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O B S T E T R I C S

Posterior reversible encephalopathy syndrome

in 46 of 47 patients with eclampsiaJustin Brewer, MD; Michelle Y. Owens, MD; Kedra Wallace, PhD; Amanda A. Reeves, MD; Rachael Morris, MD;

Majid Khan, MD; Babbette LaMarca, PhD; James N. Martin Jr, MD

OBJECTIVE: We sought to investigate the concurrence of posterior re-

versible encephalopathy syndrome (PRES) with eclampsia and to de-

scribe the obstetric, radiological, and critical care correlates.

STUDY DESIGN: This was a single-center, 2001-2010 retrospective

cohort study of all patients with eclampsia who underwent neuroimag-

ing via magnetic resonance imaging (MRI) or computerized tomography

(CT) with or without contrast.

RESULTS: Forty-six of 47 of eclamptic patients (97.9%) revealed PRES

on neuroimaging using 1 or more modalities: MRI without contrast, 41(87.2%); MRI with contrast, 27 (57.4%); CT without contrast,16 (34%);

CT with contrast, 7 (14.8%); and/or magnetic resonance angiography/

magnetic resonance venography, 2 (4.3%). PRES was identified within

the parietal, occipital, frontal, temporal, and basal ganglia/brainstem/

cerebellum areas of the brain. Eclampsia occurred antepartum in 23

patients and postpartum in 24 patients. Headache was the most com-

mon presenting symptom (87.2%) followed by altered mental status

(51.1%), visual disturbances (34%), and nausea/vomiting (19.1%). Se-

vere systolic hypertension was present in 22 patients (47%).

CONCLUSION: The common finding of PRES in patients with eclampsia

suggests that PRES is a core componentof thepathogenesis of eclamp-

sia. Therapy targeted at prevention or reversal of PRES pathogenesis

may prevent or facilitate recovery from eclampsia.

Key words: cerebral imaging, eclampsia, posterior reversible

encephalopathy syndrome

Cite this article as: Brewer J, Owens MY, Wallace K, et al. Posterior reversible encephalopathy syndrome in 46 of 47 patients with eclampsia. Am J Obstet Gynecol

2013;208:468.e1-6.

Posterior reversible encephalopathysyndrome (PRES) was first de-scribed in 1996 by Hinchey et al.1 In this

case series of 15 patients, the authors de-

scribed a condition markedby headache,altered mental status,seizures, andvisual

changes. These patients were also found

to display extensive white-matter changes

suggestive of posterior cerebral edema.

This group first named this syndrome re-

versible posterior leukoencephalopathy

syndrome, but it has also been known by

manyother names including PRES, hyper-

perfusion encephalopathy, brain capillary

leak syndrome, and hypertensive enceph-alopathy.1 PRES has been associated with

many conditions including eclampsia, se-

vere hypertension, autoimmune disease,

treatment with cytotoxic medications,

posttransplantation immunosuppression,

and infection with sepsis to name a few.2

Generalized seizures are often the

most common clinical manifestation of

PRES, but patients will also present with

signs of encephalopathy such as altered

mental status, headaches, nausea, and

vomitting.2-4 Visual disturbances are

also common, varying from mild blurry

vision to complete cortical blindness.3

Hypertension is associated with the ma-

jority of cases, although blood pressure

may be normal or only mildly elevated in

up to 20-30% of cases.5 Inthe seriesof 36

patients presented by Lee et al, 3 the

mean systolic blood pressure was 187

mm Hg (range, 80240 mm Hg) within

24 hours of presentation. Laboratory

findings can also vary, depending on theunderlying associated condition.

Neuroimaging findings of PRES have

been described in scores of eclamptic pa-

tients since the 1996 report of Hinchey etal,1 usually in single case reports or small

case series. How often PRES occurs inassociation with eclampsia is unknown.To our knowledge, there is no large pa-

tient series exploringthe relationship be-

tween eclampsia and the concurrence of

PRES. The purpose of this study was to

determine what percentage of eclamptic

women at our institution displayed find-

ings of PRES when neuroimagingstudies

were undertaken. We also soughtto deter-

mine which treatment modalities were

used to manage these patients and to ex-

plore how well these interventions had animpact on overall patient outcome.

MATERIALS AND METHODS

This project was a single-center, retro-

spective cohort study inclusive of the

years 2001-2010, which was approved by

the institutional review board at the Uni-

versity of Mississippi Medical Center.

Inclusion criteria were pregnancy or

within6 weeks postpartum;neuroimag-

ing via magnetic resonance imaging(MRI) or MRI and/or magnetic reso-

From the Division of Maternal-Fetal Medicine,Department of Obstetrics and Gynecology,Winfred L. Wiser Hospital for Women andInfants (Drs Brewer, Owens, Wallace, Reeves,Morris, LaMarca, and Martin), and theDepartment of Radiology andNeurology/Neurosciences (Dr Khan), Universityof Mississippi Medical Center, Jackson, MS.

Received Sept. 28, 2012; revised Jan. 4, 2013;accepted Feb. 5, 2013.

This study was supported by the Division ofMaternal-Fetal Medicine, Department ofObstetrics and Gynecology, University ofMississippi Medical Center.

The authors report no conflict of interest.

Reprints not available from the authors.

0002-9378/$36.00

2013 Mosby, Inc. All rights reserved.

http://dx.doi.org/10.1016/j.ajog.2013.02.015

Research www.AJOG.org

468.e1 American Journal of Obstetrics &Gynecology JUNE 2013
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nance angiography (MRA) and/or com-

puterized tomography (CT) performed

during hospitalization; and diagnosis of

eclampsia. Exclusion criteria included not

being pregnant or longer than 6 weeks

postpartum; no diagnosis of eclampsia;

MRI or MRA neuroimaging not per-

formed during hospitalization; diagnosis

of cerebral hemorrhage; known seizuredisorder; and later diagnosis of seizure

from a source other than eclampsia.

We investigated all women considered

to have eclampsia who underwent neu-

roimaging studies upon admission to

our tertiary care referral hospital. Cases

to be investigatedwere determined based on

a discharge diagnosis of eclampsia. The

appropriate charts were collected, and

the women who underwent neuroimag-

ing were selected for study. The majority

of these patients underwent imagingwithin the first 24 hours after admission.

The medical records of patients with ec-

lampsia who underwent cranial imaging

were identified, evaluated, and pertinent

data extracted. If neuroimaging was not

undertaken for an eclamptic patient, no

further data accrual was undertaken.

Imaging analysis

The imaging modalities used includedMRI, MRA, and CT both with and with-

out contrast. The diagnosis of PRES was

made by radiologists using the standard

radiological criteria for PRES. PRES has

a unique MRI and CT imaging appear-

ance, which is demonstrated as subcorti-

cal and gyral T2-weighted and fluid at-

tenuated inversion recovery (FLAIR)

signal hyperintensities that become

more diffuse as the extent of edema in-

creases. Focal areas include symmetric

multilobar/hemispheric edema with pre-dominant involvement of parietal and

occipital lobes. In addition, frontal lobes

and the inferior temporal-occipital junc-

tion are also focal areas, less commonly

the cerebellum.5 This group of women

included both antepartum and postpar-

tum eclampsia.

Statistical analysis

Maternal race, gravida, mode of delivery,

systolic hypertension, imaging modality,

site of lesions, and treatment modality

was analyzed via a 2 analysis. Maternal

age, body mass index (BMI), gestational

age at delivery, days in-house, and the

time to return to normalcy were ana-

lyzed using a Student ttest. Data are ex-

pressed as mean SD. A P .05 was

considered significant.

RESULTS

Forty-seven of 123 women considered to

have eclampsia (38.2%) underwent neu-

roimaging studies during the 10 year pe-

riod of 2001-2010 at our academic insti-

tution. The findings from all 47 patients

who underwent neuroimaging are re-

ported in the current study. Among the

47 study subjects were 23 women with

antepartum eclampsia and 24 women

with postpartum eclampsia. In cases of

postpartum eclampsia, on average, thepatient experienced her first seizure onday 6 (range, 0 14 days).

There was not a significant difference

in self-reported maternal ethnicity be-

tween women with antepartum and

postpartum eclampsia (P .729; Table

1). Neither were there anysignificant dif-

ferences in maternal age (P .506), ma-

ternal BMI (P .143), or gravidity (P

.777; Table 1) between the 2 groups.

Women who had antepartumeclamp-

sia primarily delivered via cesarean sec-tion (74%), whereas 67% of the women

with postpartum eclampsia had vaginal

deliveries (P .001; Table 1). Women

with antepartum eclampsia also deliv-

ered earlier than women with postpar-

tum eclampsia (P .002; Table 1) and

had a longer hospital stay than women

with postpartum eclampsia (P .026;

Table 1).

There was a significant difference in

systolic pressures between women with

antepartum or postpartum eclampsia(P .001; Table 1). Significantly more

TABLE 1

Patient demographics based on when seizure occurred

DemographicAntepartum, n (%)(n 23)

Postpartum, n (%)(n 24) Pvalue

Maternal race .729.....................................................................................................................................................................................................................................

African American 19 (83) 19 (79).....................................................................................................................................................................................................................................White 3 (13) 4 (17).....................................................................................................................................................................................................................................

Hispanic 1 (4) 1 (4)..............................................................................................................................................................................................................................................

Maternal age, y 21.21 4.56 22.37 6.97 .506..............................................................................................................................................................................................................................................

Maternal BMI, kg/m2 31.36 10.07 27.46 6.61 .143..............................................................................................................................................................................................................................................

Gravida .777.....................................................................................................................................................................................................................................

Nulliparous 12 (52) 13 (54).....................................................................................................................................................................................................................................

Multiparous 11 (48) 11 (46)..............................................................................................................................................................................................................................................

Gestational age, wks 31.7 4.44 36.6 4.83 .002..............................................................................................................................................................................................................................................

Mode of delivery .001.....................................................................................................................................................................................................................................

Vaginal 6 (26%) 16 (67%).....................................................................................................................................................................................................................................

Cesarean section 17 (74%) 8 (33%)..............................................................................................................................................................................................................................................

HTN (systolic), mm Hg .001.....................................................................................................................................................................................................................................

140 4 (17) 4 (17).....................................................................................................................................................................................................................................

140-159 10 (44)a 7 (29).....................................................................................................................................................................................................................................

160-180 6 (26) 13 (54)b.....................................................................................................................................................................................................................................

180 3 (13)c 0 (0)..............................................................................................................................................................................................................................................

Days in-house 5 4.01 2.79 2.41 .026..............................................................................................................................................................................................................................................

BMI, body mass index; HTN, hypertension.

a Significant compared with women with postpartum eclampsia; b Significant compared with women with antepartum eclampsia;c Significant compared with women with postpartum eclampsia.

Brewer. PRESand eclampsia. AmJ ObstetGynecol2013.

www.AJOG.org Obstetrics Research

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women with antepartum eclampsia

(44%) had systolic blood pressures be-

tween 140 and 159 mm Hg (P .039;

Table 1) compared with women with

postpartum eclampsia, whereas 54% of

women with postpartum eclampsia had

systolic blood pressures between 160and180 mm Hg, which was significantlymore compared with women with ante-

partum eclampsia (P .0001; Table 1).

In addition, no women with antepartum

eclampsia developed systolic pressures

greaterthan180mmHg,whereas13%of

women with antepartum eclampsia had

systolic pressures greater than 180 mm

Hg (P .002; Table 1). Allstudy subjects

had singleton gestations. There were no

maternal deaths in the current study.

Headache was the most common pre-senting symptom (87.2%) followed by

altered mental status (51.1%), visual dis-

turbance (34%), and nausea/vomiting

(19.1%). A diagnosis of PRES was made

in 46 of 47 women (97.9%) who were

considered to have eclampsia. This diag-

nosis was made using 1 or more imaging

modalities including MRI without con-

trast (n 41), MRI with contrast (n

27), CT without contrast (n 16), CT

with contrast (n 7), and/or MRA/

magnetic resonance venography(n

2).There was not a significant difference inthe imaging modality used when women

with antepartum eclampsia were com-

pared with women with postpartum ec-

lampsia (P .984; Table 2). Radiological

evidence of PRES was found in multiple

sites between women who developed ec-

lampsia in the antepartum (87%) and

postpartum (88%) periods. There was

not a significant difference in the site of

lesions between the 2 groups (P .705;

Table 2).Full data regarding the use of various

treatment modalities were available for

38 of the 47 patients (80.8%) and is re-

ported in Table 2. Magnesium sulfate

given as an initial intravenous bolus fol-

lowed by a continuous infusion was uti-

lized all of these women. Supplemental

therapies included intravenous antihy-

pertensives (labetalol, hydralazine, or ni-

fedipine), diuretic agents, and potent

glucocorticoids. The corticosteroids used

in these patients included either intrave-nous (IV) dexamethasone or betametha-

sone for enhanced fetal lung maturation

or maternal treatment for concurrent

hemolysis, elevated liver enzymes, and

low platelet count (HELLP) syndrome.6

There was a significant difference in

treatment modality, in which women

with antepartum eclampsia were treated

with steroids significantly (P .001)

more often than women with postpar-

tum eclampsia.

We made an intensiveeffort in this ret-rospective study to determine the length

of time that it took for these women to

return to normalcy following the initial

eclamptic seizure and whether the use of

various treatments altered this time pe-

riod. Normalcy was defined clinically as

the absence of visual problems, head-

ache, nausea/vomiting, or altered senso-

rium. The mean time from seizure to

normalcy was 36.5 hours when a diuretic

was given, 34.8 hours when antihyper-

tensives were given, and32.9 hours whencorticosteroids (IV dexamethasone) were

utilized (range, 9 135 hours forall inter-

ventions because the patients with the

shortest and longest stays received all 3

treatments). For the 19 patients who re-

ceived corticosteroids after the initial sei-

zure, the mean time between steroid ini-

tiation and a return to normalcy was 17

hours. The Figure demonstrates the time

to return to normalcy based on antepar-

tum and postpartum eclampsia. There

was not a significant difference betweenthe groups when magnesium sulfate was

administered (P .977),with or without

antihypertensives (P .955), diuretics

(P .778), or steroids (P .829;

Figure).

COMMENT

The present series of patients is the larg-

est single institutional series of imaged

eclamptic patients with evidence of

PRES in the United States that has beenpublished to date. Consistent with the

TABLE 2

Results for MRI and CT for patients with PRES

VariableAntepartum, n (%)(n 23)

Postpartum, n (%)(n 24) Pvalue

Imaging modality used .984.....................................................................................................................................................................................................................................

MRI without contrast 20 (87) 21 (88).....................................................................................................................................................................................................................................MRI with contrast 14 (61) 13 (54).....................................................................................................................................................................................................................................

CT without contrast 8 (35) 8 (33).....................................................................................................................................................................................................................................

CT with contrast 3 (13) 4 (17).....................................................................................................................................................................................................................................

MRA/MRV 1 (4) 1 (4)..............................................................................................................................................................................................................................................

Site of lesion .705.....................................................................................................................................................................................................................................

Occipital lobe 18 (78) 17 (71).....................................................................................................................................................................................................................................

Parietal lobe 17 (74) 19 (79).....................................................................................................................................................................................................................................

Temporal lobe 6 (26) 7 (29).....................................................................................................................................................................................................................................

Frontal lobe 12 (52) 17 (71).....................................................................................................................................................................................................................................Basal ganglia/cerebellum 5 (22) 6 (25).....................................................................................................................................................................................................................................

Multiple areas 20 (87) 21 (88)..............................................................................................................................................................................................................................................

Treatment modality used (results from 0.01938 patients reported).....................................................................................................................................................................................................................................

Magnesium sulfate 19 (100) 19 (100).....................................................................................................................................................................................................................................

Antihypertensives 17 (89) 16 (84).....................................................................................................................................................................................................................................

Diuretic 13 (68) 12 (63).....................................................................................................................................................................................................................................

Steriodsa 13 (68) 6 (32)..............................................................................................................................................................................................................................................

CT, computerized tomography;MRA/MRV, magneticresonance angiography/magnetic resonancevenography;MRI, magnetic

resonance imaging; PRES, posterior reversible encephalopathy syndrome.

a Women with antepartum eclampsia were treated with steroids significantly more often than women with postpartum eclampsia.

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recently published summary of current

knowledge about PRES by Sraykov and

Schwab,2 the current study revealed sev-

eral important findings that are suitable

for emphasis. First, advanced neuroim-aging techniques such as magnetic reso-nance imaging and/or computerized to-

mography indicated the presence of

PRES in every patient with eclampsia; a

single patient without evidence of PRES

was later determined to have an under-

lying seizure disorder. Second, although

headache (87%) and visual disturbance

(34%) were common symptoms presag-

ing eclampsia and PRES, they were not

universal nor was severe systolic hyper-

tension (47%) a constant feature. Third,PRES was identified often in multiple ar-

eas of the brain, not just the occipital re-

gion, consistent with the findings of oth-

ers.7 In addition, the results from this

study reconfirms a recent study from the

Mayo Clinic, in which all eclamptic pa-

tients who underwent imaging had clin-

ical and radiological findings of PRES.8

Of great importance, the authors be-

lieve that aggressive comprehensive and

meticulous medical management may

have been a factor in facilitating com-plete maternal recovery over a usually

brief hospitalization averaging 4 days

without a single maternal death.

The evidence from our report sup-

ports the hypothesis that PRES is the pri-

mary central nervous system injury inpatients with eclampsia. Some of thechanges in normal pregnancy include

substantially increased levels of vasoan-

giogenic growth factors and cytokines

into the maternal circulation. However,

during normal pregnancy the blood-brain

barrier (BBB) adapts to prevent these cir-

culating permeability factors from enter-

ing the brain and leading to vasogenic

brainedema.9,10 Interestingly plasmafrom

preeclampticwomenhasbeenfoundtoin-

crease BBB permeability, thereby suggest-ing that an increase in BBB permeability

could permit passage of damaging antiva-

sogenic and antiendothelial proteins into

thebrain to cause theneurological compli-

cations of eclampsia.11

Because not all patients with eclampsia

exhibit significant hypertension or sub-

stantialproteinuriapriortothefirstseizure

andbecausebrain imaging with MRIprior

toseizureineclampticwomenhasrevealed

evidence of vasogenic edema,12,13 the pri-

mary explanation for the pathogenesis ofneurological symptoms and cerebral

edema formation during eclampsia is that

it represents a form of PRES like that seen

in other disease processes such as hyper-

tensive encephalopathy.14

With PRES there is a loss of autoregu-

latory capacity, BBB disruption, and

subsequent vasogenic edema around ce-rebral arteries and arterioles.15,16 So-called normotensive eclampsia may ac-

tually represent a clinical state caused by

diminished autoregulatory capacity or

enhanced permeability of the BBB or

both.17-21 In addition, PRES has been

demonstrated in a patient with severe

preeclampsia without seizure, and it has

been demonstrated to precede eclamptic

convulsion.22 These findings are sugges-

tive of PRES as an antecedent to eclamp-

tic seizure as opposed to the result of aneclamptic seizure.

The cerebral pathology of patients

with severe preeclampsia who suffer sei-

zure(s) may be due to microangiopathy

of the cerebral vessels, often with hyper-

tension contributing. Microangiopathy

and/or malfunction of the cerebral vas-

culature may be related to circulating

levels of antiangiogenic factors such as

soluble fms-like tyrosine-1 (sFlt-1) and

soluble endoglin (sEng), which have

been demonstrated to be at higher levelsin patients with eclampsia comparedwith those with severe preeclampsia.23,24

In some animals exposed to high levelsof

sFlt-1 and sEng, researchers have ob-

servedchoroid plexuswith the loss of en-

dothelial fenestrae resembling the glo-

merular endotheliosis of preeclampsia.25

Interestingly, a study by Fugate et al26

found that 45% of women with PRES also

had autoimmune disease, which impli-

cates endothelial dysfunction as a possible

pathophysiological mechanism. Womenwith preeclampsia and animal models of

preeclampsia, in which endothelial dys-

function is a key feature, also have some of

the characteristics of autoimmune disease,

such as increases in interleukin-17 and T

helper 17 lymphocytes.27,28

Treatment of eclampsia, and thus

PRES, is best accomplished using mag-

nesium sulfate; however, the effect of

magnesiumsulfate in the prevention and

treatment of eclampsia likely is multifac-

torial.29-31

In the peripheral vasculatureor cerebrovasculature, magnesium sul-

FIGURE

Treatment modality does not affect the time to return to normalcy

The time to return to normalcy after the initial eclamptic seizure was compared between women with

antepartum eclampsia and women with postpartum eclampsia. Data from 38 patients was collected

and is represented as the mean time SD.

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fate may act as a vasodilator to decrease

peripheral resistance or relieve vasocon-

striction. In the central nervous system,

magnesium sulfate may also protect the

BBB and thereby limit cerebral edema

formation as well as act through a central

anticonvulsant action.

29

Control of hypertension is also con-sidered a core management component

for PRES treatment.2 Antihypertensive

treatment using intravenous labetalol,

hydralazine, or nicardipine is usually

recommended for the prevention of se-

vere systolic hypertension of more than

160 mm Hg and/or severe diastolic hy-

pertension of more than 105-110 mm

Hg.32,33 Gradual correction to target lev-

els of 140-155 mm Hg systolic and 90-

105 mm Hg diastolic are advisable toprotect the mother and to avert compro-

mised uteroplacental blood flow. Intra-

venousdexamethasone is widelyused for

the treatment of cerebral edema, espe-

cially in patients with intracranial tu-

mors because of its long biological half-

life, its low mineralocorticoid activity,

and its well-described effect in minimiz-

ing vasogenic peritumoral edema.34-36

In addition to these clinical data, stud-

ies in experimental animals have shown

that administration of IV dexametha-sone leads to a reduction of poststrokebrain edema.37 Thus, there is accumulat-

ing evidence to suggest a possible role for

potent glucocorticoids along with mag-

nesium sulfate and blood pressure con-

trol in pregnant patients with PRES/ec-

lampsia.38 This is supported by our

findings in the present study showing

faster normalization of central nervous

system function following eclampsia

when IV dexamethasone is given for

HELLP syndrome or intramuscular be-tamethasone is given to enhance fetal

lung maturation.

The current study used MRI and CT

imaging to identify the abnormal T2/

FLAIR signals associated withPRES.Dif-

fusion-weighted imaging is also capable

of distinguishing between vasogenic and

cytotoxic edema andcan be used to iden-

tify PRES. Differentiating the underlying

etiology of PRES based on imaging alone

is not possible at this time, despite the

advanced imaging techniques (ie, brainperfusion imaging, magnetic resonance

spectroscopy), but as the current study

and others have shown, neuroimaging in

conjunction with clinical diagnosis can

help identify eclamptic patients with

PRES.8

Our study shares the same shortcom-

ings of any retrospective investigation,including selection bias. Because of lo-gistical, cost, or consideration of value to

patient management in individual cases,

only 47 of 123 eclamptic patients had

neuroimaging requested by the physi-

cians who were caring for this patient

group. In addition, we do not have infor-

mation regarding women with severe

preeclampsia who had neuroimaging.

There was no consistent protocol in

place to direct who would or who would

not undergo neuroimaging, whichintro-duces a selection bias in regard to the pa-

tients who were neuroimaged; utiliza-

tion increased during the last half of the

decade that spanned the course of study

as greater interest in the information

provided led to more frequent ordering

of the test.

It is possible that a smaller percentage

of eclamptic patients may have exhibited

PRES had all patients been studied uni-

formly. Every medical record for pa-

tients discharged with a diagnosis of ec-lampsia were scrutinized carefully toidentify all those who underwent neuro-

imaging; the same research nurse re-

cordedthe data from themedical records

of all patients and the same physicians

(J.B. and A.A.R.) interpreted the radio-

logical reports for consistency and

accuracy.

Another limitation to our study is the

fact that radiologists were not blind to the

diagnosis of the patient because this study

was done retrospectively. Future studieswill include a reanalysis of images by a ra-

diologist blinded to patient diagnoses.

For patients with eclampsia/PRES,

critical care providers inclusive of obste-

trician-gynecologists and maternal-fetal

medicine subspecialists must be cogni-

zant of similar mechanisms of disease

development between eclampsia and

PRES. In the authors opinion, this

knowledge should be translated into a

rapidly initiated, comprehensive man-

agement program including intrave-nously infused magnesium sulfate,

blood pressure control, intensive mater-

nal-fetal surveillance, meticulous medi-

cal care, timely delivery, and potent glu-

cocorticoids, especially if evidence of

HELLP syndrome is also present.

Because PRES was found in almost

100% of patients with probable eclampsia,a randomized, prospective, placebo-con-trolled, and blinded trial is now underway

for patients with eclampsia to receive IV

dexamethasone or placebo soon after an

eclamptic seizure and to assess benefit if

anywhen givenin combination with mag-

nesium sulfate therapy. f

ACKNOWLEDGMENT

We thank Pamela Blake, the research nurse inthe Department of Obstetrics-Gynecology atthe University of Mississippi Medical Center, forher hard work in reviewing and collecting datafrom the patient charts.

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