Sindrome de Charles-Bonnet
description
Transcript of 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.
-
4 Case Reports in Psychiatry
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
-
Case Reports in Psychiatry 5
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
-
6 Case Reports in Psychiatry
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
-
Case Reports in Psychiatry 7
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.
-
8 Case Reports in Psychiatry
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
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
MEDIATORSINFLAMMATION
of
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Behavioural Neurology
EndocrinologyInternational Journal of
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Disease Markers
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
BioMed Research International
OncologyJournal of
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Oxidative Medicine and Cellular Longevity
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
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
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Computational and Mathematical Methods in Medicine
OphthalmologyJournal of
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Diabetes ResearchJournal of
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Research and TreatmentAIDS
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Gastroenterology Research and Practice
Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Parkinsons Disease
Evidence-Based Complementary and Alternative Medicine
Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com