-153, G–I.
It is interesting that in this patient and the previously
described MRSA case, the MRSA abscesses first appeared on
areas that were not lasered and spread to the healing lasered skin.
Presumably these patients came into contact with a source of
community-acquired MRSA infection which manifested
remotely and then spread to the reepithelializing healing skin.
It is of further interest that the case shown in Figure 12-153
cultured MRSA in the facial infection but non-MRSA staph
from the extremity infections. This could have been two separate
infections or a misculture of the facial infection.
Herpetic Infection
Herpetic infection can lead to extreme post-laser pain and scar-
ring. The herpes virus can lie dormant and become activated by
a traumatic event such as LSR. Patients with a known history
of herpes infection must be treated carefully, with strict atten-
tion to antiviral coverage and healing observation. Herpes infec-
tion, although rare, often develops before reepithelialization is
complete. Since there is no epithelium to blister, the pathogno-
monic herpes vesicles may not appear. Significant pain in the
early post-LSR period may be a tip-off of a herpes infection.
This has been a rare occurrence in my personal experience with
several herpetic flares and only a single clinically significant
herpes infection out of hundreds of full-face cases. All LSR
patients are pretreated with prophylactic valacyclovir (500 mg
BID) beginning 48 hours pre-laser and continued on that
regimen until reepithelialization is complete. This patient shown
in Figure 12-154 was treated with prophylactic valacyclovir but
still developed significant infection. She responded well when
the antiviral medication was adjusted to zoster levels (1000 mg
twice daily). In retrospect, the patient recalled that she was
plagued by fever blisters in childhood but forgot to document
that on her medical history. She healed without scarring.
Clinically, herpes infection is diagnosed by microscopic
observation of a smear of the lesion. In a positive herpes smear,

592
Chapter 12  •  Skin Resurfacing
B
A
D
C
FIGURE 12-152.  Patient developed a post-laser methicillin-resistant Staphylococcus aureus (MRSA) infection, which is shown
at post laser days 6 (A), 13 (B), 15 (C), and 60 (D).
Tzanck cells and multinucleated giant cells are identified by
microscope (Figure 12-155).
Milia Formation
Milia represent small “whitehead” lesions that form when
keratin plugs obstruct skin pores (Figure 12-156). They are very
common after LSR and are more of a sequela than a complica-
tion. They are more frequently seen with overuse of ointments
that obstruct pores; greasy dressings should be discontinued as
soon as possible. Milia will often spontaneously resolve but are
in the meantime bothersome for patients who frequently seek
resolution. Getting patients back on Retin-A and skin care as
soon as possible will improve milia. The lesions can be treated
in several ways. They can be punctured with an 18-gauge needle
and the keratin expressed with a comedone loop, or the top of
the milia can be opened with a radiofrequency or hyfrecator
probe and the contents expressed (Figure 12-157).
Acne Flare
LSR can wreak havoc on the facial skin in terms of inflam-
mation and irritation. Due to the numerous healing and cel-
lular changes, it is not uncommon to see acne flare in some
patients (Figure 12-158). This can arise in patients who have
had long-standing acne or as a new infection in patients
without acne history. This is usually self-limiting and is
improved by starting good skin care as soon as possible after
LSR. Discontinuing greasy ointments also assists skin clearing.
Topical clindamycin can be applied, and patients can be
started on minocycline or appropriate antibiotics in more
resistant cases.

B
C
A
E
F
D
H
I
G
FIGURE 12-153.  Patient is shown 7 days post full-face aggressive CO2 laser skin resurfacing (LSR). She developed an abscess
of her forearm (A), which then spread to her trunk (B) and then to her face (C). Ten days post full-face aggressive CO2 LSR
with an abscess on her forearm (D), trunk (E), and face (F). Note the crusting and scleral injection, which is frequently seen
with Staphylococcus infections. Images at 24 days post LSR show the extremity (G), trunk (H), and face (I) MRSA infections
are resolving.

594
Chapter 12  •  Skin Resurfacing
A
B
C
FIGURE 12-154.  Patient developed a severe herpes infection about 10 days after facelift with simultaneous laser skin resurfacing.
She is shown at post laser day 15 and healed uneventfully with zoster doses of valacyclovir.
Herpes Simplex Infection
Culture
Tzanck Cells
Multinucleated Giant Cells
FIGURE 12-155.  Herpes simplex infection culture. A smear of a suspected
lesion is used to provide microscopic diagnosis of Tzanck cells and mul-
tinucleated giant cells, which confirm the herpes diagnosis.
Milia
(blocked pores with keratin)
FIGURE 12-156.  Patient exhibits post laser milia in the nasolabial fold region.
B
A
FIGURE 12-157.  Milia can easily be treated by unroofing the top of the plug with a radiofrequency needle and expressing the
contents with a comedone loop.

Chapter 12  •  Skin Resurfacing
595
A
B
FIGURE 12-159.  Patient sustained a an unusual post–laser skin resurfacing lesion that was finally determined to be from unin-
tentional nocturnal abrasion of the healing post-laser skin from her wedding ring setting. Sleeping with socks on her hands
prevented further injury.
U-shaped neck pillow which was abrading the neck skin nightly.
The irritation ceased when she switched pillows.
Appropriate wound care is imperative to prevent irritation
and infections as well as keep the patient comfortable. Insuffi-
cient moisturization is a common problem for some patients.
When the healing skin surface is not cleansed and moisturized,
it can become very irritated and itchy, which then leads to the
patient picking at the skin (Figure 12-161). A frequent office
follow-up policy is an important way to control post-laser
wound care, especially in noncompliant patients.
Picking at the peeling or healing skin is a troublesome
problem in some patients, especially those with obsessive
The healing skin is quite sensitive and easily disrupted. Some
patients will scratch at the itching skin only to abrade the epi-
thelializing skin. They must be cautioned against this. Some-
times this occurs unconsciously while sleeping, and they can
injure the skin to the point of scarring. Figure 12-159 shows a
patient who sustained an abrasion of her lasered skin by inad-
vertently scratching herself with her wedding ring. Having
patients sleep with gloves or socks on their hands can decrease
this type of unintentional injury.
Patients seem to continually find new means of irritating
healing skin and must be educated to refrain from anything that
can abrade the healing skin. The patient shown in Figure 12-160
underwent face and neck LSR and developed an unusual “infec-
tion” of her left neck. The cultures were returned as negative,
and antibiotics were ineffective. A detailed history uncovered
the fact that the patient was sleeping with an airline-type
Acne Flair
A
B
FIGURE 12-158.  Acne flare can occur in the post-laser period and is fre-
quently self-limiting with the resumption of skin care. Resistant cases can
be treated with topical and systemic antibiotics.
FIGURE 12-160.  Patient post face and neck laser skin resurfacing healing
period with what appeared to be a neck infection but was actually due to
chronic irritation from sleeping on an airline pillow, which abraded the
healing skin.

596
Chapter 12  •  Skin Resurfacing
disorders (Figure 12-162). The continual disruptions of the
healing skin can lead to scarring or hypopigmented spots and
needs to be controlled. Using antipruritic medications and seda-
tives is sometimes required.
Post–Laser Skin Resurfacing Burns and Scars
As stated earlier, almost all areas of lasered skin should be fully
healed by 14 days. Areas that do not heal by 2 to 3 weeks will
likely result in scarring (Figure 12-163). If it appears that scar-
ring to an area is imminent, meticulous wound care is a neces-
sity. The region should be soaked with hydrogen peroxide
several times a day and kept occluded with a suitable burn cream
FIGURE 12-161.  Patient is an example of poor post laser skin resurfacing
wound care and insufficient moisturization. The skin is dry and irritated,
which is not only uncomfortable but also a setup for inflammation.
FIGURE 12-162.  Example of how picking can create scarring problems
during the healing process; 99% of patients will deny active or intentional
picking, but the pattern of small abrasions or purpura is a giveaway.
FIGURE 12-163.  Patient was overtreated during lasering of a lesion on the
cheek. The delayed healing implied impending scarring. With proper
wound care, the cheek finally healed with no significant noticeable scar
but did leave an area of hypopigmentation.
Hypertrophic Scarring
Most common in the
mandibular area.
Usually from over treatment
Treat early with intralesional Kenalog
(10mg/cc), and topical steroid, silastic
sheeting, pressure, massage
Erythema and hypertorphy may
respond to 585 nm pulsed dye laser
FIGURE 12-164.  Patient was seen and treated at another office and sus-
tained severe perioral scarring from overtreatment with the CO2 laser.
Intralesional steroid injection and pulsed-dye laser treatment improved the
scar, but the patient was left with a disfiguring deformity.
such as Biafine. Even extremely ominous-appearing wounds can
heal uneventfully with proper wound care. Skin that heals with
hypertrophic scars can be managed with topical and intrale-
sional steroid injection, silicone sheeting, and sometimes pulsed-
dye laser therapy (Figure 12-164). Scars that do not seem to be
improving should be evaluated by a wound-healing specialist.
The best means of preventing post-LSR scarring is to not over-
treat patients.
The perioral region, mandibular borders, and thin lower
eyelid seem to be more prone to scarring and should be treated
judiciously (Figure 12-165). Most of the cases of severe scarring
I have seen have resulted from novice surgeons trying to emulate

Chapter 12  •  Skin Resurfacing
597
B
A
FIGURE 12-165.  Patient after –CO2 laser skin resurfacing shows no outward scarring (A), but when the skin is stretched, a
fibrotic band is noticeable (B). This would seem to imply that this region was more deeply affected and was close to forming
a significant scar. This same patient developed small scars on her lip and appears more prone to hypertrophic scarring than
the average patient.
the results or settings of more experienced surgeons or from
surgeons unfamiliar with new laser machines or settings. The
unpredictability of lasers and skin, however, can result in scar-
ring in even the most experienced hands (Figure 12-166).
Lower-eyelid retraction can occur in the early post-laser
period in any patient and is manifested when the patient gazes
upward or opens the mouth (Figure 12-167). In normal patients,
this is usually self-limiting as the skin heals and becomes more
elastic. Stretching of the lower lid skin can accelerate the return
of normal lid position. In patients who have had previous bleph-
aroplasty with skin removal or previous LSR, the extent of
lower-lid retraction can be serious and permanent, and these
patients must always be approached with conservative LSR
parameters. A detailed pre-laser history is important to identify
potential at-risk patients.
Synechiae
A relatively common but underreported post-LSR complication
is the formation of healing tissue adhesions in the lower-eyelid
skin, called synechiae. This process is well described in rhino-
plasty, gynecology, urology, general surgery, and other disci-
plines, but I could not find any case reports in the aesthetic laser
literature. A synechia can occur when two raw tissue surfaces
come in contact. When this happens, the reepithelialization
fuses the two surfaces and can create an unsightly deformity
(Figures 12-168 and 12-169). In the context of post-LSR, the
lower-eyelid skin is devoid of epithelium, and the resultant
edema can produce mounds on the lower-lid skin that can come
in contact with each other. When these two raised surfaces are
in contact, there is an invagination similar to a valley between
two mountains or a pleat. Allowed to heal, this becomes a single
FIGURE 12-166.  Patient (treated by the author) developed a small scar from
routine laser skin resurfacing treatment of the lower eyelids. The scar
responded well to intralesional injection of triamcinolone 10 mg/mL
injected monthly for several treatments. Lower eyelid retraction is also
evident when the patient gazes upward. This improved with regular
stretching.
Transient Ectropion
FIGURE 12-167.  These laser skin resurfacing patients are shown several
weeks post procedure and exhibit temporary lower eyelid retraction mani-
fested by increased scleral show while opening the mouth or gazing
upward. This type of retraction is usually temporary and is not uncommon
with aggressive skin resurfacing.

598
Chapter 12  •  Skin Resurfacing
A
B
C
FIGURE 12-168.  Images illustrate healed synechiae that were not treated in the early recovery stage of post–laser skin resurfacing
healing.
FIGURE 12-169.  Another case of bilateral synechiae after full-face CO2 laser skin resurfacing.
A
B
FIGURE 12-170.  A, The lower eyelid after postperiorbital laser skin resurfacing is shown while the patient is in the supine posi-
tion, indicating how the skin bunches to form a pleat. B, Pulling the cheek inferiorly with the finger shows the normal cheek
and lid position.
unit, usually without but sometimes with a fistulous tract. This
process is probably also accelerated due to the fact that during
the post-LSR recovery period, patients lie supine for longer
periods than normal, and without downward gravitational pull,
the cheek mass bunches up the lower-lid skin (Figure 12-170).
Sleeping with the head elevated will decrease this positional
influence.
A synechia can cause an otherwise smooth eyelid to have
bulky ridges with a depression between them. Since this process
effectively accordions the lower-lid tissue slightly, it decreases
the length of the lid and can contribute to lower-lid retraction
(Figure 12-171).
This process usually occurs early in the post-LSR recovery
and manifests by day 3 to 5. If not diagnosed and treated, the
pleat will heal and become a permanent deformity. The treat-
ment is to recognize the problem and detach the pleated skin
by pulling the synechia apart with cotton-tipped applicators and
applying ointment to prevent reattachment of the surfaces
(Figure 12-172, A). When this is performed, the adhesion will
tear, and the bleeding base of the synechia will be visible (see

Chapter 12  •  Skin Resurfacing
599
Figure 12-172, B and Figure 12-173). In addition, regular
gentle stretching of the lid skin by the patient will assist in
resolution.
I have seen this numerous times on my LSR patients, and
this may be in part due to my aggressive laser treatment of the
lower lid skin as well as the fact that many of my LSR patients
undergo multiple concomitant cosmetic procedures and there-
fore have more midface edema that can bunch the healing
lower-lid skin. One maneuver that has seemed to reduce the
incidence of post-laser synechiae is to immediately vigorously
stretch the lower-lid skin after the resurfacing procedure, and
make sure patients keep liberal ointment on the lower-lid skin
B
A
FIGURE 12-172.  The surgeon must be observant for synechia development in the very early post–laser skin resurfacing period
and detach the adhesions by traction (A). When successfully treated, bleeding tissue will be apparent where the pleat was
separated (B).
during the first week of recovery (Figure 12-174). This may
create more surface area on the lower lid as the laser causes
significant and immediate skin retraction.
If synechiae are undiagnosed and allowed to heal, patients
will complain of having worse wrinkles on the lower lids than
before the laser. Minor healed synechiae may go unnoticed or
improve with time, or the lower-lid skin can be gently stretched
in the post-LSR healing period. Major fused skin folds will need
treatment. Figure 12-175 shows a patient with bilateral syn-
echiae with the skin to be excised marked with a surgical marker.
The goal of a synechia revision is to remove the pleated tissue
to form smooth and contiguous lower-eyelid skin. Surgical exci-
sion of the skin is easily completed so long as this minor fore-
shortening of the lower eyelid will not cause retraction. This can
be determined by using a forceps to pinch the superior and
FIGURE 12-171.  A synechia, along with the skin tightening effects of laser
treatment can contribute to lower-eyelid retraction and sclera show, espe-
cially in the upward gaze.
FIGURE 12-173.  Patient developed bilateral synechiae after laser skin resur-
facing (LSR). Although this process usually happens in the first week after
treatment, this patient lived out of town and was not seen for several weeks
after the procedure. The synechiae were not fully healed and were suc-
cessfully detached.

600
Chapter 12  •  Skin Resurfacing
FIGURE 12-174.  Manually stretching the skin immediately after the laser
procedure is completed seems to have some effect in the reduction of
synechiae in my practice.
FIGURE 12-175.  Patient developed bilateral synechiae that healed with an
unsightly appearance. The proposed skin excisions are marked.
B
A
FIGURE 12-176.  The pleated skin being excised with a radiofrequency
microneedle (A) and the sutured postsurgical result with the excised skin
specimens sitting on the lower eyelids (B).
inferior margins of the proposed lower lid skin excision. If the
lower eyelid does not retract, the proposed amount of skin can
safely be excised. Figure 12-176, A shows the pleated skin exci-
sion using a radiofrequency microneedle with local anesthesia.
Figure 12-176, B shows the postrevision result, with the excised
skin sitting on the lower lids and the incisions sutured.
Hypopigmentation
All resurfacing procedures that cause peeling or exfoliation will
lighten the skin to some extent. Some of the melanocytes in the
sloughed or ablated epidermis will be shed, creating a lighter
appearance. This is a temporary phenomenon; new melanin is
continually produced. The melanocytes reside in the basal layer
of the epidermis but extend down the hair follicle, and when
the epidermis and/or upper dermis peels or is ablated (depending
upon the type and depth of the LSR), these cells must migrate
from the follicle and repopulate the new epidermis. This process
takes 8 to 12 weeks, so some transient hypopigmentation is
expected but usually improves over this time period. Deeper
peels that extend into the hair follicle damage more melanocytes,
and with a certain percentage of melanocytic reduction, hypopig-
mentation can take years to improve or may be permanent.5
True hypopigmentation is an infrequent complication that
can occur immediately or several years after a deep resurfacing
procedure. It is usually associated with overtreatment that
damages the melanocytes and was common in the days of deep
phenol peels. This can be a relatively devastating complication
for some patients, because the face and neck are distinctly dif-
ferent in color and makeup must always be worn (Figure
12-177). I am not sure there is any guaranteed means of pre-
venting hypopigmentation. Some patients appear to be more
predisposed to its development, and if one performs a high
volume of LSR, it will occasionally occur. I can say that I have
seen post-laser hypopigmentation in several patients who were
so impressed with the degree of wrinkle improvement from the
laser procedure that they accepted the pigmentation tradeoff.
These patients had always worn makeup and did not see the
requirement as a significant complication. This is generally not
true with younger patients or those who do not wear makeup
on a daily basis. In those cases, hypopigmentation is seen as a
significant complication. This complication must be adequately
addressed in the pre-laser informed consent process, because it
will occur sooner or later.
Avoiding overly aggressive LSR (especially for the novice
surgeon) can reduce the incidence of true hypopigmentation. It
is better to laser a patient moderately over two sessions than to
overtreat them in a single session.
“Pseudo” or “relative” hypopigmentation is a more common
phenomenon and is not actually a melanocytic problem but a
contrast between rejuvenated facial skin and nonrejuvenated
neck skin (Figure 12-178). I describe this condition to the
patient preoperatively by showing them the color difference
between the palmar and plantar sides of my forearm. The under-
side is lighter because it has had more actinic protection, and
the other side is darker due to more exposure and photodamage.
This helps the patient understand that the treated neck skin will

Chapter 12  •  Skin Resurfacing
601
A
B
FIGURE 12-177.  Patient was treated very aggressively for severe acne scars and developed permanent “true” hypopigmentation
from damage to the melanocytes. In addition, the surgeon who performed this procedure should have not extended the laser
treatment halfway down the neck, but rather stopped the laser treatment at the mandibular border.
A
B
FIGURE 12-178.  Patient with “pseudo” or “relative” hypopigmentation. She has significant photodamage and existing hyperpig-
mentation of her neck. The laser skin resurfacing procedure has rejuvenated her facial skin to a normal color, but this stands
out against the untreated neck. This is not from severe melanocytic injury.
be lighter than the untreated neck skin. Simultaneous light laser
or peeling of the neck when performing full-face LSR can miti-
gate skin color demarcation between the treated face and
untreated neck but will not be impressive in patients with severe
neck photodamage because the neck can simply not be treated
safely and deeply enough to match the treated facial skin (Figure
12-179). When a laser surgeon evaluates a patient with a very
tan or pigmented neck, the patient must be made aware of this
future color and texture discrepancy.
Avoiding aggressive resurfacing toward the mandibular
border and feathering the lasered skin reduces the chance of
significant hypopigmentation. Judiciously hiding the lower
facial laser limit in the mandibular shadow also reduces the
demarcation line. Relative hypopigmentation will frequently
improve as the face heals and time passes. In addition, not treat-
ing tanned skin and using proper pre- and post-laser skin con-
ditioning with Retin-A and hydroquinone 4% can lighten the
neck skin and make the difference less noticeable.

602
Chapter 12  •  Skin Resurfacing
Another important consideration when performing LSR of
the face is the treatment of aesthetic subunits as opposed to
full-face treatment. As tempting as it is to treat only the perioral
region, the nasolabial folds, or any other subunit, I don’t feel it
is a good idea. Treated areas stand out against untreated facial
skin. If a patient presents with severe perioral wrinkles and
requests isolated LSR to that area, I explain the associated
problem and offer them the option of aggressively treating the
perioral region with a less aggressive full-face laser treatment to
better blend the result. As noted earlier, my only exception to
this rule is periorbital LSR; the orbits are recessed and do not
stand out as much against the rest of the face in the average
patient. In patients with significant photodamage, however,
even eyelid LSR can leave a disparity of color and texture next
to the untreated skin (Figure 12-180). I very commonly laser
the upper and lower lids without full-face laser when perform-
ing blepharoplasty, but it is important to stay within the limits
of the bony orbit. Lasering a larger area can produce a masklike
difference between the lighter lasered skin and the nonlasered
FIGURE 12-179.  Simultaneous conservative laser or peel treatment of the
neck can help reduce the difference between the lasered face and
untreated neck, but the neck cannot be treated aggressively and may
require several treatments to blend in severe cases.
FIGURE 12-180.  Patient shows extended relative hypopigmentation after
blepharoplasty with lower-lid skin resurfacing. This is a rare situation,
and performing a full-face light resurfacing would blend this disparity and
would have been a better choice for this patient.
FIGURE 12-181.  When lasering the periorbital region without full-face treat-
ment, it is important to not laser outside the limits of the bony orbit, or a
masklike appearance can result from the contrasting lighter lasered skin
and darker unlasered skin.
bordering skin. The patient shown in Figure 12-181 illustrates
the consequences of lasering outside of a subunit and is an
example of the potential for a masklike appearance due to
hypopigmentation.
References
1. Obagi ZE, Obagi S, Alaiti S, Stevens MB: TCA-based blue peel: a standard-
ized procedure with depth control. Dermatol Surg 25:773–780, 1999.
2. Hevia O, Nemeth AJ, Taylor JR: Tretinoin accelerates healing after trichlo-
roacetic acid chemical peel. Arch Dermatol 127:678–682, 1991.
3. Obagi S, Bridenstine J: Chemical skin resurfacing. In Niamtu J III, editor:
Cosmetic Facial Surgery: Oral Maxillofac Surg Clin North Am, Vol 12,
number 4, November, Philadelphia, 2000, Saunders, pp 541–553.
4. Niamtu J III: Digitally processed ultraviolet images: a convenient, afford-
able, reproducible means of illustrating ultraviolet clinical examination.
Dermatol Surg 27(12):1039–1042, 2001 Dec.
5. Rubin
M:
Manual
of
chemical
peels,
Philadelphia,
1995,
Lippincott-Raven.
6. Personal communication, Susan Obagi, M.D. 2006.
7. Anderson RR, Parrish JA: Selective photothermolysis: precise microsurgery
by selective absorption of pulsed radiation. Science 220(4596):524–527,
1983 Apr 29.
8. Price CR, Glaser DA, Carinol PJ: In Niamtu J III, editor: Cosmetic Facial
Surgery: Oral Maxillofac Surg Clin North Am, Vol 12, number 4, Novem-
ber, Philadelphia, 2000, Saunders, Philadelphia, 2000, Saunders, pp
567–578.
9. Chapas AM, Brightman L, Sukal S, et al: Successful treatment of acneiform
scarring with CO2 ablative fractional resurfacing. Lasers Surg Med
40(6):381–386, 2008 Aug.
10. Alster TS, Tanzi EL, Lazarus M: The Use of Fractional Laser Photother-
molysis for the Treatment of Atrophic Scars. Dermatol Surg 33:295–299,
2007.
11. Fife DJ, Fitzpatrick RE, Zachary CB: Complications of fractional CO2
laser resurfacing: four cases. Lasers Surg Med 41(3):179–184, 2009 Mar.
12. Avram MM, Tope WD, Yu T, Szachowicz E, Nelson JS: Hypertrophic
scarring of the neck following ablative fractional carbon dioxide laser resur-
facing. Lasers Surg Med 41(3):185–188, 2009 Mar.
13. David L, Ruiz-Esparza J: Fast healing after laser skin resurfacing. The
minimal mechanical trauma technique. Dermatol Surg 23(5):359–361,
1997 May.

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14. Ruiz-Esparza J, Barba Gomez JM, Gomez de la Torre OL, David L:
Erythema after laser skin resurfacing. Dermatol Surg 24(1):31–34, 1998
Jan.
15. Lent WM, David LM: Laser resurfacing: a safe and predictable method of
skin resurfacing. J Cutan Laser Ther 1(2):87–94, 1999 Apr.
16. Ross EV, Mowlavi A, Barnette D, Glatter RD, Grevelink JM: The effect of
wiping on skin resurfacing in a pig model using a high energy pulsed CO2
laser system. Dermatol Surg 25(2):81–88, 1999 Feb.
17. Fitzpatrick RE, Tope WD, Goldman MP, Satur NM: Pulsed carbon dioxide
laser, trichloroacetic acid, Baker-Gordon phenol, and dermabrasion: a com-
parative clinical and histologic study of cutaneous resurfacing in a porcine
model. Arch Dermatol 132(4):469–471, 1996 Apr.
18. Alster TS, Kauvar AN, Geronemus RG: Histology of high-energy pulsed
CO2 laser resurfacing. Semin Cutan Med Surg 15(3):189–193, 1996 Sep.
19. Gardner ES, Reinisch L, Stricklin GP, Ellis DL: In vitro changes in non-
facial human skin following CO2 laser resurfacing: a comparison study.
Lasers Surg Med 19(4):379–387, 1996.
20. Weinstein C: Carbon dioxide laser resurfacing. Long-term follow-up in
2123 patients. Clin Plast Surg 25(1):109–130, 1998 Jan.
21. Fitzpatrick RE, Goldman MP, Satur NM, Tope WD: Pulsed carbon dioxide
laser resurfacing of photo-aged facial skin. Arch Dermatol 132(4):395–402,
1996 Apr.
22. Lowe NJ, Lask G, Griffin ME, Maxwell A, Lowe P, Quilada F: Skin resur-
facing with the Ultrapulse carbon dioxide laser. Observations on 100
patients. Dermatol Surg 21(12):1025–1029, 1995 Dec.
23. Burkhardt BR, Maw R: Are more passes better? Safety versus efficacy
with the pulsed CO2 laser. Plast Reconstr Surg 100(6):1531–1534, 1997
Nov.
24. Niamtu J: To debride or not to debride? That is the question. Rethinking
char removal in ablative CO2 laser skin resurfacing. Dermatol Surg
34:1001–1012, 2008.
25. Nanni CA, Alster TS: Complications of carbon dioxide laser resurfacing.
An evaluation of 500 patients. Dermatol Surg. 24(3):315–320, 1998
Mar.
26. Personal communication, Suzan Obagi, M.D. 2009.
27. Perl TM, Cullen JJ, Wenzel RP, et al: Intranasal mupirocin to prevent
postoperative Staphylococcus aureus infections. N Engl J Med 346(24):1871–
1877, 2002.

604
13 
Neurotoxins in Cosmetic
Facial Surgery
I
f there is one single treatment that has revolutionized cos-
metic facial surgery over the past century, it would have to
be botulinum toxin type A. Although not the only neuro-
toxin complex available, Botox was the first botulinum toxin
approved by the U.S. Food and Drug Administration (FDA) in
the United States and will always be the granddaddy of neuro-
toxins. Surgeons, patients, and the media are in constant search
of a procedure that produces significant effects with insignifi-
cant recovery, but it rarely happens. Most products, surgeries,
or devices that promise results without recovery time are prob-
lematic, and expectations exceed outcomes. Not so with Botox.
It is the most common cosmetic treatment in the world and for
good reason. This drug is easy to administer, has no downtime,
and produces long-lasting cosmetic effects.
Botulinum Toxin Type A: History
and Physiology
The history of cosmetic botulinum is interesting. Botulism, or
sausage poisoning as it was originally termed, was first seriously
studied following an outbreak in Wildbad, Germany, in 1793.
The outbreak involved 13 people, 6 of whom died, and was
associated with consumption of a locally produced blood
sausage. Following this outbreak, the number of reported cases
of sausage poisoning rapidly increased, prompting a study of the
disease by local health officer, Justinius Kerner (1829). He
described 230 cases, most of which were attributed to the con-
sumption of sausage. The illness became known as botulism after
“botulus,” the Latin word for sausage.
Many years later, Van Ermengem (1897) investigated an
outbreak of botulism involving 34 individuals who had con-
sumed raw, salted ham served at a gathering of amateur musi-
cians in Ellezelles, Belgium. In the investigation of this outbreak,
Van Ermengem established that botulism was an intoxication,
not an infection, and that the toxin was produced by a spore-
forming obligate anaerobic bacterium, Clostridium botulinum.
He also found that toxin was rapidly inactivated by heating and
was only toxic to certain animal species.
A later outbreak in Darmstadt, Germany, associated with
canned white beans established that there was a second type of
botulism. The originally identified strain was type A, and the
Van Ermengem strain was probably type B (Landmann 1904).
As the Clostridium bacterium was studied and the toxin
isolated, it was largely controlled by the U.S. government and
considered for chemical warfare but reportedly could not be
aerosolized. The government allowed academic investigation in
the late 1940s. Dr. Allen Scott (Figure 13-1, A) had the biggest
part in the medical progression of the drug, and around the
early 1980s the drug, called Oculinum at the time, was used in
studies as a treatment for strabismus and blepharospasm. Dr.
Jean Carruthers is an oculoplastic surgeon in Vancouver, BC,
and was part of the research using botulinum toxin A for the
treatment of blepharospasm. She noticed that the drug was suc-
cessful in treating the muscular disorder, but some patients were
returning without lateral canthal wrinkles on the treated side
and were inquiring about using it to “make the wrinkles go
away” on the nontreated side. Dr. Jean shared this experience
with her husband, Dr. Alastair Carruthers, an accomplished
dermatologist who was intrigued with this finding (see Figure
13-1, B). One day, Dr. Alastair electively injected one of his
employees in the glabellar region with the botulinum toxin, and
the first cosmetic treatment of Botox was born.1
After significant investigation and trials, the drug was
approved by the FDA in 1989 for the treatment of strabismus
and blepharospasm and used off label for cosmetic treatments.
In 1991, Speywood, now Ipsen Ltd. (Maidenhead, Burkshire,
UK) had their preparation of botulinum toxin A approved as
Dysport outside the United States. The year 2000 saw FDA
approval of Botox for cervical dystonia, and in the same year
botulinum toxin B (Elan, Inc. now Solstice Neurosciences,
Dublin, Ireland) was approved and marketed in the United
States as Myobloc. In 2002, Allergan achieved FDA approval of
Botox for glabellar rhytids and in 2004 received FDA approval
for the treatment of axillary hyperhidrosis. Myobloc’s popularity
was short lived. With the exception of treating patients who
were resistant to botulinum toxin A, it did not emerge as sig-
nificant competition for Allergan’s Botox. A new botulinum
toxin A preparation called Xeomin was developed by Merz
(Merz Pharma, Frankfurt, Germany) and is unique as it claims
to be free of complexing proteins. It was approved for use in
Canada in 2009 and at the time of this writing is in the FDA
pipeline.
Botulism is not an infectious disease but rather a type of food
poisoning caused by eating food in which C. botulinum has
grown and produced toxin. Botulinum toxin has been called
“the most poisonous of all poisons”2 and molecule for molecule
is the most lethal substance known to man. The U.S. supply of
When this chapter was written, only Botox Cosmetic (Allergan Inc., Irvine, CA) was available
in the United States as an FDA-approved neurotoxin for the treatment of hyperfunctional
lines of the face. Dysport, now known globally as Dysport (Medicis Pharmaceutical Corp.,
Scottsdale, AZ) was approved in April 2009. In this chapter, however, all references to “units”
apply to Botox unless otherwise indicated. It is important for injectors to realize that the
potency and measuring schema of various neurotoxins may vary and must be differentiated
prior to usage.

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
605
reconstituted is stored in the same manner. BTA is ordinarily
incapable of crossing the blood-brain barrier and generally
exhibits no systemic effects.7 BTA is a neurotoxin and exhibits
it effects on the neuromuscular junction by inhibiting the
release of acetylcholine (ACh) , which causes weakness or flaccid
paralysis (Figure 13-2).
The storage or synthesis of ACh is not affected by BTA; its
action affects the vesicle-bound ACh.8 BTA paralyzes all striated
muscle exposed to this neurotoxin. The normal presynaptic
membrane contains membranous vesicles poised to release their
neurotransmitter cargo of ACh at the motor end plate (see
Figure 13-2). This process requires a calcium influx and special-
ized proteins such as SNAP 25 and syntaxin, which make up a
“snare complex” that drives the vesicles to the nerve membrane.
Normally the vesicles allow passage of ACh through the nerve
botulinum toxin A (BTA) that lasted for 2 decades was synthe-
sized in a 150-mg batch by Schantz in 1979.3 This batch of
crystalline BTA was dubbed batch 11-79. BTA is one of the
eight known toxic serotypes produced by Clostridium botulinum
that have been purified (A, B, C1, C2, D, E, F, and G). Seven
of the eight serologically distinct toxins can produce neuromus-
cular blockade, although type A is the most potent. This purified
serotype of BTA is available in the United States as Botox (Aller-
gan Inc., Irvine, CA) and Dysport (Medicis Inc., Scottsdale,
AZ) and is supplied in a hemagglutinin complex in the form of
a freeze-dried powder ready for dilution with preserved normal
saline.
Due to the extreme potency of this exotoxin, the 100-mg
Botox vial content is barely visible as a light coat of precipitate
adherent to the floor of the glass vial. The FDA requires speci-
fications of 100 plus or minus 30 units per vial. Allergan indi-
cates specifications closer to 100 plus or minus 10 units per vial.
These variations may affect the clinical action, onset, and dura-
tion of the treated areas and must be kept in mind: 20 units of
Botox are equipotent to 60 units of Dysport, Dysport and these
differences must be kept in mind when interpreting the litera-
ture.4 Having said this, each different type of Botulinum toxin
A is different and technically no official conversion rate exists.
In my clinical experience and opinion I equate 20 units of Botox
to 60 units of Dysport and hence a 3:1 ratio. It is commonly
said that there is a 2.5 : 1 ratio of units between Dysport and
Botox, but in my personal experience a more accurate conver-
sion is 1 Botox unit is equal to 3 Dysport units. The LD50 for
BTA in mice is 1 unit and is expressed as the amount of toxin
injected intraperitoneally that kills 50% of a group of Swiss-
Webster female mice weighing 18 to 20 grams.5 The LD50 for
humans has been calculated at 2500 to 3000 units for a 70-kg
person for a lethal dose of 40 U/kg.6 Since the usual therapeutic
dose for the treatment of hyperfunctional muscle lines is 25 to
50 Botox units, a 100× margin of safety exists. The packaged
exotoxin is stored in a conventional refrigerator and once
B
A
FIGURE 13-1.  A, Dr. Alan Scott is shown at the Smith-Kettlewell Eye Research Institute in San Francisco in 1982. B, From left
to right are Dr. Alastair Carruthers, April Niamtu, Dr. Jean Carruthers, and Dr. Joe Niamtu.
Nerve ending
Acetylcholine release
Muscle
FIGURE 13-2.  In the normal situation, acetylcholine (ACh) mediates nerve
transmission at the neuromuscular junction by releasing vesicles of ACh
across the neuronal membrane into the synaptic cleft and synaptic junc-
tion, which bind to specific receptor sites on the muscle and produce
contraction. (Copyright Allergan Inc., Irvine, CA.)

606
Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
neoneurogenesis allows complete recovery of the transmission
pathway and resultant muscle function.9
Resistance to BTA is rare and has been reported with repeated
large doses of the exotoxin.10 Resistance from prolonged usage
with strabismus treatments appears to increase with the use of
more than 300 units within a 30-day period.11 Botulinum toxin
serotypes B and F are similarly potent to type A and are being
studied for use on patients who have developed immunity to
toxin type A.12 Contraindications for BTA include known
hypersensitivity to any component of the preparation (including
human albumin), systemic neuromuscular diseases, or the use
of aminoglycoside or spectinomycin antibiotics which are
known to effect neuromuscular transmission and potentiate the
effects of BTA.6 Scott13 reported a study of nine pregnant
females, one of whom had a premature delivery thought to be
unrelated to the treatment. Neurotoxins are never used on preg-
nant or lactating patients.
Dysport, Dysport, has been used outside the United States
for 15 years. It is approved in 73 countries for various therapeu-
membrane into the synaptic cleft and through the synaptic
junction to bind with specific receptors on the striated muscle,
hence causing muscle contraction. When a neurotoxin is
injected, the toxin contacts the motor end plate, binds to the
neuron (Figure 13-3, A), becomes internalized in vesicles, and
moves throughout the neuron (see Figure 13-3, B). The light
chain of the toxin (which contains the zinc-dependent protease)
produces proteolytic cleavage of the snare complex proteins and
prevents the release of ACh at the vesicle membrane, resulting
in neuromuscular blockade (Figure 13-4). The binding of the
molecule to the motor end plate is permanent; it takes 24 to 48
hours for the therapeutic condition of weakness or paralysis to
ensue due to this chemical denervation. The reason for the delay
is the time required for the storage vesicles of ACh within the
presynaptic motor end plate to be depleted. Although the
binding of the ACh is permanent, the paralytic effect only
persists for 2 to 6 months. The reason for this temporary action
is the formation of new axonal sprouts, thus reestablishing the
neurotransmitter pathway (Figure 13-5). This process of
Muscle
Nerve ending
Acetylcholine release
BTX-A binding to neuron
Nerve cell membrane
Vesicle containing internalized BTX-A
B
A
FIGURE 13-3.  The toxin binds to the neuronal membrane (A) and becomes internalized in vesicles (B). (Copyright Allergan Inc., Irvine, CA.)
Cleaved proteins
Vesicles cannot fuse with membrane
FIGURE 13-4.  The light chain of the toxin cleaves the snare complex pro-
teins, which prevents the acetylcholine (ACh) vesicles fusing with the
neuronal membrane. Since no ACh can reach the muscle receptors,
neuromuscular blockade results. (Copyright Allergan Inc., Irvine, CA.)
Sprouts
Muscle
FIGURE 13-5.  Binding of the toxin and prevention of the release of acetyl-
choline is permanent, but muscle function returns after months as the
result of the formation of new axonal sprouts, thus reestablishing the
neurotransmitter pathway. (Copyright Allergan Inc., Irvine, CA.)

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
607
patients, I think they are missing great marketing and patient-
relation opportunities.
The most commonly treated areas in my practice are the
glabella, the lateral canthal regions, and the frontalis in that
order. Most patients present for multiple treatment areas, and
most patients are regular users and average 90-day retreatments.
The “rule of 3” is explained to all patients. The drug will take
effect by 3 days, will maximize by 3 weeks, and will last about
3 months. Obviously this is variable from patient to patient.
The main depressors of the brow are the paired procerus,
corrugator supercilii, and medial orbicularis muscles (Figure
13-6). The sole elevator of the brow is the paired frontalis
muscle, and the lateral orbicularis muscles are the main con-
tributors to “crow’s feet” wrinkles. This musculature works in
conjunction to perform the very complex orchestra of facial
expression (Figure 13-7).
Some mimetic muscles have bony origins with dermal inser-
tions and commonly interdigitate and in some areas (glabella,
modiolus) are interfaced with numerous muscles. These muscles,
through continual flexing of the skin, produce rhytids perpen-
dicular to the muscular action. With years of muscular move-
ment, the frown lines, horizontal forehead wrinkles, and lateral
canthal (crow’s feet) wrinkles become deeper and more notice-
able. Theoretically if there is no muscle movement, rhytids do
not form, as evidenced in patients with stroke or nerve injury.
Taking this into account, the younger a patient begins to receive
neurotoxin treatment, the less chance they have of forming
wrinkles. For those patients with existing wrinkles, regularly
paralyzing the muscles has a preventive effect.
Botox is shipped as a small, thin precipitate on the surface
of the vial (Figure 13-8) and is commonly reconstituted with 1
to 5 mL of preserved saline. This is operator dependent and
tic indications and in 23 countries for the treatment
of glabellar or hyperkinetic facial lines.14 Numerous studies
have been published in the literature regarding this preparation.
One early open-label U.S. study researched a cohort of 1200
patients receiving as many as 5 treatments of Dysport over a
13-month period. The results were strikingly similar to Botox
in that the average onset time for effect was 3 days, and the
mean duration was 90 days.14 The adverse events associated
with this study of over 4000 treatments were not grossly dif­
ferent from Botox studies.14 One difference that must be kept
in mind is that the units of delivery of Botox Cosmetic and
Dysport are not equipotent. Practitioners must differentiate
between the dosages of these different drugs when treating
patients.
Numerous preparations of botulinum toxin are vying for
FDA approval in this country, and there is no doubt that each
successive textbook published will include newer preparations
and indications.
Clinical Usage of Botulinum Toxin A
I have written numerous articles on the clinical usage of Botox
for cosmetic facial treatment, and although my treatment has
changed in terms of dilution, my basic injection patterns have
remained consistent.15-21 Even though Botox injections are the
most popular cosmetic treatment in the world, many patients
still do not understand the differences between Botox (or
Dysport) and injectable fillers. Realizing this, the surgeon and
staff must educate patients on what the drug and treatment will
do and won’t do. Like all cosmetic procedures, the consent
process is paramount for successful treatment and patient rela-
tions. It must be made clear in writing that neurotoxin treat-
ments vary in effect and duration from patient to patient, and
that some patients will not respond to treatment. The novice
injector will soon find out that some patients will complain that
their “Botox did not work” because they can still move their
forehead, or the drug did not last long enough, or they had
unwanted paralysis. The patient may expect free touchup,
retreatment, or a refund because their expectations were not
met. For all these reasons, the patient must be made aware of
the common effects, unwanted effects, expected duration or lack
thereof, complications, patient and surgeon responsibilities, and
any financial data that may be relevant. Although many doctors
charge by the area, I prefer to charge by the unit. This makes
treatment and retreatment simple and understandable for the
patient. They are charged for what they receive, and touchups,
when required, are simple math. In addition, some patients
require more drug than others because they have larger muscles
or higher hairlines.
I am a Diamond level injector, which means that I personally
use over 700 vials of Botox per year and I am one of the
largest solo injectors in the United States. As a consultant for
Allergan and Medicis, I have trained hundreds of doctors from
virtually every specialty in the cosmetic use of BTA. Use of
Botox and Dysport is very simple and predictable. I personally
inject every patient myself and cherish this opportunity as
well-spent doctor/patient relations. There have been many
Botox patients who turned into eyelid or facelift patients.
Although many surgeons employ physician extenders to inject
2
1
3
4
FIGURE 13-6.  The main muscles of facial expression commonly treated
with injectable neurotoxin. The paired muscles include the procerus (1),
the corrugator supercilii (2), the medial orbicularis (3), and the sole elevator
of the forehead, the frontalis (4).

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Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
problem with the 1-mL dilution is that it is much easier to waste
the toxin; misplaced drops are more concentrated and therefore
expensive. The 2.5-mL dilution has proven most convenient. It
is not the dilution that makes a difference, but rather the
number of units being delivered.
I prefer 12-inch 32-gauge needles (0.26 × 13 mm) and feel
their expense is a well-justified price for a less painful injection
(Figure 13-11) (Airtite Inc., 1-800-231-7762). It is notable that
the more expensive syringes of clear, smooth plastic have much
smoother plunger activity thanks to the lubricated stopper (1
mL Luer-Lok Tip Reference #309628, BD Inc., Franklin Lakes,
NJ). These are much smoother than the cheaper opaque poly-
ethylene syringes with smaller plunger tips, which are more
“jerky” and less precise in terms of injection control. This is
especially critical when very small units are administered in
precise areas such as the lower eyelid.
Allergan provides Botox in single-use vials of either 50 or
100 units and originally recommended that the product be
discarded at 4 hours; however, the new package insert allows 24
hours after reconstitution. Studies in the literature have shown
that 40-day-old reconstituted Botox produces clinical effects up
to 40 days.22 Many practitioners will keep reconstituted toxin
in the refrigerator for several days or weeks without apparent
loss of potency.
We label every Botox syringe with an appropriate orange
label so these syringes are not mistaken for local anesthetic
(which has occurred). In addition, a very convenient innovation
has been the purchase of small, compact countertop refrigera-
tors. These units are about $100 and not only act as refrigerators
but also can be used as heating units for IV fluids and the like.
Using these small appliances has made our fast-paced Botox
practice much more efficient. The units are aesthetic and occupy
a small footprint (Figure 13-12). We use them in our steriliza-
tion suite to store our unopened neurotoxin (Figure 13-13) and
also keep them in each room where we inject (Figure 13-14).
This has saved hours of running around to fetch syringes for use
in one of the injection suites and has been a much-appreciated
convenience.
based on the surgeon’s preference. I personally use a 2.5-mL
dilution (Figure 13-9). This makes the math easy. There are 100
units of Botox in a vial. I use an 18-gauge needle to inject 2.5
mL of preserved saline into the vial and mix the solution by
gently shaking the bottle. The top of the vial is then removed
with a bottle opener, and the solution is drawn up in 1-mL
Luer-Lok syringes (Figure 13-10). This is done with an 18-gauge
needle and never with the fragile needles that will be used for
injection. Five syringes are filled to 0.5 mL, which equals 20
units or 4 units per 0.1 mL. This means that each syringe con-
tains 20 units of toxin, and the five syringes total 100 units.
Since 20 units are used to treat the average area, this dilution
and associated math is simple for staff, doctor, and patients. It
is also important to purge the syringes so that the initial injec-
tion does not include air instead of neurotoxin.
I have experimented with dilutions from 1 to 10 mL, and
regardless of dilution have never noticed a difference in effect,
onset, or duration in patients. The problem with larger dilutions
is that they leave large injection wheals that are unsightly. The
Brow opposers
Brow elevators
Brow depressors
FIGURE 13-7.  Complex upper facial movements are produced by the
action of the brow depressors and frequently associated with negative
emotions.
FIGURE 13-8.  Botox arrives as a precipitate in an empty stoppered vial.
FIGURE 13-9.  A 2.5-mL dilution of preserved normal saline has proven to
be a convenient dilution for my practice. This allows 5 syringes, each
containing 20 units of the neurotoxin.

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
609
to mark out the points of injection with a surgical marker and
a ruler or caliper prior to injecting.
When considering needle placement, it is important that the
offending muscles are not necessarily directly under the wrinkle.
Because of variances among patients, the most accurate way to
inject is to ask the patient to animate the area to be injected
and observe the main area of muscle action. Injecting in the
main area of muscle activity is the preferable place for injection.
For experienced injectors, the glabellar, frontalis, and lateral
canthal region injections are almost standardized. The area of
maximum muscle contraction is generally consistent, and by
injecting in a common pattern, the average person can be
injected without flexing for the injector.
A common question from novice injectors is “At what level
is the neurotoxin injected?” Botox or Dysport should be injected
Treatment of Glabellar Rhytids
The procerus, corrugators, and medial orbicularis collectively
produce the common “frown lines” in the central brow region.
The two creases seen in this area are frequently referred to as the
11. The common injection pattern of this region involves five
injections placed in a manner to decrease contraction of the
depressors. The most important pearl when injecting in the
periorbital region is to keep all injections 1 cm from the bony
orbital rim. Some injectors choose to inject closer to the orbit,
but I can testify that in many thousands of injections adhering
to the “10 mm away from the orbit” rule, I have never experi-
enced a true eyelid ptosis (Figure 13-15). I have, however, seen
it happen to other injectors when neurotoxin is injected too
close to the orbital rim. For the novice injector, it is a good idea
A
B
FIGURE 13-10.  A bottle opener is used to remove the stopper and retaining band from the reconstituted vial so the solution
can be conveniently removed in syringes. This method also prevents waste.
A
B
FIGURE 13-11.  A Luer-Lok 1-mL syringe with a 32-gauge needle has proven advantageous for accurate and painless
injection.

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Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
FIGURE 13-12.  The countertop refrigerator has been a welcome addition
to a busy injection practice and aesthetically fits into the décor.
FIGURE 13-13.  Medications requiring refrigeration, such as Botox, are con-
veniently kept in the countertop refrigerator until needed.
A
B
FIGURE 13-14.  A countertop refrigerator (with syringes loaded) is kept in each injection suite and has greatly facilitated the
process of patient injection and minimized unnecessary staff excursions.
intramuscularly, since that is the site of intended drug action.
Early accounts instructed injectors to insert the needle to peri-
osteum and then draw back half the way. This is a poor practice
for several reasons: the periosteum is innervated, it is painful,
and it also will dull the needle quickly. The mimetic muscles are
subcutaneous with dermal insertions and are superficial.
Depending upon the amount of subcutaneous fat in the region,
the muscle mass can be shallower or deeper. A general rule is to
insert the 12-inch needle about one-third of its length for the
average patient. In reality, neurotoxins have a great affinity for
muscle and even if injected intradermally will generally produce
the desired effect. A common mistake of novice injectors (espe-
cially those used to giving intramuscular injections on the body)
is to hold the syringe between their index finger and thumb
similar to holding a pencil. They puncture the skin and then
have to regrasp the inserted syringe to find the plunger, which
is an awkward maneuver. It is better to inject with the thumb
on the plunger and the index and second fingers on the hilt of
the syringe.
The main injection sites for glabellar rhytids are a central
injection into the procerus, an injection in the region of each

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
611
corrugator supercilii, and a single injection at the action of the
medial orbicularis oculi muscle bilaterally (Figure 13-16). I
prefer 20 to 25 units to treat this region; when using 25 units,
each treatment site receives 5 units. While many patients mani-
fest the procerus action as a single area, it is not unusual to see
some patients scowl and observe two separate procerus ridges.
For the single ridge seen when scowling, 5 units can be placed
centrally; in the case of two separate ridges, 2.5 units can be
placed in each ridge (Figure 13-17).
Although 20 units of Botox or 60 units of Dysport are gener-
ally sufficient to improve the frown muscles in the average
patient, some patients may require double this dose for efficacy.
This is very common in men or women with very active depres-
sor muscles. Patients must also understand that lines etched into
the dermis are not going to go away but will probably be
improved as the resting tension is relaxed. Filler injection may
be necessary to improve the dermal lines. Patients must also
understand in the preinjection consent process that a given
dosage of toxin in a given patient may result in complete paraly-
sis or only a decrease in the amount of muscle movement. If a
patient is expecting paralysis without any movement, they must
understand that it may require additional amounts of the drug.
10 mm
10 mm
10 mm
10 mm
B
A
FIGURE 13-15.  A, Injecting 10 mm away from the bony orbit will ensure safety and prevent unwanted toxin diffusion. B, Same
principle of the 10-mm safety zone.
5
5
5
5
5
FIGURE 13-16.  Five injections of 5 units each are used to treat the average
patient to improve frown lines by deactivating the brow depressors.
Another relatively common phenomenon is when a patient
is asked to frown or scowl, and they recruit both the depressors
and the central frontalis (Figure 13-18). This is most frequent
in the patient who “does not know how to frown.” Hard to
believe that when asked to scowl, some patients do not under-
stand the muscles used to convey that emotion and when asked,
exhibit this biphasic expression. If they are handed a mirror and
asked to repeat the frown or scowl, most often they will use the
pure depressors. If they continue to exhibit this multiple-area
depressor/frontalis action, it must be explained to them that
they will need both regions treated.
Treating “Bunny” Lines
So-called “bunny lines” are formed by flexing the upper fibers
of the nasalis muscle on the lateral nose (Figure 13-19). These
lines can be strictly from the nasalis muscle (Figure 13-20, A)
or from a combination of heavy procerus action in conjunction
with the nasalis (see Figure 13-20, B). Regardless of causation,
this area is easily treated by injecting 2-unit aliquots in the
circled areas in the figure, which are of course different from
patient to patient. Care is used to inject well above the nasola-
bial fold to avoid affecting lip function. Some patients may not
exhibit nasalis activity until their glabella is treated and then
recruit the nasalis muscles when attempting to frown.
Frontalis Treatment
The frontalis is a more variable site than the glabella because
hairlines and forehead height are so dramatically different from
patient to patient (Figure 13-21). A patient with a very low
hairline and short forehead may need very little neurotoxin,
whereas a patient with a receding hairline or an elongated
forehead may need more than the average patient. In fact,
a patient with a very short forehead and low hairline may
experience frontalis paralysis when the treatment is limited to
the glabella.
When treating the frontalis, it is important to remember that
this is a paired sheet of muscle that can be very thin (Figure
13-22). The actual horizontal forehead rhytids have little to do
with the position of the muscle, especially in the midline where
many patients have no frontalis. The horizontal rhytids in the
skin are perpendicular to the actual muscle, so the treatment is

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Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
since the effect will spread. When treating the frontalis, a “field”
of muscle area is being treated, much in the same way one
injects local anesthetic wheals.
Since the frontalis is a thinner muscle, especially in females,
less neurotoxin is required to decrease function. The common
dose is 2 to 4 units (Figure 13-24). For patients with very thin
skin and muscle, 2 to 3 units per injection may be effective, but
for patients with thicker skin and muscle, 4 to 5 units per injec-
tion area may be necessary (Figure 13-25).
When I began injecting Botox in the mid 1990s, the frontalis
was the second most commonly requested treatment area after
the glabella. Over the past 5 years, I have seen the frontalis
region drop to third, with the lateral canthal region now the
second most commonly requested treatment area. I believe the
prime reason is that when the glabella and frontalis are treated,
a patient can lose much of the ability to animate or express
themselves. When Botox injections became popular, patients
truly wanted no muscle movement in the upper face. This
became known as a “done” look and has lost popularity. Another
reason is that many patients (especially females) go through
their waking hours with their brows subconsciously elevated.
For many women, it is almost impossible for them to relax their
brows. Any surgeon that performs brow lift procedures and
attempts a relaxed preoperative picture can testify to this. If
these patients have a component of dermatochalasis, it is not as
apparent when their brows are subconsciously elevated. If the
performed by spreading out the toxin over the active regions of
the muscle. The injection should be spread out enough to cover
all the active muscle area of the broad, thin sheets of the fron-
talis. It must be kept in mind that when a neurotoxin is injected,
the effect fans out like a bull’s eye from the center of the injec-
tion for about 10 mm (Figure 13-23). When injecting the
frontalis, there is no need to space the injections closer than this,
2.5
2.5
5
B
A
FIGURE 13-17.  A, A single procerus furrow when frowning. B, Double furrows are seen in some patients. I prefer to inject the
single furrow with 5 units and use 2.5 units for each furrow in the case of double furrows.
A
B
FIGURE 13-18.  Some patients will exhibit a biphasic animation by recruiting both the depressors and the central frontalis when
asked to frown or scowl.
FIGURE 13-19.  The nasalis muscle overlies the lateral nose and when
flexed elevates the nose and produces “bunny lines.”

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
613
B
A
FIGURE 13-20.  A, This patient has pure nasalis wrinkling. B, This patient has a combination of wrinkles from an active procerus
and nasalis. The circles indicate 2-unit injections of Botox.
B
A
FIGURE 13-21.  Patient with a low, short hairline (A) may take much less neurotoxin than one with the inverse (B).
FIGURE 13-22.  As seen in a mini open brow lift, the right frontalis is a very
thin sheet of muscle and in this case is absent in the midline. The arrows
point to a sensory nerve branch.
FIGURE 13-23.  Each neurotoxin injection can spread out concentrically
from 10 to 15 mm. The amount of diffusion may differ from one toxin
formulation to another. The key to treating an entire area like the forehead
is to space the injections far enough apart to account for the diffusion to
cover the entire desired treatment area.

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Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
frontalis is overtreated and they can no longer perform this
habitual elevation, it gives the appearance of excess upper eyelid
skin, and when the patient attempts to apply eye shadow but
can’t raise their brow, they are doubly upset. They immediately
assume they have the complication of eyelid ptosis, but the
problem is that they have lost the effect of the subconscious
brow elevation.
This phenomenon must be explained in the consent process
if dermatochalasis is present. If there is a question about excess
upper-lid skin or if the patient is a chronic brow raiser, then I
use what I call the brow-sparing injection pattern. In this treat-
ment, the frontalis is treated normally, but the areas with the
question marks in Figure 13-26 are not injected. If the patient
was younger does not have excess upper lid skin, these areas
would normally be treated, but are spared in older patients or
those with excess upper lid skin. By sparing these areas of fron-
talis muscle, the patient is still able to raise the brow.
If a patient has never received neurotoxin treatment and
requests both frontalis and glabellar treatment, it may be judi-
cious to limit the initial treatment to a single area, because the
abrupt loss or decrease in animation in the first-time patient can
be disconcerting.
3
3
3
3
3
3
3
3
FIGURE 13-24.  Smaller doses of 2 to 3 units may be adequate for thin-
skinned females with small muscle mass. Typical injection pattern with
indicated units per injection site is shown.
B
A
FIGURE 13-25.  A, For a patient with fine rhytids and less active frontalis muscle, 2 to 3 units per injection site is adequate. B, This patient shows thicker
skin and heavier muscle action and may require 4 to 5 units per site to prevent movement.
Much attention has been given to the so-called Botox brow-
lift. In this scenario, the glabellar region is treated (and some-
times part of the frontalis) and essentially inactivates the brow
depressors. This allows portions of the sole brow elevator (the
frontalis) to remain active and hence may produce slight brow
elevation. Although some of the most famous and well-known
injectors subscribe to the phenomenon, I contest the accurate
reproducibility of this treatment. I don’t contest that one can
paralyze the glabella and not the frontalis (or part of the fron-
talis) and see some brow elevation in before-and-after pictures.
What I do disagree with is that the frontalis magically pulls up
the brow. I believe that in many of these before-and-after pic-
tures, the patient is aware of the anticipated outcome, is prob-
ably subconsciously trying to elevate their brow, and even when
paralyzed, some conscious lifting occurs. Also, if both the
depressors and the elevator are selectively treated, there is usually
still some active muscle the patient can control.
In many pictures I have seen, glabellar paralysis actually
lowers the medial brow, and this produces the illusion of the
lateral brow being elevated. I am not saying that some minor
lifting of the brow is impossible, but I stand by my statement
that it is not a consistent reproducible effect that can be reliably
produced on every patient. I do believe there is another option
that can improve the chances of some brow elevation, and that
is to inject that lateral orbicularis oculi lateral to the temporal
crest (Figure 13-27). The anatomy of this area is such that the
frontalis muscle ends at the temporal crest. This means that
there is no brow elevator in this region, yet there is active depres-
sor action from the lateral orbicularis oculi muscle. Close obser-
vation will show that in some patients, smiling and squinting
will actually pull down the lateral brow, due in part to the lateral
orbicularis oculi action (Figure 13-28). By injecting the lateral
orbicularis in this area, the lateral brow may be relaxed to a point
of slight elevation. This injection requires 2 to 3 units on each
side and is placed at the lateral brow tail.
Lateral Canthal Treatment
As I said, the lateral canthal region has become the second most
requested treatment area in my practice. Crow’s feet rhytids
form perpendicular to the concentric lateral orbicularis oculi

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
615
one area where the injection can be made extremely superficial,
almost intradermal, and the neurotoxin will find the underlying
muscle.
The general treatment in this region is to place 3 to 4 units
in 3 to 4 areas in a semilunar configuration at the lateral canthus
(Figure 13-29). Use caution when injecting below the level of
the inferior orbital rim. The toxin can spread to the lip elevators
and produce dysfunctional perioral animation. Figure 13-29
shows the typical lateral canthal injection pattern. Caution is
used when injecting the most inferior area. Novice injectors
should inject here and below with caution because diffusion can
affect lip elevation.
X
FIGURE 13-27.  The sole elevator of the brow, the frontalis muscle, does
not extend lateral to the temporal crest. The lateral orbicularis, however,
can produce a downward pull on the brow. Injecting the lateral orbicularis
oculi may relax the downward pull and contribute to some lateral brow
elevation.
B
A
FIGURE 13-28.  The lateral orbicularis oculi can pull the lateral brow inferiorly during smiling and squinting. Inactivating this region
with neurotoxin may contribute to elevation of the lateral brow even though there is no opposing frontalis in the region.  
A, Lateral brow at repose. B, Brow tail pulled inferiorly during animation.
?
?
?
?
FIGURE 13-26.  The “brow-sparing” method does not inject the areas
marked with question marks in older patients, patients who chronically
elevate, or those with dermatochalasis. By sparing these areas of frontalis,
most patients can still adequately raise their brows.
muscle. This can be a variable region in terms of expected
results. If the patient has underlying muscle activity that signifi-
cantly contributes to the wrinkling, an effective treatment result
is anticipated. If the lateral canthal wrinkles are mostly from
skin wrinkling, a less significant treatment result may be seen.
Unlike the glabella or frontalis, injecting the lateral canthal
region may not produce dramatic improvement of the
wrinkles.
The most important pearl to remember when treating this
region is to keep all injections at least 10 mm lateral to the
lateral orbital rim (see Figure 13-5, A). Another very important
point is that this region is notorious for very large and superficial
veins, especially in thin females, and is subject to significant
bruising that can last for weeks. When injecting in this region,
absolute attention is required; wearing magnifying loupes can
be helpful. One can inject around the veins or even under them,
but close observation is essential to prevent ecchymosis. This is

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Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
Midfacial Treatment
The orbicularis oculi muscle is divided into pretarsal, preseptal,
and orbital portions. During smiling and animation, contrac-
tion of the pretarsal orbicularis diminishes the palpebral aper-
ture. This can produce a “jelly-roll” deformity where the
contracted muscle produces a subciliary bulge. This bulge can
be mistaken for fat (Figure 13-31). It can be treated by injecting
2 units of Botox in the pupillary midline about 3 mm below
the ciliary margin. This treatment can assist in reducing the
muscle bulge as well as open up the palpebral aperture at rest
and when smiling, producing a more wide-eyed or alert appear-
ance. Caution must be used when treating this area, especially
by the novice injector. Overtreatment can affect the ability to
close the eye and result in keratoconjunctivitis sicca (dry eye
syndrome). Neurotoxin treatment should not be attempted in
the lower lid of patients with significant lower eyelid laxity
(abnormal snap or pull test) and with caution in patients who
have had cosmetic procedures such as lower-lid skin excision or
aggressive laser resurfacing that could have foreshortened the lid
skin. Decreasing the muscle function of an already compro-
mised lower eyelid can be problematic.
If the novice injector has trouble injecting small 1- to 2-unit
aliquots, overtreatment is a possibility. Placing only the amount
of drug to be used in the syringe can prevent excessive injection.
Some practitioners utilize 0.3-mL insulin syringes with preat-
tached 30-gauge needles and dilute the Botox with a single mL
of saline. In this case, the insulin syringe increments correspond
to single units (Figure 13-32, B).
Nasal Indications
Nostril Flare
Some individuals habitually dilate their nostrils by activating
the lower nasalis fibers. Although a rarely requested procedure
in my practice, treatment of alar flare is occasionally
A situation present in some patients is elongated lateral
canthal rhytids that can extend almost to the ear. It must be
discussed with the patient that in order to improve the “lateral”
lateral canthal wrinkles, an additional round of injections may
be necessary (Figure 13-30). Since these areas may overlie the
zygomaticus muscles, a smaller dose of Botox is recommended.
The golden rule of neurotoxin treatment is you can always add
more, but you can’t take it away!
2
3
3
3
FIGURE 13-29.  Neurotoxin injections to improve lateral canthal rhytids are
typically made in a semilunar configuration 10 mm lateral to the lateral
orbital rim; 10 Botox units is a common total dose for each side. Injection
site 2 indicates lower limit for novice injectors; below that area, it is possible
to affect lip elevator musculature. Novice injectors should use one half this
amount.
3
3
3
2
2
2
FIGURE 13-30.  The medial dots indicate the standard “3 by 3” (three units
in three areas) for Botox injection at the lateral canthal region. The lateral
row of dots indicate treatment points of 2 units for the extended crow’s
feet wrinkles seen in some patients. More cautious treatment is performed
laterally to avoid extension into other facial musculature.
FIGURE 13-31.  The pretarsal orbicularis produces a subciliary bulge when
the muscle is activated. This is bothersome to some patients and can be
treated with neurotoxin injection.

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
617
requested by a patient self-conscious about the way this habit
affects face-to-face communication. Alar flare can be treated by
injecting 2 to 4 units of Botox into the lower nasalis fibers as
they follow the lateral alae (Figure 13-33).
Nasal Tip Elevation
Another obscure treatment is neurotoxin elevation of the nasal
tip. Some of the applications we describe follow the analogy, “If
you have a new hammer, the whole world is a nail,” I treat
hundreds of Botox patients each year, and in a decade have never
had a request for nasal tip elevation. The theory with this treat-
ment is to deactivate the depressor septae, the muscle that
contributes to nasal tip depression or associated droop. An injec-
tion of 2 to 3 units is placed just below the columella and is
said to elevate the nasal tip.23 Caution must be used, especially
with patients with long upper lips or low vermilion show,
because this injection can contribute to lip ptosis.
Nasolabial Fold Treatment
It is very tempting to use neurotoxins for common aging-related
facial changes, including nasolabial folds, which appear in the
later third decade. These lines extend from the nostrils to the
lateral perioral region. Some practitioners advocate injecting
the levator labii superioris alaeque nasi with 2.5 units of Botox
bilaterally at the level of the bony lateral nasal rim (Figure
13-34). This muscle is the most medial mimetic muscle and is
responsible for the last several millimeters of lip elevation in
smile; it is a strong contributor to nasolabial folds. The theory
in treating this muscle is that it may relax the fold. In my experi-
ence, the relaxation is minimal, and the dysfunctional anima-
tion or relative lip elongation is not worth the limited cosmetic
effect (Figure 13-35).
This same application is used to treat “gummy smiles,” the
excessive show of maxillary gingiva in repose or smiling. In
normal individuals, several millimeters of gingiva are seen at full
smile, but in patients with hypertrophic gingiva or vertical
maxillary excess (excessive downgrowth of maxilla), 5 to 10 mm
of gingival show can been seen with smile or animation. This is
a very unaesthetic situation for these patients, and the proper
treatment, depending upon the condition, is maxillary impac-
tion surgery or gingivoplasty. Treating the lip elevators has been
B
A
FIGURE 13-32.  A, Subciliary lower-lid pretarsal injection with a 32-gauge needle. B, Injection with the specialized 0.3-mL insulin
syringe.
FIGURE 13-33.  Botox injection of the inferior nasalis fibers that contribute
to nasal flare. Typically 2 to 4 units are injected on each lateral ala.
FIGURE 13-34.  The injection point for a dose of 2.5 units of Botox to affect
the nasolabial fold or excessive gingival display.

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Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
men can also have vertical rhytids, the severity is much less, in
part because of the presence of denser hair follicles.
Treating this area warrants conservative treatment because
the margin of error between mitigating wrinkles and affecting
normal lip function is slight. This is an area best treated (espe-
cially by novice injectors) in several appointments instead of a
single appointment. I routinely treat perioral vertical rhytids by
injecting 2 units of Botox at the regions of wrinkling visible
when puckering. This generally represents two to four areas on
each lip. Some patients require additional areas of injection
(Figure 13-36). The injections are placed very superficially and
sometimes intradermally. The patient is then asked to return in
2 weeks, and if more treatment is warranted, a second series of
injections can be performed. It must be kept in mind that
responses to neurotoxin treatment in the upper face can be very
dramatic, but responses in the middle and lower face are much
more subtle, and patients must understand the difference. It is
impossible to make all vertical rhytids go away without com-
promising the function of the lips. I most frequently combine
the vertical lip rhytid treatment with lip fillers. This is a winning
combination: Botox makes the filler last longer by decreasing
muscle activity and complements the filler by relaxing the
underlying musculature. Personally, I prefer to treat the vertical
rhytids first and have the patient return 10 days later for the
filler, although they can be done concomitantly.
Treating the Depressor Anguli Oris
The depressor anguli oris (DAO) muscle is shaped like an
inverse fan. It originates at the mandibular border and inserts
into the modiolus at the oral commissure (Figure 13-37). Con-
sistent with previously discussed procedures that sound better
on paper than they work in vivo is the treatment to upturn the
corners of the mouth. The theory is that deactivating the DAO
allows the levator anguli oris to be unopposed and elevate the
used by various specialties to disguise excessive gingival display.
The mechanism is that the lip elevators are compromised by the
neurotoxin, and the lip is not elevated to its normal position.
Although effective, the problem with this treatment is that the
animation may look dysfunctional or even stroke-like, because
the upper lip becomes elongated and does not elevate totally.
For some patients, the tradeoff is worth it, for others it is not.
The best way to determine who will be happy and who will not
is to begin with small portions of neurotoxin and slowly ease
into the final result. There is a fine line between less movement
and not enough movement. Although multiple articles exist
about successful patient treatment and acceptance for excessive
gingival display,24-27 I have been unable to consistently please
patients with this treatment; admittedly, this may be operator
induced.
Perioral Treatment
One of the true joys of Botox or Dysport treatment is the ability
to literally sculpt and define regional anatomy. Fifteen years ago,
neurotoxins were all about the glabella, but over the last decade,
applications have multiplied. A search of scientific literature will
show neurotoxin treatment for almost every specialty, and I
believe we are just scratching the surface. The use of Botox in
the perioral region is a popular procedure in my practice. I must
admit that when I first began treating this area, I was not
impressed with the changes, but then I noticed that almost every
patient treated for vertical lip rhytids continued their treatment
on a regular basis because they felt it did make a difference, and
the patient is always right.
“Lipstick lines,” which are vertical rhytids that result from
the underlying orbicularis oris muscle function, can be acceler-
ated by smoking, heredity, photodamage, playing a musical
instrument, or chronic whistling. When lipstick is applied, it
“feathers” up or down these lines and is very obvious. Although
B
A
FIGURE 13-35.  Before (A) and after (B) photos showing a patient treated with paranasal Botox injections to lessen the nasolabial
fold. The effect on the patient’s smile is evident, and she chose to not repeat the treatment.

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
619
FIGURE 13-37.  The action of the depressor anguli oris (DAO) is to depress
the corner of the mouth. The DAO is in red and the depressor labii inferioris
(DLI) is in blue. (Adapted from Patton KA, Thibodeau GA: Anatomy and
physiology, ed 7, St. Louis, Mosby, 2010.)
1u
2u
2u
2u
2u
B
A
FIGURE 13-36.  A, The Botox injections are placed at the regions of wrinkling visible when puckering. This patient required five
injections of 1 to 2 units. B, An actual injection. For those practitioners not experienced in this area, the best means of treat-
ment is to inject a single unit in each region and have the patient return in 3 weeks for another round of injections. Placing 2
units per area will cause oral muscular dysfunctions.
oral commissure. This is another example of assuming that
deactivation of a depressor can result in anatomic lifting due to
the uncontested action of the respective elevator. Again, I am
very skeptical that this maneuver (like the Botox brow lift) can
measurably and reproducibly produce noticeable change. I rou-
tinely see before-and-after slides of “successful” elevation of the
corners of the mouth but have yet to see an after picture where
there was not some hint of patient animation. The patients are
smiling! A miniscule smile, but nonetheless there is a change in
animation between the two pictures. Alternatively a picture is
shown with DAO treatment, but the patient has neurotoxin and
lip filler, and I believe the filler is what makes a difference. As
with the Botox brow lift, if a patient knows (and most do) that
they have had a procedure to uplift the corners of the mouth,
it is not uncommon for them to want to please the examiner,
and it is sometimes difficult to take a picture in total repose. In
any event, I have personally photographed numerous patients
in a controlled manner after solitary DAO treatment and have
never been able to obtain clinically significant before-and-after
pictures. I have seen improvement with the combination of
DAO treatment, lateral oral commissural treatment, and lip
augmentation, but I cannot attribute this improvement to the
DAO deactivation. Regardless of my personal observations, I do
have many patients who routinely return to the office for peri-
oral and DAO Botox treatment.
A simple means of locating the DAO is to ask the patient to
show their lower teeth and observe the muscle action under the
skin (Figure 13-38, A). When injecting the DAO, it is best to
inject the midbelly of the muscle. The depth of this muscle is
similar to other mimetic muscles. The marginal mandibular
nerve runs deep to this muscle and is a good reason for super-
ficial injection. A dose of 2.5 to 5 units is injected in each DAO
(see Figure 13-38, B). The platysma muscle, which also inserts
near the DAO and has a depressor effect on this area, is probably
partially treated in some injections.
A caveat of DAO injection is the possibility of inadvertent
injection of the depressor labii inferioris (DLI; see blue area on
Figure 13-37). The DLI is a depressor of the lower lip closer to
the midline. If this muscle is injected or if the drug diffuses to
this area, significant lip dysfunction can occur.
Mentalis Treatment
The paired mentalis muscles originate at the mandibular sym-
physis and insert into the dermis of the chin region. When the
mentalis (and the depressor labii) is activated during speech or

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Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
chewing, dimpling can occur in the chin skin; this is referred
to as peau d’orange, or orange peel. It is bothersome to some
patients and can be effectively and reproducibly improved with
small doses of neurotoxin. Superficial conservative treatment is
performed because overtreatment can affect lower-lip aesthetics
and function. Although generally a dramatic treatment result,
even conservative treatment can affect puckering and pronun-
ciation of P sounds. This is more a concern with deep injection,
and since the muscle acting on the dermis is at question, injec-
tions should be superficial. I generally inject 2 to 3 units spread
equally at the areas of deepest dimpling (Figure 13-39). It is
preferable to inject less rather than more and to be conservative,
repeating the injection a week or two later. Remember, it only
takes seconds to give more drug, but it takes months for it to
wear off.
With all the aforementioned perioral treatments, it must be
kept in mind that slight dysfunction may occur. If there is a
positive cosmetic outcome, most patients don’t mind the
minimal change in muscle function. Patients who make a living
using their mouths (singers, public speakers, scuba divers, musi-
cians, etc.) should not be treated. Even the slightest changes in
muscular function may be detrimental to their careers.
Masseter Treatment
The masseter muscles are thick, strong muscles and primary
elevators of the mandible. These muscles may become hypertro-
phic from heredity or overuse in jaw clenching or nocturnal
bruxism. The hypertrophic masseter can produce a misshapen
face with wide prominence from the earlobes to the mandibular
angle. Many patients present solely for cosmetic purposes to
slim the face. Neurotoxin treatment of the masseter is one of
the most common cosmetic procedures in Asia because many
Asians have developmentally large masseter muscles. Other
patients request masseter treatment for pain and hyperfunc-
tional reasons. The powerful masseter can exert very high
forces on the teeth, jaw, and temporomandibular joint (TMJ).
This can cause micro- and macrotrauma and contribute to
complex pain and degenerative syndromes. Collectively the
pain, muscle spasm, and dysfunction may be referred to as
B
A
FIGURE 13-38.  A, Approximate position of the depressor anguli oris (DAO) can be visualized when asking the patient to show
their lower teeth or pull down the corner of their mouth. B, Injecting 2.5 to 5 units of Botox at the midbelly of the DAO can
decrease its action of depressing the oral commissure.
B
A
FIGURE 13-39.  A, Dimpled appearance of the chin from the action of the
mentalis. Circles indicate the region of 1- to 2-unit Botox injections. B, A
clinical injection.

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
621
region is marked. Generally the three or four most prominent
regions are identified and injected (Figure 13-42).
Most masseter treatments require two to four injection
regions. A good starting point is 5 to 10 units per region on
each side. My average dosage is 20 units of Botox on each side.
The patient is seen again 2 weeks later and reevaluated. If the
aesthetic or pain goal is reached, no further treatment is required;
if the muscle is still in need of reduction, the treatment is
repeated. The endpoint for the cosmetic patient is facial slim-
ming and for the TMD patient, decreased bite force and pain
control. The treatment on this big muscular complex generally
lasts longer than other treatment areas, and most patients will
return in 4 to 6 months. Patients who return for regular treat-
ment undergo masseter atrophy and can be seen with less
frequency.
Platysma Band Treatment
The aging neck undergoes numerous changes, including platys-
mal banding. The visible bands represent lose neck skin with
ptotic medial or lateral platysmal borders (Figure 13-43).
Although the definitive treatment is platysmaplasty, the neck
bands can be mitigated with neurotoxin injection.
Large-dose therapy for neck enhancement has been
reported,29 but the muscles of deglutition and the larynx lie deep
to the platysma, so even small doses of neurotoxin must be
delivered with precision. Dysphagia requiring nasogastric
intubation has been described with as little as a 60-unit dose.27
The procedure is conservatively performed by injecting 2 to
4 units of Botox extremely superficially just under the dermis
(or intradermally) every 1.5 to 2 cm along the platysma band.
myofascial pain dysfunction (MPD) or temporomandibular dys-
function (TMD). These patients frequently clench and grind
their teeth in their conscious and unconscious hours. This
induces muscle spasm and hypertrophy, loss of tooth structure,
and possible degenerative changes in the TMJ. These patients
are more interested in pain reduction, muscle spasm resolution,
the ability to open and close their mouth, and pain-free chewing
and oral function.
Regardless of causation, the masseter treatment is the same.
This large, thick, dual-bellied muscle can handle larger doses of
neurotoxin when compared to the thinner upper facial muscles
(Figure 13-40). Quoting from Gray’s Anatomy of the Human
Body28:
The Masseter is a short thick muscle, somewhat quadrilateral in
form, consisting of two portions, superficial and deep. The superficial
portion, the largest part of the muscle, arises by a thick tendinous
aponeurosis from the malar process of the superior maxilla, and from
the anterior two-thirds of the lower border of the zygomatic arch: its
fibres pass downwards and backwards, to be inserted into the lower
half of the ramus and angle of the lower jaw. The deep portion is much
smaller, more muscular in texture, and the direction of its fibres is
forwards; it arises from the posterior third of the lower border and
whole of the inner surface of the zygomatic arch and is inserted into
the upper half of the ramus and coronoid process of the jaw. The deep
portion of the muscle is partly concealed, in front, by the superficial
portion; behind, it is covered by the parotid gland. The fibres of the
two portions are united at their insertion.28
Whereas 1 to 2 units of Botox may be used on the orbicularis
oculi or oris, I have injected each masseter with up to 50 units
of Botox in severe cases. The treatment sequence begins by
identifying the most prominent area of the masseter by asking
the patient to clench their teeth (Figure 13-41). With the teeth
clenched, the most prominent region is marked with a surgical
marker. The maneuver is repeated, and the next most prominent
FIGURE 13-41.  Clenching the teeth and hence flexing the muscle will define
the hypertrophic areas of the masseter. The main outline of the masseter
is traced with the dotted line, and the separate subprominent areas are
identified with the blue color. Most patients exhibit multiple areas of muscle
prominence, and generally 5 to 10 units are injected deep into the muscle.
FIGURE 13-40.  The masseter is a thick muscle with origins at the zygomati-
comalar regions and insertions on the inferior and posterior mandibular
border.

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Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
conditions. A good example is the Bell’s palsy patient who has
lost animation unilaterally. Before the advent of neurotoxin
treatment, these patients were pretty much forced to go through
life with uneven and asymmetric animation. Selective paralysis
has allowed many of these situations to be harmonized by treat-
ing the active side to prevent or harmonize movement (Figure
13-45). Many other conditions involving the mimetic facial
muscles can be treated in a similar manner (e.g., the asymmetric
smile and brow). The risorius, zygomaticus, and orbicularis oris
muscles can be treated to weaken the hyperfunctional side of an
As the band approaches the clavicle, it is very thin and may only
require 1 to 2 units, but as it approaches the mandibular border,
it frequently thickens and requires a larger dose of 4 to 5 units.
Generally, dosage is limited 15 to 20 units per side per treatment
(Figure 13-44). The potential problems of neck weakness, dys-
phagia, and the like make it preferable to perform multiple
treatment sessions with conservative dosage.
Facial Asymmetry
Injectable neurotoxins have open new doors for patients with
facial asymmetries secondary to nerve injury or developmental
B
A
FIGURE 13-42.  A, Multiple regions of muscle prominence and tenderness. B, These regions being injected.
FIGURE 13-43.  The aging neck produces defined platysma bands that can
respond to neurotoxin treatment.
FIGURE 13-44.  Botox in 2- to 4-unit increments is injected very superficially
every 1.5 to 2 cm for a maximum of 15 to 20 units on each side.

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
623
In several patients, no positive effects were noticed. I further
explain to these patients that my headache treatment includes
total treatment of the glabella, frontalis, and lateral canthus, as
well as selected injections in the areas where the headaches
begin, end, or cluster. The patient is told that this treatment is
very similar to cosmetic treatment for wrinkles and in the best
case scenario, they will have no headaches and no wrinkles, and
in the worst case scenario, they will have no wrinkles. I never
overpromise with pain or headache treatments. I use the same
theory and techniques for MPD and TMJ patients.
As stated, the entire upper face is treated in the same manner
as the cosmetic patient, and the regions where the headache stars
are more heavily treated. Tender points or trigger points com-
monly treated with 5 units of Botox are shown in Figures 13-46
to 13-48.
Hyperhidrosis/Frey Syndrome
The eccrine sweat glands are innervated by fibers from the sym-
pathetic nervous system, in which acetylcholine is the main
neurotransmitter. As discussed earlier in this chapter, botulinum
toxin acts mainly on the cholinergic synapses and inhibits the
release of ACh.40 This has opened up new doors for the treat-
ment of palmar, plantar, and axillary hyperhidrosis. This same
technology can be applied to such facial pathology as Frey syn-
drome (gustatory sweating).41 The auriculotemporal branch of
the mandibular nerve carries sympathetic fibers to the sweat
glands of the scalp and parasympathetic fibers to the parotid
gland. As a result of severance and inappropriate regeneration,
the fibers may switch courses, resulting in gustatory sweating,
or sweating in the anticipation of eating, instead of the normal
salivary response. It is often seen in patients with trauma or
surgery to the preauricular region or those who have undergone
endoscopic thoracic sympathectomy, a surgical procedure where
part of the sympathetic trunk is cut or clamped to treat sweating
of the hands or blushing. The subsequent regeneration or nerve
sprouting leads to abnormal sweating and salivating. It can also
include discharge from the nose when smelling certain food.
Due to the involvement of ACh-mediated transmission,
botulinum toxin can interrupt the process of inappropriate
asymmetric smile, and the frontalis can be similarly treated to
lower a hyperfunctional brow or a normal-functioning brow in
a Bell’s palsy patient. Other conditions resulting from hyper-
functional muscles can be controlled with injection, as can
spastic conditions.
With this type of treatment, there is always a tradeoff between
having one side paralyzed and having both sides paralyzed. In
some patients, depending upon the area, the tradeoff is positive.
In other situations or in other regions, a weakening of the
normal side is preferable to paralysis.
Neurotoxins for Facial Pain/TMD
Treatment/Headache
As eluded to in the section on masseter treatment, various
myofascial pain syndromes exist that present with tender
muscles and trigger points. Although this is far from an exact
science, it is well known that muscle pain and spasm can be
improved by inactivating or stimulating trigger point regions.
One of the most positive incidental findings associated with
neurotoxin treatment has been the drug’s effect on improving
headaches and muscle pain. Although the exact mechanism of
headache improvement remains unknown, neurotoxin injection
is a well recognized and welcomed therapy for migraine and
other types of headache.30-39
I have numerous patients who present for neurotoxin head-
ache treatment and could care less about the cosmetic role of
the treatment. I explain to all potential headache treatment
patients that I cannot guarantee the neurotoxin will improve or
cure their headaches. I have experienced enough positive results,
however, to tell them in good faith that the intensity and/or
frequency of their headaches is likely to improve. My experience
with migraine and other types of chronic headache has been
very positive. Unlike cosmetic patients, who may wait weeks or
months for retreatment after their Botox wears off, the headache
patients are at my doorstep as soon as the effects of their injec-
tions are gone. The experience I can report is strictly anecdotal,
but the neurotoxin treatment has stopped migraines in some
patients and in most others decreases frequency and/or intensity.
B
A
FIGURE 13-45.  A, This patient presented with a paralysis of her left frontalis and a very active right frontalis. B, To equilibrate
the animation, the normal side was treated with 10 units of Botox.

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Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
Complications of Neurotoxin Treatment
Complications from neurotoxins are temporary, but a patient
with lip incompetence or double vision for 3 months will be
unhappy nonetheless. Many complications are actually sequelae,
and all of this must be discussed with patients in the consent
process.
The main complication with cosmetic neurotoxin treatment
is patient misunderstanding of what the expected effect will be.
Many patients do not understand the difference between neu-
rotoxins and fillers. It is not uncommon for some patients to
complain that they still have a skin wrinkle after treatment. It
is important to inform patients preinjection that rhytids that
are etched into the dermis may be less noticeable but will not
sweating. The first order of treatment is to attempt to precisely
identify the involved areas. This can be conveniently performed
by applying an iodine solution (Betadine Surgical Prep works
well) over the suspected region and allow it to dry. The patient
is then given a lemon wedge or sour candy, and after several
minutes cornstarch is dusted over the area; the presence of
moisture (sweat) will react with the iodine and turn a blue/black
color (Figure 13-49). Once the offending region is identified,
the involved skin can be treated with small doses of botulinum
toxin, keeping in mind what essential muscles lie in
approximation.
Case Presentations
Figures 13-50 to 13-69 illustrate diverse cosmetic improvement
in multiple head and neck aesthetic applications.
B
A
FIGURE 13-46.  This patient presented with myofascial pain dysfunction and had headaches in the temporalis region. His tem-
poralis muscles were prominent (A) and in spasm and were greatly relieved by Botox injections in that the region (B).
FIGURE 13-47.  In addition to the normal upper facial cosmetic Botox treat-
ment (white dots), ancillary injections (blue dots) are performed in the
commonly affected regions, which differ from patient to patient.
Trapezius
Occipitalis
Splenius capitis
FIGURE 13-48.  Trigger points and tender points can be effectively treated
with 5-unit injections in the region of commonly implicated muscles,  
including the occipitalis, splenius capitis, and trapezius. (Modified from
Muscolino JE: The muscle and bone palpation manual with trigger points,
referral patterns, and stretching, St. Louis, Mosby, 2009.)
Text continued on page 632.

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
625
FIGURE 13-49.  This patient presented after a facial surgical procedure with
the chief complaint of sweating around the sideburn region when eating.
The starch/iodine test identified the offending region, which was treated
with 1 to 2 units of Botox injected intradermally in the affected area.
A
B
FIGURE 13-50.  This 40-year-old female was treated with 20 units of Botox
in the glabellar region.
A
B
FIGURE 13-51.  This 76-year-old male was treated with 35 units of Botox in the glabellar region.

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Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
A
B
FIGURE 13-52.  This 43-year-old female was treated with 25 units of Botox in the glabellar region.
A
B
FIGURE 13-53.  Patient was treated with 8 units of Botox
for “bunny lines.”
B
A
FIGURE 13-54.  This 32-year-old female was treated with 20 units of Botox for frontalis wrinkles. Note that in the postinjection
picture (B), despite resolution of the wrinkles, she can still raise her eyebrows.

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
627
A
B
FIGURE 13-55.  This 27-year-old female was treated with 20 units of Botox for frontalis wrinkling.
A
B
FIGURE 13-56.  This 45-year-old female was treated with 20 units of Botox for frontalis wrinkling.
A
B
FIGURE 13-57.  This male patient was treated with 25 units of Botox for frontalis wrinkling.

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Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
A
B
C
D
FIGURE 13-58.  This 45-year-old female was treated with 10 units of Botox on each lateral canthal region for improvement of
crow’s feet wrinkles.
A
B
FIGURE 13-59.  This male patient was treated with 12 units of Botox on each lateral canthal region.

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
629
B
A
D
C
FIGURE 13-60.  This male patient was treated with two sessions of 1 unit of Botox 3 mm below the lash line in the center of the
lower eyelid. He is shown in repose (A–B) and smiling (C–D). Notice the improvement in the orbicularis oculi hypertrophy, as
well as the increase in the palpebral aperture opening, especially in the repose image.
A
B
FIGURE 13-61.  This female patient was treated with 2.5 units in the paranasal regions for nasolabial fold improvement. Although
minor improvement is seen in the high fold, I do not routinely provide this treatment.

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Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
A
B
FIGURE 13-62.  This 46-year-old female was treated with 2.5 units of Botox in the paranasal region to decrease the amount of
gum and tooth exposure at smile. Although the treatment was effective, the normal smile animation is adversely affected, and
this is one reason why I rarely perform this treatment.
B
A
D
C
FIGURE 13-63.  A–B, This female patient was treated with four injections across the upper lip of 2 units of Botox for a total of
8 units. She is shown in repose with improvement of the vertical lip rhytids (B). The slight decrease in orbicularis oris resting
tension improved the rhytids. C–D, The treatment of 8 units of Botox in the upper lip produces a noticeable improvement in
vertical rhytids when puckering.

Chapter 13  •  Neurotoxins in Cosmetic Facial Surgery
631
A
B
FIGURE 13-64.  This female patient has a history of teeth clenching and bruxism. Each masseter was treated with 20 units of
Botox spread out in three regions. She is shown several weeks after treatment. She is clenching her teeth in both images.
B
C
A
FIGURE 13-65.  This female patient presented for treatment of jaw spasm and pain. A, Preinjection. B, One week after treatment
with 20 units of Botox on each side. Notice that only part of the masseter belly has been improved, and significant active
muscle is apparent. C, A second treatment of an additional 10 units on each side was performed.
B
C
A
FIGURE 13-66.  A, An Asian male who presented for facial slimming with Botox. B, Patient 1 month after injection. He continued
injections on a 3-month basis and is shown 1 year after the first treatment (C) with an even more dramatic result. Long-term
treatment of this region appears to produce longer-lasting atrophy of this large muscle mass.