Painful traumatic trigeminal neuropathy. Diagnosis and ...

Rev Esp Cir Oral Maxilofac. 2021;43(3):109-116

Caso clínico

Painful traumatic trigeminal neuropathy. Diagnosis and treatment: about two clinical cases

*Autor para correspondencia:Correo electrónico: [email protected] (Christian Droguett Tidy).DOI: 10.20986/recom.2021.1226/2020

A B S T R A C T

Neuropathic pain is originated as a direct consequence of an injury or disease that affects

the somatosensory system, which is a chronic, debilitating condition that affects a significant

number of patients. The causes of neuropathic pain are diverse, and trauma is one of them.

In this article the Painful Traumatic Trigeminal Neuropathy (PTTN) is reviewed. Two clinical

cases are presented. The first is a 43-year-old female with PTTN, who was diagnosed nine

months after reduction and osteosynthesis of a left zygomatomaxillary fracture. The second

case corresponds to a 62-year-old male who presented with a left suborbital PTTN also after

a zygomatomaxillary fracture and its reduction and osteosynthesis surgery. In the first case,

the patient achieved a 70 % of reduction in pain after 6 months of treatment using multimodal

analgesia with pregabalin, carbamazepine and amitriptyline. The second patient achieved

complete resolution of pain with multimodal therapy using carbamazepine, amitriptyline,

and lidocaine patches after two months of treatment. Therapy through multimodal analgesic

scheme provides a favorable prognosis, however achieving a total resolution of the patient’s

pain is a difficult objective to achieve, and a significant reduction of 30% or more in the

patient´s VAS is considered a success of the effectiveness of the therapy.

1130-0558/© 2021 SECOM CyC. Publicado por Inspira Network. Este es un artículo Open Access bajo la licencia CC BY-NC-ND (http://creativecommons.org/licenses/by-nc-nd/4.0/).

I N F O R M AC I Ó N D E L A R T Í C U L O

Keywords:

Neuropathic pain, traumatic painful trigeminal neuropathy, maxillofacial trauma.

Historia del artículo:

Recibido: 17 de noviembre de 2020Aceptado: 27 de marzo de 2021

Christian Droguett Tidy1*, Jorge Lolas Millard2 y Constanza Labbé Martínez2

1Department of Oral and Maxillofacial Surgery. Hospital del Trabajador. Oral and Maxillofacial Surgeon. Specialist in Pain Manage-ment. Faculty of Medicine. Universidad de Chile. Santiago, Chile. 2Department of Oral and Maxillofacial Surgery, Universidad de los Andes, Santiago, Chile

www.revistacirugiaoralymaxilofacial.es

Publicación Ofi cial de la SECOM CyC Sociedad Española de Cirugía Oral y Maxilofacial y de Cabeza y Cuello

Editorial 85 ¿Cuál es la relación entre hiperplasia condílea y la disfunción

temporomandibular?

Originales 90 Tumores malignos de las glándulas salivales: estudio retrospectivo

de los pacientes tratados en el Hospital La Paz entre 2008 y 2018 96 Fracturas faciales, manejo quirúrgico y resultados en un hospital

de tercer nivel

Casos clínicos101 Condilectomía baja intraoral para el tratamiento de hiperplasia condilar.

Reporte de un caso105 Quiste de la cuarta hendidura branquial. Caso clínico y revisión

de la literatura109 Painful traumatic trigeminal neuropathy. Diagnosis and treatment:

about two clinical cases117 Parálisis facial secundaria a absceso parotídeo. Revisión de la literatura

a propósito de un caso122 Lesiones � broin� amatorias tumefactas. A propósito de un caso

Volumen 43 / Número 3

2021Julio / Septiembre

Revista Española de

Cirugía Oral y Maxilofacial

R E S U M E N

El dolor neuropático es originado como consecuencia directa de una lesión o enfermedad que

afecta al sistema somatosensorial, lo cual es una condición crónica, debilitante, que afecta a un

número significativo de pacientes. Las causas de dolor neuropático son diversas y el trauma es

Neuropatía trigeminal traumática dolorosa. Diagnóstico y tratamiento: a propósito de dos casos

Palabras clave:

Dolor neuropático, neuropatía trigeminal traumática dolorosa, trauma maxilofacial.

110 REV ESP CIR ORAL MAXILOFAC. 2021;43(3):109-116

INTRODUCTION

Neuropathic pain can be caused by damage produced at any point in the nociceptive pathway, from the nociceptors to the cortical neurons of the brain1. Depending on the location of the damage, neuropathic pain can be classified as central or peripheral; according to its distribution as localized or diffuse; According to its etiology, it is classified as metabolic, second-ary to ischemia, secondary to inflammation, paraneoplastic, neurodegenerative or traumatic2,3.

Painful Traumatic Trigeminal Neuropathy (PTTN) occurs in 3.3 % of patients with trigeminal nerve injury. In patients with fractures of the zygomatic-maxillary complex, anesthesia or hypoesthesia is frequently observed at examination of terri-tory corresponding to the innervation of infraorbital nerve. However, the development of persistent neuropathic pain occurs only in 3.3 % of cases1,2.

Injury to a nerve delivers negative symptoms in an early stage such as anesthesia, hypoesthesia, or hypoalgesia. Later, it presents positive symptoms such as formication paresthe-sia, which corresponds to abnormal activity of Ab fibers, and pain. The latter can be spontaneous or provoked, which can be of a burning nature, which suggests discharges of type C nociceptors, or lancinating, which suggests ectopic discharges originating in the axon of the A delta fiber1,3.

PTTN, unlike essential trigeminal neuralgia, usually pres-ents as a persistent pain although it may have paroxysmal attacks on a painful basis; it is normally of a burning nature, although it may also have a lancinating component, and reaches a moderate to severe intensity3. Patients usually com-plains of swelling, heat or cold, and erythema in the area that hurts4,5. It shares other characteristic of all neuropathic pain, such as having a strict distribution to the affected dermatome and presenting allodynia and/or hyperalgesia.

According to the International Headache Society there are the following diagnostic criteria for PTTN:

1. Unilateral facial and/or oral pain that meets criterion 3.2. History of identifiable trauma to the trigeminal nerve,

with positive and/or negative clinical signs, these evi-dences of trigeminal nerve dysfunction.

3. Causality is demonstrated by the following two cri-teria:

a) The pain follows the same distribution of the affected trigeminal nerve branch.

b) The pain occurs between the third and sixth month after the trauma.

4. Absence of explanation for another diagnosis6.The management of neuropathic pain should be early and

multimodal in nature, considering all therapeutic alternatives, both pharmacological and non-pharmacological7.

The management of PTTN generally follows the recom-mendations for peripheral neuropathic pain, where membrane stabilizers and tricyclic antidepressants are the main drugs8 (Tables II, III and III).

A small number of patients may have very little or no response to pharmacological treatment and neurosurgical procedures appear as an alternative to this group of patients. These include radiofrequency rhizotomy, stereotaxic radiosur-gery, open section of trigeminal nerve roots, and deep cerebral or cortical electrostimulation, but reports have shown dispa-rate results for different conditions of neuropathic and non-neuropathic pain of the face9.

CASE REPORTS

First case of a 43-year-old female (Figure 1.A) patient with a left zygomatic fracture, for wich she underwent surgery for reduction and osteosynthesis. Nine months later, the patient consulted for pain assessed according to the visual-analog-scale (VAS) as 8 on the left side of the face, wich described it as lancinating in the skin of the left genial region and the left side of the upper lip. At the touch of the area she reported 10 in VAS, and hypoesthesia of the left suborbital skin, left side of the upper dentoalveolar region. The finding of mechanical allodynia manifested by touch of the innervation territory cor-responding to the left infraorbital nerve was evident.

The postoperative control image (Figure 1.B) showed a sin-gle osteosynthesis plate located in the zygomatomatoalveo-lar-buttres on the same side. Was diagnosed as a PTTN that affected the left suborbital nerve. With this, treatment with pregabalin was started with an initial dose of 75mg/day, after two weeks was has decrease in the severity of pain of 2 points in VAS was achieved, the dose was increased to 75 mg every 12 hours and carbamazepine 200mg per day was added to take as a single intake at the end of the day. After one month, the patient experienced pain relief that reached 50 % reduction in the value of VAS. Five months later a pain relief of 50 %

una de ellas. En este artículo se revisa la neuropatía trigeminal traumática dolorosa (PTTN). Se

presentan dos casos clínicos. La primera es una mujer de 43 años con PTTN que fue diagnosticada

nueve meses después de la reducción y osteosíntesis de una fractura cigomatomaxilar izquierda.

El segundo caso corresponde a un varón de 62 años que consultó con una PTTN suborbitaria

izquierda también tras una fractura cigomatomaxilar y su cirugía de reducción y osteosíntesis.

En el primer caso clínico la paciente logró una reducción de un 70 % de su sintomatología a los

6 meses de tratamiento mediante terapia farmacológica multimodal con pregabalina, carbama-

zepina y amitriptilina. El segundo paciente logró una resolución completa del dolor con carbama-

zepina, amitriptilina y parches de lidocaína, después de 2 meses. La terapia mediante esquema

analgésico multimodal proporciona un pronóstico favorable, sin embargo, lograr una resolución

total del dolor del paciente es un objetivo difícil de lograr, y una reducción significativa del 30 %

o más en la EVA del paciente se considera un éxito de la efectividad de la terapia.

REV ESP CIR ORAL MAXILOFAC. 2021;43(3):109-116 111

Tabl

e I.

Firs

t-li

ne

dru

gs f

or t

he

trea

tmen

t of

PT

TN

in

th

e m

axil

lofa

cial

ter

rito

ry.

Firs

t-li

ne

of

trea

tmen

tSu

bcla

ssM

ech

anis

m o

f ac

tion

Rec

omm

end

ed

dru

gU

se in

neu

rop

ath

ic p

ain

Dos

age

in P

TT

N

An

tico

nvu

lsiv

ants

GA

BA

der

ivat

ives

Mem

bran

e st

abil

izer

s d

ecre

asin

g ex

cita

tory

tra

nsm

issi

on o

ver

a2d

Su

bun

it o

f C

a+2 C

han

nel

V

olta

ge D

epen

den

t

Gab

apen

tin

Rel

ief

allo

dyn

ia, h

yper

alge

sia,

bu

rnin

g,

lan

cin

atin

g p

ain

1800

to

3600

mg/

day

(3 d

oses

)In

itia

l dos

e: 6

00 -

800

mg

ever

y 8

hou

rsSt

art

of a

ctio

n: 2

wee

ksM

axim

um

eff

ect:

2 w

eeks

pos

t th

erap

euti

c d

ose

Toxi

city

: dro

wsi

nes

s, d

izzi

nes

s, a

taxi

aIn

tera

ctio

ns:

Min

imal

Preg

abal

in

Sam

e ef

fect

s as

gab

apen

tin

in

neu

rop

ath

ic p

ain

.A

dd

s an

xiet

y ef

fect

Imm

edia

te a

nal

gesi

a

300

to 6

00 m

g/d

ay (2

or

3 d

oses

)In

itia

l dos

e: 7

5 to

150

mg/

day

Star

t of

act

ion

: 2 w

eeks

Max

imu

m e

ffec

t: 2

wee

ks p

ost

ther

apeu

tic

dos

eTo

xici

ty: d

row

sin

ess,

diz

zin

ess,

ata

xia

Inte

ract

ion

s: M

inim

al

An

tid

epre

ssan

tsTr

icyc

lic

An

tid

epre

ssan

ts

Mix

ed a

nd

var

iabl

e bl

ocki

ng

Mon

oam

iner

gic

effe

ct: I

nh

ibit

ion

of

ser

oton

in a

nd

nor

epin

eph

rin

e re

up

take

in s

ynap

ses

of t

he

noc

icep

tive

pat

hw

ayG

luta

mae

rgic

eff

ect:

Alt

ers

glu

tam

ate

bin

din

g to

NM

DA

re

cep

tors

Ind

irec

t ef

fect

on

op

ioid

rec

epto

rs

thro

ugh

mon

oam

inoe

rgic

neu

ron

s an

d I

nh

ibit

ion

of

aden

osin

e re

up

take

at

syn

apse

s

Am

itri

pti

lin

Rel

ief

of c

hro

nic

pai

n b

y ce

ntr

al a

nd

p

erip

her

al m

ech

anis

ms

Trea

tmen

t of

neu

rop

ath

ic p

ain

req

uir

es

low

er d

oses

th

an a

nti

dep

ress

ant

trea

tmen

t.Se

dat

ive

effe

ctEf

fect

ive

in t

he

reli

ef o

f p

ost-

her

pet

ic

neu

ralg

ia a

nd

pai

nfu

l neu

rop

ath

y se

con

dar

y to

dia

bete

s. 1

3. L

ess

effe

ctiv

e ac

tion

in n

euro

pat

hy

du

e to

HIV

an

d

spin

al c

ord

inju

ry 1

6o a

nd

neu

rop

ath

ic

pai

n d

ue

to c

ance

r

12.5

to

75 m

g/d

ay (1

dos

e p

er d

ay)

Star

tin

g d

ose:

12.

5 to

25

mg/

day

Ad

just

1 t

ime

a m

onth

On

set

of a

ctio

n: 2

wee

ksM

axim

um

eff

ect:

4 w

eeks

Toxi

city

: An

tich

olin

ergi

c ef

fect

s (d

ry

mou

th, c

onst

ipat

ion

, uri

nar

y re

ten

tion

), bl

ocki

ng

effe

cts,

sed

atio

n,

wei

ght

gain

, arr

hyt

hm

ias

and

sei

zure

s be

fore

ove

rdos

eIn

tera

ctio

ns:

CY

P in

du

cers

an

d

inh

ibit

ors

Loca

l an

esth

etic

sA

mid

es

Na+

2 ch

ann

el b

lock

in a

ctio

n

pot

enti

alSl

ows

dow

n a

nd

blo

cks

acti

on

pot

enti

al f

rom

per

iph

eral

af

fere

nts

Lid

ocai

ne

Top

ic li

doc

ain

e: r

elie

f of

all

odyn

ia a

nd

p

osth

erp

etic

neu

ralg

iaU

sefu

l in

init

ial t

reat

men

t u

nti

l rea

chin

g ef

fect

ive

dos

e of

mu

ltim

odal

an

alge

sic

trea

tmen

t

Patc

hes

5 %

(700

mg

in a

qu

eou

s ad

hes

ive

base

)1

pat

ch e

very

12

to 2

4 h

ours

Toxi

city

: Min

imal

, mil

d s

kin

rea

ctio

ns

Low

pla

sma

leve

lsIn

tera

ctio

ns:

Cla

ss I

an

tiar

rhyt

hm

ics,

H

epat

ic m

etab

olis

m


Tabl

e II

. Sec

ond

-lin

e d

rugs

for

th

e tr

eatm

ent

of P

TT

N i

n t

he

max

illo

faci

al t

erri

tory

.

Seco

nd

-lin

e of

tr

eatm

ent

Subc

lass

Mec

han

ism

of

acti

onR

ecom

men

ded

d

rug

Use

in n

euro

pat

hic

pai

nD

osag

e in

PT

TN

An

tid

epre

ssan

ts

Sele

ctiv

e se

roto

nin

-n

orad

ren

alin

e re

up

take

in

hib

itor

s (S

NR

Is)

Mod

erat

ely

sele

ctiv

e bl

ocki

ng

of s

erot

onin

an

d

nor

epin

eph

rin

e

Du

lox

etin

e

Ch

ron

ic p

ain

rel

ief

Fibr

omya

lgia

tre

atm

ent

Seco

nd

lin

e fo

r n

euro

pat

hic

pai

n

man

agem

ent

Gre

ater

tol

eran

ce t

han

tri

cycl

ic

anti

dep

ress

ants

(th

ey la

ck

anti

his

tam

ine,

alp

ha

adre

ner

gic

bloc

ker

and

an

tich

olin

ergi

c ef

fect

s)

Du

lox

etin

e:30

mg/

day

firs

t w

eek

un

til r

each

ing

60 m

g/d

ayV

enla

fax

ine:

75 t

o 22

5 m

g/d

aySt

art

37.5

mg/

day

firs

t w

eek

un

til r

each

ing

75 m

g/d

ayO

nse

t of

act

ion

: 2-4

wee

ksM

axim

um

eff

ect:

4 w

eeks

Toxi

city

: An

tich

olin

ergi

c ef

fect

s, r

isk

of g

lau

com

a an

d

live

r fa

ilu

re (d

ulo

xeti

ne)

, sed

atio

n, h

yper

ten

sion

(v

enla

faxi

ne)

Inte

ract

ion

s: s

ome

inh

ibit

ion

of

CY

P 2D

6 (D

ulo

xeti

ne,

d

esve

nla

fxin

e)

Ven

lafa

xin

e

Op

ioid

s

Wea

k ag

onis

t op

ioid

(u)

Mix

ed e

ffec

t: W

eak

u

agon

ist,

mod

erat

e se

roto

nin

re

up

take

inh

ibit

or a

nd

wea

k n

orep

inep

hri

ne

tran

spor

ter

inh

ibit

or

Tram

adol

Ad

juva

nt

opio

id in

ch

ron

ic p

ain

sy

nd

rom

esM

edic

atio

n f

or m

oder

ate

pai

nA

dju

van

t fo

r im

med

iate

pai

n r

elie

f in

m

ult

imod

al t

reat

men

t of

pai

n o

f fi

rst

lin

eEf

fect

in n

euro

pat

hic

pai

n,

pol

yneu

rop

ath

ies,

pos

ther

pet

ic

neu

ralg

ia a

nd

neu

rop

ath

ic p

ain

du

e to

m

elli

tus

dia

bete

sM

ust

be

sup

ple

men

ted

wit

h a

nti

emet

ic

med

icat

ion

in c

ase

of n

ause

a

50 t

o 40

0 m

g/d

ay (3

dos

es)

Star

tin

g d

ose:

50-

100

mg/

day

Toxi

city

: Sei

zure

s, d

izzi

nes

s, c

onst

ipat

ion

, nau

sea,

vo

mit

ing,

ris

k of

ser

oton

in s

ynd

rom

eR

isk

of a

buse

, tw

enty

Inte

ract

ion

s: R

isk

of s

erot

onin

syn

dro

me

Stro

ng

opio

ids

Stro

ng

agon

ists

of

μ

rece

pto

r, a

ffin

ity

vari

able

by

δ an

d κ

rec

epto

rs

Mor

ph

ine

Met

had

one

Fen

tan

yl

Inte

nse

pai

nA

dju

nct

in g

ener

al a

nes

thes

ia a

nd

se

dat

ion

(fen

tan

yl, r

emif

enta

nil

, m

orp

hin

e)Pu

lmon

ary

edem

a (m

orp

hin

e on

ly)

Mai

nte

nan

ce in

pro

gram

s re

hab

ilit

atio

n

(met

had

one

only

)In

ch

ron

ic n

euro

pat

hic

pai

n, a

wea

k u

ag

onis

t is

pre

fera

ble

Tit

hab

le d

ose

acco

rdin

g to

cas

eIm

med

iate

eff

ect

Som

e av

aila

ble

in lo

ng-

last

ing

tran

sder

mal

pat

ches

.D

ura

tion

: 1-4

h e

xcep

t m

eth

adon

e, 4

-6 h

Toxi

city

: res

pir

ator

y d

epre

ssio

n, s

ever

e co

nst

ipat

ion

, ad

dic

tion

liab

ilit

y, s

eizu

res,

uri

nar

y re

ten

tion

, nau

sea

/ vo

mit

ing,

del

iriu

mIn

tera

ctio

ns:

Sed

ativ

e h

ypn

otic

s (r

esp

irat

ory

dep

ress

ion

), A

nti

psy

chot

ic a

gen

ts (i

ncr

ease

d s

edat

ion

an

d

card

iova

scu

lar

effe

cts)

, mon

oam

ine

oxid

ase

inh

ibit

ors

(hyp

erp

yrex

ic c

oma

and

art

eria

l hyp

erte

nsi

on)


Tabl

e II

I. T

hir

d-l

ine

dru

gs f

or t

he

trea

tmen

t of

PT

TN

in

th

e m

axil

lofa

cial

ter

rito

ry.

Th

ird

-lin

e of

tr

eatm

ent

Subc

lass

Mec

han

ism

of

acti

onR

ecom

men

ded

d

rug

Use

in n

euro

pat

hic

pai

nD

osag

e in

PT

TN

An

tico

nvu

lsan

ts

Na+

2 ch

ann

el

bloc

kers

Na+

2 ch

ann

el b

lock

ers

and

in

hib

itio

n o

f gl

uta

mat

e re

leas

e by

n

euro

ns

of t

he

cen

tral

ner

vou

s sy

stem

. tw

enty

Rap

id o

ral a

bsor

pti

on, m

axim

um

le

vels

in 4

-5 h

ours

Car

bam

azep

ine

Use

in t

onic

-clo

nic

cri

sis

foca

l an

d f

ocal

bil

ater

al, u

se in

n

euro

pat

hic

pai

n.

Firs

t le

vel o

f ev

iden

ce f

or

esse

nti

al t

rige

min

al n

eura

lgia

, bu

t it

s ef

fica

cy f

or P

TT

N is

d

isp

ute

d w

ith

lim

ited

res

ult

s in

so

me

stu

die

s

800-

1200

mg/

day

; th

e m

axim

um

dos

eG

rad

ual

incr

ease

For

neu

rop

ath

ic p

ain

100

to

200m

g ev

ery

12 h

ours

is

reco

mm

end

edTo

xici

ty: n

ause

a, d

iplo

pia

, ata

xia,

hyp

onat

rem

ia, h

ead

ach

eIn

tera

ctio

ns:

ph

enyt

oin

, val

pro

ic a

cid

, flu

oxet

ine,

ve

rap

amil

, an

tibi

otic

s m

acro

lid

es, i

son

iazi

d,

pro

pox

yph

ene,

dan

azol

, ph

enob

arbi

tal,

pri

mid

one,

am

ong

oth

ers

Ox

carb

azep

ine

Sim

ilar

eff

ects

an

d m

ech

anis

m

of a

ctio

n a

s ca

rbam

azep

ine.

300

mg/

day

to

600m

g ev

ery

12 h

ours

Th

e cl

inic

al d

ose

of o

xcar

baze

pin

e m

ay n

eed

to

be 5

0 %

h

igh

er t

han

th

at o

f ca

rbam

azep

ine.

Few

er in

tera

ctio

ns

rep

orte

d

Prob

able

Na+

2 ch

ann

el b

lock

ing

mec

han

ism

Lam

otri

gin

e

Use

in f

ocal

sei

zure

s,

gen

eral

ized

ton

ic-c

lon

ic

seiz

ure

s, a

bsen

ce s

eizu

res,

oth

er

gen

eral

ized

sei

zure

s; d

epre

ssio

n

Bip

olar

.It

s ef

fect

iven

ess

in c

ontr

olle

d

tria

ls w

as p

oor

and

its

pot

enti

al

skin

tox

icit

y gi

ves

it a

th

ird

leve

l of

Ch

oice

for

th

e m

anag

emen

t of

neu

rop

ath

ic p

ain

100

to 3

00 m

g/d

ayIn

itia

l dos

e is

25

mg/

day

, an

d in

crea

ses

to 5

0 m

g/d

ay a

fter

2 w

eeks

; su

bseq

uen

tly,

th

e d

egre

e ca

n a

dva

nce

by

50 m

g/d

ay e

very

1-2

wee

ks u

p t

o a

regu

lar

mai

nte

nan

ce d

ose

225-

375

mg

/ d

(in

tw

o d

ivid

ed d

oses

)In

pat

ien

ts r

ecei

vin

g va

lpro

ate,

th

e st

arti

ng

dos

e of

la

mot

rigi

ne

shou

ld b

e re

du

ced

to

12.5

-25

mg

ever

y ot

her

d

ay, w

ith

incr

ease

s of

25-

50 m

g/d

ay e

very

2 w

eeks

as

nee

ded

at

a u

sual

mai

nte

nan

ce d

ose

of 1

00-2

00 m

g/d

ayTo

xici

ty: d

izzi

nes

s, h

ead

ach

e, d

iplo

pia

, ras

hIn

tera

ctio

ns:

val

pro

ic a

cid

, car

bam

azep

ine,

oxc

arba

zep

ine,

p

hen

ytoi

n, p

hen

obar

bita

l, p

rim

idon

e, s

ucc

inim

ides

, se

rtra

lin

e, t

opir

amat

e

Spre

ad

spec

tru

mU

nkn

own

mec

han

ism

Val

pro

ic a

cid

Use

ton

ic-c

lon

ic s

eizu

res

wid

esp

read

cri

sis

par

tial

, ab

sen

ce s

eizu

res,

myo

clon

ic

seiz

ure

s, o

ther

gen

eral

ized

se

izu

res;

mig

rain

e p

rop

hyl

axis

It

s m

ech

anis

m o

f ac

tion

is s

till

u

nkn

own

. No

grea

ter

effe

ctiv

enes

s th

an p

lace

bo h

as

been

fou

nd

in s

ome

poo

r q

ual

ity

stu

die

s

15 m

g/kg

wit

h o

ne

titr

atio

n s

low

un

til t

her

apeu

tic

dos

e.

Dos

es o

f 25

-30

mg/

kg/d

Toxi

city

: nau

sea,

tre

mor

, wei

ght

gain

, los

s of

hai

r,

tera

toge

nic

, hep

atot

oxic

Inte

ract

ion

s: p

hen

obar

bita

l, p

hen

ytoi

n, c

arba

maz

epin

e,

lam

otri

gin

e, f

elba

mat

e, r

ifam

pin

, eth

osu

xim

ide,

pri

mid

one

Top

iram

ate

Mu

ltip

le a

ctio

nTo

pir

amat

e

Foca

l cri

sis,

cri

sis

gen

eral

ized

p

rim

arie

s, L

enn

ox s

ynd

rom

e-G

asta

ut;

pro

ph

ylax

is o

f m

igra

ine

100

mg/

day

Init

ial d

ose

25-5

0 m

g /

day

an

d g

rad

ual

incr

ease

Toxi

city

: dro

wsi

nes

s, c

ogn

itiv

e sl

owin

g co

nfu

sion

, p

ares

thes

ias

Inte

ract

ion

s: p

hen

ytoi

n, c

arba

maz

epin

e, c

ontr

acep

tive

s or

al, l

amot

rigi

ne,

lith

ium

(Con

tinu

e in

the

nex

t pa

ge)


Tabl

e II

I (C

ont.

). T

hir

d-l

ine

dru

gs f

or t

he

trea

tmen

t of

PT

TN

in

th

e m

axil

lofa

cial

ter

rito

ry.

Th

ird

-lin

e of

tr

eatm

ent

Subc

lass

Mec

han

ism

of

acti

onR

ecom

men

ded

d

rug

Use

in n

euro

pat

hic

pai

nD

osag

e in

PT

TN

An

tid

epre

ssan

ts

Sele

ctiv

e se

roto

nin

re

up

take

in

hib

itor

s (S

SRIs

)

Hig

hly

sel

ecti

ve b

lock

ing

of t

he

sero

ton

in t

ran

spor

ter

litt

le e

ffec

t on

th

e n

orep

inep

hri

ne

tran

spor

ter.

Acu

te in

crea

se in

se

roto

ner

gic

syn

apti

c ac

tivi

ty

slow

er c

han

ges

in v

ario

us

sign

alin

g p

ath

way

s an

d

neu

rotr

oph

ic a

ctiv

ity

Paro

xet

ine

Cit

alop

ram

Maj

or d

epre

ssio

n,

anxi

ety

dis

ord

ers

• p

anic

dis

ord

er•

obse

ssiv

e-co

mp

uls

ive

dis

ord

er•

dis

ord

erp

ostt

rau

mat

ic s

tres

s•

vaso

mot

or s

ymp

tom

sp

erim

enop

ausa

l•

eati

ng

dis

ord

erT

hir

d-l

ine

use

in n

euro

pat

hic

p

ain

Var

iabl

e d

ose

Toxi

city

: sex

ual

dys

fun

ctio

n, r

isk

of s

erot

onin

syn

dro

me

wit

h iM

AO

Inte

ract

ion

s: s

ome

inh

ibit

ion

of

CY

Ps (fl

uox

etin

e 2D

6, 3

A4,

fl

uvo

xam

ine

1A2,

par

oxet

ine

2D6)

Tetr

acyc

lic,

m

onoc

lycl

ic

Incr

ease

d a

ctiv

ity

of

nor

epin

eph

rin

e an

d d

opam

ine

(bu

pro

pio

n) •

NET

>SS

RI

inh

ibit

ion

(am

oxap

ine,

map

roti

lin

e)In

crea

sed

rel

ease

nor

epin

eph

rin

e, 5

-HT

(mir

taza

pin

e)Pr

esyn

apti

c re

leas

e of

ca

tech

olam

ines

, bu

t n

o ef

fect

on

5-

HT

(bu

pro

pio

n) •

th

e A

mox

apin

e an

d M

apro

tili

ne

rese

mbl

e tr

icyc

lics

Bu

pro

pio

nT

hir

d li

ne

use

Var

iabl

e d

ose

Exte

nsi

ve li

ver

met

abol

ism

.To

xici

ty: l

ower

s th

e se

izu

re t

hre

shol

d (a

mox

apin

e,

bup

rop

ion

).In

tera

ctio

ns:

CY

P2D

6 in

hib

itor

Oth

erN

euro

toxi

ns

(Cap

saic

in)

Inte

ract

ion

wit

h t

he

van

illo

id

rece

pto

r V

R1

of t

ype

C s

enso

ry

fibe

rs a

ctiv

ate

the

van

illo

id

rece

pto

rs o

f th

e sk

in a

nd

ge

ner

ate

thei

r yo

u s

ee p

ain

, st

ingi

ng

and

late

r an

alge

sia

Th

is r

ecep

tor

is a

non

-sel

ecti

ve

cati

on c

han

nel

, wit

h a

hig

h

per

mea

bili

ty f

or c

alci

um

+2

Prom

otes

th

e re

leas

e an

d in

hib

its

the

bios

ynth

esis

an

d a

xon

al

tran

spor

t of

su

bsta

nce

P, w

hic

h

lead

s to

a d

eple

tion

of

subs

tan

ce

P in

th

e ce

ntr

al a

nd

per

iph

eral

n

ervo

us

syst

em p

rod

uce

s re

vers

ible

des

ensi

tiza

tion

of

C-fi

ber

sen

sory

en

din

gs.

It c

an c

ause

a d

egen

erat

ion

of

the

ner

ve fi

bers

of

the

epid

erm

is.

Cap

saic

in

Th

ere

is m

oder

ate-

qu

alit

y ev

iden

ce t

hat

hig

h-

con

cen

trat

ion

(8 %

) cap

saic

in

pat

ches

can

pro

vid

e m

oder

ate

pai

n r

elie

f, o

r be

tter

, to

a m

inor

ity

of p

atie

nts

wit

h

pos

ther

pet

ic n

eura

lgia

, an

d v

ery

low

-qu

alit

y ev

iden

ce t

hat

th

ey

ben

efit

pat

ien

ts w

ith

HIV

n

eura

lgia

an

d d

iabe

tic

per

iph

eral

neu

rop

ath

y.T

hir

d li

ne

of t

reat

men

t in

n

euro

pat

hic

pai

n m

anag

emen

t

Top

ical

: 0.0

25-0

.075

%, a

pp

lica

tion

eve

ry 6

to

8 h

ours

in t

he

affe

cted

are

a.8

% h

igh

con

cen

trat

ion

pat

ches

.In

80

% o

f ca

ses,

th

ere

may

be

a bu

rnin

g or

sti

ngi

ng

sen

sati

on in

th

e ar

ea o

f ap

pli

cati

on, i

rrit

ativ

e er

yth

ema,

d

ry s

kin


was maintained but had isolated episodes of increased pain severity which maintained its characteristics. It was decided to add amitriptyline in doses of 12.5 mg per day. At the seventh month after the start of the therapy, the patient reported relief of the severity of the pain giving a 2 in VAS, which meant an improvement of 70 %.

The second clinical case corresponds to a 62-year-old male patient (Figure 2.A), who suffered an accident wich resulted in a left side maxillary-zygoma fracture. He underwent surgery in another maxillofacial-surgery service, and three months later he began with a persistent lancinating sub-eyelid pain on the same side as the fracture, which reached a 5 in VAS and reached 9 with touch of the area or with movements of facial mimic muscles. Also had anesthesia in the same area of the pain that was present since the accident. On examination, the patient had allodynia to the touch of the left sub-palpebral territory, left nasal wing, and anterior area on the left side of the maxilla.

The CT scan (Figure 2.B) showed an operated left side zygo-matomaxillary fracture, with osteosynthesis installed in the left frontozygomatic suture, infraorbital rim, zygomatomaxil-lary buttres and a mesh that covered the left infraorbital hole.

Given the described disposition of the mesh, it made sus-pect a possible compression of the suborbital nerve, so it was decided to remove it. At the surgery, the compression exerted on the affected nerve was verified. The patient was treated with pregabalin at a dose of 75 mg every 12 hours and lido-caine patches to be used 1 every 24 hours in the affected ter-ritory. One month after starting this treatment, the patient evolved favorably, reporting a VAS assessment of 4. Consider-ing it still compromised the quality of life of the patient, ami-triptyline was added in a single daily dose of 25 mg/day, after which, evolving favorably after one month reporting complete pain relief, assessing it according to VAS as 0.

DISCUSSION

The low incidence of neuropathic pain in these cases has been explained because of the trigeminal nerve experienc-ing markedly lower ectopic discharges compared to other

peripheral nerves10. As pathophysiological considerations for neuropathic pain in the cases described, we can explain its occurrence through the formation of a neuroma or areas of demyelination in the suborbital nerve, given the bone dis-placement caused by the fracture.

We could argue that the best treatment is the prevention of neuropathic sequelae after trauma. This means that the indication for surgery should be considered promptly after having suffered the accident in maxillofacial fractures that compromise any branch of the trigeminal nerve, which at first will manifest with a negative neurological clinical sign (anes-thesia, hypoesthesia or hypoalgesia), although the bone dis-placement is less, trying to achieve an anatomical reduction. This give a favorable anatomical territory to allow or provide an opportunity for a repair of the affected nervous trunk to occur, thus avoiding areas of demyelination or the formation of a neuroma.

The treatment of this condition must be done with drugs of first line or in combination with others of second or third line, always considering the strategy of multimodal analgesia because of its effectiveness in pain control with lower incidence of side effects. The consequences in the quality of life of the patients who suffer PTTN can be devastating, given this, it’s essential that the maxillofacial surgery teams be trained in the diagno-sis and treatment of this type of condition, in order to achieve timely and effective treatment.

R E F E R E N C E S

1. Baad-Hansen L, Benoliel R. Neuropathic orofacial pain: Facts and fiction. Cephalalgia. 2017;37(7):670-9. DOI: 10.1177/ 0333102417706310.

2. Peñarrocha MA, Peñarrocha D, Bagán JV, Peñarrocha M. Post-traumatic trigeminal neuropathy. A study of 63 cases. Med Oral Patol Oral Cir Bucal. 2012;17(2):297-300. DOI: 10.4317/me-doral.17401.

3. Haviv Y, Zadik Y, Sharav Y, Benoliel R. Painful traumatic trigem-inal neuropathy: an open study on the pharmacotherapeutic response to stepped treatment. J Oral Facial Pain Headache. 2014;28(1):52-60. DOI: 10.11607/jop.1154.

Figure 1. Case 1. A. 43-year-old female patient with a left maxillary-zygomatic fracture. B. Postoperative control CT-3D

reconstruction. Figure 2. Case 2. A. 62-year-old male patient with a left

side maxillary-zygomatic fracture. B. CT-3D reconstruction showing an operated left side zygomatomaxillary fracture.


4. Correa-Illanes Gerardo. Neuropathic pain, classification and management for general practitioners. Rev. Medica Clínica las Condes. 2014;25(2):189-99. DOI: 10.1016/S0716-8640(14)70030-6.

5. Zakrzewska JM. Multi-dimensionality of chronic pain of the oral cavity and face. J Headache Pain. 2013;14(1):37. DOI: 10.1186/1129-2377-14-37.

6. Fernández R, Ahumada M, Muñoz R, Urra X, Yáñez MV, Velasco M, et al. Guidelines for Definition and Management of Local-ized Neuropathic Pain (LNP): Chilean Consensus. Revista El Dolor. 2011;20(55):12-31.

7. Attal N, Cruccu G, Baron R, Haanpää M, Hansson P, Jensen TS, et al. EFNS guidelines on the pharmacological treatment of neuropathic pain: 2010 revision. Eur J Neurol. 2010;17(9):1113-e88. DOI: 10.1111/j.1468-1331.2010.02999.x.

8. Haanpää M, Attal N, Backonja M, Baron R, Bennett M, Bou-hassira D ,et al. NeuPSIG guidelines on neuropathic pain as-sessment. Pain. 2011;152(1):14-27. DOI: 10.1016/j.pain. 2010.07.031.

9. Broggi G, Franzini A, Leone M, Bussone G. Update on neu-rosurgical treatment of chronic trigeminal autonomic ceph-alalgias and atypical facial pain with deep brain stimula-tion of posterior hypothalamus: results and comments. Neurol Sci. 2007;28(Suppl. 2):138-45. DOI: 10.1007/s10072-007-0767-3

10. Benoliel R, Zadik Y, Eliav E, Sharav Y. Peripheral painful trau-matic trigeminal neuropathy: clinical features in 91 cases and proposal of novel diagnostic criteria. J Orofac Pain. 2012;26(1):49-58.

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