Life and Limb: Battlefield Medicine from WWII to Today

September 29, 2017

Amputee_Combat_VeteranBy Eric Jeffrey Nisenbaum, MD

Peer Reviewed

Mr. O is a 93-year-old man with a past medical history notable for severe Alzheimer’s dementia and amputation of the left upper extremity secondary to wounds received in WWII who was brought in from his nursing home with fever and dyspnea for two days.  His physical exam was notable for inspiratory crackles at the right lung base.  His CBC was notable for an elevated WBC with left-shift and a chest x-ray revealing a right lower lobe infiltrate. He was treated empirically for health care-associated pneumonia with antibiotics and was subsequently discharged back to his nursing home. 

“I’m going to apologize in advance for my father.  If he starts cursing at you it’s not just the dementia, he’s always been like that.”  I had called Mr. O’s son to let him know of his father’s admission, but also to find out all the things about Mr. O that he – trapped in the end stages of dementia – was unable to tell me himself.  With a preface like that, I knew I was in for an interesting conversation.  As the phone call progressed, his son spoke with an impressive frankness, describing his conflicted feelings regarding a man he described as a “prototypical 1950’s father” – a provider dedicated to his family, but also an emotionally cold, functioning alcoholic.  However, while I left the conversation with a much clearer picture of who my patient had been before dementia robbed him of much of his identity, what stuck with me most was a detail his son had dropped seemingly off-handedly – that Mr. O had lost his arm fighting in the Battle of the Bulge.

Hanging up the phone, I was struck for the umpteenth time by how unique an experience it is to work at the VA.  Here was a man, now approaching the end of his life, who fought in one of the most iconic battles of a war that for my generation exists more as a legend writ large in film and literature than as a historical event.  And not only had he fought, but he had sacrificed an arm, and spent the next 70 years living his life and raising a family with a constant physical reminder of the battle and its consequences.  I couldn’t help but wonder – what was it like to lose an extremity during WWII, and how might things have been different if Mr. O had suffered his injury in a modern warzone instead of on the battlefields of Europe in 1945?

One the biggest differences for Mr. O would have been the speed in which he received care in the immediate aftermath of his wounding.  As military medicine has evolved over the 20th and now 21st century, there has been incredible progress in optimizing the delivery of care.  During WWII, the average time between a soldier being wounded and the initiation of first aid was 5 hours, while the average time to initiation of surgery was 15.2 hours.[1] In comparison, a soldier wounded during the Iraq war would have been almost immediately resuscitated by a trained combat lifesaver, evacuated to a battlefield surgical center staffed with vascular and orthopedic surgeons within 90 minutes, and then ultimately flown to a US military hospital for definitive repair within 3 days.[2]

Of course, another critical difference would be in the quality of care Mr. O would have received.  Since WWII, a vast number of advances in the fields of vascular surgery, microsurgery, and infectious disease among others has allowed for the reconstruction of limbs that previously would have required amputation.[3] During WWII, 49.6% of amputations among US troops were primarily attributable to vascular injury, a number that dropped to 20.5% by the Korean War and has continued to decrease since.2 From an infectious disease perspective, WWII was well underway before the first patient was successfully treated with penicillin in 1942, and in fact the D-Day invasion in 1944 marked the first time antibiotics were used in the treatment of US troops in any significant quantity.2  In comparison, modern troops are able to receive focused, culture-guided antibiotic therapy with a wide array of drugs, though it is worth noting that multidrug-resistant organisms have been a significant cause of morbidity and mortality among US troops in Iraq and Afghanistan.[4]

However, while decreasing rates of mortality from extremity injury in every war since WWII reflects the effectiveness of these advances in care, rates of amputation have paradoxically increased.[5]  This phenomenon can be primarily accounted for by two factors.  On one hand, the aforementioned improvements in care mean soldiers who in the past would never have survived their wounds are now able to be saved, yet may still require amputations.6  On the other hand, the increasing use of powerful explosive weaponry means soldiers are suffering more severe wounds than in the past, with the extremities disproportionally affected as a result of the commonplace use of body armor which protects the torso but leaves the extremities vulnerable.[6]

I will likely never know the exact scenario under which Mr. O lost his arm.  Yet given the fact that he survived his wound – despite the aforementioned deficiencies in available care – and did so without any other apparent injury, it is easily possible that with the benefit of modern medical care, his arm could have been reconstructed rather than amputated.  However, the Catch-22 is that if he had been fighting on a modern battlefield, his wound almost certainly would have been more severe.  Ultimately, the history of battlefield medicine is in many ways the story of the constant struggle between modern medicine and modern warfare, a metaphorical arms race arising as the inevitable consequence of a literal arms race.

Dr. Eric Jeffrey Nisenbaum, resident physician, NYU Langone Health

Peer reviewed by Amar Parikh, MD, Associate Editor, Clinical Correlations and Chief Resident in Internal Medicine at NYU Langone Health

Image courtesy of Wikimedia Commons


  1. DeBakey ME, Simeone FA. Battle Injuries of the Arteries in World War II. Ann Surg. 1946 Apr; 123(4): 534–579.
  1. Manring MM, Hawk A, Calhoun JH, Andersen RC. Treatment of War Wounds:  A Historical Review.  Clin Orthop Relat Res. 2009 Aug; 467(8): 2168–2191
  1. Bumbasirevic M, Stevanovic M, Lesic A, Atkinson H. Current Management of the Mangled Upper ExtremityInt Orthop. 2012 Nov; 36(11): 2189–2195.
  1. Calhoun JH, Murray CK, Manring MM. Multidrug-Resistant Organisms in Military Wounds from Iraq and AfghanistanClin Orthop Relat Res. 2008 Jun; 466(6): 1356–1362.
  1. Kirkup J. Elective Amputation: From 1846 to Modern Times. A History of Limb Amputation. London: Springer, 2010. 83-95.
  1. Belmont PJ, Schoenfeld AJ, Goodman G. Epidemiology of Combat Wounds in Operation Iraqi Freedom and Operation Enduring Freedom: Orthopaedic Burden of DiseaseJ Surg Orthop Adv. 2010 Spring;19(1):2-7. 




Is it Time to Skip the Gym?

January 15, 2014

By Robert Mocharla, MD

Peer Reviewed

No. Sorry. Despite such reasonable excuses as – “I forgot my iPod”, “It’s pouring rain”, or “Game of Thrones is on” — an exhaustive literature search will not reveal a shred of evidence that you or most of your patients should skip daily exercise. However, a subset of your patients should indeed be skipping workouts regularly. The group referred to consists of endurance athletes (e.g. cyclists, swimmers, long-distance runners, competitive athletes). While this may not describe the majority of our patients, growing evidence suggests that overtraining can actually be maladaptive to overall health in certain individuals.

The question of too much exercise was first asked many years ago when it was noticed that, despite rigorous training schedules, the performance of certain athletes actually began to decline months into their training routines. The athletes burned out. But why? Common sense tells us that the more exercise we engage in, the better shape we will be in. Surprisingly, this is not always the case, and until recently, little was known about this phenomenon.

An entity known as Overtraining Syndrome (OTS) has gained widespread acceptance as the cause of deteriorating athletic performance [1]. OTS has been an active area of research since the early 1990s when it was noticed that not only can athletic performance in endurance athletes decline over time, but these athletes can also experience biochemical, psychological, and immunological abnormalities [2]. Currently, there is not a universally accepted theory as to the cause of OTS. One theory with growing evidence is the “Cytokine Hypothesis” [3]. It purports that repetitive joint and muscle trauma seen with excessive physical training elicits a response similar to that seen in chronic inflammation. Inflammatory cytokines at sites of injury activate monocytes, which then release pro-inflammatory IL-1ß, IL-6, and TNF-?. The body then enters a catabolic, inflammatory state. As such, one might hypothesize a chronic inflammatory state would be evident via biochemical markers (i.e. anemia, ESR, CRP). However, to date, no studies have been able to show a relationship between OTS and any of these biomarkers of chronic inflammation. In part, this is why a diagnosis of OTS is often difficult to reach (and always should be one of exclusion after other systemic processes are ruled out) [4].

Another theory involves dysregulation of the Hypothalamic-Pituitary Axis (as seen in amenorrheic female athletes). During exercise, the body acutely releases cortisol, epinephrine and norepinephrine as a means to enhance cardiovascular function and redistribution of metabolic fuel. However, these hormones quickly return to baseline levels following a workout. Interestingly, endurance athletes suffering from burnout show higher baseline cortisol levels [5]. This may then lead to negative effects on normal metabolism, healing, and immunity. In fact, studies have shown an increased susceptibility to infection in overtrained athletes, although the mechanism is not fully understood [6,7]. Studies have not been able to identify differences in leukocyte number or distribution among overtrained vs healthy athletes, and the true etiology may rather be related to impaired functionality of immune cells. It is important to note that the body’s normal response to intermittent exercise is overall adaptive. When allowed adequate time to recover, inflammatory cytokines and hormones decrease to normal levels. The body is then able to adapt to repeated exercise by increasing muscle mass and capillary density, endothelial cell function, and glucose utilization among other things [8]. It is the lack of recovery time that is problematic in OTS.

The most common initial manifestation of OTS involves mood changes. An otherwise emotionally stable athlete may become increasingly depressed, chronically fatigued, unable to sleep, have decreased appetite, and lose interest in competition [9]. Unfortunately, patients are rarely recognized in this stage and often go on to develop the hallmark of the syndrome, deteriorating athletic performance. Muscle and joint pain are often present as well. Depending on the severity, symptoms can last anywhere from a few weeks to years [10]. Even when declining performance is evident, there are no diagnostic criteria or laboratory tests that can confirm a suspicion of OTS. For now, the diagnosis is purely clinical. A high index of suspicion must be kept for all at-risk groups. While competitive athletes are most classically thought of as high-risk, OTS should also be considered in recreational athletes (who may unknowingly advance their training regimen too hastily). The primary focus of management is rest. Each case must be managed individually with regard to the symptom cluster experienced by the patient. It is recommended that patients rest at least a full 3-5 weeks with minimal to no athletic training [11]. Selective serotonin reuptake inhibitors are increasingly being used to combat mood and appetite symptoms [12]. After recovery, a cyclical workout routine should be established with adequate recovery time between cycles. Patients should be advised to consume a high carbohydrate diet to help facilitate recovery between workouts (upwards of 60-70% of caloric intake) [13]. Fortunately, athletes can and do recover after the appropriate interventions and precautions are made.

It is difficult to predict who will develop or re-experience OTS since the threshold of exercise tolerance varies widely among athletes. Therefore, patient education and prevention are critical. Studies estimate that up to 10% of vigorously training athletes have or will experience OTS [4]. Athletes should be questioned about their exercise routines and informed about the dangers and warning signs of over-training. Any evidence of psychiatric disturbance or decreased performance should prompt a discussion on the possibility and management of OTS.

Dr. Robert Mocharla is a graduate of NYU School of Medicine

Peer reviewed by Richard Greene, MD, Internal Medicine, NYU Langone Medical Center

Image courtesy of Wikimedia Commons


1. Budgett R. The overtraining syndrome. British Journal of Sports Medicine. 1990; 24:231–6.

2. O’Toole, M. Overreaching and overtraining in endurance athletes. Overtraining in Sport. R.B. Kreider, A.C. Fry, M.L. O’Toole, eds. Champaign IL: Human Kinetics Publishers, Inc., 1998; 3-18.

3. Smith, LL. Cytokine hypothesis of overtraining: a physiological adaptation to excessive stress? Medicine & Science in Sports & Exercise. 2000; 32 (2): 317-31.

4. Meeusen R, Ducios M, Foster C, et al. Prevention, diagnosis, and treatment of the overtraining syndrome: joint consensus statement of the European College of Sport Science and the American College of Sports Medicine. Med Sci Sports Exerc. 2013; 45(1):186-205,_Diagnosis,_and_Treatment_of_the.27.aspx

5. O’Connor, P.J. et al. Mood state and salivary cortisol levels following overtraining in female swimmers. Psychoneuroendocrinology. 1989; 14 (4), 303-310.

6. Mackinnon, LT. Chronic exercise training effects on immune function. Medicine & Science in Sports & Exercise. 2000; 32 (7 Suppl): S369-76.

7. Heath, G. W., E. S. Ford, T. E. Craven, C. A. Macera, K. L. Jackson, and R. R. Pate. Exercise and the incidence of upper respiratory tract infections. Medicine & Science in Sports & Exercise. 1991; 23:152–157.

8. Mandroukas K, Krotkiewski M, Hedberg M, et al. Physical training in obese women. Effects of muscle morphology, biochemistry and function. Eur J Appl Physiol Occup Physiol. 1984;52:355-61.

9. W.P. Morgan, D.R. Brown, J.S. Raglin, P.J. O’Connor and K.A. Ellickson, Psychological monitoring of overtraining and staleness. Medicine & Science in Sports & Exercise. 1987; 21:107–114.

10. Lehmann, M., U. Gastmann, K.G. Petersen, N. Bach, A. Siedel, A.N. Khalaf, S. Fischer, and J. Keul. Training-overtraining: Performance, and hormone levels, after a defined increase in training volume versus intensity in experienced middle and long-distance runners. British Journal of Sports Medicine. 1992; 26:233-242.

11. Koutedakis, Y., Budgett, R., Fullman, L. The role of physical rest for underperforming elite competitors. British Journal of Sports Medicine. 1990; 24(4):248-52.

12. Armstrong LE, VanHeest JL. The unknown mechanism of the overtraining syndrome: clues from depression and psychoneuroimmunology. Sports Med. 2002;32:185-209.

13. Costill DL: Inside Running: Basics of Sports Physiology. Indianapolis: Benchmark Press; 1986.














Does Running Cause Knee Osteoarthritis?

September 14, 2013

By Karin Katz, MD

Faculty Peer Reviewed

Post-summer is here. Despite the heat and what feels like 100% humidity, the East River Path is packed with runners. No amount of car fumes pouring onto the path could stop those in training. Others are circling the 6-mile-loop around Central Park. Or, if you are bored of running the typical routes, for a few Saturdays, Park Avenue will be shut down for automobile traffic. New Yorkers love to run (well, some do). And while unforeseen circumstances led to a cancellation of the NYC Marathon in 2012, in 2011, almost 47,000 people ran those well-known 26 miles. Given the epidemic of obesity, we should be celebrating this phenomenon! But, is there any reason to advise our patients to be cautious of such strenuous weight-bearing activity? Osteoarthritis is thought of as a disease of “wear and tear” on the joints. Is running a risk factor for developing osteoarthritis? If so, is the damage worse for marathon runners? Maybe we should be advising our patients to stick to water aerobics.

Approximately 19-28% of adults aged 45 or older have knee osteoarthritis (OA) [1]. OA is a degenerative joint disease characterized by articular cartilage failure, although all structures of the joint are involved in the pathologic process. Risks for developing osteoarthritis include systemic factors (age, female gender, genetic susceptibility), intrinsic joint vulnerabilities (previous damage such as meniscal tears, muscle weakness, increased bone density, malalignment), and joint stressors (such as obesity). Individuals who are overweight or obese may have three times the risk of incident knee arthritis [2]. While the risk that obesity confers on osteoarthritis is well established, the impact of exercise on weight-bearing joints is complex. Exercise in different forms has been shown to prevent, cause, accelerate, or treat osteoarthritis.

Let’s start slow with a study on the effects of walking on the development of knee osteoarthritis. Felson et al. published a longitudinal study of the Framinghmam Offspring cohort to evaluate the long-term effect of recreational exercise on the development of knee OA in older adults [3]. A total of 1,279 subjects were included with a mean age at baseline of 53 years. Most reported walking for exercise. Subjects were asked about their knee pain and anteroposterior and lateral knee radiographs were obtained. Nine years later, subjects were reexamined for osteoarthritis. The primary outcomes of the study included incident radiographic OA, symptomatic OA, and tibiofemoral joint space loss. Walking (categorized as less than 6 miles per week, or greater than or equal to 6 miles per week) was not associated with an increased or decreased risk of radiographic or symptomatic OA compared to subjects who did not walk for exercise. Joint space loss was also unaffected by this activity.

Moving on to running, a study in the American Journal of Preventative Medicine investigated differences in the progression of knee OA in middle- to older-aged runners compared to healthy non-runners over two decades [4]. This study included 45 long distance runners and matched controls with a mean age of 58 years. Most of these runners had been running for over a decade. The study examined radiographic knee OA (specifically tibiofemoral disease) by serial radiographs. At the start of this study, members of the runner’s club were running for an average of 214 minutes per week. By the completion of the trial, their running time decreased by 55%. A small proportion of the controls ran for exercise at baseline, but almost all had stopped running by the time the final radiograph was obtained. In the analysis, long-distance running was not associated with accelerated incidence or severity of radiographic OA over a mean observation time of 11.7 years. While this study has a number of limitations, perhaps the greatest one is that there was no analysis of subjects’ clinical symptoms. It is also important to note that the running group was slightly younger with a slightly lower BMI compared to the control group. These differences could have confounded the results. Finally, one must also wonder, why did the runners stop running? What if a runner acquired a knee injury and had to cut down their usual workout? In such cases, longer follow-up might be necessary to detect the development of OA in “retired” runners.

Another study in the American Journal of Sports Medicine showed that formerly competitive runners did not have higher rates of arthritis in their hips, knees or ankles when compared to nonrunners [5]. This retrospective study included Danish male runners who qualified for county teams from 1950 to 1955. The study was published in 1990. Only 30 subjects were included, and were assessed using pain scores, clinical examination and x-rays. There was no difference between runners and non-runners with regard to narrowing of the joint space or osteophytosis in the lower extremity joints. There was also no difference in range of motion of the joints. Some of the runners experienced pain, but clinical and radiographic findings in this particular group were considered normal. While this study is also not without limitations, it is small, retrospective, and much of the data is subjective- it is interesting to look at the effects of long-distance running on the joints over an extended period of time in this athletic population.

Although there are other conflicting data, the medical literature generally does not support the idea that running contributes to the degeneration of articular cartilage [6]. Nonetheless, more advanced imaging techniques raise more questions about this potential association. A cohort study by Luke et al. used advanced MRI techniques to detect changes that could signify early osteoarthritis [7]. The loss of proteoglycan or glycosaminoglycan may be the initiating event in OA; this study used imaging markers to detect proteoglycan loss and collagen breakdown. In this investigation, the knee cartilage of 10 asymptomatic individuals was evaluated before and after a marathon (26.2 miles) using 3-T MRI techniques. A 3-T MRI is an MRI with a 3.0 tesla strength magnet, an advanced imaging technique that has been used assess the biochemical degradation of articular cartilage. Marathon runners were between the ages of 18 and 40 years and were matched to non-runners. The subjects had not participated in a marathon for at least 4 months. The inclusion criteria also included a BMI of less than 30. Runners had their first MRI within 2 weeks before the marathon, then had repeat imaging post-marathon (within 48 hours) and at 10 to 12 weeks after the race. One imaging technique used to describe the biochemical composition of cartilage is called a T1rho measurement. This measurement has been proposed for detecting damage to the proteoglycan-cartilage matrix. The study by Luke et al. demonstrated a significant increase in T1rho values on the post-marathon MRIs of runners. The T1rho values remained elevated 3 months later. Another MRI mapping technique for assessing biochemical changes in the joint is T2 MRI, which characterizes water content and collagen degradation. T2 signals were increased immediately after the marathon, but returned to baseline at 3 months. While this study shows that the biomechanics of knee joints change as a result of marathon running, these changes are not necessarily detrimental to the individual or their joints. The T1rho technique was previously validated in patients with OA, and the T2 relaxation time measurements has also been found to be a reliable means of detecting early degenerative changes of the cartilage. However, whether changes in T1rho and T2 after running lead to joint degeneration over time is not known. In addition, it is not clear how these changes correlate with patients’ symptoms [8,9].

Another interesting article assessing OA with advanced MRI techniques showed moderate exercise in subjects at high risk for OA was associated with joint composition changes that could have chondroprotective effects on the knee [10]. In this study, 45 subjects who underwent a partial medial meniscus resection (a group considered high risk for developing OA) were randomized to undergo a 4-month long supervised exercise regimen or to receive no intervention. The primary outcome was an estimate of cartilage glycosaminoglycan (GAG) content using delayed gadolinium-enhanced MRI techniques. The investigators found that the exercise group showed an improvement in cartilage quality. This suggests that the biochemical changes of exercise on the joint can be protective, rather than harmful.

At present, there is not enough long-term data to suggest that running is a risk factor for knee osteoarthritis. In addition, if patients are counseled that running is bad for their knees, this may deter them from physical exercise and deprive them of the benefits of staying active. An important consideration, however, is that in a patient with a prior knee injury, your advice may differ. Knee injury has been shown to confer a four-fold increased risk of developing knee osteoarthritis, and 50% of individuals with an ACL or meniscus tear may develop knee OA [2,11]. There is limited data to guide counseling patients on the prevention of OA after knee injury. The study by Roos et al. would suggest that some exercise is better than no exercise in such patients [10]. However, it is important to keep in mind that the exercise regimen in that study was supervised, and these patients were not running marathons. Athletes with a history of a knee injury who continue long-distance running may have a very different clinical course of disease.

Although there are more questions to be answered, this summer there’s no reason to tell your healthy runners to stick to the swimming pool and quit training for their next marathon.

Karin Katz, MD is a second-year internal medicine resident at NYU Langone Medical Center

Peer reviewed by Michael Pillinger, MD, Associate Professor, Department of Medicine, Rheumatology Divison, NYU Langone Medical Center


1. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II. Arthritis Rheum. Jan 2008;58(1):26-35.

2. Blagojevic M, Jinks C, Jeffery A, Jordan KP. Risk factors for onset of osteoarthritis of the knee in older adults: a systematic review and meta-analysis. Osteoarthritis Cartilage. Jan 2010;18(1):24-33.

3. Felson DT, Niu J, Clancy M, Sack B, Aliabadi P, Zhang Y. Effect of recreational physical activities on the development of knee osteoarthritis in older adults of different weights: the Framingham Study. Arthritis Rheum. Feb 15 2007;57(1):6-12.

4. Chakravarty EF, Hubert HB, Lingala VB, Zatarain E, Fries JF. Long distance running and knee osteoarthritis. A prospective study. Am J Prev Med. Aug 2008;35(2):133-138.

5. Konradsen L, Hansen EM, Sondergaard L. Long distance running and osteoarthrosis. Am J Sports Med. Jul-Aug 1990;18(4):379-381.

6. Willick SE, Hansen PA. Running and osteoarthritis. Clin Sports Med. Jul 2010;29(3):417-428.

7. Luke AC, Stehling C, Stahl R, et al. High-field magnetic resonance imaging assessment of articular cartilage before and after marathon running: does long-distance running lead to cartilage damage? Am J Sports Med. Nov 2010;38(11):2273-2280.

8. Li X, Benjamin Ma C, Link TM, et al. In vivo T(1rho) and T(2) mapping of articular cartilage in osteoarthritis of the knee using 3 T MRI. Osteoarthritis Cartilage. Jul 2007;15(7):789-797.

9. Nishii T, Kuroda K, Matsuoka Y, Sahara T, Yoshikawa H. Change in knee cartilage T2 in response to mechanical loading. J Magn Reson Imaging. Jul 2008;28(1):175-180.

10. Roos EM, Dahlberg L. Positive effects of moderate exercise on glycosaminoglycan content in knee cartilage: a four-month, randomized, controlled trial in patients at risk of osteoarthritis. Arthritis Rheum. Nov 2005;52(11):3507-3514.

11. Ratzlaff CR, Liang MH. New developments in osteoarthritis. Prevention of injury-related knee osteoarthritis: opportunities for the primary and secondary prevention of knee osteoarthritis. Arthritis Res Ther. 2010;12(4):215.




An Evaluation of Basic Running Techniques: A Guide for Health Practitioners and the Novice Runner

September 11, 2013

By Austin Peters, MD

Faculty Peer Reviewed


Running injuries are common, afflicting greater than two-thirds of frequent runners each year[1]. Despite the abundance of available resources, there are no clear guidelines to extend to patients on the subject of proper running technique in order to avoid repeat or worsening injuries. Though specialized intervention may be in order for more severe cases, novice runners and those who have not been active in the sport for some time may benefit from basic instructional advice. The purpose of this article is to provide clinicians with a first line intervention for such patients in order to minimize injuries and improve results.

Starting at the beginning

At its most basic, runners have 2 options when it comes to placing one foot ahead of the other:

1. The forefoot/midfoot strike (FFS) – impacting the ground on one’s toes or the balls of one’s feet (Figure 1c).

2. The rear foot/heel strike (RFS) – extending one’s heel to meet the ground first, and rolling forward onto the toes (Figure 1a and 1b).

Figure 1. Foot strike methods and resulting generated forces.

This figure, borrowed from Lieberman et. al. in Nature 2010 (as per Nature Publishing Group’s licensing policy for educational material), compares rear foot (1a, 1b) and fore foot (1c) strike methods as well as the force generated by each. Notice the impact transient generated by barefoot rear foot striking (1a), which is reduced when wearing shoes (1b). No impact transient is generated with fore foot striking (1c).

The primary differences between these two approaches are the force of the impact, the transference of energy, and the duration of ground contact. In each of these categories, FFS is superior to RFS[2-5]. Ardigo et. al. compared speed, step frequency, step length and oxygen consumption in 8 active male runners using either FFS or RFS[2], Hayes et. al. evaluated by video 181 runners in competition[4],and Cavanagh et. al. and Lieberman et. al. performed biomechanical comparisons of the two techniques[3,5]. In short summation, when the heel hits the ground first, there is a brake-like effect, and a greater collision and contact time between the leg and the ground. Alternatively, a forefoot impact induces a more rounded and rolling motion, reducing recoil from hitting the ground as well as actual ground contact time, and thus friction. An important caveat for this comparison is that, at slower speeds, FFS is less biomechanically fluid and efficient than RFS[2]. This may induce novice runners to prefer RFS, as it is initially less exhausting and more similar to the familiar motion of walking. No large, randomized studies have been performed comparing injury rates in these two foot strike methods. However, in the (?observational?) studies available, FFS was shown to be associated with a significantly lower injury rate, improved performance, and reversal of chronic running injuries compared to RFS[6-8]. Cheung et. al. and Diebal et. al. performed case studies of 3 runners and 10 runners, respectively, with overuse injuries, converting them from RFS to FFS, and found a resulting decrease in symptoms[6,8]; Daoud et. al. retrospectively compared injury rates of 52 runners based on foot strike patterns and found twice the rate of stress injuries in RFS runners[7].


If the shoe fits

Runners face an overwhelming variety of shoe options, more so recently with the burgeoning minimalist/barefoot running movement. Large scale comparative studies between shoe types (and no shoes at all) are lacking. Yet, consistent trends are evident. A recent study by Franz et. al. comparing 12 male runners demonstrated that increased shoe weight led to increased oxygen demand; it also showed that shod runners had reduced oxygen demand compared to barefoot runners[9]. Taken on its own, this study would suggest a clear benefit for using lightweight running shoes. However, several biomechanical studies have been put forth espousing the benefits of minimalist footwear (e.g. Vibram FiveFingers, Nike Free) and barefoot running, particularly in their tendency to force the runner to adapt to FFS technique[5,10]. Simply put, heavily cushioned shoes are more forgiving to foot strike variations (Figure 1a and 1b), preventing immediate impact injuries, but doing nothing to reduce the more gradual injuries associated with RFS, such as medial stress syndrome (shin splints) and plantar fasciitis[11,12]. Runners converting to barefoot/minimalist style should take caution to avoid starting out running distances comparable to those they were running in cushioned shoes as intrinsic foot muscles and secondary muscle groups (especially the gastrocnemii) will require strengthening and conditioning, and the sudden transition could lead to new stress injuries[13].

Stride and style

Though there is no single correct method of running, several elements appear to be universal. Reduced stride length and increased stride frequency are associated with fewer injuries and less oxygen demand than overextended and overemphasized strides[14,15]. Arm swinging – specified as alternating forward extension of the arm when the ipsilateral leg is extending backwards – is also associated with decreased oxygen demand. Finally, maintaining one’s back straight allows for greater lung capacity than hunching forward[16]. Of note, all of these characteristics are central to barefoot running techniques (e.g. POSE method, Chi running and 100-up). These techniques may be worth exploring for specific style suggestions, but no comparative studies have ever been conducted regarding their perceived benefits of injury reduction and performance improvement.

From this author’s own experience, uphill running requires inherent stride and step modifications that best reflect proper form for injury avoidance and improved performance (shorter stride, FFS, straight back) and may offer inexperienced runners a way of identifying specific mechanical aspects to improve upon. Furthermore, a focus on rapid hip flexion with a forward lean, as opposed to generating force from a rearward push, allows for core muscles to generate most of the power of running, instead of relying on ground impact to do the same (with the resulting stresses of such impact) (Multimedia 1).

Multimedia 1. A video guide to proper running technique.

This video is presented by Dr. Mark Cucuzzella, Director of the Natural Running Center, located in West Virginia. The featured runner is barefoot to illustrate recommended foot and leg placement, but also to demonstrate the viability of barefoot running itself. Notice the impact pattern of the runner’s feet. At 3:27, the runner is demonstrating the drill central to the 100-up method, with its emphasis on hip flexion rather than rearward pushing; combined with a forward lean, this motion generates movement with comparably reduced ground impact. Towards the end of the piece, Dr. Cucuzezella points out the mechanical differences between forefoot striking and rear foot striking.


For all its simplicity, running carries a shockingly high rate of injury. Yet as sedentary lifestyle-associated morbidities rise worldwide, health professionals would do well to stress the benefits of aerobic exercise – especially running – due to it accessibility and recreational value. The techniques evaluated in this paper are intended to guide the clinical practitioner in reducing commonly seen running injuries so that more people can run farther for a longer frame of time in their lives and receive all the subsequent health benefits therein implied.

Austin Peters is a former medical student at NYU School of Medicine

Peer reviewed by Richard E. Greene, MD, Medicine,  NYU Langon Medical Center

Image courtesy of Wikimedia Commons


1. van Gent RN, Siem D, van Middelkoop M, et al. Incidence and determinants of lower extremity running injuries in long distance runners: a systematic review. Br J Sports Med. Aug 2007;41(8):469-80; discussion 480.

2. Ardigo LP, Lafortuna C, Minetti AE, Mognoni P, Saibene F. Metabolic and mechanical aspects of foot landing type, forefoot and rearfoot strike, in human running. Acta Physiol Scand. Sep 1995;155(1):17-22.

3. Cavanagh PR, Lafortune MA. Ground reaction forces in distance running. J Biomech. 1980;13(5):397-406.

4. Hayes P, Caplan N. Foot strike patterns and ground contact times during high-calibre middle-distance races. J Sports Sci. Aug 2012;30(12):1275-83.

5. Lieberman DE, Venkadesan M, Werbel WA, et al. Foot strike patterns and collision forces in habitually barefoot versus shod runners. Nature. Jan 28 2010;463(7280):531-5.

6. Cheung RT, Davis IS. Landing pattern modification to improve patellofemoral pain in runners: a case series. J Orthop Sports Phys Ther. Dec 2011;41(12):914-9.

7. Daoud AI, Geissler GJ, Wang F, et al. Foot strike and injury rates in endurance runners: a retrospective study. Med Sci Sports Exerc. Jul 2012;44(7):1325-34.

8. Diebal AR, Gregory R, Alitz C, Gerber JP. Forefoot running improves pain and disability associated with chronic exertional compartment syndrome. Am J Sports Med. May 2012;40(5):1060-7.

9. Franz JR, Wierzbinski CM, Kram R. Metabolic cost of running barefoot versus shod: is lighter better? Med Sci Sports Exerc. Aug 2012;44(8):1519-25.

10. Squadrone R, Gallozzi C. Biomechanical and physiological comparison of barefoot and two shod conditions in experienced barefoot runners. J Sports Med Phys Fitness. Mar 2009;49(1):6-13.

11. Milner CE, Ferber R, Pollard CD, Hamill J, Davis IS. Biomechanical factors associated with tibial stress fracture in female runners. Med Sci Sports Exerc. Feb 2006;38(2):323-8.

12. Pohl MB, Hamill J, Davis IS. Biomechanical and anatomic factors associated with a history of plantar fasciitis in female runners. Clin J Sport Med. Sep 2009;19(5):372-6.

13. Giuliani J, Masini B, Alitz C, Owens BD. Barefoot-simulating footwear associated with metatarsal stress injury in 2 runners. Orthopedics. Jul 2011;34(7):e320-3.

14. Goss DL, Gross MT. A review of mechanics and injury trends among various running styles. US Army Med Dep J. Jul-Sep 2012:62-71.

15. Hogberg P. How do stride length and stride frequency influence the energy-output during running? Arbeitsphysiologie. 1952;14(6):437-41.

16. Anderson T. Biomechanics and running economy. Sports Med. Aug 1996;22(2):76-89.

Reviewer Comment:

Running is an excellent and inexpensive form of exercise, but many providers who are not themselves runners feel uncomfortable recommending it to patients given the high rate of injury. This article offers a nice outline for providers to begin thinking about running: form, shoes and styles. The embedded video gives a provider a nice overview of the biomechanics of running. Each runner is different, and injuries may happen, but it is an excellent form of exercise and this article offers providers a place to start discussing it with their patients. –Richard E. Greene, MD


Olympics and Medicine By The Numbers

October 7, 2012

By Tracey Liebman

Faculty Peer Reviewed

The summer games may be over, but we’re still entertained by the 2012 Olympics! Here are a few medicine-related fun facts about the London Games.

Demographics of Summer 2012 Olympics:

10,500 athletes, 70,000+ volunteers, 20,000 media and journalists, 10+ million spectators [1]

Medical care:

26 million dollars provided by the National Health Service (NHS) to build the state-of-the-art medical building in the Athletes’ Village for the Olympics [2]

500 people expected to use the medical clinic each day [2]

46 sports medicine doctors, 80 other specialists on call at the clinic [2]

95% of cases expected to be minor illnesses or injuries [2]


1055 injuries reported in 2008 Beijing Summer Olympics, 72.5% of injuries occurred during competition [3]

11.2% of athletes in 2010 Vancouver Winter Olympics reported injuries [4]

Top 10 biker in prior Olympics, British cross-country mountain biker suffered from a fractured ankle after falling on rocks during the race [5]

162 kg lift attempted by South Korean weightlifter, but athlete ended up with a dislocated elbow [6]

7th place in floor routine, World Champion gymnast Jordyn Wieber was found to have a possible stress fracture in her leg [7]


1364 food, swab, cloth, and water samples collected from London vendors to evaluate for good hygiene procedures in preparation for the Olympics. 8% of food samples and 52% of water samples were of unsatisfactory quality [9]

3-5% projected increased demand for medical care in London during the Olympics 22761253 [10]

1100 cases of measles in England and Wales in the past year – thus, Americans were strongly encouraged to be vaccinated prior to traveling to Olympics [11]

Athletes and doping:

6.8% of young elite athletes admitted to doping in a 2010 anonymous survey, though doping tests only reveal 0.81% prevalence of doping [12]

3 cross country skiers at 2002 Salt Lake City Olympics found to have darbopoeitin in their urine. Their 8 medals were sanctioned [13]

5 athletes disqualified from 2008 Beijing Olympics for using a long-acting 3rd-generation EPO [13]

47,361 square feet of space for one new anti-doping laboratory in London, functioning 24 hours/day [14]

6000 blood and urine tests predicted to be carried out during London Olympics [15]

150 antidoping scientists carrying out the tests [15]

2 sports in London games in which beta blockers are prohibited: shooting and archery [16]

31-year-old shot-putter disqualified in London Olympics and stripped of her gold medal due to testing positive for the steroid metenolone [17]

23-year-old Syrian 400-meter hurdler disqualified from London Olympics for using stimulant methylhexaneamine [18]

73-kg-class, 23-year old American Judo competitor disqualified from London Olympics due to testing positive for marijuana [19]

23 athletes provisionally suspended, 7 athletes disqualified during London Olympic Games [20]


8 to 12,000 – number of calories reportedly consumed daily by Olympian Michael Phelps [8]

Tracy Liebman is a medical student (Internal Medicine), NYU Langone Medical Center

Peer Reviewed by Neil Shapiro, Editor-In-Chief, Clinical Correlations



2. Torjesen I. Olympic site polyclinic “will be most tangible health legacy” of games, says medical chief. BMJ 2012;344:e4334.

3. Junge A, Engebretsen L, Mountjoy ML, et al. Sports injuries during the Summer Olympic Games 2008. The American journal of sports medicine 2009;37:2165-72.

4. Willis C, Elviss N, Aird H, Fenelon D, McLauchlin J. Evaluation of hygiene practices in catering premises at large-scale events in the UK: Identifying risks for the Olympics 2012. Public health 2012;126:646-56.





9. Willis C, Elviss N, Aird H, Fenelon D, McLauchlin J. Evaluation of hygiene practices in catering premises at large-scale events in the UK: Identifying risks for the Olympics 2012. Public health 2012;126:646-56.

10. Torjesen I. Doctors will see increased demand during Olympics despite preparations. BMJ 2012;345:e4585.

11. Tanne JH. US travellers to the London Olympics are warned about contracting measles. BMJ 2012;344:e2357.

12. Striegel H, Ulrich R, Simon P. Randomized response estimates for doping and illicit drug use in elite athletes. Drug and alcohol dependence 2010;106:230-2.

13. Fitch K. Proscribed drugs at the Olympic Games: permitted use and misuse (doping) by athletes. Clin Med 2012;12:257-60.

14. Kayser B, Broers B. The Olympics and harm reduction? Harm reduction journal 2012;9:33.

15. Hunger M. Would-be cheats face barrage of tests at London Olympics. BMJ 2011;343:d5847.






Class Act: Is there clinical evidence for the use of chondroitin sulfate in the treatment of osteoarthritis?

October 17, 2008

images1.jpgClass act is a feature of Clinical Correlations written by NYU 3rd and 4th year medical students. Prior to publication, each commentary is thoroughly reviewed for content by a faculty member.

Commentary by Jillian Borman, MS-4, Reviewed by Svetlana Krasnokutsky, MD, Clinical Instructor, NYU Department of Medicine

Osteoarthritis (OA) is one of the most common causes of joint pain in the aging population. The pain of OA, which is generally worsened with joint use and alleviated with rest, is typically described as a deep ache localized to the affected joint. (1) Using the National Health and Nutrition Examination Survey I (NHANES I) and the 2005 population estimates from the Census Bureau, it has been estimated that 26.9 million adults over the age of 25 years are afflicted with clinical OA of at least one joint. This estimate is up from the 1995 estimate of 21 million.(2) The prevalence of osteoarthritis in the United States will likely continue to rise due to the aging population and the fact that people are living longer than ever before.

While there are a variety of options for symptomatic treatment, which range from weight loss and non-steroidal anti-inflammatory drugs (NSAIDs) to glucocorticoid injections and total joint replacement, not all patients are helped by these treatments. Recently many patients have turned to chondroitin sulfate, a widely available dietary supplement, which is currently not approved by the U.S. Food and Drug Administration for use in OA. Chondroitin sulfate, the predominant glycosaminoglycan found in articular cartilage, allows the cartilage to withstand tensile stresses during loading conditions. In vitro, chondroitin sulfate acts as a competitive inhibitor to prevent enzymes from degrading the cartilage, increases proteoglycan production, and counters the destructive effect of interleukin 1ß.(3) Administration of chondroitin sulfate exogenously is thought to have an anti-inflammatory effect, though its efficacy in the treatment of OA remains controversial due to the lack of consistent findings among reliable scientific studies.(4)

In 2006, the New England Journal of Medicine published the results of a randomized, multicenter, double blind, placebo-controlled trial that studied the efficacy of chondroitin sulfate in the treatment of OA. The study included more than 1,500 participants with symptomatic knee osteoarthritis with a primary outcome measure of a 20 percent decrease in knee pain at 6 months. The investigators found that the rate of response to chondroitin sulfate was not significantly higher than the rate of response to placebo in the analysis of the primary outcome. However, participants using chondroitin sulfate had a significant decrease in the incidence of joint swelling, effusion, or both. Furthermore, in a subgroup of patients with moderate to severe knee pain, results for the primary outcome demonstrated that when chondroitin sulfate was used with glucosamine, the combination was significantly more effective than placebo.(5)

The Annals of the Rheumatic Diseases published the results of another randomized, multicenter, double-blind, placebo-controlled study in 2007 that included over 300 patients with symptomatic knee osteoarthritis. The primary outcome measures used by these investigators were the mean variation of pain on activity and the mean variation of Lequesne’s Index Score at the end of the 6 months of treatment compared with the score at inclusion. Lequesne’s Index Score allows patients to score pain or discomfort, stiffness, difficulty performing daily activities, and their maximum walking capacity. The results failed to show that chondroitin sulfate was effective on the two primary outcome measures, though it was slightly more effective than placebo on quality of life.(6)

A 2007 meta-analysis examined the effects of chondroitin sulfate in 20 randomized or quasi-randomized trials of 3846 patients with knee or hip OA.(7) When all 20 trials, which had a high degree of heterogeneity, were evaluated, chondroitin was statistically significantly more effective than placebo in terms of pain relief (patients were also allowed other analgesics/anti-inflammatory medications). However, when only the studies that used an intention-to-treat analysis were examined (3 largest studies, 1553 subjects), chondroitin had no effect on symptoms. Effects of chondroitin on the rate of cartilage loss have also been examined in some of the studies comprising this meta-analysis. The chondroitin-treated groups had statistically significantly less radiographic joint space narrowing compared with placebo groups in combined results from five trials. The effects, however, were small and of uncertain clinical significance.

In summary, chondroitin sulfate should not be a first-line therapy for OA at this juncture, but may be considered in patients with moderate–to-severe disease who have failed other treatments. Patients should also be advised that when chondroitin sulfate is used in combination with glucosamine, its efficacy may be improved. The current evidence for treating OA with chondroitin sulfate continues to be limited and further research needs to be completed, though it appears that any possible benefit will be small.


1. Brandt KD. Osteoarthritis. In:Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL. Harrison’s Principles of Internal Medicine, 16th ed. New York, NY: McGraw-Hill; 2005:2036-2045.

2. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II. Arthritis Rheum 2008;58:26-35.

3. Fioravanti A, Collodel G. In vitro effects of chondroitin sulfate. Adv Pharmacol 2006; 53:449-465.

4. Toshihiko T, Sakai S, Akiyama H, Linhardt RJ. Immunological activity of chondroitin sulfate. Adv Pharmacol 2006;53:403-415.

5. Clegg DO, Reda DJ, Harris CL, et al. Glucosamine, chondroitin sulfate, and the two in combination for painful knee osteoarthritis. N Engl J Med 2006;354:795-808.

6. Mazieres B, Hucher M, Zaim M, Garnero P. Effect of chondroitin sulfate in symptomatic knee osteoarthritis: a multicentre, randomized, double-blind, placebo-controlled study. Ann Rheum Dis 2007; 66:639-645.

7. Reichenbach S; Sterchi R; Scherer M; Trelle S; Burgi E; Burgi U; Dieppe PA; Juni P. Meta-analysis: chondroitin for osteoarthritis of the knee or hip. Ann Intern Med 2007;146:580-90.

Clinical Question: How do you manage plantar fasciitis?

July 19, 2007

Feet 2Commentary by Cathy Cruise, M.D. Director Department of Veterans Affairs Care Coordinator, Chair Rehabilitation Council

Case: A 25 year old woman with no significant past medical history presents to walk-in clinic complaining of several days of right heel pain. She notes that the pain is quite sharp and worst when walking. It is so severe that she has skipped her morning run for three consecutive days. She has tried taking acetaminophen which has provided minimal symptom relief. Physical exam reveals mild swelling and point tenderness over the right heel. You suspect that she has plantar fasciitis, but are unsure how to proceed.

The differential diagnosis of heel pain includes plantar fasciitis, bone spurs (which often coexist with plantar fasciitis), tendonitis of the posterior tibialis or flexor digitorum longus and bursitis. Heel pain may also be derived from pathologic processes affecting the calcaneus, such as stress fractures, malignancy, reactive arthritis, Paget’s Disease and sarcoidosis. This patient most likely has plantar fasciitis based on her history.

Plantar fasciitis is characterized by moderate to severe heel pain, worse in the morning, or when initiating activity. It is due to repetitive microtrauma to the plantar fascia of the foot, leading to pain and inflammation. It can be diagnosed by history and physical exam.

The treatment of plantar fasciitis is conservative. In order to allow the fascia to heal, patients should decrease the amount of walking, running and jumping that they do. Proper footware is essential and should include well-cushioned soles and possibly a heel pad. Soft medial arch supports may be beneficial to prevent over-pronation. High heels are to be avoided, as they can lead to shortening of the Achilles tendon. Patients with suspected plantar fasciitis may be referred to Podiatry, Rehab or Orthopedics for selection of appropriate heel and arch supports. The Rehab service can also instruct patients on an exercise program aimed at stretching the plantar fascia and Achilles tendon. Icing, ultrasound and deep friction massage are other modalities that are sometimes employed.

In terms of medical therapy, NSAIDs may provide some relief by decreasing inflammation. Most cases of plantar fasciitis will completely resolve within 6-12 weeks. For persistent cases, cortisol injections can be considered. In the rare instances when relief is not obtained by conservative methods, the plantar fascia can be surgically released from the calcaneus.

The efficacy of preventive measures is not known; however patients should be advised to wear shock absorbent shoes, stretch prior to a work out and control their intensity of running.

Image courtesy of Conrad Nutschan, Wikimedia Commons

Class Act: Is there evidence to support chiropractic care of low back pain?

July 18, 2007

Welcome to Class Act, a new feature of Clinical Correlations. Class act will feature posts written by NYU 3rd and 4th year medical students. These posts will focus on evidenced based answers to clinical questions related to patients seen by our students in the clinics or on the wards. Prior to publication, each commentary is thoroughly reviewed for content by a faculty member. Enjoy…

Commentary by Brian Liem, MSIV

A 52 year old male with no medical problems presents to your clinic with a 10 year history of chronic intermittent back pain. Over the past few months, his pain has increased in severity and frequency. Radiological examination reveals degenerative changes in the lumbar spine, particularly at L4-L5. Would the patient benefit from chiropractic intervention?

Low back pain is the 5th leading reason for medical office visits in the US and is the leading cause of work-related disability.1 Fifty-six percent of office visits for back pain are to family practitioners and internists, 25 percent to orthopedic surgeons, 7 percent to neurosurgeons, and 4 percent to neurologists, and the rest to chiropractors and other healthcare professionals.2 While the standard practice for treating lower back pain is generally with activity modification, analgesics and physical therapy, spinal manipulative therapy, otherwise known as chiropractic care, has gained popularity throughout the years.

From a chiropractor’s perspective, low back pain is a function of restricted movement in the spine. In spinal manipulation, practitioners apply high velocity manual loading to the spine using short or long leverage methods in order to increase spine mobility.3 Many patients with chronic low back pain will seek chiropractic care, but what is the evidence that chiropractic care is even effective in treating low back pain?

One randomized control study in UK of 1334 patients compared treatment of low back pain with “best care” in general practice to spinal manipulation added to “best care.” At three months post-treatment, those patients who were given the additional spinal manipulation had improved Roland Morris disability scores.4 At twelve months there continued to be improvements, although less dramatic.

However, in a meta-analysis of 39 randomized control trials comparing spinal manipulation to commonly used, but not necessarily proven, therapies (i.e.: analgesics, back school (diathermy), physical therapy, light massage, bed rest, topical gels, corsets), spinal manipulative therapy was found only to be superior to sham therapy or therapies judged to be ineffective or even harmful.5 Researchers found no evidence that spinal manipulation was more effective than standard treatments for low back pain.

Read more »

Bedside Rounds: What is Lasegue’s Sign?

July 10, 2007

LasegueCommentary by Judith Brenner MD, Associate Program Director, NYU Internal Medicine Residency Program

A 66 year old woman with a history of dyslipidemia and remote tobacco use presents with a sudden onset of pain located in her posterior left thigh radiating down her left leg below the knee. The pain began during the course of an upper respiratory illness with a cough. The pain is burning in quality and is bothersome day and night. NSAIDs have been taken and relieve the pain temporarily.

What is Lasegue’s sign and when would you find it useful?

“Lasegue’s sign” is another name for the straight leg maneuver used in the diagnosis of lumbosacral radiculopathy. It is named after the French clinician, Charles Lasegue, whose student described the maneuver and named it after his mentor. To perform the straight leg test, the clinician lifts the extended leg of a patient in a supine position. A positive response occurs when the pain pattern of the lumbar radiculopathy is reproduced. The test should be stopped when the pain is reproduced or maximum flexion is achieved. It is believed that the pain is reproduced because of stretching of the sciatic nerve and its roots when the leg is flexed. The sensitivity and specificity of the maneuver is reported in McGee’s Evidence Based Physical Diagnosis as 73-98% and 11-61%, respectively. More useful than the straight leg maneuver is the crossed straight leg test. This test has a lower sensitivity but a specificity that approaches 90%. The crossed straight leg maneuver is performed by raising the unaffected leg in a similar manner to the straight leg test. The examiner looks for the reproduction of radicular pain with elevation of the opposite leg. This test is reported by McGee to have a higher specificity and, thus, a higher likelihood ratio (LR=4.3).

The differential diagnosis of a positive straight leg test includes: disc protrusion with impingement of nerve roots below L4; meningismus; any intraspinal lesion such as tumor below L4; malignant disease or osteomyelitis of the ilium or upper femur; ankylosing spondylitis; fractured sacrum and more.

Read more »

Should You Recommend Surgery or Conservative Care for Disc Herniation?

November 29, 2006

In the November 22nd issue of JAMA, the results of two studies from the Spine Patient Outcomes Research Trial (SPORT) on lumbar disk surgery for persistent radicular pain are reported.  Both these studies sought to assess the efficacy of surgery for lumbar disk herniation as compared to nonoperative treatment, including counseling, anti-inflammatory medications, injections, and physical therapy. It is important to note that specific inclusion criteria were radicular pain as well as imaging showing disk herniation.  Because a large number of study participants declined randomization, the trial included both a randomized cohort and an observational cohort who met all inclusion criteria but opted to designate their own treatment rather than being randomized. The results of theses studies are published as companion articles. Outcomes included changes from baseline as measured by a health survey with bodily pain and physical function scales, as well as satisfaction with symptoms and self-reported improvement.  Read more »

Improving Stroke Recovery-The EXCITE Trial

November 9, 2006

The EXCITE trial was the lead article in last week’s JAMA. It looks at a 2 week program of contstraint induced movement therapy vs. usual care in patients suffering a cva within the previous 3-9 months. Pt’s in the treatment arm wore a restraining mitt on the less-affected hand and engaged in tasks/behaviors with the hemiplegic hand. This group was compared to a control group with usual care. Measures of performance time and motor function ability all showed clinically relevant improvements that persisted out to 1 year.

Commentary By Rob Staudinger, M.D. Program Director, NYU Neurology Residency, Associate Chief of Neurology at the Veterans Affairs NYHHS.

Stroke is the leading cause of disability in the US. Currently used rehabilitation treatments generally are based on empirical approaches rather than validated therapies. The EXCITE (Extremity Constraint Induced Therapy Evaluation) trial is interesting in several ways. It is the first multisite randomized study to demonstrate the efficacy of a rehabilitative intervention. It included patients who had the first stroke in the previous 3-9 months and therefore suggests that more recovery after a stroke is possible than we currently teach. The study included only patients with limited disability and it remains to be seen if this approach, based on the concept of neuronal plasticity, holds promise for more severely affected patients.

Wolf SL, et al “Effect of Constraint-Induced Movement Therapy on Upper Extremity Function 3 to 9 Months After Stroke: The EXCITE Randomized Clinical Trial” JAMA 2006; 296 (17): 2095-2104.