ndersen er an - Gundersen Health System

Th e 

validity of clarke sign in assessing anterior knee pain 

Volume 5, Number 1 

July 2008 

Gundersen 

Lu t h e r a n 

M e d i c a l J o u r n a l 

original research article 

The Effect of Functional Exercise Training on Functional Fitness 

Levels of Older Adults 

reviews 

Childhood Onset of Anorexia Nervosa 

Wernicke Encephalopathy: Is the Gundersen Lutheran Alcohol 

Detoxification Protocol Sufficient? 

case reports 

African Tick Bite Fever and Crocodile Meat–Associated 

Salmonellosis Coinfection in a Returning Traveler 

The Tensilon Test: A Case Report 

History of medicine 

Surgeon General William A. Hammond (1828-1900): Successes 

and Failures of Medical Leadership 

reprise 

Carotid-subclavian Arterial Reconstruction: Concomitant Ipsilateral 

Carotid Endarterectomy Increases Risk of Perioperative Stroke 

Gundersen Lutheran Medical Journal • Volume 5, Number 1, July 2008 2

Th e 

Gu n d e r s e n 

Lu t h e r a n 

1 

M e d i c a l J o u r n a l 

Contents 

Editor’s Message 

David E. Hartman, PhD, BC-ANCDS(A) 

3 

LETTER TO THE EDITOR 

Response to “Civil War Medicine: The Toll of Bullets and Bacteria” 

Douglas Lanska, MD, MS, MSPH, FAAN 

4 

9 

13 

17 

19 

21 

29 

ORIGINAL RESEARCH ARTICLE 

The Effect of Functional Exercise Training on Functional Fitness Levels of Older Adults 

Denise Milton, MS, PT; John P. Porcari, PhD, RCEP; Carl Foster, PhD; Mark Gibson, MS, ATC, PT; Brian Udermann, 

PHD, ATC, FACSM; John Greany, PhD, PT 

REVIEWS 


Alissa R. Reierson; Daniel D. Houlihan, PhD 

Wernicke Encephalopathy: Is the Gundersen Lutheran Alcohol Detoxification Protocol Sufficient? 

Jennifer S. Mattingley, MD; Linda C. Groon, MD 

CASE REPORTS 

African Tick Bite Fever and Crocodile Meat–Associated Salmonellosis Coinfection in a Returning Traveler 

Swapna Narayana, MBBS; Leah I. Metz, MD; Todd J. Kowalski, MD 


Balaji Vishwanat, MD 

HISTORY OF MEDICINE 

Surgeon General William A. Hammond (1828-1900): Successes and Failures of Medical Leadership 

Jeffrey S. Sartin, MD; Douglas Lanska, MD, MS, MSPH, FAAN 

reprise 

Carotid-subclavian Arterial Reconstruction: Concomitant Ipsilateral Carotid Endarterectomy 

Increases Risk of Perioperative Stroke 

Gina M. Risty, MD; Thomas H. Cogbill, MD; Clark A. Davis, MD; Pamela J. Lambert, RN, BSN

editor 


Department of Neurology 

Speech Pathology 

managing editor 

Cathy Mikkelson Fischer, MA 

Gundersen Lutheran Medical Foundation 

editorial board members 

William A. Agger, MD, FACP 

Department of Internal Medicine 

Section of Infectious Disease 

Director of Research 


Robert H. Caplan, MD, FACP, FACE 


Section of Endocrinology 

David H. Chestnut, MD 

Department of Anesthesiology 

Director of Medical Education 


Associate Dean for the Western Academic 

Campus 

University of Wisconsin School of Medicine 

and Public Health 

Steven B. Pearson, MD, FACP 


Internal Medicine Residency Program Director 

Jeffrey S. Sartin, MD 



Mark L. Saxton, MD, FACS 

Department of Surgery 

Pediatric Surgery 

Brian E. Udermann, PhD, ATC, FACSM 

Department of Exercise and Sport Science 

University of Wisconsin–La Crosse 

support staff 

Deborah Brostrom 

Research Manager 


Sarah Fillbach 

Marketing & Communication Specialist 

Marketing & Corporate Communications 

Barb Beeson 

Graphic Designer 


Beth Frechette 

Marketing & Communication Specialist 


ad hoc reviewers 

Marlene A. Bannen, PhD 

Laurence C. Berg, MD 

Joseph B. Binegar, MD 

Wayne A. Bottner, MD, FACP 

Mark E. Domroese, MD, PhD 

Gregory G. Fischer, MD 

Ronald S. Go, MD 

Richard D. Hutter, MD 

Roger W. Kwong, MD 

Michael H. Mader, MD 

Amanda L. Strosahl, MD 

Kathy A. Trumbull, MD 


Gundersen Lutheran Medical Journal publishes material related to the life sciences. We welcome submission of original research, reviews, case reports, 

commentaries, and letters. Please consult our “Instructions for Authors,” provided on our Website, for submission and manuscript preparation 

guidelines. Direct questions or submit manuscripts for consideration to 

Gundersen Lutheran Medical Journal 


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1836 South Avenue 

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Telephone: (608) 775-6648 

Fax: (608) 775-1565 

Email: glmjeditor@gundluth.org 

Website: http://www.gundluth.org/journal 

Gundersen Lutheran Medical Journal is a peer-reviewed journal published by Gundersen Lutheran Medical Foundation, 

1836 South Avenue, La Crosse, WI 54601. Copyright 2008 by Gundersen Lutheran Medical Foundation. All rights reserved. 

Individuals may photocopy parts of the Journal for educational purposes. The Journal is archived on the Gundersen Lutheran Medical Journal Website. 

Permission for use of the Journal for other purposes must be obtained in writing from the Editor. Gundersen Lutheran Medical Journal accepts no 

responsibility for statements made by contributors.

Editor’s Message 

With this issue of the Gundersen Lutheran Medical Journal comes a change of season and 

a timely ode: 

Spring has sprung, 

The grass has riz, 

I wonder where the flowers is. 

The boid is on the wing— 

Absoid! 

Of course the wing is on the boid! 

— Anonymous, New York Times, March 1948 

This issue incorporates works by several authors from outside Gundersen Lutheran 

Health System. This may be a reflection, in part, of both the breadth of distribution and 

readership that the Journal provides. I would welcome any suggestions to help ensure that 

this trend continues! 

Dr Douglas Lanska, a practicing neurologist with Veterans Affairs Medical Center, 

Great Lakes Healthcare System, in Tomah, Wisconsin, comments on Dr Jeffrey Sartin’s 

article concerning Civil War medicine published in our last issue. Then Dr Lanska 

and Dr Sartin join forces to provide interesting insights into Dr William Hammond’s 

contributions to medical care during the 1800s. 

Ms Denise Milton and several colleagues from the University of Wisconsin–La Crosse 

offer both a timely and important original research project concerning exercise and 

functional fitness in older adults. I think many of you, particularly those who care for 

older patients, will find this report relevant to patient care. 

Ms Alissa Reierson and Dr Daniel Houlihan from the Minnesota State University – 

Mankato offer an interesting review of childhood anorexia nervosa that should have 

relevance for those caring for pediatric patients and their families. 

Drs Jennifer Mattingley and Linda Groon discuss Wernicke encephalopathy and 

challenge those who care for patients with alcohol addiction to examine the current 

intervention protocol. Congratulations also to Dr Mattingley, who will begin a 

fellowship in pulmonary medicine, critical care, and sleep medicine at Mayo Clinic on 

July 1. Upon completion of her training, Dr Mattingly will return to join Gundersen 

Lutheran’s staff. 

We have 2 thought-provoking case reports in this issue. Drs Swapna Narayana, Leah 

Metz, and Todd Kowalski report a case of African tick bite fever and salmonellosis, 

and Dr Balaji Vishwanat describes use of the Tensilon test for differential diagnosis of 

myasthenia gravis. 

Finally, this issue’s Reprise features a publication from the Department of Surgery. 

Authors Dr Gina M. Risty, et al published their article about the increased risks for 

1

perioperative stroke with carotid-arterial reconstruction and concurrent ipsilateral carotid 

endarterectomy in Surgery; we reprint it here with permission. 

I hope that you enjoy this issue of the Gundersen Lutheran Medical Journal . Your contributions 

are welcomed, encouraged, and needed to keep this periodical alive! Please feel free to contact me 

or Cathy L. Fischer, MA, Managing Editor, with your questions, concerns, or suggestions. 


Editor 


2 Gundersen Lutheran Medical Journal • Volume 5, Number 1, July 2008

William Hammond’s Contributions 

To the Editor: 

I 

read the interesting article by Jeffrey Sartin on Civil 

War medicine. 1 I would like to correct and augment the 

information concerning Surgeon General William Hammond. In 

particular, Hammond was instrumental in founding the American 

Neurological Association (ANA), not the Annals of Neurology. 2-6 

Hammond was a colorful and controversial character with 

both considerable attributes and faults 3-5 : “a brilliant organizer 

and administrator, an outstanding teacher and apostle of 

neurology, a mediocre but prolific scholar, and an audacious, 

contentious, boastful, and arrogant individual.” 3 Despite critics, 

Hammond made important contributions to military hygiene, 

the development of specialty hospitals and professional medical 

societies, and neurology in general. As Surgeon General of the 

Army during the Civil War, Hammond reformed the medical 

service of the Union army, actively promoted hygienic principles 

for soldiers, and established various specialty hospitals, including 

the US Army Hospital for Diseases of the Nervous System on 

Turner’s Lane in Philadelphia, where Mitchell, Morehouse, 

and Keen undertook their pioneering studies of nerve injuries. 3 

After the war, Hammond was appointed Professor of Diseases 

of the Mind and Nervous System at Bellevue Medical College, 

developed a thriving clinical practice in New York, helped foster 

the development of exclusive neurology specialty societies and 

medical journals, wrote the first American textbook of neurology, 

founded the New York State Hospital for Diseases of the Nervous 

System (1873), and worked tirelessly to enhance public awareness 

of neurology and neurological disease. 3,5 

Hammond was the primary impetus behind the founding of 

the ANA — the first national neurological association in the world 

and the sole professional organization that was critical to the early 

development of American neurology. 2-4,6 On December 14, 1874, 

in a letter to selected colleagues across the country, Hammond 

with 6 other founding members proposed the organization of the 

ANA, which was ultimately founded in 1875 with an additional 

29 charter members. Initial members were drawn primarily from 

New York, Boston, Philadelphia, and Chicago. At the first meeting 

in New York City, lasting 2 days, the scientific presentations 

included Hammond’s presentation of his original case of athetosis. 

Hammond later served as president of the ANA in 1882. 

From its inception, the ANA had a publication committee that 

directed the publication of the transactions of the annual meeting 

as a freestanding publication, the Transactions of the American 

Neurological Association. 2,3 These Transactions, published annually 

from 1875 to 1981, were meant to document the actual proceedings 

of the annual meeting and provide a forum for publication of 

articles in full format. The Journal of Nervous and Mental Diseases, 

which began in 1876 as a continuation of the Chicago Journal of 

Nervous and Mental Diseases, was also affiliated with the ANA at 

that time. The Journal of Nervous and Mental Diseases continues 

to the present, but was not associated with the ANA after 1918 

because it had shifted its orientation to psychoanalysis. The Annals 

of Neurology, which began in 1977 (ie, long after Hammond’s 

death), is now the journal affiliated with the ANA (as well as the 

Child Neurology Society). 3 

Douglas J. Lanska, MD, MS, MSPH, FAAN 

Staff Neurologist, Veterans Affairs Medical Center, Tomah, 

Wisconsin; Professor of Neurology, University of Wisconsin School 

of Medicine and Public Health, Madison; Chair, History Section, 

American Academy of Neurology, Minneapolis, Minnesota 

REFERENCES 

1. Sartin JS. Civil War medicine: the toll of bullets and bacteria. Gund Luth Med J. 

2007;4(2):79-83. 

2. Goetz CG, Chmura TA, Lanska D. Part 1: The history of 19th century neurology 

and the American Neurological Association. Ann Neurol. 2003;53 Suppl 

4:S2-S26. 

3. Lanska DJ. Development of neurology as a specialty in the United States. In: 

Lanska DJ, ed. AAN course 6PC.001: Historical Development of Neurology as a 

Specialty. Minneapolis, MN: American Academy of Neurology; 2007. 

4. Lanska DJ, Goetz CG, Chmura TA. Seminal figures in the history of movement 

disorders: Huntington, Osler, and Hammond: part 11 of the MDS-sponsored 

History of Movement Disorders Exhibit, Barcelona, Spain, June 2000. Mov 

Disord. 2001;16:749-753. 

5. Lanska DJ. William Hammond, the dynamometer, the dynamograph. Arch 

Neurol. 2000;57:1649-1653. 

6. Lanska DJ. Characteristics and lasting contributions of 19th-century American 

neurologists. J Hist Neurosci. 2001;10:202-216. 

Editor’s Note: Having discovered a mutual interest, Dr Lanska and 

Dr Sartin collaborated on an article about Dr Hammond for this issue 

of the Gundersen Lutheran Medical Journal, pages 21-28. 


Authors: 

Denise Milton, MS, PT 

John P. Porcari, PhD, RCEP 

Carl Foster, PhD 

Mark Gibson, MS, ATC, PT 

Brian Udermann, PhD, ATC, 

FACSM 

Department of Exercise and 

Sport Science 


La Crosse, Wisconsin 

John Greany, PhD, PT 

Department of Physical Therapy 



Steven R. Murray, DA 

Department of Human Performance 

and Wellness 

Mesa State College 

Grand Junction, Colorado 

The Effect of Functional Exercise Training on 

Functional Fitness Levels of Older Adults 

ABSTRACT 

Functional fitness implies the ability to perform activities of daily living (ADLs) safely and 

independently. The purpose of this study was to determine if 4 weeks of functional exercise 

training would result in improvements in functional fitness levels of older adults. Twentyfour 

physically active adult volunteers aged 58 to 78 years were randomly assigned into 

an experimental group (functional exercises) and a control group (traditional exercises). 

Both groups were tested before and after the training period using the Fullerton Functional 

Fitness Test for Older Adults. At the completion of the study, the experimental group had 

significant improvements (P < .05) in lower body strength (13%), upper body strength (14%), 

cardiorespiratory endurance (7%), agility/dynamic balance (13%), and shoulder flexibility 

(43%) compared with the control group. No significant improvements were observed in 

hamstring flexibility. The results of this study indicate that a short course of functional exercise 

training can lead to improvements in several components that contribute to functional fitness 

levels of older adults. The functional exercise circuit used in this study was shown to be simple, 

inexpensive, easy to individualize, and one that could be performed conveniently at home, in an 

exercise facility, or in a clinic. 

Address for correspondence: 

John P. Porcari, PhD 

Department of Exercise and Sport 

Science 

141 Mitchell Hall 



Telephone: (608) 785-8684 

email: porcari.john@uwlax.edu 

F 

unctional fitness and functional exercise are popular 

buzzwords in mainstream media, and functional fitness 

programs are becoming more prevalent in gyms and fitness 

centers. 1 Rickli and Jones 2 define functional fitness as “the ability 

to do activities of daily living (ADLs) safely and independently 

without undue fatigue.” While improved physical function of older 

adults as a result of traditional strength and power training is well 

documented in the literature, 3-10 few studies have been published 

that specifically examine the changes in functional fitness of older 

adults in response to functional exercises. 11,12 

Functional independence implies the ability to independently 

perform the ADLs required to live alone. However, the sedentary 

lifestyle of older adults leads to muscle weakness, loss of mobility, 

and difficulty performing ADLs. This ultimately reduces their 

ability to live independently. 13,14 According to the US Bureau of 

the Census, the percentage of Americans aged 65 and older has 

risen from 4.1% in 1900 to 12.7% in 1999, and is expected to 

reach 20% by 2030. 15 Accordingly, developing exercise programs 

that improve functional fitness and contribute to prolonged 

independent living for this growing population is a critical task. 

Strength gains due to training have been shown to be due to 

both enhanced neural recruitment and hypertrophy of the trained 

muscle. Initial strength gains (ie, within the first 3-5 weeks) are 

thought to be primarily attributable to neural adaptations, 16 

with hypertrophy playing the major role thereafter. Bemben and 

Murphy 17 showed no significant age effects on the occurrence of 

neural adaptations, as relative strength gains after 14 days of training 

were the same for young women (20 years) compared with older 

women (58 years). Additionally, Laidlaw et al 9 found significant 

strength gains in older adults (aged 60-90 years), presumably 

attributable to neural adaptations, since they were observed after 

only 4 weeks of strength training. 

Despite studies that show early responses to strength training, 

the research on effects of functional exercise training have 

assessed responses only to programs of at least 12 weeks duration. 

Whitehurst et al 12 conducted a nonexperimental investigation 

(no control group) on the effects of a 12-week functional exercise 

circuit on older adults (aged 68-78 years). They found the circuit 

to be suitable and safe, and observed functional improvements. 

DeVreede et al 11 conducted a 12-week randomized controlled 

trial and found significantly increased functional fitness scores in 

women 70 years and older who performed functional exercises 

versus women who performed traditional resistance exercises. 


Effect of Functional Exercise Training 

Research documenting initial strength gains attributable 

to neural adaptations suggests that functional improvements, 

which are partially measured by strength gains, may also occur 

after a short course of functional exercise training. Identifying 

early improvements in functional fitness is important as it may 

motivate older adults to persist with a functional exercise program 

to maintain fitness. 

The purpose of this study was to determine if there were 

significant improvements in functional fitness levels in older adults 

after 4 weeks of participation in a functional exercise program. 

METHODS 

Approach to the Problem 

This study tested the hypothesis that performing a short course 

of functional exercise training would result in improved functional 

fitness in older adults. The independent variable was exercise type. 

The experimental group performed functional exercises, while the 

control group performed traditional exercises. All subjects were 

regular exercisers, so the control group simply continued with their 

usual routines. Functional fitness scores were measured before and 

after a 4-week training period to assess changes in both groups. 

Subjects 

The subject population consisted of 24 volunteer men and 

women aged between 58 and 78 years. The subjects were randomly 

assigned to 1 of 2 groups: a functional exercise group (experimental: 

n = 12) and a traditional exercise group (control: n = 12). All 

subjects were actively participating, with physician approval and 

referral, in the La Crosse Exercise and Health Program (LEHP) 

at the University of Wisconsin-La Crosse (UWL). Subjects had a 

variety of cardiac, metabolic, and orthopedic conditions; however, 

subjects were excluded if they had conditions precluding them from 

performing the functional exercises prescribed in this study (eg, 

marked balance deficits affecting gait, extreme obesity, and inability 

to perform 12 minutes of continuous activity). Subjects were 

recruited by flyers distributed to members of the LEHP. Interested 

individuals were interviewed to determine their availability and 

suitability for the study and to confirm their medical history. Each 

subject provided informed consent prior to participation. The 

protocol was approved by the Institutional Review Board for the 

Protection of Human Subjects at UWL. 

Procedures 

Functional fitness levels were assessed for all subjects before 

and after the 4-week training period. Testing was conducted 

using the Fullerton Functional Fitness Test for Older Adults 

(FFT) developed by Rikli and Jones. 2,18 The FFT consists of the 

following 6 components: 30-second chair stand for lower body 

strength, bicep curls for upper body strength, 6-minute walk 

for cardiovascular endurance, chair sit-and-reach for hamstring 

flexibility, back scratch for shoulder flexibility, and 8-foot up-andgo 

for balance and agility. 

The experimental group participated in functional exercise 

sessions 3 days per week for 4 consecutive weeks. Subjects were 

required to attend at least 10 sessions to be retained in the study. 

Each session consisted of a 5-minute warm-up, a circuit of 12 

functional exercises, and a 10-minute cool-down. Each functional 

exercise was performed for 1 minute, and the entire circuit was 

completed 3 times. Subjects were instructed to exercise at a moderate 

intensity level (11-14 using the Borg Rating of Perceived Exertion 

Scale 19 ). Resistance, repetitions, and speed were progressed based 

on the ability and comfort level of each subject, while maintaining 

a moderate intensity level. The subjects in the control group were 

instructed to continue with their usual physical activities during 

the 4-week study period. 

Functional Exercise Circuit 

The functional exercise circuit is a modified version of the circuit 

developed by Whitehurst et al 12 consisting of 12 exercises, which 

were each performed for 1 minute, with 15-second transitions 

between each exercise. Resistance was added as tolerated, using 

various levels of sand-filled milk jugs to approximate weights of 

common household items (one-half to 10 pounds). As the exercises 

became easier to perform, the level of difficulty was increased by 

adding weight or making modifications to the exercise, to achieve 

and maintain moderate intensity. It is important to note that 

although the exercises were generally similar to those used in the 

FFT, they were not identical. This should reduce concerns related 

to the specificity of testing and training overlap. 

Unilateral balance. Subjects stood on each leg for 30 seconds, 

while using the upper extremities for support by holding on to 

the back of a chair. The spine was kept in a neutral position, 

the abdominals were held tight, and subjects were instructed to 

avoid knee hyperextension. The level of difficulty was increased 

by removing upper extremity support, flexing the hips so that the 

thighs were parallel to the floor, adding head rotations and arm 

motions, or closing both eyes. 

Golfer’s lift. Subjects stood on 1 leg, with the knee straight 

but not hyperextended. They then flexed forward at the hip and 

reached toward the floor, while extending the nonweightbearing 

leg behind the body. They then returned to upright position. The 

spine was kept in a neutral position and the abdominals were held 

tight throughout the movement. Repetitions were performed for 

30 seconds on 1 leg and then on the other. An increased level of 

difficulty was achieved by adding small weights in the hands. 

Squat with arms forward. Standing in place, subjects squatted 

slowly up and down for 60 seconds. The arms were kept slightly 

forward, the knees were kept behind the toes, and the abdominals 

were held tight throughout the movement. An increased level of 

difficulty was achieved by deepening the squat, extending the arms 

out to be parallel to the floor, or holding a weight in front of the 

body with both hands. 

Wall push-ups. Subjects faced the wall with their feet a 

comfortable distance away from the base of the wall. The feet and 

hands were shoulder width apart, and the body was aligned with 

a neutral spine. Subjects were instructed to slowly lean toward 

the wall and then push away. Repetitions were performed for 1 

minute. Intensity was increased by performing knee push-ups or 

full push-ups on the floor. 

Lateral squats. Subjects stepped sideways and squatted, while 

keeping their trunk aligned, and then returned to an upright 

position. This motion was then repeated to the opposite side, 

alternating sides for 1 minute. The level of difficulty was increased 


y progressing from shallow squats to deeper squats and by holding 

weights in the hands. 

Forward/backward leans. Subjects faced a wall with their 

arms crossed over their chest. They leaned toward the wall, while 

sustaining neutral trunk alignment, and tried to hold this position 

for 30 seconds. They returned to the upright position, turned 

around with their backs to the wall, and performed the same 

exercise by leaning backward toward the wall, holding the position 

for 30 seconds. 

Squat with diagonal reach. Subjects stood with their feet shoulder 

width apart and performed squats while alternately reaching with 

both hands down toward the lateral aspect of 1 ankle and then 

reaching up past the contralateral shoulder for 30 seconds. This 

movement was repeated toward the other ankle and up past 

the contralateral shoulder for an additional 30 seconds. Higher 

levels of difficulty were achieved by holding a weight using a 

bilateral grip. 

Walk around obstacle. Subjects walked for 1 minute on a level 

surface while maneuvering around cones placed on the floor in a 

figure-8 pattern. 

Overhead press. Subjects stood with their feet shoulder width 

apart and performed bilateral overhead presses. During the exercise, 

they were instructed to maintain a neutral trunk alignment, 

avoiding hyperextension of the trunk and knees. Weights were 

added as tolerated, using a bilateral hand grip. An increased level 

of difficulty was achieved by standing on 1 leg during the exercise 

for 30 seconds and switching to the other leg for the remaining 

30 seconds. 

Rotation Lunges. Subjects began the exercise by facing forward 

and feet shoulder width apart. While maintaining good posture, 

subjects rotated to the right and lunged with the right foot 

approaching the 5 o’clock position. They then returned to the 12 

o’clock position, rotated to the left, and lunged with the left foot 

approaching the 7 o’clock position. Subjects performed lunges to 

alternate sides for 1 minute. The level of difficulty was increased by 

holding a small hand weight in each hand as tolerated. 

Lunge and chop. Subjects started in a partial forward lunge 

position and, using a bilateral grip, held a small weight near the 

lateral aspect of the forward ankle. Subjects then rose upright and 

rotated their trunk, while raising the weight in the hands from the 

low lateral position to up and over the opposite shoulder. They 

returned to the starting position and repeated the exercise for 30 

seconds. Mirrored repetitions were then performed with the other 

foot forward for the next 30 seconds. 

Stair climb. Subjects climbed up and down a flight of steps for 

1 minute. The height of the steps was 10 inches. 

Statistical Analysis 

Standard descriptive statistics were used to characterize the 

subject population. 

Differences between the control and the experimental groups 

at the beginning of the study were compared using independent 

t tests. Because there was a significant difference in body weight 

between the experimental and control groups at the beginning of 

the study, analysis of covariance (ANCOVA) was used to analyze 

pre and post differences between groups using body weight 

as the covariate. Alpha was set at P < .05 to achieve statistical 

significance. 

Table 1. Physical Characteristics of Study Participants by Group 

Variable 

Control Group 

Experimental 

Group 

Age, mean (SD), y 64.3 (7.60) 68.2 (7.16) 

Height, mean (SD), in 66.3 (2.55) 66.2 (3.35) 

Weight, mean (SD), lb 178.7 (28.56) 154.9 (31.60) a 

Abbreviation: SD, standard deviation. 

a 

Significantly different from the control group (P < .05) 

RESULTS 

Of the 24 initial subjects, 9 experimental and 9 control 

subjects completed the study, leaving 6 women and 3 men in each 

group (Table 1). Three experimental subjects did not complete the 

study due to illness or poor tolerance of the functional exercises, 

and 3 control subjects were unavailable for posttesting. Average 

attendance for the experimental group was 10.7 sessions out of a 

possible 12. 

The results of each component of the FFT are presented in 

Table 2. The experimental group showed greater improvements 

than the control group in 5 of the 6 test parameters. Statistically 

significant improvements were seen in chair sit-to-stand, bicep 

curls, the 6-minute walk, back scratch, and 8-foot up-and-go. There 

were no significant improvements in the chair sit-and-reach. 

DISCUSSION 

The main outcome of this study was the finding that 4 weeks 

of functional exercise training significantly improved upper 

body strength (14%), lower body strength (13%), cardiovascular 

endurance (7%), agility/dynamic balance (13%), and shoulder 

flexibility (43%) compared with the control group. We found no 

significant improvements in hamstring flexibility. 

The results of the current study compare favorably with 2 other 

functional training studies found in the literature. It should be 

noted that direct comparisons between studies is difficult due to 

different testing batteries and to differences in subject populations. 

For instance, deVreede et al 11 used the Assessment of Daily Activity 

Performance (ADAP) for pretesting and posttesting, Whitehurst 

et al 12 used a combination of tests, and we used the FFT. 2 

Similar to the current study, deVreede et al 11 found significant 

improvements in balance and coordination (22%), cardiovascular 

endurance (18%), and lower body strength (18%). They did 

not find increases in upper body strength, shoulder flexibility, or 

the 8-foot up-and-go, which we did observe. Whitehurst et al 12 

found significantly improved 8-foot up-and-go scores (8.4%), 

comparable to the current study. Unlike the current study, they 

did not find a statistically significant improvement in 6-minute 

walk distance; however, the relative improvement in 6-minute 


Effect of Functional Exercise Training 

walk distance in their subjects was virtually identical to that in 

the current study (7% versus 7.4%, respectively). Contrary to the 

current study, Whitehurst et al found significant improvements in 

hamstring flexibility (14%). They used the standard sit-and-reach 

test, whereas we used the chair sit-and-reach test. The increase in 

hamstring flexibility in their study was 1.6 inches, and in our study 

the increase was 1.2 inches. Thus, even though the improvement in 

our group of subjects was not significant, the absolute improvement 

was comparable to that reported by Whitehurst et al. 

The goal of a functional fitness training program is to improve 

the ability to perform ADLs. An improvement in the ability to 

perform ADLs should make life easier for individuals and allow 

them to maintain their independence. We did not directly assess 

the psychological consequences of the increase in functional 

fitness; however, comments made by the subjects suggested that 

participants experienced carry-over benefit to common everyday 

tasks. Several of the subjects commented that they found it easier 

to “reach for things,” had “better balance,” and 1 subject found 

it easier to “look over [her] shoulder while backing up [her] car.” 

These comments are consistent with the findings of Whitehurst 

et al, 12 whose subjects had increased physical functioning and 

vitality scores, as assessed by the Medical Outcomes Study 36-Item 

Short Form Health Survey (SF-36). Similar results were reported 

in chronically ill patients who were living in an assisted living 

facility. 20 Patients reported greater feelings of independence and a 

greater quality of life that coincided with measured improvements 

in flexibility, grip strength, and mobility. 

A factor that makes the current findings even more meaningful 

is that subjects in the current study were already regular exercisers. 

All of the subjects were doing 30 to 45 minutes of aerobic exercise 

3 days per week, as well as 10 to 15 minutes of resistance training. 

Based on published age-specific and sex-specific norms for the FFT, 21 

the subjects in the current study exceeded the 80th percentile for 

each item. Comparisons between subjects in other studies, such as 

those of Whitehurst et al, 12 provide further evidence of the fitness 

of our subjects. Subjects in the 2 studies were of similar age, yet 

subjects in the current study performed the pretesting 8-foot upand-go 

test in 5.50 seconds, versus 7.92 seconds for their subjects. 

Initial 6-minute walk distances were also very different, with our 

subjects initially walking 618 yards, compared with 365 yards for 

their subjects. 

A possible limitation of any study investigating functional 

exercises is that the training exercises closely resemble the testing 

protocol. For example, the warm-up sequence included standing 

hamstring stretches for flexibility. One of the tests on the FFT, the 

chair sit-and-reach test, is designed to assess hamstring and low 

back flexibility. Thus, it can be seen that the training and testing 

movements were similar, but not identical. The key point is that 

concerns about specificity of training/testing protocols in this type 

of study should not be a major issue. If the testing battery is valid, 

Table 2. Pretest and Posttest FFT Scores of Control and Experimental Groups 

Variable 

Group Pretesting Posttesting Change 

Chair sit-to-stand, mean (SD), repetitions 

Control 


Bicep curls, mean (SD), repetitions 

Control 


6-minute walk, mean (SD), yds 

Control 


15.0 (3.7) 

13.8 (3.1) 

15.1 (2.7) 

13.8 (2.6) 

641 (79.1) 

618 (62.4) 

14.9 (3.4) 

-.1 

15.6 (2.6) a +1.8 

14.6 (3.4) 

-.5 

15.7 (3.1) a +1.9 

+2 

643 (83.9) 

+43 

661 (67.1) a 

Chair sit-and-reach, mean (SD), in 

Control 


-4.8 (3.5) 

-5.3 (4.8) 

-4.4 (3.9) 

-4.1 (3.9) 

-.04 

-.8 

Back scratch, mean (SD), in 

Control 


8-foot up-and-go, mean (SD), sec 

Control 


Abbreviations: FFT Functional Fitness Test; SD, standard deviation. 

a 

Significantly different from the control group (P < .05). 

-2.6 (3.4) 

-3.7 (5.8) 

5.1 (.53) 

5.5 (.77) 

-2.7 (3.6) 

-.1 

-2.1 (4.9) a +1.6 

5.1 (.75) 

0 

4.8 (.50) a -.7 


it should mimic common ADLs. Accordingly, the training 

regimen should be designed to enhance the performance of 

those specific, everyday ADL movements. 

PRACTICAL APPLICATIONS 

Overall, this study found significant improvements in 

functional fitness after only 4 weeks of functional exercise 

training. Seeing benefits in such a short time may encourage 

older adults to initiate and continue a functional exercise 

program, especially when the benefits carry over to their 

ability to perform ADLs. Additionally, the training circuit 

was designed using only exercises that could be performed at 

home, with little need for space or equipment. Empty milk 

jugs and soda bottles filled with sand were used as weights; the 

single and double hand grips utilized for many of the exercises 

simulated the grips necessary to grasp common household 

items; and the reaching and bending exercises mimicked 

many body postures common to daily tasks. Additionally, 

each exercise can be easily modified to make it more or 

less challenging, thereby tailoring the circuit to meet 

individual needs. 

REFERENCES 

1. Shaw G. Functional fitness: working out for real life situations. WebMD 

Web site. Available at: http://www.webmd.com/fitness-exercise/guide/ 

working-out-for-real-life-functions. Published August 12, 2003. Accessed 

March 11, 2008. 

2. Rikli RE, Jones CJ. Development and validation of a functional fitness test 

for community-residing older adults. J Aging Phys Act. 1999;7(2):129-161. 

3. Barry BK, Carson RG. The consequences of resistance training for 

movement control in older adults. J Gerontol A Biol Sci Med Sci. 

2004;59(7):M730-754. 

4. Chandler JM, Hadley EC. Exercise to improve physiologic and functional 

performance in old age. Clin Geriatr Med. 1996;12(4):761-784. 

5. Cress ME, Buchner DM, Questad KA, Esselman PC, deLateur BJ, Schwartz 

RS. Exercise: effects on physical functional performance in independent 

older adults. J Gerontol A Biol Sci Med Sci. 1999;54(5):M242-248. 

6. Henwood TR, Taaffe DR. Improved physical performance in older adults 

undertaking a short-term programme of high-velocity resistance training. 

Gerontology. 2005;51(2):108-115. 

7. Hunter GR, McCarthy JP, Bamman MM. Effects of resistance training on 

older adults. Sports Med. 2004;34(5):329-348. 

8. King AC, Pruitt LA, Phillips W, Oka R, Rodenburg A, Haskell WL. 

Comparative effects of two physical activity programs on measured and 

perceived physical functioning and other health-related quality of life outcomes 

in older adults. J Gerontol A Biol Sci Med Sci. 2000;55(2):M74-83. 

9. Laidlaw DH, Kornatz KW, Keen DA, Suzuki S, Enoka RM. Strength 

training improves the steadiness of slow lengthening contractions performed 

by old adults. J Appl Physiol. 1999;87(5):1786-1795. 

10. Miszko TA, Cress ME, Slade JM, Covey CJ, Agrawal SK, Doerr CE. Effect 

of strength and power training on physical function in community-dwelling 

older adults. J Gerontol A Biol Sci Med Sci. 2003;58(2):171-175. 

11. de Vreede PL, Samson MM, van Meeteren NL, Duursma SA, Verhaar HJ. 

Functional-task exercise versus resistance strength exercise to improve daily 

function in older women: a randomized, controlled trial. J Am Geriatr Soc. 

2005;53(1):2-10. 

12. Whitehurst MA, Johnson BL, Parker CM, Brown LE, Ford AM. The 

benefits of a functional exercise circuit for older adults. J Strength Cond Res. 

2005;19(3):647-651. 

13. Jette AM, Branch LG, Berlin J. Musculoskeletal impairments and physical 

disablement among the aged. J Gerontol. 1990;45(6):M203-208. 

14. LaCroix AZ, Guralnik JM, Berkman LF, Wallace RB, Satterfield S. 

Maintaining mobility in late life. II. Smoking, alcohol consumption, physical 

activity, and body mass index. Am J Epidemiol. 1993;137(8):858- 869. 

15. Duncker AM, Greensberg S; Administration on Aging. A Profile of 

Older Americans: 2000. http://aoa.gov/PROV/Statistics/profile2000.pdf. 

Accessed May 16, 2008. 

16. Moritani T, deVries HA. Neural factors versus hypertrophy in the time 

course of muscle strength gain. Am J Phys Med. 1979;58(3):115-130. 

17. Bemben MG, Murphy RE. Age related neural adaptation following 

short term resistance training in women. J Sports Med Phys Fitness. 

2001;41(3):291-299. 

18. Miotto JM, Chodzko-Zajko WJ, Reich JL, Supler MM. Reliability and validity 

of the Fullerton Functional Fitness Test: an independent replication study. 

J Aging Phys Act. 1999;7(4):339-353. 

19. American College of Sports Medicine, Whaley MH, Brubaker PH, Otto 

RM, Armstrong LE. ACSM’s Guidelines for Exercise Testing and Prescription. 

7th, 30th Anniversary ed. Philadelphia, PA: Lippincott Williams & 

Wilkins; 2006:366. 

20. Hessert MJ, Gugliucci MR, Pierce HR. Functional fitness: maintaining 

or improving function for elders with chronic diseases. Fam Med. 

2005;37(7):472-476. 

21. Rikli RE, Jones CJ. Functional fitness normative scores for communityresiding 

older adults, ages 60-94. J Aging Phys Act. 1999;7(2):162-181. 


Authors: 

Alissa R. Reierson 

Daniel D. Houlihan, PhD 

Minnesota State University –Mankato 

Mankato, Minnesota 


Daniel D. Houlihan, PhD 

Psychology Department 

Office WH 261 

23 Armstrong Hall 

Minnesota State University–Mankato 

Mankato, MN 56001 

Telephone: (507) 389-6308 

email: daniel.houlihan@mnsu.edu 


ABSTRACT 

Extensive research concerning the presentation and treatment of adolescents and adults 

diagnosed with anorexia nervosa can be found within the literature. Conversely, the research 

regarding early-onset anorexia is limited. Children presenting with anorexia nervosa may 

display qualities and experience challenges disparate from those of their older counterparts. 

This review of the literature examines these differences and their significance regarding the 

diagnosis, treatment, and outcome of early-onset anorexia nervosa. 

T 

he rates of individuals seeking treatment for anorexia 

nervosa (AN) have risen in recent years. 1,2 This increase 

may be attributable more to the attention AN has received, rather 

than to a genuine rise in the incidence of the disorder. However, 

in conjunction with this increase in individuals seeking treatment 

comes an increase in prepubertal individuals experiencing AN-type 

symptoms. 

It is estimated that early-onset AN accounts for nearly 5% of 

all AN cases. 3 Within the literature, AN is considered early-onset 

if individuals are 13 to 14 years old or are prepubertal. 4-6 Only a 

small proportion of the eating disorders literature has addressed 

this younger population. 7,8 Many studies fail to differentiate 

between early-onset and late-onset AN, which may be problematic 

because of the differences between early-onset and late-onset AN. 

For example, compared with individuals with late-onset AN, those 

with early-onset AN are more likely to be male and more likely 

to belong to families with high socioeconomic status. Individuals 

with early-onset AN also are usually physically and psychologically 

less mature than their peers. 4,9 These differences are significant 

and can affect the diagnosis, course, and treatment outcome. The 

following review will focus on differences between early-onset and 

late-onset AN with regard to diagnosis, characteristics, physical 

risks, treatment, and outcome. 

Discrepancies in Diagnosis 

Anorexia nervosa is the willful refusal to maintain a body 

weight that is within 85% of a healthy weight for an individual’s 

height and age. Along with this refusal, people with AN display 

a fear of becoming overweight. 10 They make extreme attempts at 

avoiding weight gain, which may include an extremely restricted 

diet and/or excessive exercising. Accompanying this fear of weight 

gain, individuals with AN don’t recognize that they are dangerously 

thin. Their perception of their body weight or shape is distorted. 

Consequently, they may be 15% or more under their ideal weight, 

but still believe that they need to lose weight. 10 

The criteria for AN have been subject to much debate, 

especially for prepubertal children and those under 13 years of 

age. 5 Conflicting reports on children’s presentation of AN are 

found within the literature. Some researchers have found that 

children who are referred for AN-type symptoms often do not 

have a distorted body image. 11,12 Most of these children have not 

yet reached puberty and may simply fear that they will gain weight 

as their bodies change. Therefore, they do not necessarily believe 

they are currently overweight, yet they have gone to great lengths 

to not gain weight. 12 Consequently, the characteristic distortion in 

body image, weight, and shape may develop later, as children go 

through puberty and their bodies change and the social appeal of 

their appearance becomes a factor. 

Other differences between early-onset and late-onset AN have 

been noted, as well. 6 For example, Matsumoto and colleagues 

found that fewer early-onset than late-onset AN patients had 

extremely low weight. 6 Similarly, others have found that the 

average weight of children with early-onset AN was only 5% below 

their ideal weight. 11 This less severe weight loss may be because 

younger individuals are still in the early stages of AN. 11 Still other 

researchers have found that children often lose weight more rapidly 

than adolescents and adults do. 7 Perhaps because their weight loss 

occurs in a shorter period of time, and because they are usually more 

supervised than adolescents and adults, younger children present 

to a physician or psychologist earlier than other AN patients do. 

However, it should be noted that some researchers have reported 

no differences between early-onset and late-onset AN. 13 

The question remains whether the weight criterion and 

a distorted body image are essential for the diagnosis of AN in 

preadolescence. Imposing the weight and distortion criteria on 

children who present for assessment may underestimate the 

number of children who are experiencing severely disordered 

eating patterns. In younger children, it is easier to attribute 

symptoms to something less serious, such as being a picky eater. 

This misattribution is especially true when children have not 

met the weight loss criterion and do not have a distorted body 

image. 14 Yet many of these children will eventually be diagnosed 

with AN. In their study, Lask and colleagues found that girls with 

early-onset AN had a higher rate of physician visits within the 5 

years preceding diagnosis than did girls with no history of mental 

health problems. 14 Indeed, just 1 visit to the physician for eating, 

weight, or shape concerns was a strong predictor of a subsequent 

diagnosis of AN. 14 Early diagnosis is important because the longer 


an individual has been anorexic, the more challenging it is to 

intervene. 9 Thus, in the case of prepubertal children, optimal 

outcome may require lenient use of the weight loss and distorted 

body image criteria. 

Common Co-Occurring Conditions 

Whereas psychological aspects of AN in adolescents and adults 

have been examined extensively, their correlates in childhood 

AN have not. 15 Individuals with AN are usually high achieving 

and have perfectionist qualities. 16 They show high compliance to 

the demands of others and have a high level of self doubt. 16 Like 

their older counterparts, prepubertal individuals with AN show 

these same characteristics, but more intensely. 4 The intensity 

of these personality characteristics at such a young age may be 

connected with earlier onset of AN. Therefore, the intensity of 

such characteristics and their association with early-onset AN need 

further examination. 

Prepubertal children with AN can also have a sense of what is 

called pseudomaturity, that is, they appear to be responsible and 

trustworthy beyond their years. As Arnow and colleagues argue, 

this illusion of maturity can be problematic. 4 Such patients may 

seem outwardly more mature and able to handle serious problems, 

when in reality it is difficult for them to cope with even small 

amounts of stress. They also may believe themselves capable of 

handling these problems without assistance, which could trigger 

stress and exacerbate AN symptoms. 3 

Both early-onset and late-onset AN are associated with high 

levels of depression. 15 This correlation is not surprising, considering 

the criteria included in the Diagnostic and Statistical Manual of 

Mental Disorders and the personality characteristics associated with 

this disorder. 9 AN is characterized by dissatisfaction with one’s body 

and a drive for perfection, which — especially in combination with 

their tendency to withdraw from social networks — puts these 

patients at risk for depression. 

Physical Risks 

Children are typically more easily emaciated than teenagers and 

adults. 6 Consequently, being even 5% below their ideal weight can 

have serious medical consequences. At initial evaluation, children 

often present with the same medical problems as older individuals. 3 

They are often seriously malnourished and dehydrated, which 

puts them at risk for immediate medical problems, such as low 

body temperature and hypotension. 17 And because they are in a 

critical period of growth and bone development, malnourishment 

places them at increased risk of hindered development. 7,9 During 

treatment, patients recovering from early-onset AN often 

experience amplified growth, although they rarely reach their full 

growth potential. 9,18 Consulting with a physician to monitor these 

physical symptoms is essential. 

In order to ameliorate the effects malnutrition has on growth, 

immediate intervention is necessary. But when interviewing the 

parents of early-onset AN patients, researchers heard repeatedly 

that parents did not know enough about AN. 19 When parents 

noticed behavioral change in their children, they often associated 

it with something other than AN, such as starting puberty or 

testing parental boundaries. They also reported their belief that 

general practitioners did not know enough about signs of an eating 

disorder. In fact, like the parents, general practitioners often first 

attributed the child’s symptoms to something other than AN. 19 

Likewise, others have noted that general practitioners tended 

to overlook eating disorders as a diagnosis, especially when the 

children were younger. 14 Signs of early-onset AN, therefore, need 

to be identified so that the problem can be detected early. 

Treatment 

Many studies examining the efficacy of treatments for AN 

in adolescents and adults can be found in the literature. 20 Most 

researchers suggest using a multidimensional approach to therapy, 

which can be expanded to a variety of individuals with AN. 21 The 

2 main components in this multidimensional approach, cognitivebehavior 

therapy and family therapy, have been effective in the 

treatment of AN. 8,21,22 There is a dearth of research, however, on 

treatments for children diagnosed with AN. 

Once a diagnosis is made, the initial treatment question 

is whether the individual needs to be hospitalized. 23 Severe 

dehydration, self-injurious behavior, and failure to progress 

in outpatient treatment are all signs the individual should be 

hospitalized. 

Inpatient treatment should focus on achieving a healthy weight, 

and behavior therapy is often the most effective way to do that. The 

components of behavior therapy typically used are reinforcement 

and meal planning. 22,24 Immediate increase in weight is important 

because of the medical risks that accompany low weight. Researchers 

also believe that increasing the weight of individuals may help with 

some of the psychological symptoms — such as depression, anger, 

and hysteria — associated with AN. 25 Another component of 

behavior therapy often used in the treatment of AN is getting the 

individual involved in activities that give the individual something 

other than the eating disorder upon which to focus. Also, they 

help augment socialization. Homework assignments may assist 

the patient with tracking participation in and emotional response 

to activities. Homework may also be given to help the individual 

express assertiveness and decision making with family members. 20 

Treatment should also focus on taking control away from 

the child. 23,24 The parents need to work together to take control 

away from their child, especially when it comes to meal planning. 

Getting parents to compromise and work together may require 

couples therapy. 23 With younger children, autonomy is not as 

much of a concern in treatment. For younger patients, parents 

likely will still have control over their eating; when they get older, 

increasing their responsibility will be important. Addressing family 

conflict is also an important therapeutic intervention. Since AN is 

often associated with problematic relations within the family; it is 

important to address the conflict in treatment. 26 

In a study examining the use of family therapy for individuals 

with early-onset AN, family therapy consisted of giving control back 

to the parents so they could then re-feed their child and helping 

the parents gradually give the patient age-appropriate control over 

his/her eating. 8 The outcomes of children and adolescents going 

through family-based therapy were comparable. Children’s weight 

and height increased significantly during this treatment, with only 

1 of 31 patients being below 85% of their ideal body weight at its 

completion. Children’s eating restraint, eating concerns, and body 


Childhood Anorexia 

shape concerns also decreased dramatically. The only aspect that 

did not decrease was weight concerns, which parallels the results of 

studies of adolescents receiving similar therapy. 8 

More research is needed in order to find out whether behavior 

and family therapy are effective for children with AN. Children 

with AN present differently from other AN patients, so they might 

respond to treatment differently, as well. For example, because 

children tend to rely on their parents more than do adolescents 

and adults, family therapy might be more effective in children 

than in older AN patients. Addressing family issues and control 

may have great implications in the treatment of early-onset of 

AN. Another consideration for children with AN is the eventual 

onset of adolescence and puberty, a period of transition that can be 

difficult for AN patients. Even patients who have been treated for 

AN and are doing well might benefit from booster sessions during 

this period. 

Outcome 

Research on the outcome of individuals with early-onset 

AN has shown conflicting results. 9,27 One study used a modified 

version of the outcome status ratings Morgan and Russell used on 

adults with AN to examine children with a 2- to 5-year followup. 

Outcome was based on the individual’s ratings on 5 different 

scales: nutritional status, menstruation, mental state, psychosocial 

adjustment, and psychosexual adjustment. 27,28 Overall outcome 

was based on these 5 scales. 27,28 The child study found that 11 

(70.6%) of the 17 subjects had an overall “good” outcome. 27 

Outcome based solely on mental state or menstruation had the 

highest number of individuals in the “poor” category (n = 4). 27 Poor 

ratings in these categories signified a grossly abnormal mental state 

and virtually absent menstruation. 27,28 Another study also reported 

that a small majority of individuals with early-onset AN were 

categorized as having a good outcome (57%). In follow-up 2 of 

18 patients reported suicide attempts, which is very concerning. 29 

Likewise, in a study done by Theander, 9 2 individuals in the earlyonset 

group had died at follow-up — 1 at 24 years after onset, and 

the other at 20 years after onset. In comparison, no individuals in 

the late-onset group had died. The patient who died 24 years after 

onset had been doing well for 12 years following treatment. 9 Thus, 

follow-up studies 2 to 5 years after treatment may not reflect longterm 

outcomes for some patients. 

In his 1982 review of the literature, Swift concluded that 

there was insufficient evidence to show that the outcome of earlyonset 

AN patients was better or worse than that of late-onset AN 

patients. 30 Many studies done to date do not directly compare earlyonset 

patient results to those of late-onset patients, thus making 

it difficult to directly compare the 2 groups. However, based on 

his review of the literature, Swift concluded that the long-term 

outcome of early-onset patients was equivalent to that of other AN 

patients. 30 In a comparison follow-up of individuals with earlyonset 

and late-onset AN, it was found that 45% of individuals 

with late-onset AN were “good” at examination 4 to 10 years later, 

while 2% had died. These results echo the findings of another 

follow-up study examining early-onset AN patients. 31 

The assertion that outcomes for early-onset and late-onset AN 

patients are similar is not promising. The results are especially 

concerning when one considers that the longer an individual has 

symptoms of AN, the more difficult it is to intervene. 9 Intervention 

occurred at a young age for the subjects examined in these outcome 

studies. But if AN symptoms are not recognized and treatment 

sought, the course of the disorder may be irreversible and produce 

detrimental effects years later. 

Conclusion 

Diagnosis is an important issue with AN. More leniency in 

the criteria for diagnosis of early-onset AN may allow intervention 

before the disorder progresses to a point where there are irreversible 

side effects. In order to intervene as early and as effectively as 

possible, however, more research is needed on treatment that 

targets younger individuals with AN. 

Although early-onset patients represent a minority of AN 

patients, the illness can have serious and irreversible health 

consequences. 15 Future research should seek to clarify the 

differences between early-onset and late-onset AN and to identify 

the most effective treatments for AN patients of all ages. 

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2. Lucas AR, Crowson CS, O’Fallon WM, Melton LJ 3rd. The ups and downs of 

anorexia nervosa. Int J Eat Disord. 1999;26(4):397-405. 

3. Bostic JQ, Muriel AC, Hack S, Weinstein S, Herzog D. Anorexia nervosa in a 

7-year-old girl. J Dev Behav Pediatr. 1997;18(5):331-333. 

4. Arnow B, Sanders MJ, Steiner H. Premenarcheal versus postmenarcheal anorexia 

nervosa: a comparative study. Clin Child Psychol Psychiatry. 1999;4(3):403- 414. 

5. Nicholls D, Chater R, Lask B. Children into DSM don’t go: a comparison of 

classification systems for eating disorders in childhood and early adolescence. Int J 

Eat Disord. 2000;28(3):317-324. 

6. Matsumoto H, Takei N, Kawai M, et al. Differences of symptoms and standardized 

weight index between patients with early-onset and late-onset anorexia nervosa. 

Acta Psychiatr Scand. 2001;104(1):66-71. 

7. Peebles R, Wilson JL, Lock JD. How do children with eating disorders differ 

from adolescents with eating disorders at initial evaluation? J Adolesc Health. 

2006;39(6):800-805. 

8. Lock J, le Grange D, Forsberg S, Hewell K. Is family therapy useful for treating 

children with anorexia nervosa? Results of a case series. J Am Acad Child Adolesc 

Psychiatry. 2006;45(11):1323-1328. 

9. Theander S. Anorexia nervosa with an early onset: selection, gender, outcome, and 

results of a long-term follow-up study. J Youth Adolesc. 1996;25(4):419-429. 

10. American Psychiatric Association Task Force on DSM-IV. Diagnostic and 

Statistical Manual of Mental Disorders : DSM-IV-TR. 4th rev ed. Washington, 

DC: American Psychiatric Association; 2000. 

11. Nielsen GB, Lausch B, Thomsen PH. Three cases of severe early-onset eating 

disorder: are they cases of anorexia nervosa? Psychopathology. 1997;30(1):49-52. 

12. Robins PM, Putnam PH. From the children’s corner: a comparison of childhood 

variant disorders of eating and early-onset eating disorders. Eat Disord. 

1999;7:149-156. 

13. Cooper PJ, Watkins B, Bryant-Waugh R, Lask B. The nosological status of early 

onset anorexia nervosa. Psychol Med. 2002;32(5):873-880. 

14. Lask B, Bryant-Waugh R, Wright F, Campbell M, Willoughby K, Waller G. 

Family physician consultation patterns indicate high risk for early-onset anorexia 

nervosa. Int J Eat Disord. 2005;38(3):269-272. 


15. Lask B, Bryant-Waugh R. Early-onset anorexia nervosa and related eating 

disorders. J Child Psychol Psychiatry. 1992;33(1):281-300. 

16. Strober M. A comparative analysis of personality organization in juvenile anorexia 

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17. Mitchell JE, Pomeroy C, Adson DE. Managing medical complications. In: 

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18. Lantzouni E, Frank GR, Golden NH, Shenker RI. Reversibility of growth 

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19. Cottee-Lane D, Pistrang N, Bryant-Waugh R. Childhood onset anorexia nervosa: 

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21. Garner DM, Garfinkel PE, Bemis KM. A multidimensional psychotherapy for 

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Adolesc. 1996;25(4):563-568. 

Amblyrhynchus cristatus 

(marine iguana, endemic to the Galapagos) 

Photograph by Gregory G. Fischer, MD 

Gundersen Lutheran 


Authors: 

Jennifer S. Mattingley, MD 

Internal Medicine Residency 

Gundersen Lutheran Medical 

Foundation 


Linda C. Groon, MD 


Gundersen Lutheran Health System 



Jennifer Mattingley, MD 



Foundation 



Telephone: (608) 782-7300 

Fax: (608) 775-4511 

email: jsmattin@gundluth.org 

W 

Wernicke Encephalopathy: 

Is the Gundersen Lutheran Alcohol Detoxification 

Protocol Sufficient? 

ABSTRACT 

ernicke encephalopathy (WE) is an acute neuropsychiatric 

condition resulting from thiamine deficiency. 

It is classically characterized by a symptom triad of ataxia, mental 

status changes, and ocular abnormalities, although all 3 need 

not be present for the diagnosis. Up to 19% of patients with 

WE have none of the classic triad of symptoms at presentation 

and may present with irritability and fatigue alone. 1-3 Late-stage 

findings include hyperthermia, increased muscle tone, and 

choreic dyskinesias. 4,5 

Thiamine deficiency is common in alcoholics, and therefore 

diagnosis and treatment of WE is often focused on care during 

alcohol detoxification. However, WE has also been well described 

in patients with Crohn disease, anorexia nervosa, acquired immune 

deficiency syndrome (AIDS), hyperemesis gravidarum, and in 

patients who have undergone chemotherapy or gastric bypass 

surgery. 6 Treatment is aimed at replenishing thiamine stores, 

especially to the areas of the brain most susceptible to thiamine 

deficiency. Although replacing thiamine is standard practice in 

patients with symptoms suggestive of WE and is often begun 

prophylactically in alcohol detoxification, there is increasing 

evidence that traditional dosages of thiamine replacement 

are suboptimal in improving outcomes of WE patients. We 

present a case report of a patient with WE, review the current 

literature, and discuss potential changes to standard practice of 

thiamine replacement. 

CASE REPORT 

A 35-year-old white man presented to the emergency 

department of Gundersen Lutheran Medical Center with 

complaints of inability to walk and slurred speech. He had a 

history of chronic alcohol abuse and previous alcohol withdrawal 

seizures. He stated that he believed he had a seizure 3 days prior 

We describe the case of a 35-year-old man who presented with central nervous system 

symptoms suggestive of Wernicke encephalopathy (WE). After ruling out other possible causes, 

and based upon clinical findings, WE was diagnosed. WE is caused by a thiamine deficiency 

and because thiamine deficiency is common among people who abuse alcohol, thiamine 

replacement is a component of Gundersen Lutheran’s alcohol detoxification protocol. However, 

review of the literature suggests that the current thiamine replacement regimen may not be 

sufficient, especially for patients with symptoms of WE. 

to his presentation. Since that time he had been unable to walk 

and had had multiple falls. He also stated he was unable to “see 

straight.” He was, however, ambivalent about these symptoms. 

He had continued to drink alcohol. He stated he was drinking 

“less than usual,” but was unwilling to quantify further. He also 

admitted to not eating for several days. 

On initial examination he was awake and oriented to person. 

Vitals included heart rate of 120 beats per minute and blood 

pressure of 139/102 mm Hg. The patient was afebrile. Neurologic 

examination revealed marked vertical, horizontal, and rotary 

nystagmus. Bilateral sixth cranial nerve palsies were present. 

Function of the remaining cranial nerves was intact. Strength was 

normal in the upper and lower extremities. Occasional choreiform 

movements of the left upper extremity, especially with provocation, 

were noted. Deep tendon reflexes were brisk but without clonus, 

and Babinski sign was absent bilaterally. There was marked bilateral 

upper extremity ataxia and gait ataxia. Because of truncal ataxia, he 

could not sit up without support. He had marked dysarthria with a 

paucity of spontaneous speech. Due to his marked dysarthria and 

poor level of cooperation, it was difficult to fully assess cognition. 

On skin examination, multiple areas of ecchymosis and abrasions 

were noted on his extremities, trunk, and face. 

Laboratory test results showed a white blood cell (WBC) 

count of 14 500/μL, hemoglobin concentration of 17.9 g/dL, and 

a platelet count of 102 ×10 3 /μL. Potassium was markedly depleted 

at 2.4 mEq/L. Sodium was 134 mEq/L, chloride 80 mEq/L, and 

magnesium 2.0 mEq/L (decreased to 1.3 mEq/L within 48 hours). 

Other electrolyte and glucose values were within reference range. 

Aspartate aminotransferase (AST) and alanine aminotransferase 

(ALT) concentrations were marginally elevated at 73 U/L and 51 

U/L, respectively (Table). International normalized ratio (INR) 

was slightly elevated at 1.2. Findings from noncontrast computed 


tomographic scan of the head were normal. Findings from 

subsequent magnetic resonance imaging of the head performed the 

following day were also without specific abnormality. No infectious 

etiology was identified, and his electrolytes were replaced. 

Given the clinical findings and exclusion of other causes 

of central nervous system dysfunction, WE was diagnosed. 

Within hours of the patient’s admission, his nystagmus and 

Laboratory Test Results Upon Admission 

Analyte Value Reference Range 

WBC count, /μL 14 500 4500 -11 000 

Hemoglobin 

concentration, g/dL 

17.9 14.0 -17.5 

Platelet count, ×10 3 /μL 102 150-350 

Potassium concentration, 

mEq/L 

Sodium concentration, 

mEq/L 

Chloride concentration, 

mEq/L 

Magnesium 

concentration, mEq/L 

2.4 3.5-5.0 

134 136 -142 

80 96 -106 

2.0 1.3 -2.1 

AST concentration, U/L 73 10 -30 

ALT concentration, U/L 51 10 -40 

Abbreviations: WBC, white blood cell; AST, aspartate 

aminotransferase; ALT, alanine aminotransferase. 

SI conversions: To convert WBC count to ×10 9 /L, multiply by 0.001; 

hemoglobin to g/L, multiply by 10.0; platelet count to ×10 9 /L, 

multiply by 1.0; potassium, sodium, and chloride to mmol/L, 

multiply by 1.0; magnesium to mmol/L, multiply by 0.50; AST to 

μkat/L, multiply by 0.0167; ALT to μkat/L, multiply by 0.01667. 

opthalmoplegia had resolved. Thiamine 100 mg intravenously 

(IV) had been administered in the emergency department prior 

to admission per the existing alcohol detoxification protocol of 

thiamine 100 mg orally, by IV, or intramuscularly (IM) daily for 

3 days. Initial inpatient orders were to continue thiamine 100 mg 

IV daily for 3 days, again per the existing protocol. Prompted by 

review of literature on WE, however, within 24 hours his thiamine 

dosage was increased to 250 mg IV 3 times daily for 5 days. He 

then received thiamine orally during the remainder of his 3-week 

hospital stay. His ataxia improved but did not completely resolve. 

At the time of discharge the patient was still unable to walk due 

to ataxic gait, and his upper extremity ataxia remained prominent, 

as well. He continued to be dysarthric. Neuropsychiatric testing 

demonstrated significant memory deficits with mild immediate 

recall deficits and severe short and long delayed recall deficits. 

DISCUSSION 

Wernicke encephalopathy is an acute syndrome classically 

characterized by ataxia, altered mental status, and ocular 

abnormalities of nystagmus and ophthalmoplegia. Carl Wernicke 

first described it as a superior hemorrhagic polioencephalitis in 

1881. He reported case studies of 3 patients, all of whom died 

within 2 weeks of presentation. Two of the patients were men 

with chronic alcoholism, while the third patient (a woman) had 

persistent vomiting secondary to pyloric stenosis from sulphuric 

acid ingestion. 7 In the 1940s, Campbell and Russell were the first 

to implicate thiamine deficiency as the underlying etiology of the 

encephalopathy. 8 

Based upon postmortem studies identifying typical brainstem 

lesions, WE has a prevalence of 0.8% to 2.8% in the general adult 

population of the United States and 12.5% in the population that 

misuses alcohol. 1,9,10 This is a much higher incidence than what 

is diagnosed clinically. As only 10% of patients with WE present 

with the classic triad of signs, it is suggested that up to 90% of 

individuals with WE go undiagnosed. 1,11 There is a definite male 

predominance (1.7:1). 12 Ethnic-specific differences in presentation 

of thiamine deficiency also exist. Europeans more commonly 

develop encephalopathy and peripheral neuropathy (dry beriberi), 

while the majority of Asians manifest with cardiovascular effects 

(wet beriberi). 13 

Thiamine deficiency leads to pathologic lesions within the 

brain, especially the periaqueductal grey matter, mamillary bodies, 

and medial thalamus, all of which have a high thiamine content 

and metabolism. 14 Neuronal cells convert thiamine to thiamine 

pyrophosphate, the metabolically active form, which is essential 

for ATP synthesis, myelin sheath production, and synthesis of 

neurotransmitters. 15 Within 4 days of developing deficient thiamine 

levels, there is marked decrease in activity of alpha-ketoglutaratedehydrogenase 

within astrocytes. By 7 days there is reduction in 

activity of transketolase and subsequent increase in nitric oxide 

from endothelial cell dysfunction. This leads to astrocytic and 

neuronal edema and disruption of the blood-brain barrier. Within 

2 weeks of thiamine deficiency there is evidence of neuronal DNA 

fragmentation and necrosis, which leads to irreversible lesions 

16 -26 

within the brain. 

Average thiamine requirement for an adult is 0.5 mg of thiamine 

per 1000 kcal (4184 kilojoules) although needs are significantly 

higher in children and in patients who are critically ill, pregnant, 

or lactating. 27 Requirements are also related to carbohydrate 

intake as well as total caloric intake. 28 Diets high in carbohydrates 

increase the demand for thiamine because it is vital in carbohydrate 

metabolism. Chronic alcoholics are often malnourished with 

suboptimal thiamine intake and have decreased ability for vitamin 

storage in the liver, while alcohol itself increases the need for 

carbohydrate metabolism. 29 Thus, chronic alcoholics can often 

become significantly thiamine depleted. 

Absorption of thiamine occurs in the duodenum by an 

active, carrier-mediated, and rate-limited process. Therefore, 

the maximum amount of thiamine that can be absorbed from a 

single oral dose is ~ 4.5 mg. 30 In alcoholics, enteral absorption of 

thiamine is diminished and erratic. 29 Alcohol alone can decrease 

intestinal absorption of thiamine by 50%; malnutrition can 


gundersen lutheran alcohol detoxification protocol 

decrease absorption by up to 70%. 30 Hence, enteral replacement 

of thiamine in a patient with WE is inadequate. 

At the blood-brain barrier, thiamine is transported by both 

passive and active carrier-mediated mechanisms. 31 At normal plasma 

concentrations, thiamine influxes into the brain almost entirely via 

the carrier-mediated process at a rate essentially equal to that of 

thiamine turnover. However, by creating a large plasma:central 

nervous system concentration gradient, thiamine stores can be 

readily replaced within the brain by passive transport alone. As 

enteral absorption of thiamine is limited, IV or IM administration 

should be used to obtain adequate plasma concentrations. 30 

Several studies by Cook, Thomson, and colleagues 29,30,32-35 

support the use of a much higher dosage of parenteral thiamine 

than what has been traditionally utilized. They have recommended 

that patients who are at risk or who have clinical evidence of 

WE receive a minimum dosage of 500 mg of IV thiamine 3 times 

daily for 3 days. When there is an effective response, thiamine 

should be continued at 250 mg IV daily for an additional 3 to 5 

days, or until clinical improvement ceases. Traditional dosages of 

100 mg to 200 mg of thiamine per day were found to be insufficient 

to replete thiamine stores, improve clinical findings, or prevent 

permanent neurologic damage or death. The estimated mortality 

for inadequately treated WE is 20%. 30,32 Moreover, almost 80% 

of patients with untreated or undertreated WE develop Korsakoff 

syndrome, a permanent disorder of anterograde and retrograde 

amnesia with confabulation as a prominent feature. 12 

Identifying patients with WE or who are at high risk of 

developing WE is difficult. Nineteen percent of patients with 

WE have none of the classic triad of symptoms at presentation. 

Only 29% have ocular abnormalities, while only 23% have gait 

incoordination and truncal ataxia at presentation. 1 Adding to the 

difficulty is that acute alcohol intoxication and alcohol withdrawal 

can also cause mental status changes and ataxia, and indeed these 

abnormalities are often attributed to intoxication or withdrawal 

without consideration of WE. 

Several protocols have been developed in an attempt to better 

identify, and therefore treat, patients with high likelihood of WE. 

Caine et al use criteria of 2 of the classic triad of symptoms (mental 

status changes, ocular abnormalities, incoordination of gait/trunk 

ataxia) and presence of dietary deficiencies. 36 The Royal College of 

Physicians guidelines are to treat “all patients with any evidence of 

chronic alcohol misuse and any of the following: acute confusion, 

decreased conscious level, ataxia, ophthalmoplegia, memory 

disturbance, hypothermia with hypotension…, [and] patients 

with delirium tremens…” with thiamine 500 mg IV 3 times daily. 

Other at-risk patients receive prophylactic thiamine dosing of 250 

mg IV daily for 3 to 5 days. 30 

Significant magnesium deficiency is common in chronic 

alcoholics, and adequate replacement is also vital in treatment 

of WE. Magnesium serves as a cofactor required for normal 

functioning of several key thiamine-dependent enzymes of 

carbohydrate metabolism and neurochemical transmission. 

Studies by Traviesa demonstrated that patients with WE may 

well be unresponsive to parenteral thiamine administration if 

hypomagnesemia is present. 37-39 Therefore, patients at high risk 

of WE should have magnesium levels measured and aggressively 

corrected, as well. 

Gundersen Lutheran’s current inpatient alcohol detoxification 

protocol includes administering 100 mg of thiamine daily for 3 

days and gives the option of enteral, parenteral, or IM routes. 

There are no specific criteria on the current protocol to identify 

individuals who are at high risk or who manifest symptoms of 

WE and therefore would potentially benefit from higher doses of 

thiamine. Most of the alcohol detoxification patients, unless they 

are experiencing severe withdrawal symptoms requiring higher 

dosages of IV ativan, do not have IV access routinely placed. The 

majority of these patients are receiving enteral thiamine rather 

than IM as the alternative route of administration. 

The case report presented here demonstrates that an updated 

alcohol detoxification protocol could prompt earlier identification 

and treatment of patients with WE. Although this patient 

had definite improvements in his overall condition during 

hospitalization, at discharge he demonstrated memory deficits 

that were consistent with Korsakoff syndrome. Whether earlier 

administration of higher dosages of IV thiamine would have 

changed his outcome is unknown. However, WE is considered 

a medical emergency, and therefore outcome is affected not 

only by adequate amounts of thiamine replacement but also by 

the timeliness of the administration. To this end, optimally the 

protocol would direct that the first dose of high-dosage thiamine 

be given while the at-risk patient is in the emergency department. 

CONCLUSIONS 

Wernicke encephalopathy is a neuropsychiatric condition of 

thiamine deficiency that is under-diagnosed and often undertreated. 

Specifically, oral thiamine is not absorbed to an extent 

sufficient to replace thiamine stores in WE and should not be used. 

High IV or IM dosages are required to attain serum levels high 

enough for passive transport across the blood-brain barrier. 

We propose a new alcohol detoxification protocol that identifies 

high-risk patients or those demonstrating signs of WE to receive 

parenteral thiamine 500 mg 3 times daily for a minimum of 3 

days. In addition, baseline and daily magnesium levels should be 

monitored and replaced if necessary. 

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Authors: 

Swapna Narayana, MBBS 

Leah I. Metz, MD† 



Foundation 


†Dr Metz is now a Nephrology Fellow 

at University of Iowa Health Care 

Todd J. Kowalski, MD 





African Tick Bite Fever and Crocodile Meat– 

Associated Salmonellosis Coinfection in a 

Returning Traveler 

ABSTRACT 

A 44- year- old man developed fevers, myalgias, headache, and a vesicular rash after returning 

from South Africa. A presumptive diagnosis of African tick bite fever was made and doxycycline 

was started. The patient remained symptomatic, however, and stool culture eventually grew 

Salmonella enterica subsp diarizonae. Further history revealed the patient ingested crocodile 

meat during his trip. Serology eventually confirmed the diagnosis of African tick bite fever. All 

clinical symptoms subsequently resolved following courses of doxycycline and ciprofloxacin. 


Todd J. Kowalski, MD 

Mail Stop C02-007 




Telephone: (608) 775-4472 

Fax: (608) 775-4476 

email: tjkowals@gundluth.org 

A 

frican tick bite fever is an emerging infection 

among travelers, usually caused by Rickettsia africae. 1 

Salmonella enterica subsp diarizonae is a rare human pathogen 

that is typically associated with reptile exposure. 2,3 We report 

an interesting case of coinfection with African tick bite fever 

immediately followed by crocodile meat–associated salmonellosis 

in a traveler returning from South Africa. 

CASE REPORT 

A 44-year-old, previously healthy man was admitted to the 

hospital with fevers, myalgias, and headache 10 days after returning 

from a weeklong trip to South Africa. Activities during his trip 

included foot- and vehicle-based photo safaris in the Kwa Zulu- 

Natal province. Two days prior to returning home, he consumed 

crocodile meat. One day prior to returning home, he went on a 

foot safari and reported “bug bites” above his ankles the following 

day. He did not recall a tick bite. Subsequently, he developed a 

vesicular rash on his lower extremities bilaterally, and 4 days after 

returning from Africa developed systemic symptoms of fever, 

myalgias, headache, and fatigue. He denied diarrhea or abdominal 

discomfort upon admission. He took no medications except 

atovaquone/proguanil 250/100 mg for malaria chemoprophylaxis. 

He had received typhoid vaccine intramuscularly 3 years earlier 

and had completed hepatitis A and B immunization series. 

Initial physical examination revealed a temperature of 39.1˚C, 

pulse of 83 beats per minute, and blood pressure of 127/83 mm 

Hg. The only notable finding on his physical examination was a 

vesicular, punctate rash on his lower extremities bilaterally (Figure). 

Admission laboratory values included hemoglobin concentration 

of 14.0 g/dL (to convert to g/L, multiply by 10), white blood cell 

count of 4900/μL (to convert to ×10 9 /L, multiply by 0.001), and 

platelet count of 169 ×10 3 /μL (to convert to ×10 9 /L, multiply by 

1.0). Electrolyte, creatinine, and liver transaminase concentrations 

were within reference range. The results of 3 serial malaria smears, 

blood cultures, urine cultures, dengue serology, and a chest 

radiograph were unrevealing. 

Based upon the symptoms, epidemiological exposure, and 

characteristic rash, a presumptive diagnosis of African tick bite 

fever was made, and doxycycline was initiated at a dosage of 100 

mg orally twice daily. After 24 hours the patient was afebrile and 

feeling much improved. 

Hospital discharge was planned, but just prior to anticipated 

discharge the patient redeveloped a fever (temperature, 40.1˚C). The 

following day his fevers persisted, and he developed a cough, along 

Vesicular, punctate rash visible on the patient’s lower extremities. 


with abdominal bloating and cramping pain without diarrhea. His 

myalgias had resolved. A stool culture was obtained and ceftriaxone 

was started empirically to treat the possibility of typhoid fever while 

cultures were pending. The patient subsequently defervesced over 

48 hours, and all of his symptoms resolved. His stool culture grew 

S enterica subsp diarizonae. He was discharged from the hospital 

to complete a 7-day course of doxycycline and a 10-day course of 

ciprofloxacin. Results of serology by immunofluorescence assay for 

spotted fever group rickettsia antibodies converted from a negative 

titer on day 4 of illness (immunoglobulin M [IgM]

Author: 


Physician Emeritus, 

Department of Neurology 




David Hartman, PhD, 

BC-ANCDS(A) 

Mail Stop EB3-002 




Telephone: (608) 775-9000 

Fax: (608) 775-6358 

email: dehartma@gundluth.org 


Abstract 

A patient presented with symptoms and signs consistent with a diagnosis of myasthenia 

gravis (MG), a neuromuscular junction disorder. Herein, findings from the patient’s physical 

examination and results of the edrophonium chloride (Tensilon) test administered to confirm 

the MG diagnosis are reported. The symptoms and underlying pathophysiology of MG are 

described. Finally the array of tests that can be used to aid in a diagnosis of MG are reviewed. 

A 

68-year-old man presented with a 2-month history of 

weakness of his jaw, drooping of his left upper eyelid, and 

double vision. All his symptoms were intermittent in nature. His 

jaw tired after he had chewed 3 or 4 mouthfuls and would recover 

after resting for a couple of minutes. The left upper eyelid would 

be fine in the morning but would start drooping by noon and stay 

that way the rest of the day. The double vision was also prominent 

toward the end of the day. He had experienced no difficulty 

swallowing or breathing. He had experienced no weakness of his 

neck muscles. His extremities were perfectly strong. Medical history 

was significant for rheumatic fever in childhood leading to aortic 

stenosis. He required aortic valve replacement and 2 revisions. 

Complete review of systems was unremarkable. The patient was 

taking no prescription medications. 

Findings from a general physical examination were 

unremarkable. A very definite ptosis was present on the left. The 

patient had binocular diplopia on right and left lateral gaze. Jaw 

muscles were normal but easily fatigued. Mild bilateral lower motor 

neuron facial weakness was evident. Limb musculature strength 

was normal. Deep tendon reflexes were normal and the plantar 

responses flexor. There were no sensory deficits. 

An edrophonium chloride (Tensilon) test was performed 

(Figures 1 and 2). 

(1) What is the likely diagnosis? 

(2) What does the Tensilon test show? 

(3) How would you manage this patient? 

junction by antibodies to the postsynaptic acetylcholine receptors 

(AChR). Normal quanta of acetylcholine are released at the 

nerve terminal, but the response is reduced, leading to weakness. 

In contrast, the defect in Lambert-Eaton syndrome lies in the 

presynaptic nerve terminals due to antibodies directed toward 

calcium channels and the release of insufficient quanta of 

acetylcholine. 1 Cobra venom and bungarotoxin produce blockage 

of neuromuscular transmission by prolonged nondepolarization of 

the neuromuscular junction. Botulinum toxin causes blockage of 

acetylcholine release from nerve terminals. 

In MG, the extraocular, facial, jaw, bulbar, neck, and shoulder 

girdle muscles are affected, most commonly in that order. The 

extremity and respiratory muscles are also often involved. The 

muscle weakness typically fluctuates, being minimal in the 

DISCUSSION 

This gentleman presented with classical symptoms and signs 

of myasthenia gravis (MG). MG is the prototypic neuromuscular 

junction disorder. Other entities in this spectrum are Lambert- 

Eaton myasthenic syndrome, botulism, congenital MG, familial 

infantile MG, and envenomation by cobra or alpha-bungarotoxin. 

A transitory form of MG affects 10% to 20% of the newborns 

whose mothers have autoimmune MG. 

The underlying pathophysiology in MG is distortion and 

simplification of the end-plate membrane in the neuromuscular 

Figure 1. Ptosis of the left upper 

and right lower lid is evident. 

Figure 2. Following injection of 

the edrophonium chloride, the 

ptosis is resolved. The frontal 

and nasolabial creases are more 

prominent due to improved tone 

in the facial muscles. 


morning and getting more noticeable toward the end of the day. 

Since MG is an autoimmune disease, patients tend to have an 

increased incidence of other disorders, such as rheumatoid arthritis, 

Hashimoto thyroiditis, and pernicious anemia. 

The Tensilon test can be very useful in the bedside diagnosis 

of MG. Ideally the test should be done in a double-blind fashion 

to improve objectivity. Edrophonium chloride is a short-acting 

cholinesterase inhibitor and will rapidly improve neuromuscular 

deficits due to MG. Ten mg of the drug in 1- cc doses are 

administered intravenously over about a minute. It is important 

that readily observable deficits are present so that any improvement 

that occurs is appreciated. The effect lasts about 5 minutes. The 

usual side effects are lacrymation, sweating, abdominal cramps, 

bradycardia, and occasionally hypotension, all resolving within 

5 minutes. The author dilutes 1 cc of the drug with 1 cc of the 

patient’s blood and administers a 2-mg test dose. If there are no 

adverse effects, the remainder of the drug is given over the next 

minute. Electrocardiographic monitoring is not necessary. 

Another rapid and easy test for MG involves applying ice to 

the ptotic eyelid for a few minutes. Cooling maintains the sodium 

channels open for a longer period, thus enhancing the action 

potentials at the neuromuscular junction. This is the underlying 

principle that aggravates the symptoms of myotonia. The converse 

of this is also the reason for aggravation of symptoms in multiple 

sclerosis when the body temperature rises above normal. 

Laboratory tests can aid in diagnosis. Antibodies against AChR 

are found in most patients with MG. Antistriational antibodies are 

also found in patients who have thymic hyperplasia or thymoma. 

The antibody titers, however, do not correlate with the severity of 

the clinical illness. 

A small subset of patients with MG do not have AChR 

antibodies but may have antibodies to muscle-specific tyrosine 

kinase (MuSK). These patients tend to have more prominent 

bulbar and respiratory muscle involvement and do not respond 

well to cholinesterase inhibitors. 2 

Since there is high incidence of thymic hyperplasia and of 

benign or malignant thymoma in patients with autoimmune MG, 

a computed tomographic (CT) scan of the chest should be obtained 

on all patients. Our patient’s CT scan revealed a thymoma. 

Repetitive nerve stimulation studies and single-fiber 

electromyography can also aid in diagnosis of MG. 

The immediate treatment of MG consists of an oral 

anticholinesterase-inhibiting drug such as pyridostigmine 

bromide. 3 The use of immunosuppressive drugs such as 

corticosteroids, azathioprine, cyclophosphamide, cyclosporin, 

mycophenolate mofetil, and rituximab may be necessary in some 

patients. Myasthenic crises usually respond well to plasmapheresis 

or intravenous immunoglobulin therapy. Thymectomy is 

indicated for thymoma and should be considered in all patients 

not responding to conventional medical therapies. 

Drugs known to cause neuromuscular blockage should be 

avoided. Other drugs that have a potential for aggravating the 

symptoms of MG include quinine, quinidine, procainamide, 

aminoglycosides, beta blockers, and calcium channel blockers. 

Induction of autoimmune MG by D-penicillamine 4 and statins 5 

is well documented. 

REFERENCES 

1. O’Neill JH, Murray NM, Newsom-Davis J. The Lambert-Eaton myasthenic 

syndrome. A review of 50 cases. Brain. 1988;111(Pt 3):577-596. 

2. Sanders DB, El-Salem K, Massey JM, McConville J, Vincent A. Clinical aspects of 

MuSK antibody positive seronegative MG. Neurology. 2003;60(12):1978-1980. 

3. Keesey JC. Clinical evaluation and management of myasthenia gravis. Muscle 

Nerve. 2004;29(4):484-505. 

4. Albers JW, Hodach RJ, Kimmel DW, Treacy WL. Penicillamine-associated 

myasthenia gravis. Neurology. 1980;30(11):1246-1249. 

5. Purvin V, Kawasaki A, Smith KH, Kesler A. Statin-associated myasthenia gravis: 

report of 4 cases and review of the literature. Medicine. 2006;85(2):82-85. 

Pelican 

Photograph by David E. Hartman, PhD 



Authors: 






Douglas Lanska, MD, MS, MSPH, 

FAAN 

Veterans Affairs Medical Center 

Great Lakes Healthcare System 

Tomah, Wisconsin 

Professor of Neurology 

University of Wisconsin School of 

Medicine and Public Health 

Madison, Wisconsin 

Surgeon General William A. Hammond 

(1828-1900): 

Successes and Failures of Medical Leadership 

Abstract 

A controversial character in his day, William A. Hammond made a number of lasting 

contributions to the medical profession in the second half of the 19th century. Here we 

recount the highlights and the lowlights of Hammond’s long and lively career. 



Mail Stop C02-007 




Telephone: (608) 782-7300 

Fax: (608) 775-5542 

email: jssartin@gundluth.org 

Having rushed up the stairs of his Washington home 

with characteristic alacrity, on January 5, 1900, 

William Alexander Hammond, MD, collapsed with an acute 

coronary occlusion that would soon prove fatal. Thus ended the 

life of a remarkable physician and man of science, whose long 

career spanned the transition of medicine from a relatively crude 

and ineffective empiricism to a profession based on scientific 

principles. He is best remembered today as the unfortunate victim 

of Washington politics, being the only Army Surgeon General to 

suffer the indignity of a court-martial and removal from office in 

1863. Nevertheless, he had an illustrious career as a seminal figure in 

American neurology, and his innovative organizational leadership 

produced new military and civilian specialty hospitals, significant 

improvements in military medical care, a ground-breaking history 

of medical care during the Civil War, and various other institutions 

and professional medical organizations. 

Hammond’s leadership successes were balanced by significant 

failures, and more than a century after his death his legacy remains 

complicated and controversial. Hammond was indeed a colorful 

and complex character with both considerable attributes and 

faults: a brilliant organizer and administrator, and an outstanding 

teacher and apostle of neurology, but at best a mediocre if prolific 

scholar. More problematically, he came across as an audacious, 

contentious, boastful, and arrogant individual 1 with “a voice so 

powerful that it could be heard up-wind in a hurricane.” 2 In his 

appetites and endeavors Hammond symbolized the best and worst 

of American culture as it barreled through the latter half of the 

19th century. 

Early Career 

William Hammond was born on August 28, 1828, in Annapolis, 

Maryland, and grew up in Harrisburg, Pennsylvania. By the age of 

20 he had completed his medical training at the University of the 

City of New York. In July 1848 he married his first wife, Helen 

Nisbet, and began his service in the Army in the distant post of 

New Mexico Territory. His various postings throughout the West 

afforded him a steady income for his burgeoning family, soon to 

include 3 children, as well as the opportunity to learn medicine 

and engage in scientific inquiries in an arena far removed from the 

constraints of the eastern medical establishment. 3 

He approached his work with precision and imagination, and 

his reputation as a medical officer in the Army and as a scientific 

investigator blossomed throughout the 1850s. He had at least 24 

publications on various topics — particularly nutrition, physiology, 

and toxicology — during that decade. His military service was 

interrupted for a while in 1852, as he manifested the first signs 

of the peculiar and disabling cardiac condition that would trouble 

him intermittently for the next 8 years. In 1857 he won the 

American Medical Association’s essay prize for his entry on “The 

Nutritive Value and Physiological Effects of Albumen, Starch, 

and Gum,” based on experiments and observations with himself 

as the test subject. 4 Toward the end of his early Army career in 

1858 he spent an extended medical leave in Philadelphia, where 

he collaborated with other young physicians, including Silas Weir 

Mitchell (1829-1914), in establishing an elite research society, 

the Philadelphia Biological Society. His association with Mitchell 

would later bear fruit in the advancement of the field of neurology 


in America. By 1860 Hammond resigned his military commission 

to take a position with the University of Maryland Medical School 

in Baltimore. 

Court-martial for a Surgeon General 

Hammond was well on his way to a promising career in 

academic medicine when the conflagration between northern and 

southern states came to a head. In 1861 the young faculty member 

witnessed a mob attack on members of the 6th Massachusetts 

Infantry Regiment as they marched through Baltimore following 

the reoccupation of Fort Sumter. Hammond treated several soldiers 

and performed trephination on a young man struck in the head by 

a brick, who nevertheless died. 5 Thus, through chance Hammond 

attended one of the first fatalities of the Civil War. In May 1861 

Hammond volunteered again for service in the United States Army 

(Figure 1). Though initially assigned to mediocre posts with a low 

rank incommensurate with his previous 11 years of outstanding 

military service, he worked diligently and was soon made an 

Inspector of Hospitals in the eastern Atlantic area. 6 

Figure 1. Brigadier General William A. Hammond, Surgeon General 

of the United States Army. (Wet collodion glass plate in Brady 

National Photographic Art Gallery, Washington, DC. Courtesy of 

the National Library of Congress Prints and Photographs Division, 

Washington, DC.) 

His reports to the newly-established but influential U.S. 

Sanitary Commission were so impressive that prominent 

members, including landscape architect Frederick Law Olmsted, 

began to promote the 34-year-old doctor as a replacement for the 

elderly and incompetent Surgeon General Clement Finley. 7 As a 

result, Hammond became deeply involved in the arcane world of 

Washington politics, using it to his benefit as he catapulted into 

the most powerful medical position in the country at that time. 

In April 1862 he was awarded the post with a rank of brigadier 

general, and the American Medical Times exulted that “No man 

could be selected who so happily combines in his professional 

relations the confidence and esteem of both the Medical Staff of 

the Army, and the profession of the country.” 8 

As Surgeon General, Hammond reformed the medical service 

of the Union army, actively promoted hygienic principles for 

soldiers, 9 and established various specialty hospitals to treat 

injured soldiers. After colleague S. Weir Mitchell expressed interest 

in cases with neurological disorders, Hammond set aside a ward 

for neurological cases, and when the neurology ward “overflowed 

with cases” Hammond ordered the establishment of the U.S. Army 

Hospital for Diseases of the Nervous System, which opened on May 

5, 1862, and operated until October 22, 1864, in Philadelphia. 

The hospital was eventually moved to a site on Turner’s Lane with 

beds for 400 men. There, Mitchell conducted pioneering studies 

of gunshot wounds and other injuries of the peripheral nerves with 

the assistance of George Reed Morehouse and William Williams 

10 –12 

Keen, both then acting assistant surgeons. 

Never one to dither or harbor second thoughts, Hammond 

seized the opportunities presented to him, installing young and 

energetic new department heads in place of the “Old Guard.” 

Among these was Jonathan Letterman (1824-1872), who was 

promoted from assistant regimental surgeon to medical director 

of the Army of the Potomac. Hammond’s instructions to his 

subordinates were clear: “Red tape was out; efficiency and results 

would be all that counted.” 13 His approach was perhaps necessary 

and was certainly dramatically effective, but in the process his 

arrogance, his overbearing manner, and his failure to build 

coalitions and seek the input of subordinates in the face of major 

organizational changes alienated many prominent officers in the 

Army War Department. 

Hammond recognized the incredible inefficiencies and gross 

underfunding of the Army Medical Department as the first problems 

to be addressed. He streamlined procurement policies and lobbied 

for increased funding from Congress. His success is reflected in 

the fact that the allocated budget went from $90 000 in 1860 to 

over $10 000 000 in 1863. 14 Personnel policies were overhauled 

as well, and he pushed for the recruitment of large numbers of 

military and civilian contract doctors to take care of the appalling 

number of casualties that the conflict produced. At the same time, 

Hammond standardized the rank of military medical officers and 

insisted on strict guidelines for their acceptance into the Army. His 

proposals for a professional ambulance corps and an independent 

board of Inspectors General met with more opposition, but were 

eventually implemented with Congress’ reluctant acquiescence. 

The latter board proved to be a source of great friction with a 

number of Washington’s power brokers and eventually contributed 

to Hammond’s fall from grace. 


successes and failures of medical leadership 

Other forward-looking and successful Hammond initiatives 

during the Civil War included the centralization of military 

hospital authority; the initiation of a massive program for 

building large pavilion-style hospitals, which were state-of-theart 

in the 1860s; and streamlining and standardizing procedures 

for discharging disabled men from the service. In between official 

duties he found time to publish an extended treatise on public 

health for the military, a book which quickly became a standard 

text. 9 Hammond proposed a military medical school, an idea 

which was not to reach fruition until 1893 as the Army Medical 

School. Two of his ideas were far-ranging, indeed, and represent an 

important legacy for medicine in general: The Medical and Surgical 

History of the War of the Rebellion, a 13-volume set chronicling in 

great detail the medical issues confronted during the war; 14 and the 

Army Medical Museum, a collection of pathological specimens that 

evolved into the renowned Armed Forces Institute of Pathology. In 

1878, Hammond wrote, “There are few things in my professional 

career in which I take more pride than that the ideas of the Army 

Medical Museum and of the Medical and Surgical History… were 

conceived by me.” 15 

His early work was highly praised by soldiers’ advocacy groups. 

As Reverend Henry Whitney Bellows (1814-1882), the first 

President of the U.S. Sanitary Commission, wrote in 1862, “I am 

more and more pleased with Dr. Hammond. His views are large, 

his mind active & prompt — his action at present embarrassed by 

almost insuperable difficulties. But he is cutting his way out.” 16 

Such a positive view of Dr Hammond’s accomplishments was 

not universal, however. Many critics found him abrupt, tactless, 

and pompous. In May 1863 Hammond issued a memorandum 

outlawing use of the popular medicinal compounds calomel (a 

mercurial agent) and tartar emetic (an emetic) by military doctors, 

and found almost universal disapproval of his actions. Political 

wrangling over the composition of the newly formed corps of 

Inspectors General further poisoned the atmosphere. 

His biggest enemy was Edwin McMasters Stanton (1814 –1869), 

the U.S. Secretary of War, who had opposed Hammond’s 

appointment from the beginning. In late 1863 opposition to the 

Surgeon General reached a critical mass within the War Department, 

and Stanton engineered a subtle coup. He ordered Hammond on 

an extended tour outside of Washington, and during Hammond’s 

absence installed his own favorite, Joseph K. Barnes (1817–1883), 

the head of the Inspectors General. On September 3, 1863, by 

special order of the War Department, Barnes was “empowered to 

take charge of the bureau of the Medical Department of the army 

and to perform the duties of Surgeon General during the absence 

of that office [ie, Hammond].” 17,18 Hammond was outraged at the 

charges of fraud and mismanagement that were leveled at him and 

demanded a court-martial, a move that proved to be a mistake. 

The court was essentially hand-picked by Stanton and his allies, 

and the testimony was flimsy and trumped up, if not perjurous. 

Hammond was found guilty of “irregularities” in the purchase 

of medical supplies and convicted of “conduct unbecoming an 

officer” and given a dishonorable discharge on August 28, 1864. 18 

While the New York Times opined that discharge was “too mild 

a punishment… for utter villainy,” 5 for the most part the medical 

community was supportive of Hammond and considered the 

outcome a travesty. Barnes ultimately became the Surgeon General 

on August 22, 1864, a position he held until 1882. 

A Successful Private Practice 

Dr Hammond’s life and career after the undeniable humiliation 

of his court-martial and dishonorable discharge disproved the 

famous maxim attributed to F. Scott Fitzgerald that “There are 

no second acts in American lives.” Hammond’s finances were in 

shambles, but friends helped him get established in New York City, 

where he inaugurated an increasingly lucrative clinical practice 

focusing on diseases of the brain and psyche (Figure 2). 

In the 2 decades following the Civil War, Hammond’s medical 

practice flourished, and in his best years he was 1 of the highest-paid 

physicians in the country. He had a large house on West 54th St. in 

New York City that was filled with antiques, rare books, and works 

Figure 2. William A. Hammond in civilian neurological practice after 

the Civil War. (Courtesy of the National Library of Medicine.) 

of art where he frequently held court over exclusive dinner parties 

and large soirees. At a time when general practitioners struggled 

financially, Hammond’s estimated annual earnings of $60 000 

($840 000 in current dollars) far surpassed almost all contemporary 

physicians. As noted by fellow neurologist Charles Loomis Dana, 

“Hammond put neurology in New York on its feet economically 

by his amazing audacity of charging $10 [approximately $140 in 

modern currency] as his fee, and showing the bills on his table.” 19 

Not content with purely scientific pursuits, he turned his hand 

to novels, publishing 9 works during his lifetime. They generally 

represented typical Victorian melodramas, many referring to 

scientific topics and 1 alluding to his professional crisis of 1863. 20 

He was married twice, with 2 children who lived to adulthood. 


By all appearances Hammond had a comfortable family life, 

and on one novel he collaborated with his beloved daughter, 

Clara. 21 His son, Graeme, followed his footsteps and became a 

well-respected neurologist. In the 1870s William Hammond 

pursued a strong interest in forensic medicine and testified in a 

number of high-profile cases, always for the defense and typically 

involving insanity pleas. 22 Hammond’s testimony often included 

results of measurements he had taken of the defendant using a 

dynamograph, an instrument that measured muscle power but was 

used by some physicians as a diagnostic aid. 23 His testimony was 

controversial and even criticized as fraudulent; certainly by modern 

standards much of it was unscientific and ill-founded, but there is 

little doubt that his ideas came from a singular and strongly held 

medical Weltanschauung (world view). 

Contributions to the Development of Neurology as 

a Specialty 

Hammond made major contributions to the early development 

of neurology as a medical specialty in the United States. In brief, 

he helped foster the development of exclusive neurology specialty 

societies and medical journals; he wrote the first American textbook 

of neurology; 24 he founded the New York State Hospital for Diseases 

of the Nervous System (1870), an innovative charitable and 

educational venture that was short-lived but established a model 

for specialty care in the nascent field of neurology; and he founded 

the New York Post-Graduate Medical School and Hospital (1882, 

incorporated 1886), the first of such graduate medical schools 

in the United States, and a precursor to the modern neurology 

residency. 25 He developed or adopted new neurological diagnostic 

technologies, including the dynometer and dynamograph (although 

often with inadequate theoretical or empirical foundation). 26 

And, importantly, Hammond worked tirelessly to enhance public 

awareness of neurology and neurological disease. 

Hammond was the primary impetus behind the founding of 

the American Neurological Association (ANA) — the first national 

neurological association in the world and a critical contributor to 

the early development of American neurology. 27 On December 14, 

1874, in a letter to selected colleagues across the country, Hammond 

with the 6 other founding members (R. Bartholow, M. Clymer, J. 

S. Jewell, E. C. Seguin, J.J. Putnam, and T. M. B. Cross) proposed 

the organization of the ANA, which was ultimately founded in 

1875 with an additional 29 charter members. Initial members 

were drawn primarily from New York, Boston, Philadelphia, and 

Chicago. At the first meeting in New York City, lasting 2 days, the 

scientific presentations included Hammond’s presentation of his 

original case of athetosis. Hammond later served as president of 

the ANA in 1882. 

During his career, Hammond held various neurology 

professorships, including those at the Bellevue Hospital Medical 

College, the College of Physicians and Surgeons, the University of 

the City of New York, and the New York Post - Graduate Medical 

School (the latter which he helped establish). 1 He also helped 

found the New York Neurological Society, as well as organizations 

devoted to the burgeoning field of forensic medicine. 28 He was an 

editor for a number of medical journals, including the Quarterly 

Journal of Physiological Medicine and Medical Jurisprudence (which 

he founded), the New York Medical Journal (which he helped 

found), the Maryland and Virginia Medical Journal (which he 

founded), and the Journal of Nervous and Mental Disease. He wrote 

widely on medical topics, including general texts on neurology 

and psychiatry, and monographs on cerebellar physiology and 

pathology, cerebral hyperemia, spinal irritation, sleep disorders, 

impotence, venereal diseases, hygiene, and medico-legal issues, 

among others. 

In 1871 Hammond published his magnum opus, Treatise on 

Diseases of the Nervous System, the first comprehensive textbook of 

neurology published in America, which eventually went through 

9 printings and which remains the most highly cited 19th - century 

American neurology textbook. 29 In his textbook and in separate 

articles 30 Hammond described a condition that he called athetosis 

(from the Greek term for without fixed position, subsequently 

sometimes referred to as Hammond’s disease), “characterized by an 

inability to retain the fingers and toes in any position in which 

they may be placed, and by their continual motion.” 31 There 

were associated “pains in the spasmodically-affected muscles, and 

especially complex movements of the fingers and toes, with a 

tendency to distortion,” with a slower, sinuous quality compared 

with chorea, and without any associated weakness (Figure 3). Based 

on Thomas Willis’ 200 -year-old concept that the corpus striatum is 

the seat of motor power, Hammond speculated that “one probable 

seat of the morbid process [in athetosis] is the corpus striatum.” 

Only several years earlier Hammond’s British contemporaries 

William Broadbent 32 and John Hughlings Jackson 33 had implicated 

the striatum in chorea — localizations that would prove essentially 

correct, though somewhat serendipitously. Hammond’s localization 

was ultimately supported by the autopsy on the original case that 

Figure 3. Hand posture of athetosis from the first edition of 

Hammond’s textbook in 1871 and corresponding pathology as 

reported by his son, Graeme Hammond, in 1893. 36 



was reported by his son, Graeme Hammond, in 1890. 34 There 

was indeed a lesion involving the lenticular nucleus, the posterior 

thalamus, and part of the internal capsule (Figure 3). Graeme 

Hammond “called attention to the fact that the motor tract was 

not implicated in the lesion, and claimed that this case was further 

evidence of his theory that athetosis was caused by irritation of the 

thalamus, the striatum, or the cortex, and not by a lesion of the 

motor tract.” 

Despite the confirmation of a proposed clinicopathological 

association, athetosis was, and remains, controversial, being 

considered by many late 19th - and 20th - century neurologists as a 

form of posthemiplegic chorea or part of a continuum between chorea 

and dystonia 35-38 Charcot, in particular, dismissed Hammond’s 

athetosis as “simply choreiform movements” or as “only a variety 

of post-hemiplegic hemichorea,” to which Hammond retorted, “I 

have only to say that the distinction between the two conditions 

is as well marked as between chorea and disseminated cerebrospinal 

sclerosis. In athetosis the movements are slow, apparently 

determinate, systematic, and uniform; in post-hemiplegic chorea 

they are irregular, jerking, variable, and quick. Moreover, athetosis 

is not by any means necessarily post-hemiplegic.” 36 Even modern 

authors have erroneously indicated that Hammond’s original cases 

were examples of a posthemiplegic movement disorder, but, as 

emphasized by Hammond, “In the original case there had never 

been hemiplegia, nor was there such a state in the second case, 

on which [Hammond’s] description of the disease was based.” 39 

Hammond’s cases both occurred after convulsions and loss of 

consciousness, and both were associated with some sensory loss. 

Hammond accepted that hemiplegia could be an antecedent in 

some cases, but “Where the motor tract is implicated there will be 

hemiplegia, spastic spasm, and exaggerated reflexes in addition to 

the athetosis.” 39 

Hammond also published volumes of other scientific articles 

on matters large and small; his topics included insanity, male and 

female sexuality, baldness, temperance, drugs both recreational and 

therapeutic, syphilis, psychosis, evolution, and sleep. 3 Hammond’s 

more than 400 articles and 30 published books are a testament 

to the enormous energy he put into his work, although some 

are of less than optimal quality and some were primarily for selfpromotion. 

Even into his later career, he continued to carry out 

experiments, frequently using himself as the subject, as he did for 

tests on cocaine 40 and testosterone 41 (parenthetically, he added “not 

that I thought I required the injection for any infirmity”). 

Although he was himself quite prominent, Hammond achieved 

little success in his efforts to foster the acceptance of neurology 

as a specialty among the masses of general practitioners or, for 

that matter, among the superintendents of insane asylums in the 

late 19th century. His arrogance, obstinacy, and flamboyance 

proved to be counterproductive, and some general practitioners 

and psychiatrists (or alienists as they were then called) considered 

Hammond’s fees not only exorbitant but criminal. 42 

Battles with Alienists 

Although Hammond and many 19th - century American 

neurologists practiced some psychiatry, there was at the time 

considerable animosity and antagonism between neurologists and 

the superintendents of asylums for the insane. The superintendents, 

despite being physicians, were relatively isolated from the rest of 

the medical profession, adopted primarily managerial roles, and 

dealt largely with institutionalized patients in a custodial fashion. 

Nevertheless, these superintendents were powerful, often had 

strong political ties, were supported by public funds, and controlled 

significant numbers of jobs. 

Beginning in the 1870s, Hammond and other neurologists 

repeatedly argued that psychiatric illnesses, and particularly 

neurasthenia, would be better managed by neurologists under 

an organic paradigm, but offered no clearly better alternative to 

the management of asylum patients. 43-47 Attempts by Hammond 

and other neurologists to undermine the authority of the 

superintendents and to take control of the asylums led predictably 

to open conflict between these groups. 

The conflicts between neurologists and asylum superintendents 

received increasing media attention and public notice as 

representatives of these groups testified as expert witnesses on 

opposing sides in a number of high-profile legal cases involving 

insanity pleas. 22 In the late 1870s, hostilities escalated and erupted 

in bitter verbal and printed attacks between the neurologists, 

championed by Hammond and New York neurologist Edward 

Charles Spitzka (1852-1914), and the asylum superintendents, 

championed by John Purdue Gray (1825-1886), a powerful and 

contentious individual who was an asylum superintendent from 

Utica State Hospital, New York, 1 of the 13 founders of the 

Association of Medical Superintendents of American Institutions 

for the Insane (which later became the American Psychiatric 

Association) and the editor of the American Journal of Insanity 

(now the American Journal of Psychiatry), and Eugene Grissom 

(1831-1902), who was an asylum superintendent from Raleigh, 

North Carolina, and a friend of Gray’s. 48 In May 1878 at a meeting 

of the Association of Medical Superintendents, Grissom, perhaps 

at the instigation of Gray, verbally attacked Hammond and labeled 

him a “supposed expert,” the “Benedict Arnold of his profession,” 

“[a] man lost to conscience and honor,” and “a Judas Iscariot of 

humanity, selling the blood of his children for thirty pieces of 

silver…. Now at last we shudder as we recognize that the false 

expert is no man at all, but a moral monster, whose baleful eyes 

glare with delusive light; whose bowels are but bags of gold, to feed 

which, spider-like, he casts his loathsome arms about a helpless 

prey.” 42 This diatribe was reported to have produced thunderous 

applause among the superintendents, and the speech was soon 

published (not surprisingly) in the American Journal of Insanity. 

This personal attack on Hammond resulted in an interchange 

of open letters from Hammond and Grissom presenting their 

cases and rebutting each other, followed closely by announcements 

and editorials in general medical, neurological, and psychiatric 

journals — many of which (outside of the psychiatric literature) 

supported Hammond. 49,50 For example, an editorialist in the Saint 

Louis Clinical Record concluded that “Dr. Hammond was attacked 

for expressing his opinion on the asylum question, fearlessly and 

openly as he did. . . . [It] is but natural that we should ask ourselves, 

why Dr. Hammond was singled out for attack. There can be no 

doubt, after the evidence adduced, that he has been attacked for 

being the most prominent member on the committee appointed 

to memorialize the legislatures in regard to charges made against 

asylums…. The real motive for attacking Dr. Hammond, was 


weakness on the part of the cause of the Asylum Association. It was 

much more easy to attack the record of a prominent individual, 

justly or unjustly, than to disprove facts alleged, and arguments 

advanced against a corrupt system.” 51 

Hammond himself noted “my sole cause of offense was the 

fact that I had ventured to express my views—without the 

slightest personality — on the subject of mechanical restraint 

in insane asylums. I should have asked you, what you and those 

you represented could possibly hope to gain by treating a most 

important subject, not with reasoning, but with vituperation so 

foul that it would disgrace the inmates of a brothel…. I should 

have dwelt upon the fact that if this be your line of defense, you 

grossly mistake the temper and the understanding of the American 

people; for though no prophet, I perceive very clearly that what 

Pinel and Conolly did for France and England [in providing 

humane care for those with mental illness], some one will do for 

this country, and that ere long, camisoles and Utica cribs will 

go the way of chains and dungeons…. I might have mentioned 

the wretched taste, the low professional morality, the transparent 

falsehoods which characterize your speech, and the utter disregard 

of the ethics of your profession which prompted you to publish it 

in a common newspaper.” 52 Hammond went so far as to publicly 

diagnose Grissom as “insane.” 

To address growing concern over the management of the 

asylums, a New York State Senate Investigative Committee 

held hearings on asylum reform in 1880, with testimony from 

Hammond and Spitzka, and from the psychiatrists. However, the 

neurologists failed to establish exclusive expertise for treatment of 

the insane, nor did they present a viable improvement over the 

status quo. Furthermore, the commission—selected as it was based 

on political connections — was biased toward the superintendents, 

or as Hammond put it, the commission “could not have been more 

favorable to the superintendents if the latter had themselves, as 

was very likely, selected the names of the appointees.” 53 As a result, 

little positive reform came from the hearings, and the psychiatrists 

maintained control over the asylums. 

At the trial of Charles Jules Guiteau (1841-1882) in 1881 

following Guiteau’s assassination of President James Garfield 

(1831-1881), the position of the neurologists was further weakened 

when they testified for the defense. Hammond, Spitzka, and 

other neurologists testified that Guiteau was insane and suffered 

from “reasoning mania,” while Gray — the chief prosecution 

witness — testified that Guiteau was sane. 54 Guiteau was found 

guilty and hung. Although the neurologists were later shown to 

be correct— a subsequent autopsy of Guiteau showed evidence of 

what would today be diagnosed as neurosyphilis — their position 

was certainly unpopular. In further ironic twists, Gray was shot 

to death by one of his mentally ill patients several months after 

his testimony, and Grissom did himself become insane from 

neurosyphilis and committed suicide in 1902. 55,56 

Later Career and Legacy 

In 1888 Hammond gave up his New York practice and 

started a private sanatorium in Washington, DC. He undertook 

the study of various animal extracts and their effect on human 

disease states, with an entrepreneurial as well as scientific interest 

in his enterprises. The asylum proved to be a virtual money-pit, 

while most of Hammond’s business schemes, such as his interest 

in proprietary nostrums, came to naught and embroiled him in 

financial and legal entanglements. As one contemporary wrote 

after Hammond’s demise, “Scheme after scheme… would arise in 

his mind, for he was optimistic almost to the verge of the visionary, 

but some defect that a more prudent man would have guarded 

against too often barred their fruition.” 57 His writings during this 

period focused mainly on promoting animal and plant extracts 

for relief of a variety of ailments. 3 While he perhaps focused 

too much on what might politely be termed quack theories, 

he continued to ruminate on the physical correlates of sleep, 

criminality, and insanity. 

In 1898 Hammond sought to revisit the issue of his courtmartial 

and loss of military pension. While he saw the annulment 

of the verdict in 1879, after a review of the original evidence by 

Congress, his pension was not restored. By 1898 he had run out of 

money and rather desperately petitioned Congress for a restoration 

of his military pension or to be placed on active duty as a medical 

officer in the Spanish-American War (at the rather ripe age of 70); 

however, his request was politely declined. 5 

William Hammond was thus a singular figure, a man of 

voluminous energy with a passion for science and, indeed, for 

life. His accomplishments rank with those of the finest American 

physicians of his time, and his leadership and innovations during the 

Civil War alone changed the face of military medicine and ensured 

that many thousands of lives were saved that would otherwise 

have been lost. As an organizational leader he had few peers. His 

personality reflected the extroverted ambition of the Victorian 

period in America, where innovative leaders like Hammond were 

striving for new approaches to old problems despite being hampered 

by more conservative contemporaries. Hammond typified some 

of the excesses of that era, as well, such as a hyperbolic emphasis 

on technology and an overconfidence bordering on arrogance. 

Although he actively dabbled in politics and finance, his talent in 

these areas was lacking, and his shortcomings caused him much 

grief. Perhaps the chief criticism of Hammond from a scientific 

point of view is that he lacked the necessary rigor in his thinking. 

Though he loved inquiry and investigation, he was unable to 

distinguish the truly significant from the merely interesting, and 

as a consequence he held a number of execrable theories even 

after diligent research by others had proven them fallacious. In 

this respect his confident though erroneous courtroom testimony 

regarding insanity actually damaged the evolving legal theory on 

this subject. 

Perhaps the most apt and concise judgment on William 

Hammond came from a colleague, Frank P. Foster, who eulogized 

that Dr Hammond “came very near being a great man.” 57 

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Specialty. Minneapolis, MN: American Academy of Neurology; 2007. 

2. Haymaker W. William Alexander Hammond (1828 -1900). In: Haymaker W, 

Schiller F, eds. The Founders of Neurology; One Hundred and Forty-Six Biographical 

Sketches by Eighty -Eight Authors. 2d ed. Springfield, IL: Thomas; 1970:448. 



3. Key JD, Blustein BE. William A. Hammond, MD (1828 -1900): The Publications 

of an American Neurologist. Rochester, MN: Davies Press; 1983:7-14. 

4. Hammond WA. Experimental researches relative to the nutritive value and 

physiological effects of albumen, starch, and gum, when singly and exclusively 

used as food, being the prize essay of the American Medical Association for 1857. 

Trans Am Med Assoc. 1857;10:511-587. 

5. Freemon FR. The first career of William Alexander Hammond. J Hist Neurosci. 

1996;5(3):282-287. 

6. Blustein BE. Preserve Your Love for Science: Life of William Hammond, American 

Neurologist. Cambridge and New York: Cambridge University Press; 1991:53 -54. 

7. Adams GW. Doctors in Blue: The Medical History of the Union Army in the Civil 

War. New York: H. Schuman; 1952. [Facsimile Reprint No. 84. Dayton, OH: 

USA Press of Morningside; 1985:24- 41.] 

8. Anonymous. Editorial. Am Med Times. 1862;4:239. 

9. Hammond WA, Rutkow IM. A Treatise on Hygiene: With Special Reference to 

the Military Service. Philadelphia: J. B. Lippincott & Co; 1863. [Reprint: San 

Francisco: Norman Publishing; 1991.] 

10. Mitchell SW. On the diseases of nerves, resulting from injuries. In: Flint A, 

ed. Contributions Relating to the Causation and Prevention of Disease, and to 

Camp Diseases; Together with a Report of the Diseases, etc., among the Prisoners at 

Andersonville, Ga. Vol 1. New York and Cambridge: US Sanitary Commission; 

Riverside Press; 1867:412 - 468. 

11. Mitchell SW, Morehouse GR, Keen WW. Gunshot Wounds, and Other Injuries of 

Nerves. Philadelphia: J. B. Lippincott & Co; 1864. 

12. Mitchell SW. Injuries of Nerves and their Consequences. Philadelphia: J. B. 

Lippincott; 1872. 


War. New York: H. Schuman; 1952. [Facsimile Reprint No. 84. Dayton, OH: 

USA Press of Morningside; 1985:32.] 

14. US Surgeon General’s Office, Barnes JK, Woodward JJ, Smart C, Otis GA, 

Huntington DL. The Medical and Surgical History of the War of the Rebellion. 

(1861- 65). Washington: Gov’t Print. Off.; 1870. 

15. Hammond WA. Quoted by: Blustein BE. Preserve Your Love for Science: Life 

of William A. Hammond, American Neurologist. Cambridge and New York: 

Cambridge University Press; 1991:71. 

16. Bellows HW. Quoted by: Blustein BE. Preserve Your Love for Science: Life 

of William A. Hammond, American Neurologist. Cambridge and New York: 

Cambridge University Press; 1991:61- 62. 


War. New York: H. Schuman; 1952. [Facsimile Reprint No. 84. Dayton, Ohio: 

USA Press of Morningside; 1985:39 - 41.] 

18. Blustein BE. Preserve Your Love for Science: Life of William Hammond, 

American Neurologist. Cambridge and New York: Cambridge University Press; 

1991:86 - 93. 

19. Dana CL. Early neurology in the United States. JAMA. 1928;90:1421-1424. 

20. Hammond WA. Robert Severne, his Friends and his Enemies. Philadelphia: J. B. 

Lippincott; 1867. 

21. Hammond WA, Lanza CH. Tales of an Eccentric Life. New York: Appleton; 1886. 

22. Patten A, Patten BM. William A. Hammond, the dynamograph, and bogus 

neurologic testimony in old New York. J Hist Neurosci. 1997;6(3):257- 263. 


Neurol. 2000;57(11):1649 -1653. 

24. Hammond WA. A Treatise on Diseases of the Nervous System. New York: D. 

Appleton and Company; 1871. 

25. Pappert EJ. Training opportunities for the nineteenth-century American 

neurologist: preludes to the modern neurology residency. Neurology. 

1995;45(9):1771-1776. 


Neurol. 2000;57(11):1649 -1653. 

27. Goetz CG, Chmura TA, Lanska D. Part 1: The history of 19th century neurology 

and the American Neurological Association. Ann Neurol. 2003;53 Suppl 

4:S2 - S26. 

28. Haymaker W. William Alexander Hammond (1828 -1900). In: Haymaker 

W, Schiller F, eds. The Founders of Neurology; One Hundred and Forty - Six 

Biographical Sketches by Eighty-Eight Authors. 2d ed. Springfield, IL: Thomas; 

1970:445 - 449. 

29. Lanska DJ. Characteristics and lasting contributions of 19th-century American 

neurologists. J Hist Neurosci. 2001;10(2):202-216. 

30. Hammond WA. Athetosis. Medical Times Gazette (London). 1871;2:747-748. 

31. Hammond WA. Athetosis. In: A Treatise on Diseases of the Nervous System. New 

York: D. Appleton and Company; 1871:654. 

32. Broadbent WH. On the pathology of chorea. Br Med J. 1869 ; 86 : 

345 - 347- 369 - 371. 

33. Jackson JH. Observations on the physiology and pathology of hemi-chorea. 

In: Taylor J, Holmes G, Walshe FMR, eds. John Hughlings Jackson: Selected 

Writings. Vol 2. Nijmegen, The Netherlands: Arts and Boeve Publishers; 

1868/1932/1996:238 - 245. 

34. Hammond GM. Pathological findings in the original case of athetosis. J Nerv 

Ment Dis. 1890;17:555. 

35. Mitchell SW. Post-paralytic chorea. Am J Med Sci. 1874;68:342 - 352. 

36. Gowers WR. On “athetosis” and post-hemiplegic disorders of movement. Med 

Chir Trans. 1876;59:271-326. 

37. Gowers WR. A Manual of Diseases of the Nervous System. London: J and A 

Churchill; 1888. 

38. Charcot JM. On athetosis. In: Sigerson G, trans. Lectures on Diseases of the 

Nervous System: Delivered at La Salpêtrière. Vol 2. London: New Sydenham 

Society; 1881:390 - 394. 

39. Hammond WA, Hammond GM. Athetosis. In: A Treatise on Diseases of the 

Nervous System. New York: D. Appleton and Company; 1893:324. 

40. Hammond WA. Cocaine and the so-called cocaine habit. NY Med J. 

1886;44:637- 639. 

41. Hammond WA. Experiments relative to the therapeutical value of the expressed 

juice of the testicles when hypodermically introduced into the human system. 

NY Med J. 1889;50:232-234. 

42. Grissom E. True and false experts. Am J Insanity. 1878;35:1- 36. 

43. American Neurological Association. Minutes of the first annual meeting of the 

American Neurological Association, New York, 1875. Papers of the American 

Neurological Association Collection, Dorothy Carpenter Medical Archives, 

Wake Forest University School of Medicine, Winston Salem, NC. 

44. Spitzka EC. Merits and motives of the movement for asylum reform. J Nerv Ment 

Dis. 1878;5:694- 714. 

45. Spitzka EC. Reform in the scientific study of psychiatry. J Nerv Ment Dis. 

1878;5:201- 229. 

46. Hammond WA. Insane Asylum Reform. New York: G. P. Putnam’s Sons; 1879. 

47. Gray LC. Resolutions on asylums. J Nerv Ment Dis. 1880;5:512 - 515. 

48. Grissom E. Mechanical protection for the violent insane. Am J Insanity. 

1877-1878;34:27-58. 

49. Anonymous. Book notices and reviews. Saint Louis Clinical Record. 1878; 

5:158 -165. 

50. Anonymous. Editorial department. J Nerv Ment Dis. 1878;5:579 - 582. 

51. Anonymous. Book notices and reviews. Saint Louis Clinical Record. 1878;5: 

162 - 163. 


52. Anonymous. Book notices and reviews. Saint Louis Clinical Record. 1878;5: 

164 -165. 

53. Blustein BE. “A hollow square of psychological science”: American neurologists 

and psychiatrists in conflict. In: Scull AT, ed. Madhouses, Mad-doctors, and 

Madmen: The Social History of Psychiatry in the Victorian Era. Philadelphia: 

University of Pennsylvania Press, 1981:254. 

54. Blustein BE. Preserve Your Love for Science: Life of William Hammond, American 

Neurologist. Cambridge and New York: Cambridge University Press; 1991:262. 

55. Werman DS. True and false experts: a second look. Am J Psychiatry. 

1973;130(12):1351-1354. 

56. Torrey EF. The year neurology almost took over psychiatry. Psychiatric Times. 

2002;19(1):5 - 6. 

57. Foster FP. William A. Hammond, M.D., L.L.D. NY Med J. 1900;71:64. 

First Moon 

Photograph by Gregory G. Fischer, MD 



Carotid-subclavian arterial 

reconstruction: Concomitant 

ipsilateral carotid endarterectomy 

increases risk of perioperative stroke 

Gina M. Risty, MD, Thomas H. Cogbill, MD, Clark A. Davis, MD, and Pamela J. Lambert, RN, BSN, 


Background. Carotid-subclavian bypass (CSB) and carotid-subclavian transposition (CST) have 

excellent long-term patency with low perioperative mortality and morbidity. Carotid endarterectomy 

(CEA) is necessary for severe ipsilateral internal carotid artery stenosis in asmall subset of these 

patients. CEA can be performed as acombined or separate procedure. This study was undertaken to 

delineate the results of CSB and CST at our institution and to determine if concomitant CEA with 

CSB or CST is safe. 

Methods. We evaluated the outcome of 36 patients with symptomatic subclavian artery stenosis treated 

surgically at asingle institution during a22-year period. Outcomes of patients undergoing CSB or 

CST with concomitant CEA were compared with those of patients undergoing CSB or CST alone. 

Available literature was reviewed to compare the rate of perioperative stroke following CSB or CST with 

concomitant CEA versus CSB or CST alone. 

Results. Twenty-one patients underwent CST and 15 patients underwent CSB. There were 2(5.6%) 

deaths and 2(5.6%) strokes within 30 days of surgery. Concomitant CEA was performed in 6CST 

patients and 2CSB patients. Both perioperative strokes occurred in patients who had concomitant 

CEA. There were no strokes in the CST or CSB alone group (P .044). In acollected review of 12 

evaluable studies plus our experience, the rate of perioperative stroke was 0.32% in 617 patients who 

underwent CSB or CST alone versus 4.73% in 148 patients who had concomitant CEA with CSB or 

CST (P .001). 

Conclusions. Both CSB and CST are safe and effective for symptomatic subclavian artery stenosis, 

with excellent long-term results. In patients also requiring CEA, the rate of perioperative stroke is 

significantly higher with acombined procedure. Consideration should be given to performing CEA 

separately from CSB or CST. (Surgery 2007;142:393-7.) 

From the Department of General &Vascular Surgery, Gundersen Lutheran Medical Center, La Crosse, Wisconsin 

Patients presenting with symptomatic subclavian 

artery stenosis are uncommon. Edwards et al. 1 reported 

that in over 5000 patients presenting with 

cerebral symptoms, only 11.7% were due to astenosis 

of the subclavian artery, the vertebral artery, 

or both. Symptoms of subclavian artery stenosis 

most frequently include arm claudication, rest 

Accepted for publication March 16, 2007. 

Reprint requests: Thomas H. Cogbill, MD, Department of Surgery, 

Gundersen Lutheran, 1900 South Avenue, C05-001, La 

Crosse, Wisconsin 54601. E-mail: thcogbil@gundluth.org. 

0039-6060/$ -see front matter 

© 2007 Mosby, Inc. All rights reserved. 

doi:10.1016/j.surg.2007.03.014 

pain, or ischemic changes of the ipsilateral hand or 

digits. 2 Vertebrobasilar symptoms may also result 

from subclavian artery steal from the vertebral artery 

or embolic events in the distribution of the 

vertebral artery. These patients may present with 

dizziness, syncope, ataxia, vertigo or bilateral blurred 

vision 3 Less commonly, patients can present with 

chest pain following coronary artery bypass grafting 

(CABG) in which an internal mammary artery graft 

originates from asubclavian artery with aproximal 

stenosis. This may cause reversal of flow in the 

internal mammary artery graft to provide flow to 

the distal subclavian artery, resulting in coronary– 

subclavian steal syndrome. 4,5 

Treatment of symptomatic subclavian artery stenosis 

has undergone significant change over the 

past several decades. Transthoracic endarterec- 

SURGERY 393 


394 Risty et al Surgery 

September 2007 

tomy and bypass procedures were initially attempted 

but fell out of favor due to unacceptably high 

perioperative morbidity and mortality. 6-8 Extrathoracic 

bypass and transposition procedures were 

then developed, resulting inasignificant reduction 

in morbidity and mortality. Most recently, percutaneous 

techniques of angioplasty and stenting are 

increasingly being used to treat symptomatic subclavian 

artery stenosis. 9,10 This study was undertaken 

to determine the immediate and long-term 

results of carotid-subclavian bypass (CSB) and carotid 

subclavian transposition (CST) performed at 

our institution. In addition, we sought to determine 

the safety of concomitant carotid endarterectomy 

(CEA) in that subset of patients with severe 

ipsilateral carotid artery stenosis. 

PATIENTS AND METHODS 

All patients with adiagnosis of subclavian artery 

stenosis (ICD-9 code 435.2) treated from June 1983 

to December 2005 were identified. Inpatient hospital 

and outpatient clinic records were then reviewed. 

Sixty-five patients were identified; 23 asymptomatic 

patients did not require any intervention and these 

patients were excluded from further analysis. Also 

excluded were 4patients who underwent endovascular 

subclavian artery angioplasty and stenting, 

and 2who underwent transthoracic aortic to brachiocephalic 

branch bypass procedures. 

Thirty-six patients included in this study underwent 

either CSB or CST. All procedures were performed 

at a single institution under general 

anesthesia. Twenty-eight (78%) procedures were 

performed by a single surgeon. Hospital charts 

and outpatient clinic records were retrospectively 

reviewed for presenting symptoms, risk factors, demographics, 

pre-operative studies, and operative 

data. Operative results, postoperative complications, 

and long-term follow-up were also determined. 

Fisher’s exact test was used to analyze the 

data after confirmation that all pertinent statistical 

assumptions were met. Level of confidence was 

defined at P .05. 

RESULTS 

Patients ranged in age from 46 to 83 years 

(mean 63.9 years). Twenty-six (72%) of the patients 

were women. Comorbid conditions included hypercholesterolemia 

in 18 (50%), hypertension in 

18 (50%), coronary artery disease in 12 (33.3%), 

diabetes mellitus in7(19.4%), previous myocardial 

infarction in 3 (8.3%), renal insufficiency in 3 

(8.3%), congestive heart failure in 2 (5.6%), 

chronic obstructive pulmonary disease in 2(5.6%), 

Table I. Presenting symptoms for 36 patients 

with subclavian artery stenosis 

Symptoms 

No. of patients 

Arm claudication 22 

Vertebrobasilar symptoms 18 

Coronary-subclavian steal 2 

Asymptomatic 1 

and previous cerebral vascular accident in 1 

(2.8%). Thirty-one (86.1%) of patients hadasmoking 

history. Presenting symptoms are shown in Table 

I, with several patients having more than 1 

presenting symptom. 

Of 36 patients, 21 (58.3%) underwent CST and 

15 (41.7%) underwent CSB with polytetrafluoroethylene 

(PTFE) grafts. Eight patients underwent 

concomitant carotid endarterectomy (CEA); 6patients 

with CST and 2patients with CSB. Operative 

time for the CSB patients ranged from 90 to 395 

minutes (mean 189 minutes). Operative time for 

the CST patients ranged from 80 to 335 minutes 

(mean 178 minutes). Length of stay ranged from 

1to27 days for CSB patients (median, 5days); and 

1to14 days for CST patients (median, 3days). 

Over the 22-year period, the average length of stay 

steadily decreased. There were no statistically significant 

differences between the 2 groups when 

operative times or length of stay were compared. 

Two of 36 patients died within 30 days of surgery 

for a mortality rate of 5.6%. One patient death 

occurred in each of the CSB and CST groups. One 

patient had an uncomplicated hospital course and 

was discharged home the day following surgery, but 

died at home 3days later of an unknown cause. 

The second patient had multiple serious medical 

comorbidities including end-stage renal disease, 

chronic obstructive pulmonary disease, hypertension 

and hypercholesterolemia. Postoperatively, 

the patient developed pneumonia, myocardial infarction 

and pulmonary aspiration. This patient 

died 14 days after surgery, with multi-system organ 

failure. 

Two patients developed thoracic duct leak following 

CSB. Both were managed with re-operation 

and closure of the leak. One patient in the CSB 

group sustained a phrenic nerve injury; this resolved 

in less than 6 months with conservative 

management. A patient in the CSB group who 

developed early graft thrombosis was managed with 

successful re-operation. Although there were more 

perioperative complications in CSB patients than 

CST patients, the differences were not significant. 


Surgery Risty et al 395 


Table II. The risk of postoperative stroke in 

patients with or without concomitant carotid 

endarterectomy 

Concomitant CEA 

N 8 

No CEA 

N 28 

CEA, carotid endarterectomy. 

Perioperative 

stroke 

No perioperative 

stroke 

2 6 

0 28 

Average length of follow-up was based on the 

number of months from operation to most recent 

clinic visit. Follow-up ranged from 1to 212 months 

(mean, 66 months). Symptom resolution was determined 

by history and physical exam. One patient 

was lost to follow-up. All remaining patients (97%) 

had relief of symptoms. 

Twenty-five percent (2/8) of patients who underwent 

concomitant CEA sustained post-operative 

stroke, 1each with CST and CSB (Table II). No 

patients who underwent CSB or CST alone had a 

post-operative stroke. The risk of postoperative 

stroke in patients with concomitant CEA was significantly 

higher than the risk of stroke after CSB or 

CST alone (P .044). 

Twelve studies from the English language literature 

since 1990 had sufficient information to 

compare the rate of perioperative stroke in patients 

undergoing CST or CSB alone versus those 

who had concomitant CEA with CST or CSB 

(Table III). 11-22 There were only 2(0.34%) strokes 

in 589 patients undergoing CSB or CST alone versus 

5 (3.57%) strokes in 140 patients who had 

concomitant CEA with CST or CSB. This difference 

was significant (P .004). Adding our patients to 

these totals, there were 2 (0.32%) perioperative 

strokes in 617 patients undergoing CSB or CST 

alone versus 7(4.73%) perioperative strokes in 148 

patients who had concomitant CEA with CSB or 

CST. This difference was significant (P .001). 

DISCUSSION 

Both CST and CSB can be performed with 

relatively low rates of mortality and morbidity. 

There were two deaths within 30 days in our 

series, one after CSB and one after CST. The 

perioperative mortality rate following these two 

procedures reported in the literature has ranged 

from nil to 12%. 7,8,12,14,15,23-27 Edwards and associates 

reported 2.2% overall mortality rate after 

190 extrathoracic reconstructions, including 178 

CST. 14 Vitti et al. 15 reported one death after 124 

P 

.044 

Table III. Results of English-language literature 

review comparing the rates of perioperative 

stroke after CSB or CST alone or with 

concomitant CEA 

Reference 

Year 

CSB/CST 

alone 

CSB/CST with 

CEA 

Defraigne 11 1990 0/24 1/5 

Perler 12 1990 1/27 0/4 

Mingoli 13 1992 0/26 1/23 

Edwards 14 1994 0/177 2/10 

Vitti 15 1994 0/92 0/32 

Salam 16 1994 0/30 0/4 

vanderVliet 17 1995 0/35 0/7 

Schardey 18 1996 0/93 0/15 

Deriu 19 1998 0/30 1/10 

Toursarkissian 20 1998 1/16 0/6 

Wittwer 21 1998 0/28 0/12 

Cina 22 2002 0/11 0/12 

Total 2/589 (0.34%) 5/140 (3.57%) 

P .004 

CSB procedures. Sandmann and coworkers 27 documented 

a1.4% mortality rate in 72 patients who 

underwent CST. Procedure-related complications 

can be grouped into several categories. Thoracic 

duct leaks requiring reoperation have been described 

by many investigators. 7,14-17,21,22,27 The incidence 

of thoracic duct leak can be reduced by 

meticulous identification and ligation of the main 

duct and any small lymph channels with permanent 

suture. Phrenic nerve injury has been reported by 

many groups. 12,15-17,23,24,26 These injuries appear 

more frequently after CSB than CST. Transient and 

permanent Horner’s syndrome are not infrequent 

following both CSB and CST. 14,17,25,26 Recurrent 

laryngeal nerve dysfunction has also been described. 

12,14,15,17,26 

Long-term results after both CSB and CST were 

excellent in our series. At average follow-up of 

more than 5years, 97% of patients had relief of 

symptoms. There was only 1patient in our series 

who required thrombectomy for graft thrombosis 

and there were no late operations for restenosis. 

Many previous studies have documented impressive 

long-term patency rates after CSB and CST. 

AbuRahma and coworkers 23 reported 92% primary 

and 95% secondary patency rates at 10 years. 

Edwards et al. 14 discovered only one failure at 26 

months after 178 CST procedures. Owens and associates 

24 calculated a 96.5% patency rate at a 

mean follow-up of 26 months after CSB. Sandmann 

et al. 27 reported 95% patency rates after both CSB 

and CST. Cina et al. 22 studied 23 patients by ultrasound 

at amean of 25 months after CST; all recon- 


396 Risty et al Surgery 

September 2007 

structions were patent. Furthermore, in aliterature 

review they found patency rates of 84% and 98%, 

respectively, in 516 patients after CSB and 511 patients 

after CST. This difference was significant. At 

a mean follow-up of 59 months, the rates of freedom 

from symptoms in these two groups were 88% 

and 99%, respectively. 

In our series, there were no differences in the 

immediate or long-term results of CST versus CSB. 

There was one death in each group. Although procedure-related 

complications such as thoracic duct 

leak, phrenic nerve injury, and graft thrombosis 

occurred only in CSB patients, the difference was 

not significant. The long-term results of both procedures 

in the relief of presenting symptoms were 

excellent. However, CST offers several advantages 

over CSB. CST is performed with asingle anastomosis, 

does not require aprosthetic graft, and effectively 

removes the stenotic lesion from arterial 

flow so that it cannot serve as asource of atheromatous 

emboli. 14,26,27 Although Sterpetti and associates 

26 noted shorter operative times with CST 

versus CSB, we did not find asimilar trend. Although 

several authors quote superior long-term 

patency in CST patients, they caution that patients 

undergoing CST and CSB may not be comparable. 

14 Finally, the ability to perform CST with dissection 

limited to the area medial to the anterior 

scalene muscle puts the phrenic nerve and brachial 

plexus at less risk of inadvertent injury. For these 

reasons, CST is the procedure of choice at our 

institution for subclavian artery lesions treated surgically. 

We prefer CSB for patients with multifocal 

subclavian stenoses, more distal subclavian stenoses, 

or when reoperation is necessary. Percutaneous 

angioplasty and stenting is also being performed 

with increasing frequency at our institution. 

Arteriosclerotic lesions develop in multiple arteries 

simultaneously. Concurrent stenoses in the 

subclavian artery and ipsilateral carotid artery bifurcation 

are therefore not infrequent. Defraigne 

and associates 11 stressed the importance of treating 

the carotid stenosis at the time of CSB in order to 

prevent acarotid steal phenomenon. Mingoli and 

coworkers 13 recommended acombined approach 

of CSB or CST with concomitant CEA for correction 

of subclavian and ipsilateral carotid lesions in 

order to avoid the development of symptoms from 

each respective stenosis. They reasoned that significant 

carotid stenoses left untreated would cause 

neurologic deficits during follow-up. Edwards and 

coauthors 14 also performed concomitant CEA in 10 

of 178 patients undergoing CST. The only 2perioperative 

strokes in their series occurred in patients 

who also had CEA. We found the risk of 

perioperative stroke to be significantly higher in 

patients after concomitant CEA with CSB or CST. A 

collected review of current literature corroborated 

this finding. Adding our experience to the collected 

review totals, perioperative stroke occurred 

in only 2(0.32%) of 617 patients after CSB or CST 

alone versus 7(4.73%) of 148 patients with concomitant 

CEA (P .001). The low risk of stroke 

after CST or CSB alone has been attributed to 

several factors. Edwards et al. 14 have stressed the 

importance of collateral circulation through the 

external carotid arteries while the anastomosis is 

being performed at the proximal common carotid 

artery. Furthermore, the common carotid artery at 

this level is usually free of atheromatous plaque at 

the site of clamp placement, decreasing the risk of 

embolization. The marked increase in the risk of 

stroke after combined CEA and CSB or CST can be 

contrasted to the risk of perioperative stroke after 

CEA alone for asymptomatic, severe carotid stenoses. 

The disabling stroke rates reported in the 

ACAS and ACST studies were 1.4% and 0.7%, respectively. 

28,29 At our institution over the last 10 

years, the perioperative stroke rate after CEA for 

asymptomatic stenoses was 0.9%. 30 It is unclear why 

the addition of CEA to CSB or CST is associated 

with such asignificant increase in the risk of perioperative 

stroke. Although the increased stroke 

rate may be areflection of more severe vascular 

disease involving two arterial beds, the additive 

risks of two procedures should also be considered. 

This finding parallels the results of combined CEA 

and CABG for simultaneous carotid and coronary 

artery stenoses. Arecent meta-analysis of concomitant 

CEA with CABG concluded that the risk of 

stroke was dramatically higher compared with CEA 

and CABG performed in astaged fashion. 31 Coyle 

and associates 32 reported 18.2% 30-day risk of 

stroke or death after simultaneous CEA and CABG 

versus 6.6% when the procedures were done separately. 

Reasons proposed for the marked increase 

in stroke risk include the effects of multiple arterial 

clamping sites, prolonged operative times, and inadequate 

anticoagulation. Each of these factors 

may play arole in combined CEA and CSB or CST 

procedures. 

We agree that severe ipsilateral internal carotid 

artery stenoses should be aggressively treated for 

best stroke prevention and to prevent the rare case 

of carotid steal. However, based upon our experience 

herein along with results of contemporary literature 

review, we cannot support concomitant CEA at 

the time of CSB or CST due to asignificantly greater 

risk of perioperative stroke when compared with CSB 

or CST alone. We have changed our approach to 


Surgery Risty et al 397 


staged procedures at separate sittings. It is our 

current practice to perform CEA first under cervical 

block. Some patients with vertebrobasilar insufficiency 

may improve with CEA alone. Patients 

remaining symptomatic are treated 3to6weeks 

later by CST or CSB under general anesthesia. 

Further study of this staged approach is necessary 

to confirm if it will yield more favorable perioperative 

results. 

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4. Edwards WH. An unsuspected cause for recurrent angina: 

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5. Sechriest VF, Jaklitsch MT, McFalls EO, Ward HB, Santilli SM. 

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6. Thompson BW, Read RC, Campbell GS. Operative correction 

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CALL FOR PAPERS 

M E D I C A L J O U R N A L 

Gundersen Lutheran Medical Journal (GLMJ) is an interdisciplinary archival journal. To this end, manuscripts 

considered for publication are sought from any medical or surgical specialty or subspecialty, or any healthrelated 

field. Manuscripts may be based upon, but are not limited to, (1) original, data-driven, high quality, 

randomized or nonrandomized, controlled trials; (2) systematic reviews or meta-analyses; (3) clinical 

outcome studies; (4) tutorials; (5) case reports; (6) historical reports; and (7) letters to the editor. The Journal 

will also consider “vignette” or “how I do it” papers, pieces designed to provide the readership with “pearls,” 

rationale, and/or techniques for a given procedure or examination. They may be based upon research, upon 

clinical experience, or both. Interesting imaging studies accompanied by a brief descriptive or explanatory 

text would be appropriate, as well. 

The submission deadline for the next issue is October 15, 2008. 

Please prepare manuscripts in accordance with the most recent version of “Uniform Requirements for 

Manuscripts Submitted to Biomedical Journals” (www.icmje.org). Assistance in preparing your manuscript is 

available through the Journal office (see below). 

Submit an electronic version as an attachment via email to glmjeditor@gundluth.org or on 3.5” floppy or 

CD, along with any nondigital original figures to: 

Cathy Mikkelson Fischer, MA, Managing Editor 



C03-006B 


La Crosse, Wisconsin 54601 

QUESTIONS? 

Please contact: 

David E. Hartman, PhD, BC-ANCDS(A), Editor 

Cathy Mikkelson Fischer, MA, Managing Editor 



C03-006B 


La Crosse, Wisconsin 54601 

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journal published by Gundersen Lutheran Medical 

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