Sindrome de Charles-Bonnet

Case ReportDiagnosis and Treatment of Psychiatric Comorbidity ina Patient with Charles Bonnet Syndrome

Jasper J. Chen1,2

1 Behavioral Health Services, Cheyenne Regional Medical Center, Cheyenne, WY 82001, USA2Department of Psychiatry, Geisel School of Medicine at Dartmouth College and Dartmouth-Hitchcock Epilepsy Center atDartmouth-Hitchcock Medical Center, Lebanon, NH 03756, USA

Correspondence should be addressed to Jasper J. Chen; [email protected]

Received 27 June 2014; Revised 7 October 2014; Accepted 17 October 2014; Published 6 November 2014

Academic Editor: Thomas Hyphantis

Copyright 2014 Jasper J. Chen.This is an open access article distributed under the Creative CommonsAttribution License, whichpermits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Background. A significant proportion of patients with neurological disorders may have comorbid psychiatric symptomology, whichmay be managed by primary outpatient neurologists. Referral to their psychiatric colleagues is mediated by available consultation-liaison units and according to clinical opinion. Aims of Case Report. We present the case of a patient whose initial referral toepilepsy clinic led to a workup which ultimately diagnosed her with nonepileptic seizures (NES). In the course of her follow-up, shedeveloped intractable headaches, and worseningmood symptoms and eventually exhibited Psychotic Features for which psychiatrybecame coinvolved in her care.Major Depression with Psychotic Features and Charles Bonnet syndromewere considered as a likelycomorbid diagnoses. Her pharmacologic management on venlafaxine and quetiapine eventually caused substantial ameliorationof her psychiatric symptomology as longitudinally followed by PHQ-9 and GAD-7 scores. Conclusion. Optimal evaluation andmanagement of mental illness in patients with complex neurologic symptomology may require independent evaluation andtreatment by psychiatrists when clinically appropriate.

1. Background

Charles Bonnet syndrome (CBS) is principally characterizedby complex visual hallucinations and ocular pathology caus-ing vision loss [1]. Other characteristics include insight intothe unreality of the perceptions, absence of mental disorders,and preserved cognitive status [2]. Cognitive impairment,stroke, or early Alzheimers disease may be predisposingconditions. Furthermore, albeit the hallucinations being clas-sically purely visual [3], a small minority of patients with CBShave reported concomitant auditory hallucinations. Patientswith CBS, especially when having comorbid psychiatricsymptomology and complex medical histories, may makediagnosis and treatment challenging. They may also oftenencounter significant mood symptoms more optimallyaddressed by psychiatrists.

2. Case Report

We present the case of a 66-year-old woman referred orig-inally to Dartmouth-Hitchcock Epilepsy Center in 2010 for

seizure disorder. In her 20s, she was involved in a motorcyclecollision for which she was hospitalized for one week. Noknown traumatic brain injury (TBI) was diagnosed.Then shedeveloped migraine headaches later, becoming more severein her 30s. Also in her 30s and 40s, she developed faintingepisodes. When she was standing for a long time, she wouldtumble down and get up. If she stood quickly, she would loseher vision.Thosewere diagnosed as syncope andwere presentall her life. It also seemed to run in her family.

Then, in 2007, she developed what she thought wereseizures.They occurredwhen she was lying in bed. She wouldwake up and shake in the middle of the night. She wouldnot lose consciousness. They were diagnosed as nonepilepticseizures (NES). Of note, the patient denied having any historyof trauma, stressful life events, or other current stressors thatmight have triggered spells.

The patient initiated levetiracetam but nevertheless con-tinued having events where she started whole-body shaking,lasting 5 to 10 minutes. She described having two recentevents where she only had shaking of her right hand, arm,and face. After this event, her eyes were closed and she was

Hindawi Publishing CorporationCase Reports in PsychiatryVolume 2014, Article ID 195847, 8 pageshttp://dx.doi.org/10.1155/2014/195847

2 Case Reports in Psychiatry

very tired and slept for several hours. She had two of thoseright-sided events. All other events previously have includedwhole body shaking.

In the summer of 2008, she had an event where she waswalking to the bathroom at night, she crashed down on thefloor, had raccoon eyes and bruises, and was hospitalizedelsewhere.There she had tilt table testing, which was positiveand she was diagnosed with syncope; however, she wasalso noted to be hypertensive. She was not started on anymedications during that outside hospitalization but wasadvised to sit at the edge of the bed and stand up slowly.

She also complained of having comprehension difficultiesand poor memory, citing difficulties doing the laundry. Attimes, she was incapable of using a coffee maker that shehas used for a long time and her husband confirmed thatthose events were more frequently occurring. She had notbeen sleeping very well and had difficulties concentrating.She denied feeling depressed. Physical exam found no cog-wheeling but falling diffusely with positive Rombergs and hereyes closed. She also had difficulties performing tandem gaitbut was able to walk on her heels and toes. The plan was forher to be admitted for video EEG (VEEG) monitoring and tohave neuropsychological testing.

VEEG monitoring six weeks later in April 2010 capturedmultiple NES but no episodes with ictal correlates. She wasdischarged with outpatient follow-up outside our institution.A year later, in March of 2011, she re-presented with the chiefcomplaints of headaches and did not have any significantNES spells. At this time, it was noted that while she didnot have psychiatric care, she was taking both citalopramand clonazepam as prescribed by her primary care physician(PCP).

Half a year later in September 2011, the patient was seenwith the chief complaint of headache as well as worseningdepth perception. She was prescribed topiramate for herheadaches and considered usage of amitriptyline, althoughpatient was concerned about possibility of weight gain as hadhappened in the past. The patient was counseled on non-pharmacologic treatments of both anxiety and sleep hygiene.Nine months later in June 2012, the patient first describedhavingmore frequent falls as well as worsened headaches. Forher symptoms, she was increased on topiramate prescribedhydroxyzine for moderate headaches and zolmatriptan formore severe headaches.The patient did not exhibit significantclinical improvement.

Then, in May 2013, the patient and her family describedhaving hallucinations nearly every night, which consisted ofthe patients witnessing other people talking to each other,but never to her directly. These people never talked to her ortold her to do things. She denied these as the typical audi-tory hallucinations worrisome of primary thought disordersconsisting of running commentary about the patients ownbehavior.The auditory hallucinations were also never presentin the absence of visual hallucinations. The visual hallucina-tions were nonhostile, but the patients emotions associatedwith them were of fear due to uncertainty of the intentionsof the people she was experiencing. However, she knew thatthese people werent really there and that when she turnedon the lights, they would disappear. She also described

episodes where she was confused and had wandered about.This happened in late February and again early March 2013.Although she had been living in the same house for 37 years,it did not feel like the same house to her.

Visual symptoms included seeing blue spots under myeyes on the left as well as on my hands. Fundoscopic examrevealed floaters. The patient reported seeing cracks in thewall when looking at a white wall. The patients husbandreported that she is becoming very forgetful. These halluci-nations were thought to be associated with nortriptyline, anddosage was reduced to 10mg PO at night. It was first thoughtand documented at the end of May 2013 that the patient mayhave a neurodegenerative disease especially given significantatrophy of her frontal lobes as evidenced on magneticresonance imaging (MRI). Four months later, her falls andheadaches continued, although now she was hearing voicesthat are not threatening. The goal had been to decrease hernightly clonazepam dosage to see if this would allow halluci-nations to improve. Of all her concerns, her headaches werecausing the most misery.

At this point, referral to embedded psychiatric clinicianwithin the neurology outpatient clinic occurred. The patientmet our newly established quality improvement referralcriteria by scoring above a certain threshold on depressionscreening. Shewas seen initially at the end ofNovember, 2013.In addition to confirming her history above, it was foundthat family history was significant for early-onset Alzheimersdisease in the patients brother. Physical exam did not findany cog-wheeling, rigidity, shuffling gait, or gait instability.Mental status exam revealed appearing younger than herstated age, anxious mood and flat affect, and thought contentrevealing the belief that there are migrant French-Canadianworkers at home threatening to hurtmy familymembers. Shehad seen them at least twice or thrice.

Her Montreal Cognitive Assessment (MOCA) scorewas 20/30 (score breakdown: 3/5 on visuospatial/executive:missed trails and did not get hands of clock correct; attention:5/6: missed serial 7 subtraction; language: 2/3: did not repeatsentences perfectly with regard to pronouns, singular versusplural; delayed recall: 0/5, but recalled all five with categorycuing; orientation: 5/6. Her PHQ-9 [4] and GAD-7 [5] scoreswere 7 and 9, resp.).

It was thought that it would be exceedingly rare, althoughnot impossible, for the patient to have a new-onset psychosisat this age. However, the patients description of her symp-toms was not classically Charles Bonnet syndrome, as sheexperienced real people talking and interacting in additionto just seeing them. We decided to re-do MRI and obtaindementia workup, including B12/folate, and other basic labs,which were all unremarkable.

At our second appointment severalmonths later, we againnoticed the constellation of visual hallucinations, cognitiveimpairment, and history of multiple falls despite not havingany clear Parkinsonian features on physical exam. At thisappointment, both the patient and her family were more sig-nificantly distressed by especially the auditory hallucinationscomponent of her experiences, described as little peoplethreatening to do things to me or my family. Her PHQ-9 andGAD-7 scores had worsened to 10 and 17, respectively. MRI

Case Reports in Psychiatry 3

was unchanged compared to a year ago. It was thought atthis time that the patients distressing symptoms as well aspsychotic symptoms could benefit from trial of quetiapine,to which the patient was nave. Concurrently, we aimed todecrease clonazepam dosage from 3mg to 2mg per day overseveral weeks.

At our 3rd appointment, a month later, the patient re-ported that everybody is noticing the difference with theSeroquel (quetiapine). In fact, she described no longer hav-ing any AVH. Her quetiapine dosage had been titrated toeffect to 200mg PO QHS. Her PHQ-9 and GAD-7 scoreswere both zero. Of particular significance was also that thepatient had tapered off clonazepam completely. As a result,both her headaches and her memory complaints had alsodecreased.The patient stated that since she was doing so well,she declined formal MOCA retesting.

However, at our 4th appointment, two months since theprevious one, the patient described having horrible head-aches and having hallucinations again, described as I seepeople in the bathroom dressed in regular clothes, and theyjust stand there without talking to me. The patient andher family did not seem to think that her headaches andhallucinations were connected. She also stated that sleep wasawful despite taking hydroxyzine, melatonin, and quetiapineconcurrently. We thus decided to transition her sertraline tovenlafaxine using cross-titration.

At our 5th appointment a month and a half later, thepatient had in the interim requested increasing quetiapinefrom 200 to 300mg PO at night, and she was noticeablyimproved with both increase of quetiapine and transitionfrom sertraline to venlafaxine. In fact, her headaches werenow gone completely and her mood symptoms were alsoimproved: The new medication is a happy pill! The patientdescribed having minimal auditory and visual hallucinationswhich were no longer bothering me.

Approximately 8 months following her initial presenta-tion, the patient described things as going very well: she wasno longer waking up in the morning with any headaches andfelt comfortable with seeing little happy faces at night wheneither falling asleep or waking up. At this point, the patientsvenlafaxine dosage was 225mg PO QDay and quetiapinedosage was between 300 and 400mg PO at night. Giventhe patients historical lack of depth perception and knownhistory of floaters, it was thought that Charles Bonnet syn-drome could be considered due to response of patients AH toquetiapine but not her visual hallucinations. The patient waseducated about the possibility that she had Charles Bonnetsyndrome in addition tomeeting criteria formajor depressivedisorder with Psychotic Features and she was reassured.

Ten to twelve months following her initial presentation,the patient described having a significant improvement inmood symptoms, and clinical exam and family collateralinformation indicated her Major Depression was in remis-sion. The patients medication dosages of venlafaxine 225mgdaily and 400mg quetiapine at night were stable and didnot cause any noticeable adverse effects, and discussionabout eventually trying to find theminimally effective doseespecially in the case of the latter medication, due to con-cerns for potential metabolic and extrapyramidal adverse

effectsensued, although the patient and her family wantedto continue the current dosage given lack of any psychiatricsymptoms.

3. Discussion

Our differential diagnosis was quite broad and includedepilepsy, nonepileptic seizures (NES), depression, anxiety,pseudodementia,mild cognitive impairment/Alzheimers de-mentia, Lewy-Body dementia (LBD), Parkinsons demen-tia, formal thought disorder/schizophrenia, headache, andCharles Bonnet syndrome.

The patients history of documented NES most likelyruled out the development of new-onset epilepsy at the age of70, although partial complex seizures could possibly accountfor her history of falls. However, the patient and her familysdescription of her NES made partial complex seizures lesslikely.

In line with the conceptualization of NES, there is a possi-bility that the patients episodes of confusion and wanderingalongside the feeling of unfamiliarity of her house mightrepresent dissociative phenomena, specifically depersonal-ization, which may be associated with psychosocial stressors,although the patient was not able to clearly identify anyknown stressors.

When the patient had MOCA scores completed, pseu-dodementia was initially considered given severity of docu-mented depression and anxiety. However, the patients abilityto perform the majority of her ADLs and IADLs as well ashaving no clinically apparent anomia, aphasia, or apraxiamade mild cognitive impairment or Alzheimers less likely.

Once the patient was found to have memory and cog-nitive impairment alongside fall frequency, the diagnosis ofLewy-Body Dementia was then considered. However, of theclinical symptomatic triad of fluctuating cognitive impair-ment, extrapyramidal features, and visual hallucinations, thepatient primarily had only the latter once her clonazepamwastapered and discontinued, making LBD less likely. Further-more, the patient did not demonstrate any extrapyramidalsymptoms or clinical sensitivity to quetiapine, an atypicalantipsychotic, which definitively goes against the diagnosis ofLBD.

The patients history of frequent falls and residual daytimegrogginess was most likely attributable to her usage of night-time clonazepam. Her history of myriad falls was initiallythought to be due to a combination of either NES or syncope,both previously diagnosed, and thus their attribution toParkinsonism was thought less likely. Much less likely wasthat the patient presented with 1st onset formal thoughtdisorder at the age of 70.

The patients once or twice monthly to near daily chronicheadaches or transformed migraines were associated withflashing lights, and so the notion that her vision was com-promised at baseline (problems with depth perception) wasnot on the forefront of our conceptualization towards thepossibility of Charles Bonnet Syndrome until much later inher clinical course.


Table1:Ch

rono

logicalsynop

sisof

signs

andsymptom

s,tentatived

iagn

oses,m

edicationchanges,andrespon

sestopsycho

pharmacologictre

atment.

Date

Sign

sand

symptom

s[Tentativ

ediagn

oses]and

(differentia

ldiagn

oses)

Psycho

pharmacologicand

nonp

sychop

harm

acologic

treatments,

ifany

Respon

sestotre

atments,

ifany

1970s

Motorcycle

collisio

nrequ

iring

onew

eeks

hospitalization.Nokn

ownTB

Iwas

diagno

sed.Notethe

largetim

elag

betweenthec

ollisionandthes

ymptom

sthatfollow.

[Postcon

cussiveh

eadache]

1980s

Severe

unilateralh

eadaches

[Migraines]

Amitriptylin

ePartialeffectiver

espo

nse,bu

tpatient

discon

tinueditdu

eto

significantw

eightgain

1990s

Faintin

gepiso

des.Whenthep

atient

stood

fora

long

time,shew

ould

tumbled

ownandgetu

p.Ifshes

tood

quickly,shew

ould

lose

herv

ision

.

[Syncopeappeared

tobe

familial]

2007

Thou

ghttobe

having

seizures.Th

eseo

ccurredwhenthe

patient

was

lyingin

bed.Shew

ould

wakeu

pandshake

inthem

iddleo

fthe

night.Nolossof

consciou

sness.

[Epilepsyversus

nonepilep

ticseizures]

Levetiracetam

Con

tinuedhaving

eventswhere

thep

atient

hadwho

le-bod

yshaking,lasting5to

10minutes

andalso

shakingof

herright

hand

,arm

,and

face.Following

events,

eyes

werec

losedandshe

was

very

tired

andsle

ptfor

severalh

ours.She

hadatleast

twoof

ther

ight-sided

events.

2008

Summer

Had

aneventw

hereshew

aswalking

totheb

athroo

mat

nightand

crasheddo

wnon

thefl

oor;sheh

adraccoo

neyes

andbruisesa

ndwas

hospita

lized

[Syn

cope

diagno

sedby

tilt-table

testing;sim

ultaneou

slyno

tedto

behypertensiv

e]

Not

started

onanymedications

durin

gthatho

spita

lizationbu

tadvisedto

sitatthee

dgeo

fthe

bedandsta

ndup

slowly.

2008

Fall

Firstcom

plainedof

having

comprehensio

ndifficulties

andpo

ormem

ory,citin

gdifficulties

doingthelaund

ry.

Attim

es,she

was

incapableo

fusin

gac

offee

maker

that

sheh

asused

fora

long

timea

ndherh

usband

confi

rmed

thatthosee

ventsw

erem

orefrequ

ently

occurring.Sheh

adno

tbeensle

epingvery

welland

had

difficulties

concentrating.Shed

eniedfeelingdepressed.

Physicalexam

foun

dno

cog-wheelingbu

tfallin

gdiffu

selywith

positiveR

ombergsandhere

yesc

losed.

Shea

lsohaddifficulties

perfo

rmingtand

emgaitbu

twas

ableto

walkon

herh

eelsandtoes.

[Pseud

odem

entia

versus

dissociativ

estateversus

adverse

effecttotre

atmentw

ithclo

nazepam]

Was

onclo

nazepam

durin

gthis

time


Table1:Con

tinued.

Date

Sign

sand

symptom

s[Tentativ

ediagn

oses]and

(differentia

ldiagn

oses)

Psycho

pharmacologicand

nonp

sychop

harm

acologic

treatments,

ifany

Respon

sestotre

atments,

ifany

April

2010

VEE

Gmon

itorin

gcaptured

onlyNES

.[N

ES]

Non

e

March

2011

Patient

re-presented

inou

tpatient

clinicw

ithchief

complaint

ofheadachesa

nddidno

thavea

nysig

nificant

NES

spells.

[Headaches;N

ES]

Whileshed

idno

thave

psychiatric

care,she

initiated

both

citalopram

andclo

nazepam

asprescribed

byherp

rimarycare

physician(PCP

).

Con

tinuedto

have

falling

episo

des,dissociativ

eepisodes.

Septem

ber2

011

Seen

inou

tpatient

neurologyclinicw

ithchief

complaint

ofheadache

andworsening

depthperceptio

n[H

eadaches;N

ES]

Prescribed

topiramatefor

headachesa

ndconsidered

amitriptylin

e,althou

ghpatient

was

concernedabou

tpossib

ility

ofweightgainas

hadhapp

ened

inthep

ast.Th

epatient

was

coun

seledon

nonp

harm

acologic

treatmentsof

both

anxietyand

sleep

hygiene.

June

2012

Firstd

escribed

having

morefrequ

entfallsas

well

asworsenedheadaches

[Headaches;N

ES]

Increasedon

topiramatea

ndinitiated

hydroxyzinefor

mod

erateh

eadaches

and

zolm

atrip

tanform

ores

evere

headaches.

Did

notexhibitsig

nificant

clinicalimprovem

ent

March

toMay

2013

Nightlyhallu

cinatio

nsconsistingof

witn

essin

gother

peop

letalkingto

each

other,bu

tnever

toherd

irectly.

Thesep

eoplen

ever

talked

tohero

rtoldhertodo

things.She

denied

thesea

sthe

typicalA

Hsw

orris

ome

ofprim

arythou

ghtd

isordersc

onsistin

gof

runn

ing

commentary

abou

tthe

patientsow

nbehavior.Th

eAHs

werea

lsoneverp

resent

inthea

bsence

ofVHs.Th

eVHs

weren

onho

stile,but

thep

atientsem

otions

associated

with

them

wereo

ffeard

ueto

uncertaintyof

the

intentions

ofthep

eopleshe

was

experie

ncing.How

ever,

she

knew

thatthesep

eoplew

erentreallythereand

thatwhenshe

turned

onthelights,they

wou

lddisapp

ear.

Shea

lsodescrib

edepiso

desw

here

shew

asconfused

andhadwanderedabou

t.Alth

ough

sheh

adbeen

livingin

thes

ameh

ouse

for3

7years,itdidno

tfeel

likethe

sameh

ouse

toher.

[Dissociativ

eepisodes,Major

Depressionwith

Psycho

ticFeatures](schizop

hrenia)

Thep

atient

andherfam

ilythou

ghtthatthe

hallu

cinatio

nswe

reassociated

with

nortrip

tylin

e,anddo

sage

was

redu

cedto

10mgPO

atnight

Nosig

nificantchanges

from

redu

ctionin

nortrip

tylin

e


Table1:Con

tinued.

Date

Sign

sand

symptom

s[Tentativ

ediagn

oses]and

(differentia

ldiagn

oses)

Psycho

pharmacologicand

nonp

sychop

harm

acologic

treatments,

ifany

Respon

sestotre

atments,

ifany

Novem

ber2

013

Scored

PHQ-9

greaterthan15

tobe

considered

for

evaluatio

nwith

embedd

edpsychiatric

clinician

with

inneurologydepartment.Ph

ysicalexam

didno

tfind

any

cog-wheeling,rig

idity,shu

fflinggait,

orgaitinstability.

MSE

revealed

appearingyoun

gerthanherstatedage,

anxiou

smoo

dandflataffect,and

thou

ghtcon

tent

revealingtheb

eliefthatth

erea

remigrant

French-C

anadianworkersatho

methreatening

tohu

rtmyfamily

mem

bers.Sheh

adseen

them

atleasttwice

orthric

e.MOCA

scoreo

f20/30.

[Pseud

odem

entia],(A

lzheimers,

CharlesB

onnetsyndrom

e)

Re-did

MRI

andobtained

dementia

workup,inclu

ding

B12/folate,and

otherb

asiclabs,

which

werea

llun

remarkable.

Janu

ary2014

Had

constellatio

nof

visualhallu

cinatio

ns,cognitiv

eim

pairm

ent,andhisto

ryof

multip

lefalls

despite

not

having

anycle

arParkinsonian

features

onph

ysical

exam

.Boththep

atient

andherfam

ilywerem

ore

significantly

distressed

byespeciallytheA

Hcompo

nent

ofhere

xperiences,described

aslittlep

eople

threateningto

dothings

tomeo

rmyfamily.

Worsening

PHQ-9

andGAD-7

scores.M

RIwas

unchangedcomparedto

ayeara

go.

[Major

Depressionwith

Psycho

ticFeatures,adverse

effect

ofclo

nazepam],(Lew

y-Bo

dydementia

,Alzh

eimers,and

Prim

aryTh

oughtD

isorder)

Itwas

thou

ghtatthistim

ethat

thep

atientsdistressing

symptom

sasw

ellasp

sychotic

symptom

scou

ldbenefit

from

trialofq

uetiapine,towhich

the

patient

was

nave.Con

currently,

wea

imed

todecrease

clonazepam

dosage

from

3mgto

2mgperd

ayover

severalw

eeks.

February

2014

Everybo

dyisno

ticingthed

ifference

with

theS

eroq

uel

(quetiapine).

Nolonger

hadanyAV

H.H

erqu

etiapine

dosage

hadbeen

titratedto

effectto200m

gPO

QHS.

Her

PHQ-9

andGAD-7

scores

wereb

oth0.As

aresult,

thep

atient

statedthatsin

ceshew

asdo

ingso

well,she

declinedform

alMOCA

retesting.

[Major

Depressionwith

Psycho

ticFeatures,inpartial

remission;medication-indu

ced

falls

anddaytim

egrogginessa

ndim

paire

dconcentration

associated

with

clonazepam]

Quetiapine

titratedto

effectto

200m

gPO

QHS.

Patient

hadalso

taperedoff

clonazepam

completely

.

Both

headachesa

ndherm

emory

complaintsh

adalso

decreased.

April

2014

Described

having

horribleheadachesa

ndhaving

hallu

cinatio

nsagain:Iseep

eopleintheb

athroo

mdressedin

regularc

lothes,and

they

juststa

ndthere

with

outtalking

tome.

Thep

atient

andherfam

ilydid

notseem

tothinkthatherh

eadaches

and

hallu

cinatio

nswerec

onnected.She

also

statedthat

sleep

was

awfuld

espitetaking

hydroxyzine,melaton

in,

andqu

etiapine

concurrently.

[Major

Depressionwith

Psycho

ticFeatures;C

harle

sBo

nnetsynd

rome]

Transitionedsertralin

eto

venlafaxineu

singcross-titratio

n.

May

2014

Headaches

were

nowgone

completely

and

herm

ood

symptom

swerea

lsoim

proved:Th

enew

medicationis

ahappy

pill!Th

epatient

describ

edhaving

minim

alauditory

andvisualhallu

cinatio

nswhich

were

nolonger

botheringme.

[Major

Depressionwith

Psycho

ticFeatures,inremission;

migraines,currentlyin

remission;Ch

arlesB

onnet

synd

rome]

Patient

andfamily

hadrequ

ested

trialofincreasingqu

etiapine

from

200to

300m

gPO

atnight;

titratedvenlafaxineu

pto

225m

gPO

daily.

Noticeableimprovem

entw

ithbo

thincreaseso

fquetiapine

and

transitionfro

msertralin

eto

venlafaxine


Table1:Con

tinued.

Date

Sign

sand

symptom

s[Tentativ

ediagn

oses]and

(differentia

ldiagn

oses)

Psycho

pharmacologicand

nonp

sychop

harm

acologic

treatments,

ifany

Respon

sestotre

atments,

ifany

June

2014

Things

areg

oing

very

well:

shew

asno

longer

waking

upin

them

orning

with

anyheadachesa

ndfelt

comfortablewith

seeing

littleh

appy

facesa

tnight

wheneither

falling

asleep

orwakingup

.Given

the

patientshisto

ricallack

ofdepthperceptio

nandkn

own

histo

ryof

floaters,itwas

thou

ghtthatC

harle

sBon

net

synd

romec

ould

beconsidered

duetorespon

seof

patientsAHto

quetiapine

butn

otherv

isual

hallu

cinatio

ns.

[Charle

sBon

netsyndrom

e;Major

Depressionwith

Psycho

ticFeatures]

Atthispo

int,thep

atients

venlafaxined

osagew

as225m

gPO

QDay

andqu

etiapine

dosage

was

between300and40

0mgPO

atnight.

Thep

atient

was

educated

abou

tthep

ossib

ilitythatsheh

adCh

arlesB

onnetsyndrom

ein

additio

nto

meetin

gcriteria

for

major

depressiv

ediso

rder

with

Psycho

ticFeatures

andshew

asreassured.

Septem

ber2

014

Sign

ificant

improvem

entinmoo

dsymptom

s,and

clinicalexam

andfamily

collateralinformation

indicatedherM

ajor

Depressionwas

inremission.Th

epatientsmedicationdo

sageso

fvenlafaxine

225m

gdaily

and40

0mgqu

etiapine

atnightw

eres

tablea

nddidno

tcause

anyno

ticeablea

dverse

effects.

Thep

atient

was

nolonger

distr

essedby

theV

H.

[Charle

sBon

netsyndrom

e;Major

Depressionwith

Psycho

ticFeatures

inremission]

Disc

ussio

neventuallytrying

tofin

dthem

inim

allyeffectiv

edo

seespeciallyin

thec

aseo

fqu

etiapine,due

toconcerns

for

potentialm

etabolicand

extrapyram

idaladversee

ffects.

How

ever,the

patient

andher

family

desired

continuatio

nof

herc

urrent

medications

and

dosagesg

iven

lack

ofany

psychiatric

symptom

s.


The patients comorbid mood and anxiety symptoms aswell as her preexisting diagnosis of NESmade her psychiatricdiagnostic formulation particularly challenging. Further-more, while paranoid delusions are very rarely encounteredin patients with CBS, they have been known to be associatedwith the visual hallucinations experienced [6]. In our patientwhowas eventually tentatively diagnosedwith several comor-bid neurological diagnosesincluding headache, nonepilep-tic seizures, and Charles Bonnet syndromeattributing herpsychiatric symptomology parsimoniously to her knownneurological diagnoses provided context for psychopharma-cologic treatment.

It was thought that the patients cognitive status, auditoryhallucinations, and paranoid ideationwere unlikely attributa-ble to simply a diagnosis of Charles Bonnet syndrome. Rather,these clinical features indicated the severity of her psychiatricsymptoms such that the patient met diagnostic criteria formajor depressive disorder with Psychotic Features.

Our case therefore illustrates the evolution of a patientssymptomology and ultimate benefit of formal psychiat-ric management. Specifically, venlafaxine ameliorated ourpatients anxiety, depression, and headachewhether FDA-approved (anxiety and depression) or off-label (in the caseof headache). Quetiapine targeted the amelioration of heranxiety and AVH. Equally noteworthy was that the patientexhibited dramatic improvement following taper and even-tual discontinuation of clonazepam.

Given that the medication received by the patient wascomplex and evolved, please refer to Table 1a chronolog-ical synopsis of signs and symptoms, tentative diagnoses,medication changes, and responses to psychopharmacologictreatmentin order to clarify any drug-related side-effects.

4. Conclusion

Referral of this patient with complex neurological history toa co-located psychiatrist within the neurology departmentguided the diagnostic formulation and eventual diagnosesof the patients underlying medical and psychiatric comor-bidities. Therefore, optimal evaluation and managementof mental illness in patients with complex neurologicalsymptoms may require independent treatment by psychia-trists when clinically appropriate. Furthermore, psychiatriccomorbidities of patients with neurological disorders maybe more optimally addressed by dedicated psychiatrists co-located within neurology clinics in order to reduce utilizationand prevent avoidable reencounters [7, 8]. We advocate formore standardized referral procedures including baselineand longitudinal screening of psychiatric comorbidity usingvalidated instruments for patients seen in neurology clinics.

Conflict of Interests

The author declares that there is no relevant financial, ethical,or professional conflict of interests.

Authors Contribution

Jasper J. Chen oversaw the case report in its entirety and isfully responsible for content.

References

[1] R. J. Teunisse, J. R. Cruysberg, W. H. Hoefnagels, A. L. Verbeek,and F. G. Zitman, Visual hallucinations in psychologicallynormal people: charles Bonnets syndrome,TheLancet, vol. 347,no. 9004, pp. 794797, 1996.

[2] A. P. Schadlu, R. Schadlu, and J. B. Shepherd III, Charles Bon-net syndrome: a review, Current Opinion in Ophthalmology,vol. 20, no. 3, pp. 219222, 2009.

[3] G. J. Menon, I. Rahman, S. J. Menon, and G. N. Dutton, Com-plex visual hallucinations in the visually impaired: the CharlesBonnet syndrome, Survey of Ophthalmology, vol. 48, no. 1, pp.5872, 2003.

[4] K. Kroenke, R. Spitzer, and J. Williams, The PHQ-9: validity ofa brief depression severity measure, Journal of General InternalMedicine, vol. 16, no. 9, pp. 606613, 2001.

[5] R. L. Spitzer, K. Kroenke, J. B.W.Williams, and B. Lowe, A briefmeasure for assessing generalized anxiety disorder: the GAD-7, Archives of Internal Medicine, vol. 166, no. 10, pp. 10921097,2006.

[6] C. Makarewich and D. A. West, Charles bonnet syndrome-induced psychosis? visual hallucinations with paranoid delu-sions in a visually-impaired man, Journal of Neuropsychiatryand Clinical Neurosciences, vol. 23, no. 4, pp. 615, 2011.

[7] T. A. Caller, J. J. Chen, J. J. Harrington, K. A. Bujarski, and B.C. Jobst, Predictors for readmissions after video-EEG moni-toring, Neurology, vol. 83, no. 5, pp. 450455, 2014.

[8] J. Chen, T. Caller, J. Mecchella et al., Reducing severity of co-morbid psychiatric symptoms in an epilepsy clinic using acolocation model: results of a pilot intervention, EpilepsyBehavior, vol. 39, pp. 9296, 2014.

Submit your manuscripts athttp://www.hindawi.com

Stem CellsInternational

Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014


MEDIATORSINFLAMMATION

of


Behavioural Neurology

EndocrinologyInternational Journal of



Disease Markers


BioMed Research International

OncologyJournal of



Oxidative Medicine and Cellular Longevity


PPAR Research

The Scientific World JournalHindawi Publishing Corporation http://www.hindawi.com Volume 2014

Immunology ResearchHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014

Journal of

ObesityJournal of



Computational and Mathematical Methods in Medicine

OphthalmologyJournal of


Diabetes ResearchJournal of



Research and TreatmentAIDS


Gastroenterology Research and Practice


Parkinsons Disease

Evidence-Based Complementary and Alternative Medicine

Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com

Documents

Sindrome de Charles-Bonnet