eMedicine Specialties > Physical Medicine and Rehabilitation > Medical Diseases

Low Energy Availability in the Female Athlete

Author: Stacey Miller-Smith, MD, Staff Physician, Department of Physical Medicine and Rehabilitation, Kessler Institute for Rehabilitation, UMDNJ-New Jersey Medical School
Coauthor(s): Gerard A Malanga, MD, Founder and Director, New Jersey Sports Medicine Institute; Director of Pain Management, Overlook Hospital; Director of Sports Medicine, Sports Medicine Fellowship Director, Mountainside Hospital; Clinical Chief, Rehabilitation Medicine and Electrodiagnosis, St Michael's Medical Center; Medical Director, Consultant, Horizon Healthcare Worker's Compensation Services, Blue Cross and Blue Shield Worker's Compensation
Contributor Information and Disclosures

Updated: Jan 8, 2009

Introduction

Background

The opening of the Olympics to women in 1912 and the establishment of the Commission on Intercollegiate Athletics for Women in 1967 signified the increasing numbers of female athletes. However, the addition of the famed education amendment of 1972, Title IX, and its reinforcement in the 1988 Civil Rights Restoration Act, legally opened the door to equal opportunities and financial assistance for female athletes. Since then, female participation in athletics and the number of elite female athletes has soared.

With this increase in the number of physically active women comes the need to understand the unique physiology of the female athlete. Although further research is needed to clarify issues such as the effect of exogenous ovarian hormones (oral contraceptives) on performance, many advances have been made.

One discovery has been that chronic energy deficit in the female athlete can cause musculoskeletal and reproductive dysfunction. Despite previous theories on the causes of menstrual dysfunction and the increased risk of stress fractures in the female athlete, studies have shown that the primary mechanism of menstrual disturbance in the female athlete is low energy availability. Even normally menstruating athletes can be in a state of low energy availability and can therefore experience deleterious effects on musculoskeletal health and performance.

The limiting factor for performance during training and competition in high-intensity sports of long duration is energy intake, especially carbohydrate intake, and a direct correlation exists between carbohydrate availability and reproductive and skeletal health. It might seem logical that increased energy expenditure, such as that during athletic training and performance, increases energy intake. However, for many athletes, particularly female athletes, this is simply not the case.

When this energy deficit is intentional, it is described as disordered eating and forms part of the female athlete triad.1,2 Often the deficit is unintentional, and physicians, athletic trainers, and even the athletes themselves can remain unaware of the condition and its potentially disastrous consequences. Unintentional underconsumption and its effects are the focus of this article.

Pathophysiology

Menstrual cycle/endogenous ovarian hormones

Length of the menstrual cycle

When asked, 60% of women say that their menstrual cycle is 28 days in length, but only approximately 12% of menstrual cycles are actually 28 days long.3 The length of the menstrual cycle varies from individual to individual, from cycle to cycle, from year to year, and from decade to decade. No one knows how much of the variation in the length and quality of menstrual cycles between and within women is due to environmental and behavioral factors, such as those that occur in athletic training, and how much is due to normal aging, inborn differences, disease, and random variation.

The median length of the menstrual cycle in the general population decreases from approximately 29 days in the first year after menarche to approximately 26 days after 40 years. If eumenorrhea is defined for college-aged women to span 1 standard deviation around the mean, then it ranges from 26-32 days, and 1 menstrual cycle in this range is most likely followed by another in the same range.4

Oligomenorrhea

The term oligomenorrhea (from the Greek oligos meaning few) is usually used to refer to menstrual cycles longer than 36 days. By far, most cases of oligomenorrhea occur in the first decade after menarche and in the last decade before menopause. Because the length of their cycles is so irregular, oligomenorrheic women may have difficulty conceiving, and paradoxically, they may also be at increased risk of an unintended pregnancy because of the difficulty of predicting the day of their next ovulation.

The incidence of oligomenorrhea declines steadily from approximately 27% in the first year after menarche to approximately 3% after 30 years. It then rises to approximately 27% in the decade before menopause.3

Luteal suppression

The term luteal suppression refers to an entirely asymptomatic, subclinical menstrual disorder that is evident only by measuring ovarian steroid hormone concentrations in the blood or urine over a number of weeks. In luteal suppression, follicular development progresses more slowly than usual; therefore, ovulation occurs later in the cycle. The following luteal phase may be short, and/or progesterone concentrations may be low. Often, the overall length of the menstrual cycle is indistinguishable from that in eumenorrhea. The incidence of short luteal phase is between 30% and 45% during the first decade after menarche, after which it declines to approximately 5%.3

Anovulation

The term anovulation refers to an asymptomatic subclinical menstrual disorder in which follicular development is so impaired that ovulation does not occur. Estrogen and progesterone levels are low, but enough estrogen is produced to stimulate some proliferation of the uterine lining, and bleeding occurs when the lining is sloughed. The incidence of anovulation declines from approximately 55% to less than 5% during the first decade after menarche and increases to approximately 20% in the last decade before menopause.3

Amenorrhea

The term amenorrhea denotes the absence of menstrual cycles. A female has primary amenorrhea if she has not yet menstruated by age 16 years, even though she has undergone other normal changes that occur during puberty. The rate of primary amenorrhea in the United States is less than 0.1%.

The persistent absence of menstrual cycles beginning sometime after menarche is called secondary amenorrhea. Because ovarian follicular development, ovulation, and luteal function are not occurring in amenorrheic women, they are infertile. While recovering, however, they ovulate before menstruating, ie, before they know that their fertility is restored. Therefore, they should not rely on their amenorrhea for birth control purposes.

The prevalence of amenorrhea strongly depends on how amenorrhea is defined. When more months without menstrual periods are required, lower prevalences are reported. Studies of the general population have specified 3 months, because menstrual cycles longer than 90 days are extremely rare, even in the first and last decades of reproductive life. Large epidemiologic studies of college-aged women in which amenorrhea was defined as no menstrual cycles for 3 consecutive months have show prevalences of 2-5%.5,6,7

Typically, the first day of menstruation is considered the start of the follicular phase and day 1 of the menstrual cycle. Ovulation occurs approximately on day 14, and the luteal phase occurs between day 15 and day 28 in a 28-day cycle. The entire cycle is influenced by pulses of gonadotropin-releasing hormone from the hypothalamus, which activates follicle-stimulating hormone (FSH) and luteinizing hormone (LH) pulses from the pituitary. The FSH and LH pulses stimulate ovarian activity through follicular maturation and ovarian hormone secretion. Ovulation occurs following the LH surge.

The cells in the hypothalamus that secrete gonadotropin-releasing hormone are controlled by a variety of neurotransmitters and hormones that reflect physical and emotional conditions in the body.8

Oral contraceptives/exogenous ovarian hormones

Oral contraceptives are prescribed to female athletes for several purposes, including contraception, cycle regulation, and control of dysmenorrhea (menstrual cramps). The oral contraceptive comes in many different brands with different synthetic hormones, doses, and dosing regimens. Those currently prescribed are usually given at doses lower than those of first-generation pills; therefore, they may have fewer adverse effects.

Oral contraceptives usually contain an estrogen and a progestin. The estrogen is commonly ethinyl estradiol, at doses of 20-50 mcg per pill. The progestin is often norethindrone, norgestrel, or levonorgestrel, with typical doses of 0.05-2.5 mg per pill.

The regimens are typically monophasic or triphasic. Triphasic dosing regimens more closely simulate the natural menstrual cycle and contain lower per-cycle progestin levels than do those of their monophasic counterparts.8,9 The estradiol levels in most oral contraceptives contain approximately 3-5 times the estrogen and 1-2 times the progestin levels present in the normal menstrual cycle.10

Menstrual cycle irregularities in the female athlete

All types of menstrual disorders that occur in the general population also occur among athletes. However, they are more common among athletes, even young athletes, than in nonathletes. Approximately 31% of athletes who are not using oral contraceptives report symptomatic menstrual irregularities.8 If anything, exercise reduces dysmenorrhea, which is a common menstrual symptom and not a menstrual irregularity. More common irregularities in female athletes include primary or secondary amenorrhea, a shortened luteal phase, and oligomenorrhea.

On average, menarche appears to occur at a later age in athletes. American girls tend to get their first menstrual period between ages 12 and 13 years. Some studies have found an average age of 13.6 years in track and field athletes,11 14.2 years in Olympic volleyball candidates,12 14 years in elite figure skaters, 12.9 years in elite Alpine racers, 13.4 years in competitive swimmers,13 and 15.6 years in elite gymnasts.14

Although many studies have established that menarche often occurs later in athletes than in nonathletes, such retrospective surveys are inherently biased.15 Because the long bones continue to grow until increased estrogen levels close off the growth plates shortly after menarche and because longer bones are conducive to athletic success,16 later-maturing girls may be more athletically successful and so may choose to continue to participate in athletics, whereas earlier-maturing girls may be less successful and may therefore be socialized away from athletics.16 Thus, while athletic training may delay menarche and even though animal research suggests that this is possible, so far no studies have validated this theory.

Large-scale studies of college athletes using the same 3-month definition to directly compare data from general college-age women have yet to be performed. Smaller studies of athletes using the same 3-month definition of amenorrhea have shown a prevalence as high as 44% (in dancers) and 65% (in long-distance runners).17

The incidence of luteal suppression and anovulation is high in regularly menstruating recreational and competitive athletes. Approximately 78% of regularly menstruating female runners have luteal suppression or anovulation in at least 1 month out of 3.18

Oligomenorrhea and hyperandrogenism

Different menstrual disorders can be symptoms of the same medical condition, while oppositely, the same menstrual disorder can be a symptom of various conditions. Since the discovery in the late 20th century of progressive skeletal demineralization in amenorrheic athletes, most research has focused on amenorrhea in athletes. For inferential reasons, amenorrheic athletes have been compared with athletes who have highly regular menstrual cycles and with equally regular sedentary women. This research has identified undernutrition as the primary cause—and indeed the only demonstrated cause—of amenorrhea and luteal suppression in athletes.

By comparison, oligomenorrhea in athletes has been studied less. Findings from 2 studies suggest that in many athletes, the mechanism for oligomenorrhea may differ from that of amenorrhea. A study measuring the diurnal pattern of testosterone and pituitary hormone in female endurance athletes with menstrual disorders showed that in amenorrhea, hypothalamic inhibition due to energy deficiency appeared to play a major role; however, hyperandrogenism (increased testosterone secretion) seemed to be the major cause of oligomenorrhea.19

The 24-hour hormone profiles in amenorrheic athletes showed decreased LH pulsatility and a peak amplitude of prolactin, as well as increased baseline levels of growth hormone and cortisol. In oligomenorrheic athletes, higher diurnal testosterone secretion was observed and levels of LH, prolactin, growth hormone, and cortisol were similar to those of regularly menstruating subjects.

High testosterone levels and oligomenorrhea (and occasionally amenorrhea) are symptoms of polycystic ovary syndrome, which is thought to be the most common cause of infertility in the United States. Therefore, just as it is plausible that later-maturing girls may self-select into athletics because of the rewards they receive for developing longer bones, it is also plausible that women with eating disorders may self-select into sports in which low body weight offers a competitive advantage. Similarly, women with polycystic ovary syndrome may self-select into sports in which high testosterone levels offer an advantage. This possibility warrants focused research, because the treatment for polycystic ovary syndrome completely differs from that for undernourishment.

Effect of low energy availability on the reproductive system

Female athletes can be chronically energy deficient.20  With the exception of cross-country skiers, female endurance athletes consume approximately 70% as much energy and carbohydrates (controlled for body weight) as male athletes.21 Biochemical markers in female athletes indicate a mobilization of fat stores, slowing of the metabolic rate, and a decline in glucose utilization, with more extreme abnormalities in amenorrheic athletes and less extreme abnormalities in regularly menstruating athletes.20

Studies in humans and monkeys have shown that this chronic energy deficiency causes reproductive disturbances in many female athletes. In 1998, Loucks and colleagues demonstrated that the stress of exercise did not suppress LH pulse frequency, because the disruption of LH pulsatility in exercising women could be prevented with dietary supplementation. On the other hand, low energy availability, caused either by an increase in exercise energy expenditure or by dietary energy restriction alone, did disrupt LH pulsatility.22 This low-energy state also suppressed levels of triiodothyronine (T3), insulin, insulinlike growth factor–1, and leptin and raised levels of growth hormone and cortisol in a pattern similar to that seen in amenorrhea and luteal suppression with eumenorrhea.22

Similar effects of low energy availability on the reproductive system have been noted in men.23 One week of dietary supplementation reversed disruptions of metabolic and reproductive hormones in US Army Ranger trainees despite continued exposure to strenuous exercise, sleep deprivation, cold, heat, injuries, infections, and other stresses. Therefore, exercise (and other stresses) appears to have no disruptive effect on the reproductive system apart from the impact of energy cost on energy availability.

Curiously, LH pulsatility is less disrupted in women who exercise than in women whose energy availability is reduced by exactly the same amount because of dietary restriction. This is surprising, because no one had previously suggested that exercise might be protective against menstrual disorders. On closer examination, working muscle in energy-deprived women who exercised reduced its glucose utilization so that substantially more carbohydrate was available to the brain. This finding strengthens the hypothesis that reproductive function in women specifically depends on brain glucose availability.20

The dose-response relationship between energy availability and LH pulsatility has been investigated. LH pulsatility was found to have been disrupted below a threshold of energy availability of approximately 30 kcal/kg of lean body mass (LBM) per day. The dose-dependent effects on LH pulsatility most closely resembled the metabolic substrates glucose and beta-hydroxybutyrate and the metabolic hormones cortisol and growth hormone. This finding supports the reported hypothesis that "reproductive function reflects the availability of metabolic fuels, especially glucose, which may be signaled in part by activation of the adrenal axis."20

Menstrual function can also be restored by increasing energy availability. In female monkeys, amenorrhea induced by increasing exercise energy expenditure, with no reduction in dietary intake, was restored simply by means of dietary supplementation, without any moderation of the animals' exercise regimen.24

Effect of low energy availability on bone health

Stress fractures are common among female athletes. In one survey of competitive collegiate cross-country runners, 44% had experienced at least 1 stress fracture and 21% had suffered multiple stress fractures (Stanford B-Fit Web site). The incidence of stress fractures is greater in amenorrheic athletes, and bone density has been shown to be negatively correlated with the number of missed menstrual cycles since menarche.25

Bone is a dynamic tissue that is constantly being remodeled. This remodeling is performed by osteoclasts (which resorb old bone) and osteoblasts (which form new bone) under the control of polypeptides, steroid hormones, thyroid hormones, cytokines, and growth factors.26 The balance between resorption and formation is usually coupled so that in adults, bone mass remains stable.

The principal role of estrogen, through its action on osteoblasts and its indirect effect on osteoclasts, is to prevent bone resorption.27 In the past, some have theorized that the decreased bone densities observed in females with anorexia nervosa and in amenorrheic athletes was due solely to chronic hypoestrogenism. However, estrogen replacement in these individuals does not fully reverse the decrease in bone density.28,29,30,31 This finding prompted researchers to investigate chronic undernutrition as an estrogen-independent mechanism for decreased bone mineral density in these patients.

The effects of low energy availability on bone health are evident even in normally menstruating sedentary women. In a landmark study, Ihle and Loucks demonstrated for the first time that bone formation is impaired within 5 days of the onset of low energy availability. At levels of energy deficit milder than in bone resorption and at extreme energy restriction (10 kcal/kg LBM/d), increased bone resorption becomes uncoupled from decreased bone formation.32

The findings of the study are applicable to female athletes, because normally menstruating athletes have reported energy availabilities of approximately 30 kcal/kg LBM/d and amenorrheic athletes have reported energy availabilities of approximately 16 kcal/kg LBM/d.33

A diversity of metabolic hormones—including carboxyterminal propeptide of type I procollagen and osteocalcin—are disrupted by all levels of energy restriction.34 The dose-response relationships of insulin, T3, and insulinlike growth factor–1 closely resemble those of propeptide of type I procollagen and osteocalcin and could be involved in mediating the effect of low energy availability on bone. In addition, similar to N -telopeptide, estradiol is unaffected until energy restriction becomes severe. Because the primary role of estrogen in the skeletal system is to suppress osteoclast activity, this relationship is an expected finding.32

Similar studies on postmenopausal women showed that changes similar to those in the 10-kcal/kg LBM/d group resulted in approximately a 6% change in bone mineral density after 2 years.35

Peak bone mass is a significant predictor of risk for the development of osteoporosis.27 The decrease in bone formation and increase in resorption (uncoupling) that occurs in a severe, chronic energy-deficient state is dangerous at any age. Because approximately 50% of peak bone mass is achieved in adolescence and is completed in most women by the end of the second decade,36,37 the consequence of suppressing bone formation in adolescence can be disastrous.

Related eMedicine topics:
Amenorrhea
Amenorrhea, Primary
Amenorrhea, Secondary
Androgen Excess
Anovulation
Osteoporosis [Orthopedic Surgery]
Osteoporosis [Pediatrics: General Medicine]
Osteoporosis [Rheumatology]

Frequency

United States

Although it is difficult to ascertain the exact number of female athletes with low energy availability, the effect of this chronic state of energy deficiency is evident in the number of female athletes with musculoskeletal and reproductive disturbances.

Clinical

History

A good history should be obtained from all female athletes. In addition to the normal comprehensive history, certain components on which to focus include the athlete's nutritional, musculoskeletal, menstrual, endocrine/metabolic, psychosocial, performance, and medication history.

  • Nutritional history
    • Importantly, gather information about nutritional intake and eating patterns.
    • The components of each athlete's diet are important in terms of the quantity of protein, carbohydrate, vitamins, and minerals consumed.
    • Also important are the effect of training on an athlete's diet and the modification of the athlete's diet in times of increased training.
  • Musculoskeletal history
    • With the increase in risk of stress fractures in females with chronic energy deficit, a careful review of past and current musculoskeletal injuries in the female athlete should be conducted, with a focus on all stress fractures.
    • Any injury that results in loss of training or competition time should be considered major.
  • Menstrual history
    • Other than fracture, the most likely manifestation of severe, chronic low energy availability in the female athlete is menstrual disturbance.
    • Because many women do not volunteer information concerning menstrual disturbances, it should be specifically sought during all routine and sick visits by female athletes.
    • A complete menstrual history should be obtained. This includes the age at menarche, average length of menses, average time between menstruation, variations during times of increased training, and number of cycles per year.
    • The possibility of pregnancy should be excluded in the case of amenorrhea.
    • The patient's personal and family history of reproductive disorders, such as premature ovarian failure, should be discussed.
  • Endocrine/metabolic history
    • A history of and the risk for any endocrine abnormalities should be explored.
    • Any personal and family history of thyroid disorders, pituitary disorders, and diabetes should be sought.
    • Any family history of bone disease should be elicited.
  • Psychosocial history
    • Eating patterns should be discussed, and the Eating Disorder Inventory (EDI) may be used to screen for current and past disordered eating patterns.
    • As with all patients, alcohol, tobacco, and drug use, as well as social support, depression, anxiety, and a history of abuse, should be determined.
  • Performance history
    • During sustained energy deficiency, an athlete's strength, power, and vertical jump all decline by approximately 20%.38
    • The athlete should be questioned as to whether she has noticed any change in strength or performance.
  • Medication history
    • All medications, dietary supplements, and herbal agents should be reviewed.
    • Particular attention should be paid to medications, such as corticosteroids and anticonvulsants, that could affect bone health.
    • The use of oral contraceptives should be elicited separately because patients often do not consider this a medication.

Physical

A typical comprehensive physical examination should be performed on all female athletes, with a focus on weight, percentage body fat, and thyroid function (for evidence of hypertrophy or irregularity).

For patients with menstrual irregularities, the physical examination should screen for pathologies that could cause metabolic and hormonal abnormalities. Particular attention should be paid to the parotid glands (for evidence of hypertrophy, as in bulimia), visual-field testing for pituitary adenoma, muscle strength, and the epidermis. Skin findings might include evidence of hirsutism, vitiligo, or increased pigmentation of the palmar creases in adrenal insufficiency; easy bruising or stria in Cushing syndrome; warm, moist skin in hyperthyroidism; or any lanugo in anorexia.

A pelvic examination should be performed when appropriate and particularly when a patient presents with delayed menarche.

Causes

The appetite of an athlete is not a reliable indicator of either energy balance or specific macronutrient requirements, because no biologic imperative to match intake to expenditure appears to exist.39 Hunger is actually suppressed for a brief period after a single episode of exercise at greater than 60% maximal oxygen consumption, or VO2max.40

Food deprivation increases hunger, but the same low energy availability, when caused by energy expenditure from exercise, does not increase appetite.41 In one study, a 20% increase in energy expenditure during 40 weeks of marathon training did not result in an increase in energy intake.42,43 Even female monkeys with induced amenorrhea secondary to increased energy expenditure must be offered special treats in order to persuade them to consume enough food to restore normal menstrual function.24

Another factor in chronic energy deficiency in athletes is that body weight is not a reliable indicator of either energy or macronutrient balance. Because fat stores are associated with less body water than are protein and glycogen stores, the weight gain resulting from an increase in protein or glycogen stores more than counterbalances the weight loss resulting from the equivalent energy reduction in fat stores that occurs in low energy availability.

More on Low Energy Availability in the Female Athlete

Overview: Low Energy Availability in the Female Athlete
Differential Diagnoses & Workup: Low Energy Availability in the Female Athlete
Treatment & Medication: Low Energy Availability in the Female Athlete
Follow-up: Low Energy Availability in the Female Athlete
References
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Further Reading

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Keywords

anorexia, anorexic, eating disorder, eating disorders, osteoporosis, menstrual cycle, anorexia nervosa, athletic women, menstruation, bone density, women exercise, amenorrhea, bone loss, female athlete, women athletes, athletic woman, chronic energy deficit, menstrual dysfunction, stress fractures, sports performance, energy expenditure, athletic training, athletic performance, energy intake, disordered eating, female athlete triad, anovulation, oligomenorrhea, unintentional underconsumption, athlete's diet, musculoskeletal disturbances, reproductive disturbances, menstrual-cycle irregularities in the female athlete, primary amenorrhea, secondary amenorrhea, delayed menarche, exercise energy expenditure, luteal suppression

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Contributor Information and Disclosures

Author

Stacey Miller-Smith, MD, Staff Physician, Department of Physical Medicine and Rehabilitation, Kessler Institute for Rehabilitation, UMDNJ-New Jersey Medical School
Stacey Miller-Smith, MD is a member of the following medical societies: American College of Sports Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Gerard A Malanga, MD, Founder and Director, New Jersey Sports Medicine Institute; Director of Pain Management, Overlook Hospital; Director of Sports Medicine, Sports Medicine Fellowship Director, Mountainside Hospital; Clinical Chief, Rehabilitation Medicine and Electrodiagnosis, St Michael's Medical Center; Medical Director, Consultant, Horizon Healthcare Worker's Compensation Services, Blue Cross and Blue Shield Worker's Compensation
Gerard A Malanga, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Medical Editor

Elizabeth A Moberg-Wolff, MD, Associate Professor and Pediatric PM&R Fellowship Director, Department of Physical Medicine and Rehabilitation, Medical College of Wisconsin; Program Director, Tone Management and Mobility, Department of Physical Medicine and Rehabilitation, Children's Hospital of Wisconsin
Elizabeth A Moberg-Wolff, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
Disclosure: Medtronic Neurological Grant/research funds Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Kat Kolaski, MD, Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine
Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

 
 
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