Eating epilepsy. A narrative review

196

Eating epilepsy. A narrative reviewMariana Ruiz-León1, Marco A. Sánchez-Torres2, Sonia Luquin-de Anda2, Mónica E. Salmerón-Mercado3, and José L. Ruiz-Sandoval2,4*1Department of Neurology, Hospital Civil de Guadalajara Fray Antonio Alcalde; 2Department of Neurosciences, Centro Universitario de Ciencias de la Salud (CUCS), Universidad de Guadalajara; 3Department of Neurophysiology, Hospital Civil de Guadalajara Fray Antonio Alcalde; 4Instituto de Neurociencias Traslacionales. Guadalajara, Jalisco, Mexico

Revista Mexicana de Neurociencia

REVIEW ARTICLE

Abstract

Eating epilepsy (EE) is rare reflex epilepsy in which seizures are triggered by mechanisms related to the eating process. In this narrative review, we analyzed case series and case reports found in the literature and describe sociodemographic, se-miological, and radiological characteristics of patients with EE in the general population. Our analysis revealed that this epilepsy is more common in male patients and usually presents with focal onset seizures. There is wide variability in clinical presentation and there is not enough evidence to affirm that there is a specific food or diet that triggers the seizures. Tem-porolimbic and suprasylvian areas of the frontal and temporal lobes, particularly the insular and opercular cortex, play an important role in the pathophysiology of EE as found in neuroradiological and neurosurgical studies. As for the treatment, there is a high prevalence of pharmacoresistance and clobazam was the most used antiepileptic drug, usually as an add-on therapy.

Key words: Eating epilepsy. Eating seizures. Reflex epilepsy. Reflex seizures.

Epilepsia refleja por alimentación. Una revisión narrativa

Resumen

La epilepsia por alimentación es un tipo de epilepsia refleja poco frecuente, en donde las crisis epilépticas son detonadas por mecanismos relacionados con el proceso de alimentación. En esta revisión narrativa analizamos reportes y series de casos de este tipo de epilepsia en la población general y detallamos características sociodemográficas, semiológicas y radiológicas. Nuestro análisis reveló que la epilepsia por alimentación es más prevalente en el sexo masculino y general-mente se presenta como crisis convulsivas focales. Existe una alta variabilidad en la presentación clínica y no hay evidencia suficiente para afirmar su asociación con algún tipo de alimento o dieta específica. En los estudios complementarios se encontró relación clínico-radiológica y quirúrgica en áreas temporolímbicas y suprasilvianas de los lóbulos frontal y tempo-ral, particularmente la corteza insular y opercular, recalcando su importante papel en la fisiopatología de esta epilepsia. En cuanto al tratamiento, hay una alta prevalencia de farmacorresistencia y el clobazam fue el antiepiléptico más utilizado, generalmente en conjunto con otros fármacos.

Palabras clave: Epilepsia por alimentación. Crisis epilépticas por alimentación. Epilepsia refleja. Crisis epilépticas reflejas.

Correspondence: *José L. Ruiz-Sandoval

E-mail: [email protected]

Available online: 01-10-2021

Rev Mex Neuroci. 2021;22(5):196-207

www.revmexneurociencia.com

Date of reception: 25-01-2021

Date of acceptance: 16-03-2021

DOI: 10.24875/RMN.21000005

2604-6180/ © 2021 Academia Mexicana de Neurología A.C. Published by Permanyer. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

mailto:jorulej-1nj%40prodigy.net.mx?subject=

http://dx.doi.org/10.24875/RMN.21000005

http://crossmark.crossref.org/dialog/?doi=10.24875/RMN.21000005&domain=pdf

197

M. Ruiz-León, et al.: Eating epilepsy

Introduction

Reflex epilepsy (RE) or reflex seizures refers to epi-leptic syndromes characterized by focal or generalized seizures elicited by a specific stimulus or activity. These stimuli can be simple (visual, auditive, proprioceptive, or tactile) or complex (while eating, talking, tooth-brush-ing, bathing, etc.)1,2. RE estimated prevalence rep-resents 4-7% of all epilepsies and 21% of idiopathic generalized type, being photosensitive epilepsy the most common3.

Eating epilepsy (EE) is a rare form of RE with a prev-alence of 1:1000-2000 of all patients with epilepsy, al-though it ranges higher in Asia3-6. EE is more common in males and usually presents as focal seizures with impaired awareness which can occur before, during, and/or after eating3,4,7.

In this critical review, we aimed to answer the follow-ing questions: which are the sociodemographic, semi-ological, and radiological characteristics of EE in the general population?

Background

Eating is a complex mechanism that includes olfac-tory, taste, somatosensory, and other interoceptive in-puts, which activate brain structures such as the insular cortex, frontal operculum, orbitofrontal cortex, and the amygdala8. The hypothalamus and other com-ponents of the autonomic nervous system regulate central and peripheral homeostasis of digestion and metabolism9. These structures are of particular interest in the study of hunger, satiety, obesity, as well as eat-ing and body image disorders such as anorexia and bulimia. Moreover, all of the aforementioned structures are well recognized as trigger zones of EE in various studies8,10.

Although the pathophysiology of EE is not clear, ac-cording to case reports and small case series in the literature, plausible mechanisms for its appearance have been proposed. A genetic involvement is shown in sub-jects with mutations in genes SYNGAP12, MECP211; as well as familial EE5, associated with Rett12, Cri du Chat,13,14 and congenital or acquired bilateral opercular syndromes15,16. Ethnic origin and environmental factors such as chemical composition of food, culinary habits, feeding behavior, and emotional and psychological in-volvement may be important in EE etiology7,17. EE can present with other epileptic syndromes, structural pathol-ogies (malformations, tumors), and/or brain injury (hy-poxic brain damage, gliosis, encephalomalacia, and

meningoencephalitis)4,7,17. Therefore, it has been pro-posed that EE may be a long-term manifestation of an initial precipitating event in the past7,17.

Clinical presentation of EE is diverse. Seizures usu-ally present as focal onset with impaired awareness and less commonly with generalized onset, including atonic, myoclonic, or even autonomic types3,4,7,17. EE occurs more frequently in the context of temporal or frontal lobe epilepsies4 and it usually is symptomatic or associated with imaging abnormalities in these loca-tions (Tables 1 and 2).

In patients with EE, seizures can be caused by di-verse and heterogeneous stimuli; nevertheless, all of them are related to the feeding process, either just before, during, or after it. These triggers may involve visual and olfactory stimuli (sight and smell), digestive and autonomic functions (salivating, chewing, swallow-ing, gastric distention, and gastric acid secretion), pro-prioceptive stimuli, thinking about food, bulky meals rich in carbohydrates, and gastroesophageal re-flux2,12,17-20. Moreover, association of EE to vasovagal syncope attacks has been reported, suggesting a vagal mechanism7.

Electroencephalographic (EEG) findings can be nor-mal or present focal or diffuse epileptiform abnormali-ties3. Magnetic resonance imaging (MRI) can also be normal or present structural abnormalities specifically in temporolimbic or suprasylvian areas, particularly in the insular and opercular cortex3,4,7,12. A clinical neuro-topographic correlation can be made with EEG finding and/or imaging findings.

Although identification and avoidance of stimulus in some patients could aid in seizure control, in EE, this is not always possible, except in very specific associat-ed situations3. Some patients respond and benefit from antiepileptic drugs. Although management of choice has not yet been established, intake of clobazam before meals may be effective as add-on therapy in the man-agement of EE3,4. Kokes et al. suggest that seizures that originate from the left temporal region may be more resistant to antiepileptic management7. Some patients with therapy resistance may benefit with surgical treat-ment21 or vagus nerve stimulation22, especially those with imaging abnormalities21.

Methods

This article is based on unsystematic research in Google Scholar and PubMed for original manuscripts about “Eating epilepsy,” “Eating reflex seizures,” “Eating seizures,” “Reflex eating epilepsy,” and “Reflex eating

198

Rev Mex Neuroci. 2021;22(5)

Aut

hor/

year

Ahu

ja, 1

98023

Nag

araj

a, 1

98424

Koul

, 198

925Se

nana

yake

, 19

905

Lore

to, 2

00026

Nak

azaw

a,

2002

27Se

nevi

ratn

e,

2003

28La

bate

, 200

529Cu

kier

t, 20

1022

n3

1350

203

228

23

Sex

(M/F

)3/

08/

5N

D13

/72/

12/

013

/15

2/0

2/1

Eatin

g ep

ileps

y m

ean

age

onse

t (ye

ar)

2214

15.2

1722

.69.

518

.68.

611

Trig

gers

Eatin

gCh

ewin

g, d

rinki

ng (w

ater

), ea

ting,

sna

cks

Chew

ing,

sw

allo

win

gN

DEa

ting

Chew

ing,

eat

ing,

sw

allo

win

gEa

ting

Eatin

gEa

ting

Mea

l of t

he d

ayN

DN

DN

DLu

nch

Mea

ls, l

unch

ND

ND

ND

ND

Mom

ent o

f eat

ing/

mea

lAf

ter,

durin

gAt

the

mid

dle,

at t

he e

ndDu

ring

Afte

r (30

min

po

st m

ain

mea

l), d

urin

g

At s

ight

, be

ginn

ing,

dur

ing

Afte

r, be

fore

, du

ring

Afte

r, du

ring

Begi

nnin

g,

durin

gDu

ring

Qual

ity o

r qua

ntity

of

mea

lN

DBu

lky

mea

ls, c

onve

ntio

nal

Indi

an m

eals

ND

ND

ND

ND

ND

ND

ND

Aura

(foc

al a

war

e)N

umbn

ess

ND

Forc

ed th

inki

ng

and

mem

orizi

ng,

visu

al

hallu

cina

tion

ND

ND

ND

ND

ND

ND

Eatin

g re

flex

seizu

re

type

At, F

BTC,

FO

IAFB

TC, F

O GT

CFB

TC, F

OA, F

OIA

FBTC

, FOA

, FO

IAFB

TC, F

OIA

FOA,

FOI

A,

FTBC

, GT

FBTC

, FOI

A GT

CFO

IA, G

TFO

IA

Radi

olog

ical

abn

orm

al

findi

ngs

(CT/

MRI

/PET

/SP

ECT)

ND

ND

NR

ND

MRI

: L

vent

ricul

omeg

aly,

R

retro

trigo

nal

hype

rinte

nsity

SPEC

T: M

e‑RT

lo

be fo

cal

hype

rper

f.

MRI

: non

eSP

ECT:

R‑F

hy

perp

erfu

sion

an

d R‑

stria

te

body

hyp

oper

f.

ND

MRI

: poo

r op

ercu

lum

fo

rmat

ion

with

th

icke

ned

Co

MRI

: B

peris

ylvi

an

poly

mic

rogy

ria

Elec

troen

ceph

alog

raph

ic

abno

rmal

find

ings

Inte

ricta

l EE

G:R‑

H: d

iffus

e,

unila

tera

l Spk

an

d Sh

w.

Gene

raliz

ed

disc

harg

es.

EEG:

L‑FT

Slw

Shw

.R‑

T Sw

v bu

rsts

.Ge

nera

lized

Spk

.

Inte

ricta

l EEG

: “p

ositi

ve”,

ED.

Inte

ricta

l EE

G:B‑

MT,

B‑P

oT

Shw

and

Slw

.

vEEG

: low

vo

ltage

slo

wed

ba

ckgr

ound

Icta

l vEE

G: h

igh

volta

ge S

lw +

di

ffuse

Slw

; R‑P

o Sh

‑Slw

Inte

ricta

l vEE

G:

R‑TF

, L‑T

pa

roxy

sm; R

‑T

ED

Icta

l vEE

G: h

igh

ampl

itude

del

ta

or th

eta

Inte

ricta

l EEG

: R‑

F Sp

and

Sh

w; R

‑O S

p

ND

Icta

l EEG

: di

ffuse

Spw

, ED

+ d

iffus

e at

tenu

atio

nIn

teric

tal E

EG:

gene

raliz

ed

Spk

or

poly

‑Spw

; R‑T

sl

owin

g an

d hi

gh a

mpl

itude

Sh

w S

lw

Icta

l EEG

: B‑T

lo

be o

nset

In

teric

tal E

EG:

B‑T

spik

ing;

L‑F

C Sp

k

Tabl

e 1.

Clin

ical

cha

ract

eris

tics,

dia

gnos

is, a

nd tr

eatm

ent o

f mai

n ca

se re

port

serie

s of

pat

ient

s w

ith e

atin

g ep

ileps

y (C

ontin

ued)

(Con

tinue

s)

199


Aut

hor/

year

Ahu

ja, 1

98023

Nag

araj

a, 1

98424

Koul

, 198

925Se

nana

yake

, 19

905

Lore

to, 2

00026

Nak

azaw

a,

2002

27Se

nevi

ratn

e,

2003

28La

bate

, 200

529Cu

kier

t, 20

1022

Trea

tmen

tCB

Z, P

B, P

HTCB

Z, P

B, P

HT, P

MD.

Av

oida

nce

of b

ulky

mea

ls.

CBZ,

PB,

PHT

. Us

e of

left

hand

an

d/or

spo

on.

CBZ,

CLB

, PH

T, P

MD

CBZ,

CLB

, GBP

, GV

G, L

TG, P

B,

VPA

CBZ,

CLB

, CLZ

, PH

T, V

PA, Z

NS,

Fe

d by

ano

ther

pe

rson

, red

uced

at

tent

ion

to th

e m

eal

CBZ,

VPA

ACTH

, CBZ

, CL

Z, G

VG, N

Z,

PB, V

PA

CBZ,

CLB

, PB,

OX

C, V

PA.

+ Va

gus

nerv

e st

imul

atio

n

Phar

mac

ores

ista

nce

ND

Pres

ent i

n 10

ND

Non

ePr

esen

t in

1Pr

esen

t in

1N

DN

DPr

esen

t in

thre

e

Surg

ery

Non

eN

one

ND

Non

eN

DN

DN

one

ND

R‑TO

rese

ctio

n;

L‑F

rese

ctio

n

Aut

hor/

year

Bae

, 201

130G

ujja

r, 20

1221

Pate

l, 20

1331

Koke

s, 2

0137

Shir

ai 2

01514

Jagt

ap, 2

01632

Von

Stül

pnag

el,

2019

2

Sing

h, 2

0194

Ata

lar,

2020

33

n2

56

62

478

122

Sex

(M/F

)1/

14/

13/

34/

21/

141

/64/

411

/11/

1

Eatin

g ep

ileps

y m

ean

age

onse

t (ye

ar)

39.5

23.6

20.6

2010

.516

313

.520

Trig

gers

Eatin

gEa

ting

Eatin

g, th

ough

of

food

Chew

ing

(pro

long

ed),

drin

king

, sw

allo

win

g,

taki

ng fo

od to

th

e m

outh

Chew

ing,

eat

ing

ND

Chew

ing,

ea

ting,

or

ofac

ial

stim

uli

Eatin

gEa

ting

Mea

l of t

he d

ayN

DLu

nch,

mid

day

mea

lN

DBr

eakf

ast,

dinn

er, l

unch

. Pa

rticu

larly

Su

nday

s

Brea

kfas

t, di

nner

, lun

chN

DN

DDi

nner

, lun

ch,

no

pred

ilect

ion

ND

Mom

ent o

f eat

ing/

mea

lAf

ter

(imm

edia

tely

), du

ring

At th

e m

iddl

e, a

t the

end

, du

ring

Begi

nnin

g, a

t the

m

iddl

eBe

ginn

ing,

du

ring

Begi

nnin

g,

durin

gAf

ter,

begi

nnin

g,

at th

e en

dN

DN

DN

D

Qual

ity o

r qua

ntity

of

mea

lN

DN

DRi

ce m

ade

food

Over

eatin

g,

past

ry/s

alty

fo

od, s

olid

fo

od

ND

Rice

, w

heat

‑bas

ed

diet

ND

ND

ND

Tabl

e 1.

Clin

ical

cha

ract

eris

tics,

dia

gnos

is, a

nd tr

eatm

ent o

f mai

n ca

se re

port

serie

s of

pat

ient

s w

ith e

atin

g ep

ileps

y (C

ontin

ued)

(Con

tinue

s)

200


Aut

hor/

year

Ahu

ja, 1

98023

Nag

araj

a, 1

98424

Koul

, 198

925Se

nana

yake

, 19

905

Lore

to, 2

00026

Nak

azaw

a,

2002

27Se

nevi

ratn

e,

2003

28La

bate

, 200

529Cu

kier

t, 20

1022

Aura

(foc

al a

war

e)Bl

urre

d vi

sion

, ja

mai

s‑vu

, pa

lpita

tions

, un

plea

sant

fe

ar.

ND

ND

Dysc

ogni

tive,

“e

xper

ient

ial”

ND

Ceph

alic

se

nsat

ion,

déj

à vu

, epi

gast

ric

risin

g se

nsat

ion,

fe

ar,

som

atos

enso

ry,

verti

go, v

isua

l,

ND

Ceph

alic

se

nsat

ion,

ep

igas

tric

sens

atio

n,

gidd

ines

s,

unea

sine

ss,

Epig

astri

c,

visu

al, v

ertig

o,

Eatin

g re

flex

seizu

re

type

A, F

BTC

FBTC

, FOI

A GT

CFO

FBTC

, FOA

, FO

IAFO

AFB

TC, F

OIA,

“H

D”Ab

, At,

EM,

GTC,

M, O

c,

To

FBTC

, FOI

A,

GTFB

TC, F

OIA

Radi

olog

ical

abn

orm

al

findi

ngs

(CT/

MRI

/PET

/SP

ECT)

MRI

: non

eCT

: non

eM

RI:

L‑M

eT s

cler

osis

, L‑T

: at

roph

y, c

ortic

al le

sion

,R‑

T ho

rn d

ilata

tion.

MRI

: L‑F

P pe

risyl

vian

co

rtica

l dy

spla

sia,

R a

nd

L Sy

lvia

n an

d pe

risyl

vian

gl

iosi

s, L

F ca

lcifi

ed

gran

ulom

a.SP

ECT:

F

hypo

perf.

; F, T

+

P‑in

sula

r hy

perp

erf.

MRI

:L‑

F‑EA

m

enin

giom

a,

L‑H

sequ

el

lesi

ons.

PE

T:L‑

MeT

, L‑L

aT,

O, a

nd

mul

tifoc

al

hypo

‑m

etab

olis

m.

MRI

: pon

tine

and

cere

bella

r hy

popl

asia

MRI

: PoT

PO

poly

mic

rogy

ria.

Perit

rigon

al

hype

rinte

nsiti

es,

pach

ygyr

ia,

glio

sis.

M

e‑T

scle

rosi

s.

T ca

vern

oma.

F

dysp

lasi

a.B

peris

ylvi

an,

MRI

:F

dila

tatio

n of

ext

erna

l sp

aces

of

CSF.

MRI

:B:

per

isyl

vian

gl

iosi

s.L‑

I‑F g

liosi

s.R‑

F pe

risyl

vian

sc

lero

sis,

R‑T

sc

lero

sis.

MIR

: “n

on‑s

peci

fic”

SPEC

T: L

‑T, L

‑I‑F,

and

R‑S‑

F hy

pope

rf.PE

T: R

‑T

hypo

met

abol

ism

.

Elec

troen

ceph

alog

raph

ic

abno

rmal

find

ings

Icta

l EEG

:L‑

T on

set o

f ge

nera

lized

rh

ythm

ic

thet

a an

d de

lta a

ctiv

ity.

Inte

ricta

l vE

EG:

B‑T:

Spk

.

Inte

ricta

l vEE

G:L‑

MT

onse

t of i

sola

ted

disc

harg

es.

Inte

ricta

l EEG

:R‑

FT, R

‑TP

gene

raliz

ed S

pk,

Shw

.

Icta

l EEG

: L‑P

T,

L‑FC

, R‑F

TC

slow

ing.

R‑F

CT

beta

, the

ta

activ

ity. L

‑FCT

Sh

wIn

teric

tal E

EG:

L‑C

thet

a w

v,

L‑FC

Shw

.

Icta

l EEG

on

set:

L‑FT

, L‑T

P.In

teric

tal

EEG:

L‑FT

, L‑P

T,

and

L‑T

Spk

and

slow

ing,

L‑

H sl

owin

g.R‑

TO S

pk a

nd

slow

ing.

Icta

l EEG

: Slw

(>

T);

nega

tive‑

posi

tive

pote

ntia

ls (>

F, m

idlin

e)In

teric

tal E

EG:

ED (>

MT,

PoT

), Sp

w

Icta

l vEE

GDi

ffuse

, F‑C

, Po

TPO

and

T ED

.In

teric

tal v

EEG:

Late

raliz

ed,

unce

rtain

, and

di

ffuse

ED.

vEEG

:B

(>O)

, B‑P

O Sp

w, B

‑O

slow

ed

back

grou

nd

activ

ity

(thet

a).

Diffu

se S

pk

and

Spw

.PO

slo

win

g.

Inte

ricta

l EEG

:B‑

Po E

D, B

pe

rirol

andi

c Sp

k.L‑

FT E

D, L

‑PoT

ED

with

se

cond

ary

gene

raliz

atio

n,

L‑T

Spk.

R‑CT

ED,

R‑P

o Sp

k.

Icta

l/Int

eric

tal:

R‑FT

slo

w a

nd

Spw

Trea

tmen

tCB

Z, L

EVCB

Z, C

LZ, L

EV, L

MT,

PB,

TP

M, V

PAN

DN

DCB

Z, C

LB, L

TG,

LEV,

TPM

, VPA

, ZN

S

ND

CLB,

ESM

, LE

V, L

TG,

TPM

, VPA

, ZN

S

CBZ,

CLB

, LEV

, LC

M, O

XC,

PHB,

PHT

, TP

M, V

PA

CBZ,

LCM

, LEV

Tabl

e 1.

Clin

ical

cha

ract

eris

tics,

dia

gnos

is, a

nd tr

eatm

ent o

f mai

n ca

se re

port

serie

s of

pat

ient

s w

ith e

atin

g ep

ileps

y (C

ontin

ued)

(Con

tinue

s)

201


Aut

hor/

year

Ahu

ja, 1

98023

Nag

araj

a, 1

98424

Koul

, 198

925Se

nana

yake

, 19

905

Lore

to, 2

00026

Nak

azaw

a,

2002

27Se

nevi

ratn

e,

2003

28La

bate

, 200

529Cu

kier

t, 20

1022

Phar

mac

ores

ista

nce

ND

Pres

ent i

n 1

ND

Pres

ent i

n 5

Pres

ent i

n 2

Pres

ent i

n 16

Pres

ent i

n 6

ND

ND

Surg

ery

Non

eL‑

T lo

bect

omy

+ am

ygda

lohi

ppoc

ampe

ctom

yLe

sion

ecto

my

Non

eN

DYe

s (in

2)

Non

eN

DN

one

ACTH

: adr

enoc

ortic

otro

pic

horm

one;

At:

aton

ic; A

b: a

bsce

nse;

B: b

ilate

ral;

C: c

entro

; CBZ

: car

bam

azep

ine;

CES

: clu

ster

of e

pile

ptic

spa

sms;

CLB

: clo

baza

m; C

LZ: c

lona

zepa

m; C

o: c

orte

x; C

SF: c

ereb

rosp

inal

flui

d; C

T: c

ompu

teriz

ed to

mog

raph

y; D

A:

drop

atta

cks;

EA:

ext

ra‑a

xial

; ED:

epi

lept

iform

dis

char

ges;

EEG

: ele

ctro

ence

phal

ogra

m; E

M: e

yelid

myo

clon

ia; E

SM: e

thos

uxim

ide;

F: f

ront

al; F

OA: f

ocal

ons

et a

war

e; F

OAI:

foca

l ons

et im

paire

d aw

aren

ess;

FBT

C: fo

cal t

o bi

late

ral t

onic

‑clo

nic;

FC:

fro

nto‑

cent

ral;

fRM

I: fu

nctio

nal m

agne

tic re

sona

nce

imag

ing;

GBP

: gab

apen

tin; G

T: g

ener

alize

d to

nic;

GTC

: gen

eral

ized

toni

c‑cl

onic

; GVG

: vig

abat

rin; H

: hem

isph

ere;

HD:

hea

d dr

ops;

I: in

ferio

r; L:

left;

La:

late

ral;

LCM

: lac

osam

ide;

LEV

: le

vetir

acet

am; L

TG: l

amot

rigin

e; M

e: m

esia

l; M

: myo

clon

ic; M

RI: m

agne

tic re

sona

nce

imag

ing;

MT:

mid

‑tem

pora

l; N

D: n

o da

ta; N

R: n

o re

alize

d; N

Z: n

itraz

epam

; O: o

ccip

ital;

Oc: o

culo

ceph

alic

s; O

XC: o

xcar

baze

pine

; P: p

arie

tal;

PB: p

heno

barb

ital;

PET:

pos

ition

em

issi

on to

mog

raph

y; P

HT: p

heny

toin

; PN

ET: p

rimiti

ve n

euro

ecto

derm

al tu

mor

; Po:

pos

terio

r; PR

M: p

rimid

one;

R: r

ight

; sEE

G: s

tere

oele

ctro

ence

phal

ogra

phy;

Shw

: sha

rp w

ave;

Slw

: slo

w w

ave;

SPE

CT: s

ingl

e ph

oton

em

issi

on

tom

ogra

phy;

Sp:

spi

kes;

Spw

: spi

ke w

ave;

S: s

uper

ior;

T: te

mpo

ral;

To: t

onic

; TPM

: top

iram

ate;

vEE

G: v

ideo

elec

troen

ceph

alog

ram

; VPA

: val

proa

te; w

v: w

ave;

ZN

S: z

onis

amid

e.

Tabl

e 1.

Clin

ical

cha

ract

eris

tics,

dia

gnos

is, a

nd tr

eatm

ent o

f mai

n ca

se re

port

serie

s of

pat

ient

s w

ith e

atin

g ep

ileps

y (C

ontin

ued)

seizures;” followed by a discretionary selection of pub-lications. We included observational studies (such as case reports and case series) published between 1967 and 2020. Editorial notes, literature systematic reviews and clinical images were excluded from the study.

Results

In this review, we analyzed 18 case series and 23 case reports (Tables 1 and 2) and we included the case of a 40-year-old male patient with EE evaluated in our epilepsy clinic (T able 2).

Discussion

Due to the inherent limitations of the case report and case series, result heterogeneity is obvious, with the consequent weakness of the conclusions. Despite these limitations from the data not reported or speci-fied, the following information is relevant. We found that out of 237 patients, 126 were male and 61 were female (the sex of 50 patients was not specified by the author) with a resulting 2:1 ratio, highlighting the predominance among men. The reason why there is a clear predominance in males is unknown; we won-der if it has to do with the diagnosis approach, or if women are underdiagnosed or if there is a more com-plex pathophysiological explanation.

As for the type of seizures, the most frequently re-ported were the focal type with or without impaired awareness (Tables 1 and 2).

In both the case series and the case reports, the most common and constant trigger was by definition the act of eating itself2,4,11,13-19,21-24,26-31,33-38,42-46 but in some cases other stimuli were detailed such as chew-ing2,7,14,18,24,25,27,34,36, swallowing7,25,27,36, drinking7,24, seeing18,37,39,45, smelling11,37,39, and even thinking31,37 or talking37 about food. Orofacial stimuli2, taking food to the mouth7, hunger alone37, eating snacks24, and tasting food11 were also described.

In the case report series, other specific triggers to EE related to the type of food have also been described, including bulky meals, conventional Indian meals24, wheat-based diet, and on a rice-based diet31,32. Only 4 patients had a preference for a specific type of food (spicy food11, bread17, strawberry syrup42, and minced meat45). Furthermore, just a few authors specified the patient’s diet, so it remains unclear if EE has a relation to specific diet type.

MRI and CT findings were variable. Some abnor-malities were encephalomalacia, sclerosis,

202


(Con

tinue

s)

Tabl

e 2.

Clin

ical

cha

ract

eris

tics,

dia

gnos

is, a

nd tr

eatm

ent o

f mai

n ca

se re

ports

of p

atie

nts

with

eat

ing

epile

psy

Aut

hor/

year

Lavi

zzar

i, 19

6718

Ciri

gnot

ta, 1

97719

Robe

rtso

n, 1

97834

Fiol

, 198

635M

ateo

s, 1

99515

Kish

i, 19

9916

Sex

MF

MF

MM

Eatin

g ep

ileps

y ag

e on

set (

yr)

1216

1412

118

Trig

gers

At s

ight

, che

win

g,

eatin

gEa

ting

Chew

ing,

eat

ing

Eatin

gEa

ting

Eatin

g

Mea

l of t

he d

ayN

DM

eals

*m

ore

frequ

ent a

t br

eakf

ast

ND

Mor

e at

bre

akfa

stM

eals

ND

Mom

ent o

f eat

ing/

mea

lN

DBe

ginn

ing,

dur

ing

ND

Begi

nnin

gN

DN

D

Qual

ity o

r qua

ntity

of m

eal

ND

ND

ND

Non

eN

DN

D

Aura

(Foc

al A

war

e)N

DN

DLe

ft up

per l

imb

num

bnes

s an

d le

ft fa

cial

par

esth

esia

.

ND

ND

ND

Eatin

g re

flex

seizu

re ty

peFO

AFO

IA, H

DFO

AFO

IA, G

TCFO

, FTB

CFO

IA

Radi

olog

ical

abn

orm

al fi

ndin

gs

(CT/

MRI

/PET

/SPE

CT)

NR

NR

CT: R

ast

rocy

tom

a of

ba

sal g

angl

ia.

CT: n

one.

CT/M

RI: B

rola

ndic

op

ercu

la a

troph

y.M

RI: B

per

isyl

vian

m

alfo

rmat

ions

, po

lym

icro

gyria

.

Elec

troen

ceph

alog

raph

ic

abno

rmal

find

ings

EEG:

B‑F

sha

rp

trans

ient

s, p

ositi

ve

spik

es.

Inte

ricta

l EEG

: ge

nera

lized

slo

w

wav

es.

EEG:

infre

quen

t diff

use

spik

e‑w

ave

disc

harg

es. B

rief

low

‑vol

tage

fast

act

ivity

and

di

ffuse

pol

yspi

ke‑w

ave

disc

harg

es d

urin

g sl

eep.

Icta

l EEG

: diff

use

shar

p w

ave.

B:

low

vol

tage

fast

act

ivity

. R‑T

: ra

pid

activ

ity m

ediu

m v

olta

ge.

EEG:

R‑

FT fo

cal s

low

ing.

R‑

F de

lta fo

cus,

sp

ikes

, sha

rp w

aves

.

Icta

l vEE

G: g

ener

alize

d lo

w‑v

olta

ge fa

st fr

eque

ncie

s.

L ‑T

or R

‑T o

nset

spi

kes.

Inte

ricta

l EEG

:Ge

nera

lized

pol

yspi

ke w

ave.

R‑Po

, R‑M

T, L

‑Po,

L‑M

T sp

ikes

, and

sha

rp w

aves

.

Inte

ricta

l EEG

: R‑C

T sl

ow

Spk,

Slw

.Ic

tal v

EEG:

gen

eral

ized

low

‑vol

tage

atte

nuat

ion.

Inte

ricta

l EEG

: B‑C

P sy

nchr

onou

s Sh

w.

Trea

tmen

tPH

T, P

RMN

DPB

, PHT

CBZ,

CZP

, ESM

, PB,

PHT

, VPA

CBZ,

CLB

, VPA

ND

Phar

mac

ores

ista

nce

No

Yes

ND

Yes

No

Yes

Surg

ery

No

No

Fron

tal c

rani

otom

y +

subt

otal

rese

ctio

n of

lo

w‑g

rade

as

trocy

tom

a.

No

ND

ND

203


Tabl

e 2.

con

tinua

tion:

Clin

ical

cha

ract

eris

tics,

dia

gnos

is, a

nd tr

eatm

ent o

f mai

n ca

se re

ports

of p

atie

nts

with

eat

ing

epile

psy

(Con

tinue

d)

Aut

hor/

year

Dom

izio

, 200

620D

’Ors

i, 20

0736

El B

ouzi

di, 2

01037

Man

yam

, 201

038M

artín

ez, 2

01112

De

Palm

a, 2

01211

Sex

MM

FF

FM

Eatin

g ep

ileps

y ag

e on

set (

yr)

< 1

2544

2316

6

Trig

gers

Brea

stfe

edin

gCh

ewin

g, e

atin

g, s

wal

low

ing

At s

ight

, dis

cuss

ing

cook

ing,

eat

ing,

hu

nger

thou

ght o

r sm

ell o

f foo

d.

Eatin

gN

DEa

ting,

sm

ell,

tast

e, *

es

peci

ally

spi

cy fo

od.

Mea

l of t

he d

ayN

DLu

nch,

bre

akfa

st, d

inne

rDi

nner

, lun

ch, m

eals

, sn

acks

Mea

lsN

DN

D

Mom

ent o

f eat

ing/

mea

lAf

ter d

rinki

ng m

ilkN

DBe

ginn

ing,

dur

ing

ND

Begi

nnin

gN

D

Qual

ity o

r qua

ntity

of m

eal

Milk

ND

ND

ND

ND

ND

Aura

(Foc

al A

war

e)N

DN

DN

DN

DN

DN

D

Eatin

g re

flex

seizu

re ty

peDe

satu

ratio

n, c

yano

sis,

in

crea

se in

mus

cula

r to

ne.

At (g

ener

alize

d)FB

TC, F

OAFO

IAFO

ACE

S

Radi

olog

ical

abn

orm

al fi

ndin

gs

(CT/

MRI

/PET

/SPE

CT)

MRI

/CT:

non

eM

RI: B

ope

rcul

ar d

yspl

asia

+

corp

us c

allo

sum

hyp

opla

sia.

MRI

: L‑F

(pre

cent

ral)

hype

rinte

nsity

.M

RI: p

ost‑s

urgi

cal.

RMI:

none

RMI:

none

Elec

troen

ceph

alog

raph

ic

abno

rmal

find

ings

EEG:

R‑M

eT a

bnor

mal

w

aves

Icta

l EEG

: B‑A

n di

ffuse

Slw

Inte

ricta

l EEG

: diff

use

alph

a‑lik

e ba

ckgr

ound

+ L

‑TPO

th

eta

activ

ity a

nd S

pw.

Inte

ricta

l EEG

: non

e

*Ele

ctro

corti

cogr

aphy

: L‑

F op

ercu

lum

ep

ilept

iform

act

ivity

(a

nter

ior‑

infe

rior.

to

the

MRI

lesi

on)

Icta

l EEG

: del

ta a

ctiv

ity (>

F)In

teric

tal E

EG: L

‑H s

low

ing,

th

eta

and

delta

act

ivity

. L‑T

Sh

w.

Inte

ricta

l EEG

: F, C

ED.

Icta

l EEG

: diff

use

slow

‑wav

e co

mpl

ex, >

B‑

FC, f

ollo

wed

by

volta

ge a

ttenu

atio

n.

Trea

tmen

tPB

, ant

iaci

d th

erap

y (G

ER)

CBZ,

CLB

, CLZ

, LEV

, LTG

, OXC

, VP

ACB

Z, V

PALT

G, V

PAES

M, L

EV, V

PACL

B, V

PA, a

void

ance

of

spic

y fo

od.

Phar

mac

ores

ista

nce

No

Yes

Yes

No

No

Yes

Surg

ery

No

ND

‑Sub

tota

l res

ectio

n of

L‑

F op

ercu

lum

: Gra

de

IV g

liobl

asto

ma.

Post

‑res

ectio

n le

ft op

ercu

lar

PNET

.N

oN

o

(Con

tinue

s)

204


Tabl

e 2.

con

tinua

tion:

Clin

ical

cha

ract

eris

tics,

dia

gnos

is, a

nd tr

eatm

ent o

f mai

n ca

se re

ports

of p

atie

nts

with

eat

ing

epile

psy

(Con

tinue

d)

Aut

hor/

year

Sand

hya,

201

339Ko

ul, 2

01340

Silla

npää

, 201

441Lo

di, 2

01513

Bla

uwbl

omm

e, 2

01542

Koba

yash

i, 20

1643

Sex

MF

FM

FF

Eatin

g ep

ileps

y ag

e on

set (

yr)

8<1

<127

288

Trig

gers

Sigh

t or s

mel

l of f

ood

Brea

st fe

edin

gBr

east

feed

ing

Eatin

gEa

ting

Eatin

g

Mea

l of t

he d

ayN

DN

DN

DN

DN

DN

D

Mom

ent o

f eat

ing/

mea

lAt

sig

ht, b

efor

eBe

ginn

ing,

afte

rBe

ginn

ing

ND

ND

Begi

nnin

g, d

urin

g

Qual

ity o

r qua

ntity

of m

eal

ND

ND

ND

ND

Espe

cial

ly s

traw

berr

y sy

rup

ND

Aura

(Foc

al A

war

e)N

DN

DCr

ying

and

cou

ghin

gN

DN

DN

D

Eatin

g re

flex

seizu

re ty

peN

DFO

, GT

FBTC

CES

FOIA

CES

Radi

olog

ical

abn

orm

al

findi

ngs

(CT/

MRI

/PET

/SPE

CT)

MRI

: non

eIn

teric

tal S

PECT

: L‑

FPO

perfu

sion

ch

ange

s.Ic

tal S

PECT

: B‑F

TPO

perfu

sion

cha

nges

.

MRI

: non

eM

RI: n

one

MRI

: non

eM

RI: p

ost‑s

urge

ry

cavi

tyfM

RI: a

ctiv

atio

n of

B

insu

la, R

‑dor

sola

tera

l‑F‑

Co a

nd d

orso

late

ral‑

P‑Co

.

MRI

: cor

pus

callo

sum

dy

sgen

esis

, cer

ebel

lar

hypo

gene

sis,

cer

ebra

l as

ymm

etry

, po

lym

icro

gyria

, pe

riven

tricu

lar

hete

roto

pia,

clo

sed

lip

schi

zenc

epha

ly.

Elec

troen

ceph

alog

raph

ic

abno

rmal

find

ings

Inte

ricta

l vEE

G: L

‑FT

ED EEG‑

fMRI

: ED,

ac

tivat

ion

of L

‑FT

lobe

s, B

‑P re

gion

, M

e‑st

ruct

ures

(p

arac

entra

l lob

ule,

ca

udat

e, c

ingu

late

an

d m

edia

l fro

ntal

, lin

gual

and

med

ial

occi

pita

l gyr

us.

Inte

ricta

l EEG

: non

eEE

G: R

‑PoT

slo

win

gIn

teric

tal E

EG:

R as

ymm

etric

ba

ckgr

ound

act

ivity

of

low

er a

mpl

itude

an

d re

peat

ed

slow

‑wav

e di

scha

rges

Inte

ricta

l EEG

: slo

w

back

grou

nd a

ctiv

ity, p

oor

orga

niza

tion

Icta

l EEG

:F‑

C (>

LH) d

iffus

e irr

egul

ar

spik

e an

d sl

ow‑w

ave

com

plex

, som

e fo

llow

ed b

y de

lta rh

ythm

ic a

ctiv

ity fr

om

L‑FC

and

An

verte

x.

vEEG

: An

hipp

ocam

pus

spik

es. A

n in

sula

r in

frequ

ent

asyn

chro

nous

spi

kes.

sEEG

: AnI

insu

la

high

‑am

plitu

de s

pike

fo

llow

ed b

y lo

w‑

volta

ge h

igh‑

frequ

ency

di

scha

rge

with

se

cond

ary

spre

adin

g to

hi

ppoc

ampu

s an

d TC

o.

Inte

ricta

l EEG

: slo

w

back

grou

nd a

ctiv

ity

with

mul

tifoc

al s

pike

s L‑

H, R

‑CT

regi

on.

Icta

l EEG

: diff

use

larg

e tri

phas

ic p

oten

tials

>R

‑CTP

regi

on.

Trea

tmen

tN

DVP

APB

CLB

ND

LTG,

TPM

, VPA

Phar

mac

ores

ista

nce

ND

No

No

Yes

Yes

ND

Surg

ery

No

No

No

No

‑9 y

ears

bef

ore

EE: O

perc

ular

‑insu

lar

R‑ c

aver

nom

a re

sect

ion

‑Epi

leps

y su

rger

y: A

n in

sula

rese

ctio

n.

ND

(Con

tinue

s)

205


Tabl

e 2.

con

tinua

tion:

Clin

ical

cha

ract

eris

tics,

dia

gnos

is, a

nd tr

eatm

ent o

f mai

n ca

se re

ports

of p

atie

nts

with

eat

ing

epile

psy

(Con

tinue

d)

Aut

hor/

year

Lee,

201

644M

imur

a, 2

01745

Kisl

i, 20

1817

Ald

osar

i, 20

2046

Ruiz

-Leó

n, 2

020

(pre

sent

cas

e)

Sex

FF

FM

M

Eatin

g ep

ileps

y ag

e on

set (

yr)

6020

1930

20

Trig

gers

Eatin

gAt

sig

ht, e

atin

gEa

ting

Eatin

gEa

ting

Mea

l of t

he d

ayN

DN

DN

DN

DN

o pr

efer

ence

Mom

ent o

f eat

ing/

mea

lN

DBe

fore

, dur

ing

Mos

tly a

t the

be

ginn

ing

Mos

tly a

t the

beg

inni

ngM

iddl

e

Qual

ity o

r qua

ntity

of m

eal

ND

Spec

ially

min

ced

mea

tOn

ly w

hile

eat

ing

brea

dN

DOn

ly w

ith s

olid

food

Aura

(Foc

al A

war

e)Di

zzin

ess,

impa

ired

spee

chN

DN

DN

DDi

zzin

ess

Eatin

g re

flex

seizu

re ty

peFO

AFB

TC, F

OAFO

AFB

TC, F

OIA

FOIA

Radi

olog

ical

abn

orm

al

findi

ngs

(CT/

MRI

/PET

/SPE

CT)

MRI

: non

ePE

T: b

item

pora

l hy

pom

etab

olis

m (>

L)

ND

MRI

: B‑P

Co

ence

phal

omal

acia

ar

ea

MRI

/PET

: non

eM

RI: n

one

Elec

troen

ceph

alog

raph

ic

abno

rmal

find

ings

ND

Icta

l vEE

G:L‑

F to

MT:

rhyt

hmic

thet

a ac

tivity

follo

wed

by

gene

raliz

ed s

eizu

re p

atte

rn.

Icta

l EEG

: R‑F

T sh

arp

wav

e ac

tivity

Inte

ricta

l EEG

: non

e.

vEEG

: B‑T

ED.

Icta

l vEE

G: R

‑T rh

ythm

ic

activ

ity w

ithpe

risyl

vian

spr

eadi

ngsE

EG:

R‑An

MeT

, ins

ula,

am

ygda

la,

hipp

ocam

pus.

vEEG

: Int

erm

itten

t R‑H

slo

win

g w

aves

, pr

edom

inan

tly F

‑C a

nd w

ith n

o ep

ilept

iform

ab

norm

ality

.

Trea

tmen

tN

DN

DLE

VN

DOX

C

Phar

mac

ores

ista

nce

ND

ND

ND

Yes

No

Surg

ery

ND

ND

ND

R‑An

‑T lo

bect

omy

incl

udin

g M

e st

ruct

ures

(am

ygda

la,

uncu

s, h

ippo

cam

pus)

+

parti

al in

ferio

r ins

ulec

tom

y.

No

ACTH

: adr

enoc

ortic

otro

pic

horm

one;

At:

aton

ic; A

b: a

bsce

nse;

B: b

ilate

ral;

C: c

entro

; CBZ

: car

bam

azep

ine;

CES

: clu

ster

of e

pile

ptic

spa

sms;

CLB

: clo

baza

m; C

LZ: c

lona

zepa

m; C

o: c

orte

x; C

SF: c

ereb

rosp

inal

flui

d; C

T: c

ompu

tariz

ed to

mog

raph

y;

DA: d

rop

atta

cks;

EA:

ext

ra‑a

xtia

l; ED

: epi

lept

iform

dis

char

ges;

EEG

: ele

ctro

ence

phal

ogra

m; E

M: e

yelid

myo

clon

ia; E

SM: e

thos

uxim

ide;

F: f

ront

al; F

OA: f

ocal

ons

et a

war

e; F

OAI:

foca

l ons

et im

paire

d aw

aren

ess;

FBT

C: fo

cal t

o bi

late

ral t

onic

‑clo

nic;

FC

: fro

nto‑

cent

ral;

fRM

I: fu

nctio

nal m

agne

tic re

sona

nce

imag

ing;

GBP

: gab

apen

tin; G

T: g

ener

alize

d to

nic;

GTC

: gen

eral

ized

toni

c‑cl

onic

; GVG

: vig

abat

rin; H

: hem

isph

ere;

HD:

hea

d dr

ops;

I: in

ferio

r; L:

left;

La:

late

ral;

LCM

: lac

osam

ide;

LE

V: le

vetir

acet

am; L

TG: l

amot

rigin

e; M

e: m

esia

l; M

: myo

clon

ic; M

RI: m

agne

tic re

sona

nce

imag

ing;

MT:

mid

‑tem

pora

l; N

D: n

o da

ta; N

R: n

o re

alize

d; N

Z: n

itraz

epam

; O: o

ccip

ital;

Oc: o

culo

ceph

alog

yres

; OXC

: oxc

arba

zepi

ne; P

: par

ieta

l; PB

: ph

enob

arbi

tal;

PET:

pos

ition

em

issi

on to

mog

raph

y; P

HT: p

heny

toin

; PN

ET: p

rimiti

ve n

euro

ecto

derm

al tu

mor

; Po:

pos

terio

r; PR

M: p

rimid

one;

R: r

ight

; sEE

G: s

tere

oele

ctro

ence

phal

ogra

phy;

Shw

: sha

rp w

ave;

Slw

: slo

w w

ave;

SPE

CT: s

ingl

e ph

oton

em

issi

on to

mog

raph

y; S

p: s

pike

s; S

pw: s

pike

wav

e; S

: sup

erio

r; T:

tem

pora

l; To

: ton

ic; T

PM: t

opira

mat

e; v

EEG:

vid

eoel

ectro

ence

phal

ogra

m; V

PA: v

alpr

oate

; wv:

wav

e; Z

NS:

zon

isam

ide.

206


pachygyria, polymicrogyria, dysplasia, glioma, ven-triculomegaly, meningioma, cavernoma, astrocytoma, and other lesions2,4,7,14-16,21,22,26,29,31,32,34,36,37,43. Four authors reported positron emission tomography; three presented hypometabolism7,33,44, and one was nor-mal46. Five authors reported single-photon emission computed tomography that showed perfusion chang-es26,27,31,33,39. Two authors reported functional MRI showing activation of both insula and dorsolateral frontal and parietal cortex42 and the other showing left temporal, bilateral parietal, paracentral lobule, cingu-late, medial frontal gyrus, and lingual and medial occipital gyrus abnormalities39. EEG findings were highly variable and different in each patient (Tables 1 and 2). Two authors detailed stereoelectro-encephalography, finding affectation of the insula, hippocampus, and temporal cortex and/or amigda-la42,48]. One patient underwent electrocorticography with operculum activity37. Surgery was performed on 10 patients, consisting of left-temporal lobectomy and amygdalohippocampectomy21, right-temporo-occipital resection, left-frontal resection22, lesionectomy31, subtotal resection of low grade astrocytoma34, subto-tal resection of left-frontal operculum (grade IV glio-blastoma)37, anterior insula resection42, right-anterior-temporal lobectomy including mesial structures and partial inferior insulectomy46, and non-specified in two patients. Only three patients un-derwent vagus nerve stimulation22.

Furthermore, the presence or absence of pharma-coresistance was specified in 131 patients (55% of the reviewed patients), of which 45 (41%) presented phar-macoresistance although sex, age, or type of seizure predominance was not clear.

Conclusion

EE is not the most frequent type of RE and be-cause it can coexist with other epileptic syndromes, we speculate that EE may be under-diagnosed, so RE should be investigated in all patients with known epilepsy. It is our belief that semiology and specific activities during the eating process should be spec-ified in order to identify the possible physiological-eti-ological mechanism, which until the present day is unknown. Finally, EE can be a therapeutic challenge since each patient presents variability in age of on-set, type of stimuli and seizure, clinical course, find-ings in complementary studies, and response to management.

Funding

None.

Conflicts of interest

None.

Ethical disclosures

Protection of human and animal subjects. The authors declare that no experiments were performed on humans or animals for this study.

Confidentiality of data. The authors declare that they have followed the protocols of their work center on the publication of patient data.

Right to privacy and informed consent. The au-thors have obtained the written informed consent of the patients or subjects mentioned in the article. The cor-responding author is in possession of this document.

Supplementary data

Supplementary data are available at Revista Mexi-cana de Neurociencia online (www.revmexneurocien-cia.com). These data are provided by the corresponding author and published online for the benefit of the read-er. The contents of supplementary data are the sole responsibility of the authors.

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Eating epilepsy. A narrative review

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