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Case ReportA Case Study of Intractable Vomiting with Final Diagnosis ofNeuromyelitis Optica

Rachel Bramson1,2 and Angela Hairrell1

1College of Medicine, Texas A&M Health Science Center College of Medicine, Bryan, TX 77807, USA2Family Medicine, Scott and White University Clinic, College Station, TX 77845, USA

Correspondence should be addressed to Rachel Bramson; [email protected]

Received 30 June 2015; Accepted 21 September 2015

Academic Editor: Denis A. Cozzi

Copyright © 2015 R. Bramson and A. Hairrell. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properlycited.

This case study presents a patient living in a suburban/rural community who received appropriate referral to secondary and tertiarycare for nausea and vomiting, accompanied by waxing and waning neurological symptoms, yet proved difficult to diagnose. Thispatient is presented to draw attention to a rare neurological disorder which should be included in the differential diagnosis of nauseaand vomiting with some key neurological complaints, even in the absence of physical findings.

1. Introduction

When a previously healthy adolescent presents with nau-sea and vomiting, the most common diagnoses are viralgastroenteritis or pyelonephritis. Vague waxing and waningneurological symptoms in an adolescent may be attributed tostress or developmental issues. Here we present a patient liv-ing in a suburban/rural community who received appropriatereferral to secondary and tertiary care, yet proved difficultto diagnose. This patient is presented to draw attention toa rare neurological disorder which should be included inthe differential diagnosis of nausea and vomiting with somekey neurological complaints, even in the absence of physicalfindings. Physical findings may develop late in the course ofthe diseasemaking a heightened index of suspicion importantfor early diagnosis and treatment.

2. Patient Presentation

The patient is a 17-year-old African-American female, mul-tisport athlete in 11th grade in a rural high school. She is thesecondof four children and lives at homewith her parents andtwo siblings. She gets Bs and Cs in school and is extremelywell-liked by teachers and fellow students. She presentedto Urgent Care with abdominal pain, nausea, and vomitingwith a 19 lb. unintentional weight loss over a three-month

period and BMI of 20. Her past medical history revealednormal development, immunizations being up to date, andpyelonephritis at age 14 for which she was hospitalized. Shehad no past surgeries and no history of alcohol, tobacco, ordrug use. Her parents and siblings are healthy.

3. Clinical Findings

On initial presentation, the patient appeared healthy with nonotable physical findings. She was discharged on Zofran anda clear liquid diet. On a follow-up two days later she hadmild epigastric tenderness on physical exam and describeda problem with shaky hands and back pain radiating into theright leg off and on, worse when she runs. The neurologicalexam was normal. CBC and CMP were normal with theexception of low WBC 3400 and sodium 134. TSH waslow normal (0.5). On Beck’s Anxiety Inventory she scored11 (mild), and on Beck’s Depression Inventory she scored 1(negative).

4. Timeline

Due to the protracted course of this patient’s illness andworkup, Table 1 details her visits and care over a three-monthperiod. The following is a brief summary of her clinicalpresentation.

Hindawi Publishing CorporationCase Reports in PediatricsVolume 2015, Article ID 291390, 7 pageshttp://dx.doi.org/10.1155/2015/291390

2 Case Reports in Pediatrics

Table1:Timelineo

fpresentationanddiagno

sis.

Date

Chiefcom

plaint/history

Con

sultant

Diagn

ostic

study

Find

ings

andtre

atment

9/7/2014

Urgentcarev

isit(i)

Vomiting

(ii)U

nintentio

nalw

eightloss

Prim

arycare

Prescribingon

dansetronandfollo

w-upwith

PCPforw

eightloss

9/9/2014

PCPfollo

w-up

office

visit

(i)Gastritis

(ii)W

eightloss

(iii)Ortho

statichypo

tension

(iv)Intermittentright

lower

back

pain

with

radiationinto

ther

ight

leg

Prim

arycare

(i)Be

ck’sAnx

ietyandDepressionInventory

(ii)C

BC,C

MP

(iii)LipidPanel

(iv)T

SH

(i)Mild

anxiety

(ii)N

odepressio

n(iii)Alllabs

norm

al(iv

)Normalreflexes,muscle

tone,

coordinatio

n

9/11/2014

ERvisit

(i)Vo

miting

(ii)D

ehydratio

n(iii)Weightloss

(i)Ch

estX

-ray

(ii)C

BC,C

MP

(iii)Urin

epregn

ancy

testandUA

(iv)E

SR(v)C

RP

(i)Allno

rmal,exceptlow

prealbum

inat18

andsodium

136

(ii)G

iven

IVflu

ids

(iii)Disc

harged

onprom

ethazine

for

vomiting

andnausea

9/14–9/22/2014

Com

mun

ityho

spita

ladmittance

with

samed

aytransfe

rto

child

ren’s

hospita

l

(i)Intractablev

omiting

(ii)W

eightloss

(iii)Hypertension

(iv)5

-day

histo

ryof

hiccou

ghs

Pediatric

GI

Rightu

pper

quadrant

ultrasou

ndSm

allamou

ntof

gallbladdersludge,no

gallstones

CTabdo

men

pelviswith

contrast

Normal

EGD

(i)H.P

ylorigastritis,biop

sydiagno

sis(ii)T

ripletherapywas

initiated,changed

toIV

duetopersistentn

auseaa

ndvomiting

,completed

Colon

oscopy

with

biop

sies

Noabno

rmalities

Pediatric

neph

rology

Urin

eVMA,R

enalultrasou

ndBo

thno

rmal

Pediatric

nutrition

(i)15%weightlossin3mon

ths

(ii)2

7thpercentilew

eightfor

age

(iii)32nd

percentiles

tature

fora

geNeurology

Normalstr

ength,tone,m

ovem

ent

Case Reports in Pediatrics 3

Table1:Con

tinued.

Date

Chiefcom

plaint/history

Con

sultant

Diagn

ostic

study

Find

ings

andtre

atment

DischargeD

iagnosis:

H.pylorigastritis

medica

tion:

TripletherapyforH

.pylori:clo

nidine

patch,pantop

razole,

sucralfate

9/28–10/4/2014

ERvisit/tr

ansfe

rto

child

ren’s

hospita

l

(i)Pancreatitis

(ii)H

ypertension

History:2fleetingepiso

deso

fblurry

visio

n,lightheadedness,pain,

itching

onleftsid

eoffaces

ince

9/24,syn

cope

on9/25

with

10-secon

dlossof

consciou

sness,

difficulty

follo

wingcommands

Pediatric

neurolog

y(i)

BrainCT

(ii)B

rain

MRI

(i)Bo

thNormal

(ii)N

ormalstr

ength,tone,m

ovem

ent

(iii)PT

consultfor

instabilityin

ambu

lation

Pediatric

GI

EGDwith

biop

syfore

mesis

(i)Gastricno

dularity,H.pylorip

ositive

(ii)L

ipase4

65–1498,Lacticacid

2.7elevated

Pediatric

neph

rology

Echo

Normal

Discharged

iagnosis:

Dehydratio

n,abdo

minalpain,intractablevomiting

,syn

cope,H

.pyloriinfectio

n,neurop

athicleft

facialpain

(worsenedon

gabapentin,sosto

pped)

Medica

tion:

Clon

idinep

atch

0.1m

g/24

hrweekly,pantop

razole40

mg2x

daily,sucralfate1g

2xdaily

prn,

ondansetron8m

g2x

daily

prn

10/6/2014

PCPfollo

w-up

from

hospita

lization

(i)Pancreatitis

(ii)H

ypertension

History:lower

extre

mity

weakn

ess,

numbn

essinfin

gers,hyperesthesia

ofthefacea

ndhead,shaking

episo

des,feelingcold,m

omrepo

rts

symptom

sworsening

,had

“seizure”

inho

spita

l

(i)Lipase

(ii)W

estN

ileIG

GandIG

M(iii)ES

R(iv

)TSH

(i)Ph

ysicalexam

:normalreflexes,no

cranialn

erve

deficits,n

ormalmuscle

tone,

decreasedsensationin

extre

mities

(ii)L

absn

ormalexcept

elevatedlip

ase(277)

(iii)Coldintolerance

(iv)S

pells

(v)U

rgentreferraltoneurolog

y

10/7–9/2014

Office

visit

with

pediatric

neurolog

yresulting

inho

spita

lization

atchild

ren’s

hospita

l

History:shakingepiso

dessince

9/27

affectin

ghead

andup

per

extre

mities,occur

rand

omly,

last

second

swith

nopo

stictal

confusion,

pins

andneedles

sensationaffectin

gentirefacea

ndleftarm,itching

andbu

rningof

left

face

with

hyperpigmentatio

n,weakn

essrequirin

gwheelchair

Pediatric

neurolog

y,pediatric

GI,

adolescent

medicine,neurosurgery

Neurologicalexam

(i)Cr

anialn

ervesintact

(ii)S

ensatio

nintact

(iii)Bilateralup

pera

ndlower

extre

mities

(iv)R

ight

uppere

xtremity

strength5/5

(v)L

eftup

pere

xtremity

strength4/5

(vi)Pron

ator

drift

(vii)

Bilaterallower

extre

mities

4/5

(viii)G

aitw

eakon

leftsid

e

Con

tinuo

us24-hr.VideoEE

GNormalin

awake,drow

sy,sleepingsta

tes;7

episo

desw

ithno

EEGcorrelate

EMGandNerve

cond

uctio

nstu

dyNormal

(i)Cerulop

lasm

in(ii)V

itamin

D(iii)Cortisol

(iv)L

ipase

(v)A

NAprofi

le(vi)En

trovirus

(i)Lo

w(ii)L

ow(iii)Normal

(iv)E

levatedlip

ase(771)

(v)N

egative

(vi)Negative


Table1:Con

tinued.

Date

Chiefcom

plaint/history

Con

sultant

Diagn

ostic

study

Find

ings

andtre

atment

DischargeD

iagnosis:

(i)Left-sid

edup

pera

ndlower

extre

mity

weakn

ess

(ii)S

pells

Medica

tions:

Vitamin

Ddeficiency,hydrocortison

ecream

,ond

ansetro

n,sucralfate,vitamin

D,m

ultiv

itamin,ranitidine

10/18

/2014

PCPf/u

hospita

lization

(i)Pain

inbilateralupp

erextre

mities,chest,

lowback

(ii)S

haking

Lipase

(i)Alm

ostn

ormal(126)

(ii)M

yalgias

(iii)Parasthesia

s(iv

)Spells

(v)T

remors

(vi)Hypertension

(vii)

Urgentreferraltopediatric

neurolog

y

10/23/2014

Pediatric

neurolog

y

(i)Pain

inbilateralupp

erextre

mities,chest,

lowback

(ii)S

haking

Pediatric

neurolog

y(i)

MRI

who

lespine,with

andwith

out

contrast(perform

edon

11/3)

(ii)N

eurologicalexam

(i)Trem

ors

(ii)P

arasthesias(face,arm

s,trun

k,legs)

(iii)Non

specificm

uscle

tend

erness,possib

leweakn

ess

(iv)R

eflexes

norm

al,dow

ngoing

plantar

Muscle

norm

albu

lk,ton

e,str

ength

(v)D

ecreased

cold

face

toT4

,decreased

pinp

rickface

totoes.

(vi)Re

cent

histo

ryof

pancreatitis

10/29/2014

pediatric

GIf/u

hospita

lization

Intractablev

omiting

Pediatric

GI

Serum

copp

erNormal

11/4/2014

PCPfollo

w-up

MRI

results

(i)MRI

cervicalspine

(ii)M

RIthoracicspine,lumbarspine,

sacrum

,coccyx

(i)4×3cysticdilatio

nof

thec

entralcanal

from

C5to

T2(ii)Increased

signalinthem

edulla

oblong

ataa

ndC2

toC5

,relativee

xpansio

nof

thec

ervicalspinalcord

(iii)Syrin

gomyelia

(iv)N

ormal

11/7/2014

pediatric

neurosurgery

Abno

rmalcervicalspineM

RIHistory:decreasedactiv

itydu

eto

neck

pain,diffi

culty

startin

gurination,

hand

tremor,w

eakn

essin

allextremities,num

bnessa

ndtin

glingin

leftleg

Pediatric

neurosurgery

Neurologicalexam

(i)Ab

norm

alreflexes,increasedmuscle

tone,clonu

sinbo

thfeet,spasticg

ait

(ii)N

omuscle

atroph

y,no

cranialn

erve

orsensorydeficit,

norm

alpo

sitionand

vibrationsense,no

rmalcoordinatio

n(iii)Po

ssiblemultilevelspinalcord

tumor

(iv)R

eferredto

2ndchild

ren’s

hospita

lneurosurgery


Table1:Con

tinued.

Date

Chiefcom

plaint/history

Con

sultant

Diagn

ostic

study

Find

ings

andtre

atment

11/16–25/2014

ERvisit

and

hospita

lization

atas

econ

dchild

ren’s

hospita

l

Possiblemultilevelspinalcord

tumor

Child

neurolog

y(i)

Lumbarp

uncture

(ii)M

RIcerv.spine

(i)CS

Fpo

sitivefor

neurom

yelitisop

tica

(NMO),WBC

18,R

BC3,gram

stain

cultu

renegativ

e,IgGindex0.6,oligoclonalbands

negativ

e,AC

E1.1,N

MDAreceptor

antib

ody

negativ

e;seropo

sitivefor

NMO.

(ii)E

xtensiv

ecervicalspine

long

itudinal

myelitis;

confl

uent

ill-defined,partly

enhancing,abno

rmalintram

edullary

signal

from

pontom

edullary

junctio

nthroug

hthe

lower

cervicalcord.N

oop

ticnerve

abno

rmality.

(iii)Dystonia

(iv)T

egretol300

mg3x

daily

(v)2

days

ofIV

IG(vi)5-daycourse

ofIV

methylpredn

isone,

discharged

onprednisone

taper

Discharged

iagnosis:

(i)Neuromyelitisop

tica(

NMO)

(ii)C

ervicalm

yelopathy

(iii)Dystonia

12/3/2014

Follo

w-upwith

pediatric

neurolog

y

(i)Neuromyelitisop

tica(

NMO)

(ii)C

ervicalm

yelopathy

(iii)Second

aryParoxysm

alKinesig

enic

Dyskinesia

(PKD

)(iv

)StartCellceptw

ithslo

wincrease

togoal

of1000

mgBID

1/22/2015

Follo

w-upwith

PCP

(i)Neuromyelitisop

tica

(ii)C

ervicalm

yelopathy

(i)Weightg

ainsin

ceNovem

bero

f34lb

(ii)T

akingmycop

heno

late,carbamazepine,

prednisone

(iii)Re

ferralto

ophthalm

olog

yforb

aseline

evaluatio

nandon

goingcare


Two days after her initial presentation, she presentedto the emergency room with vomiting and dehydration.Bloodwork and chest X-raywere unremarkable except for lowprealbumin. She was treated with IV fluids and dischargedon promethazine to relieve the nausea and vomiting. Threedays later, she presented with intractable vomiting and afive-day history of hiccoughs. She was admitted to thelocal hospital and transferred the same day to the regionalchildren’s hospital. She was discharged eight days later with abiopsy-proven diagnosis of H. pylori gastritis and hyperten-sion having had multiple imaging studies, upper and lowerendoscopy, and renal and nutrition consultation for 15%weight loss in three months. Neurological exams revealednormal reflexes, strength, tone, coordination, andmovement.Discharge medication included triple therapy for H. pylori,sucralfate, clonidine patch, and ondansetron.

Six days later, she presented to the emergency roomand was transferred back to the regional children’s hospitalfor pancreatitis and hypertension with additional history offleeting blurry vision and pruritus of the left face. Workupincluded a neurology consult, brain imaging, EGD withbiopsy, and echocardiogram, all unremarkable. Neuropathicfacial pain was added to her diagnoses. Treatment continuedunchanged.

In follow-upoffice visit twodays later, the patient’smotherinsisted she was having lower extremity weakness, shakingepisodes that looked like seizures, and hypersensitivity ofthe face and head. An urgent referral to neurology resultedin hospitalization at the regional children’s hospital. Neuro-logical exam showed slightly decreased strength of the leftupper extremity and bilateral lower extremities, pronatordrift, and gait weakness on the left side. Video EEG, EMG,and nerve conduction studies were unrevealing. Wilson’sdiseasewas ruled out.Thepatient was found to have a vitaminD deficiency, normal cortisol, and negative ANA.

Nine days later in follow-up with the primary careprovider, tremors were witnessed and the patient had intensepain of the bilateral upper extremities, chest, and low back.Urgent referral to pediatric neurology resulted in an order forMRI of the whole spine with and without contrast which wasperformed eight days later.The next day, the radiology resultswere described to the patient (increased signal in themedullaoblongata, between C2 and C5, and possible diagnosis ofsyringomyelia). Three days later she saw a pediatric neuro-surgeon who suspected a multilevel spinal cord tumor andreferred her to a tertiary care children’s hospital departmentof neurosurgery. Due to difficulty scheduling an outpatientconsultation, the patient presented to the emergency roomnine days later and was admitted for a possible multilevelspinal cord tumor.

5. Outcome

At the tertiary care children’s hospital, CSF from lumbarpuncture was NMO positive with 18 WBC, 3 RBC, gramstain and culture negative, IgG index 0.6, oligoclonal bandsnegative, ACE 1.1, and NMDA receptor antibody negative.MRI of the cervical spine revealed confluent ill-defined,partly enhancing, abnormal intramedullary signal from the

pontomedullary junction through the lower cervical cordwith no optic nerve abnormality (no syringomyelia or spinalcord tumor). She was also diagnosed with extensive cervicalmyelopathy and dystonia. She was started on carbamazepine,two days of IV IG, and five days of IV methylprednisone anddischarged on a prednisone taper.

Eight days later she followed up with pediatric neurologyand started mycophenolate with the goal of a 1000mg BID.She was noted to have Secondary Paroxysmal KinesigenicDyskinesia (PKD).

Six weeks later in a follow-up with her primary carephysician, she had gained 34 pounds and was doing well onmycophenolate, carbamazepine, and prednisone.

6. Patient Perspective

Mother’s perspective: I knew something was wrong with mydaughter. It was frustrating to have to ask for testing. I amglad that we finally got a diagnosis. Nowmy daughter ismuchbetter.

7. Discussion

Physicians involved in the management of this patient werediligent in efforts to reveal the underlying cause of intractablenausea and vomiting. Several factors contributed to thedifficulty of determining the correct underlying diagnosis. (1)Nausea and vomiting were the presenting problem for onemonth. (2) The patient’s neurological symptoms presentedlate and were vague and diffuse with only subtle findings onphysical exam. While her mother reported “shaking spells,”the tremors observed appeared to be a stress response. (3)Thenormal CT and MRI of the brain were falsely reassuring thata demyelinating disorder or other neurological disease wasnot the underlying cause. (4)The patient developed neck painlate in the course of her illness. The combination of tremors,paresthesias, nonspecific muscle tenderness, and weaknessled to whole spine MRI. The cervical spine MRI revealed theabnormal findings which allowed subsequent diagnosis.

This patient’s diagnostic workup also demonstrates acritical point about interpretation of abnormal spinal cordimages: a false diagnosis of spinal cord tumor can resultin unnecessary biopsy of the spinal cord. Fortunately, theneurosurgeon referred the patient to a tertiary care settingwhere further evaluation resulted in the correct diagnosis andtreatment.

Neuromyelitis optica (NMO) is an uncommon diseasesyndrome of the central nervous system (CNS) that affects theoptic nerves and spinal cord. Individuals with NMO developoptic neuritis (pain in the eye and vision loss) and transversemyelitis (weakness, numbness, and sometimes paralysis ofthe arms and legs), along with sensory disturbances and lossof bladder and bowel control [1–5].

NMO is distinguished frommultiple sclerosis by positiveserum autoantibody NMO-IgG, which targets aquaporin 4[6–11]. Over the last nine years, the aquaporin 4 serum testhas allowed identification of a wider spectrum of clinical andradiological characteristics associated with NMO.


In 2006 [3], diagnostic criteria were developed for arelated clinical syndrome, NMOSD (NMO Spectrum Disor-der). This requires NMO-IgG seropositive status in associa-tion with a limited form of NMO or a “signature clinical syn-drome,” such as intractable nausea, vomiting, or hiccoughs[5, 12, 13].

This patient demonstrates several typical findings ofNMO, presented here to encourage clinicians to identifythis unusual constellation of symptoms. NMO should beconsidered in the differential for intractable nausea andvomiting [13]. Analysis of a multicenter study by Mealy et al.[14] provides the best current characteristics of patients withNMO and NMOSD. This study examined 187 patients whowere diagnosed with NMO or NMODS at three nationallyknown medical centers distributed across the US.

Our patient shares several characteristics with patientsin the multicenter study. As in other autoimmune disorders,females predominate (6.5 : 1) [14]. African Americans wereoverrepresented at 37% [14], while they represent only 13.2%of the US population [15]. Additionally, of those patients inthe study with brain stem lesions (𝑛 = 30/187), 80% (𝑛 =24/30) were of African descent [14]. The disproportionateprevalence ofNMO inAfricanAmericans and their increasedincidence of brain stem lesions deserve further study. How-ever, while our patient was only 17, the median age of onset inthe study group was 40 years (range: 3–81) [14].

Other common manifestations of NMO were also notedin this patient [5]. For example, most patients with transversemyelitis due to NMO have extensive longitudinal involve-ment (≥3 vertebral segments), as did our patient. Additionallythere are reported cases of generalized pruritus early in thedisease [9, 16, 17]; this patient had focal pruritus of the leftcheek which became hyperpigmented due to inflammationand scratching. This was the only clue to the itching she wasexperiencing. This patient also developed hypertension.

NMOhas yet to receive funding for a nationalmulticenterconsortium; however, a five-year multicenter analysis in2012 [14] revealed several key features of the disease thatthis patient demonstrates. Pediatricians and other primarycare providers should be sensitized to the unusual present-ing symptoms of NMO to optimize early detection andtreatment. Early detection and treatment seem to improveprognosis and reduce relapse rate.

Conflict of Interests

The authors declare that there is no conflict of interestsregarding the publication of this paper.

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[14] M. A.Mealy, D.M.Wingerchuk, B.M. Greenberg, andM. Levy,“Epidemiology of neuromyelitis optica in the United States: amulticenter analysis,” Archives of Neurology, vol. 69, no. 9, pp.1176–1180, 2012.

[15] Centers for Disease Control and Prevention, “Minority health:Black and African American populations,” 2015, http://www.cdc.gov/minorityhealth/populations/REMP/black.html.

[16] R. Govindarajan and E. Salgado, “What is the true clinicopatho-logic spectrum of neuromyelitis optica?” JAMA Neurology, vol.70, no. 2, pp. 272–273, 2013.

[17] L. Elsone, T. Townsend, K. Mutch et al., “Neuropathic pruritus(itch) in neuromyelitis optica,” Multiple Sclerosis, vol. 19, no. 4,pp. 475–479, 2013.

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