Causes Of Exercise-induced Leg Pain Research Articles

OA06 Behçet's associated myositis: an unusual cause of exercise-induced leg pain

Abstract Introduction This case describes a 29-year-old gentleman of Cypriot heritage who presented with exercise-induced bilateral lower leg pain and swelling which made it difficult for him to cycle. Symptoms progressed over months to calf pain at rest accompanied by fatigue. He subsequently presented with central visual loss in the right eye, followed by the left. The second episode of visual loss coincided with development of oro-genital ulceration and, following rheumatology review, a diagnosis of Behçet’s disease was made. The case is significant in terms of the chronicity and nature of presenting symptoms which is not typically described in this disease. Case description A 29-year-old gentleman presented with exercise-induced bilateral lower leg pain and swelling for which he was reviewed in emergency care on four occasions. He received treatment for presumed cellulitis and underwent US-doppler studies, excluding thromboembolic disease. MRI of the lower legs was requested given lack of diagnosis with ongoing symptoms. This demonstrated bilateral muscle oedema in the antero-lateral compartments and lateral gastrocnemius heads, prompting rheumatology referral. Prior to attending rheumatology, the patient developed bilateral sequential visual loss. This was attributed to right acute macular neuroretinopathy, followed by significant left posterior pole choroidal ischaemia 2 months later. Each presentation was associated with transient low-grade anterior uveitis, vitritis, and the presence of a pre-papillary vitreous infiltrate. Initial treatment included a six-week oral prednisolone taper from 60mg daily. He reported a progressive leg pain which initially occurred during cycling but later affecting his walking. He was of Cypriot heritage, with no family history of autoimmune disease. A focused history revealed oral ulceration and an acne-like pustular rash over the back. His gait was antalgic with minimal toe-off phase. Investigations demonstrated raised ESR and CRP, negative autoimmune immunology, negative myositis ENA, normal CK, and positive HLA-B51. Given these features, a provisional diagnosis of Behçet’s was made. Nerve conduction studies were requested to consider whether changes could be secondary to denervation. They displayed non-specific S1 neurogenic changes and small tibial motor amplitudes. Subsequent MRI lumbar spine excluded radiculopathy. Repeat CK remained within normal limits. Muscle biopsy was sought and performed with a clinical suspicion of atypical myositis which has previously been reported in Behçet’s. At the second episode of visual loss, he was admitted under ophthalmology and treated with intravenous methylprednisolone and azathioprine. The case was discussed with our regional centre of excellence for Behçet’s and infliximab at 5mg/kg was commenced. Discussion This case was notable for the complexity and atypical presenting features with calf pain induced by exercise likely due to atypical myositis (biopsy report still awaited at time of submission). More classical Behçet’s disease symptoms including oro-genital ulceration were significantly later. The case highlights the importance of multidisciplinary working and involving specialist centres especially when rapid escalation to biologic treatment is required. Leg symptoms are persistent but improved despite ongoing treatment with prednisolone and azathioprine with the recent addition of infliximab. Visual symptoms have stabilised and skin involvement has settled. Management Rationale At the time of first review in rheumatology clinic, high-dose steroid treatment had already been initiated; therefore, expediting the investigative aspect of his management felt most appropriate, particularly given that myositis seemed to be the predominant feature at that time. In joint consultation with neurophysiology and neurology, putting the EMG and MRI findings in context, MRI of the lumbar spine was felt necessary to exclude discogenic disease causing denervation oedema. Unfortunately, visual symptoms progressed rapidly after this, requiring admission, which precluded an earlier opportunity for biopsy but leading to quick authorisation and organisation of treatment with infliximab. Key learning points This case highlights an atypical presentation of Behçet’s disease including associated likely atypical myositis. Causes of exercise-induced leg pain in a young, fit patient need to be considered: The need for multidisciplinary discussion both across specialties and with regional centres is key in order to progress with diagnostics and treatment In sharing this case for discussion, we wish to highlight possible causes of exercise-induced calf pain and a pathway for investigation of this. Our patient had atypical myositis as the cause for his symptoms in the context of multi-system disease. Both his myositis and ophthalmology presentations were somewhat atypical but multidisciplinary working, along with the development of some further symptoms, were helpful in making the diagnosis.

Effectiveness of surgical and non-surgical management strategies in patients with chronic exertional compartment syndrome of the anterior compartment of the leg: a systematic review protocol.

The objective of this review is to evaluate the effectiveness of surgical management versus non-surgical management on pain, range of motion, intracompartmental pressure values, patient satisfaction, recurrence of symptoms, return to activity, function, strength, and sensation in patients diagnosed with chronic exertional compartment syndrome of the anterior compartment of the leg. Chronic exertional compartment syndrome is the most prevalent cause of exercise-induced leg pain in athletes. Current evidence suggests that the best methods for management include activity modification or cessation, injection of botulinum toxin into the affected compartment, or surgical intervention. Due to the limited number and quality of studies available, the evidence needs to be synthesized to pool findings from current research and to identify gaps in the literature. This review will consider studies that include people with chronic exertional compartment syndrome of the anterior compartment of the leg diagnosed through a combination of elevated intracompartmental pressure values and patient history. Studies that include patient-reported outcome measures will be included. MEDLINE, SPORTDiscus, Physiotherapy Evidence Database, MasterFILE Premier, CINAHL Complete, ProQuest Health and Medical Complete, Scopus, and Science Direct will be searched from 1956 to date. Gray literature databases will also be searched. Two reviewers will independently retrieve and screen full-text studies, critically appraise included studies, and extract data. Meta-analyses will be performed where possible. PROSPERO CRD42020189661.

Tibia stress injury and the imaging appearance of stress fracture in juvenile dermatomyositis: six patients\u2019 experiences

BackgroundTibial stress injuries are frequent injuries of the lower extremity and the most common causes of exercise-induced leg pain among athletes and military recruits. They sometimes occur in patients with pathological conditions of bone metabolism such as osteoporosis or rheumatoid arthritis, but there are previously no cases reported in juvenile dermatomyositis (JDM). Here we report 6 JDM patients who presented with shin pain, and the imaging appearance of tibial stress fractures or stress reactions.Case presentationAll 6 patients with JDM presented with shin pain or tenderness in the anterior tibia without any evidence of excessive exercise or traumatic episode. They were diagnosed with tibial stress injuries based on a combination of radiographs, three-phase bone scans, and magnetic resonance imaging (MRI), and 5 out of 6 patients had been treated with prednisone and/or methotrexate at onset of tibial stress injuries. In one patient, we could not find any abnormalities in his radiograph, but the subsequent MRI showed tibial stress reaction. In all 6 patients, the tibial stress injuries improved with only rest and/or analgesics.ConclusionWe experienced 6 children with JDM who presented with shin pain, and who were diagnosed with tibial stress fractures or stress reactions. Their underlying disease and weakness, treatment with glucocorticoid and methotrexate, or inactivity may have resulted in these tibial injuries, and made these patients more predisposed than other children. In addition to preventing JDM patients from getting osteoporosis, we need to consider stress reactions when children with JDM complain of sudden shin pain.

Botulinum toxin: A new treatment for functional popliteal artery entrapment syndrome? Five patients relieved more than one year

Functional popliteal artery entrapment syndrome (FPAES) is an uncommon cause of exercise-induced leg pain. Artery compression is mostly due to hypertrophic gastrocnemius muscles (GCM) without any anatomic abnormality. Surgical arteriolysis of popliteal artery is often proposed, sometimes with myotomy. But long-term efficacy of surgery is unknown. As botulinum toxin A (BoNT-A) injections can induce localised and partial muscular atrophy and hypotonia, we supposed that BoNT-A injections in GCM could relieve pain associated with FPAES. We describe five patients with a FPAES treated with BoNT-A and followed more than one year. Diagnostic was confirmed by provocative tests in plantar or dorsal flexion of the ankle on vascular imagery (doppler ultrasonography, computed tomography or magnetic resonance angiography). Other causes of leg pain were excluded, such as chronic exertional compartment syndrome with compartment pressure after exercise. BoNT-A was injected under electromyograph guidance in the proximal third of both heads of GCM (two sites/head), with 25 to 37.5 U of Incobotulinum toxin A or 100 to 160 US of Abobotulinum toxin A. Exercise-induced leg pain completely disappeared after treatement for all patients and they resumed their normal level of sports or physical professional activities. One patient was treated twice, eight months after the first injections, since he relapsed. There were no muscular weakness but the patient treated with the highest dose had transient asthenia and mictional disorders. Four patients are currently still asymptomatic, with a follow up between 14 and 28 months. One patient relapsed late after 50 months. BoNT-A injections could be used as a new conservative therapeutic strategy in FPAES and could reduce functional compression by improving artery-GCM impingement. This study is the first to demonstrate that BoNT-A could induce long-lasting resolution of symptoms, more than one year as previoulsy described (Hislop, 2017). It is well tolerated if the dose is well choosed.

Could botulinum toxin be a treatment for functional popliteal artery entrapment syndrome? A preliminary study

Functional popliteal artery entrapment syndrome (FPAES) is an uncommon cause of exercise-induced leg pain. Contrary to the anatomic type, there is no anatomical abnormality: entrapment is caused by hypertrophic gastrocnemius muscles (GCM). Even though arterial compression is purely functional, a surgical arteriolysis of popliteal artery is often proposed, in order to release the artery from adjacent structures. It is sometimes associated with myotomy. Studies on surgical treatment lack for cases. We hypothesize that botulinum toxin A (BoNT-A) injections in GCM could improve GCM-artery impingement by inducing localized and partial muscular atrophy and hypotonia. This retrospective study included patients with FPAES treated with BoNT-A. Clinical exam, ankle brachial pressure index after exercise, provocative tests in plantar or dorsal flexion of the ankle (Doppler ultrasonography, computed tomography or magnetic resonance angiography) were used for diagnostic. Other causes of leg pain were systematically excluded with further investigations, such as compartment pressure after exercise, low back and leg imagery. BoNT-A was injected in the proximal third of both heads of GCM, in two sites for each head, after location of the muscles by electrical stimulation. Investigations with provocative maneuvers were done after treatment. Eight patients (fourteen limbs) aged between 17 and 54 years old were included. One patient had previously unsuccessfully been treated by surgery. Mean follow up was 22.1 ± 21.2 months (6–74). Five patients had resolution of symptoms, during 70.6 ± 74.3 weeks (17–216). Two patients are currently still asymptomatic. Three patients relapsed. Adverse events were moderate systemic events (two patients) and subjective muscular weakness (two patients). Ankle brachial index, Doppler ultrasonography or tomography angiography improved or normalized in three patients, all successfully treated. Long-lasting resolution of symptoms in five patients could indicate that BoNT-A injections reduce functional compression. However, treatment failed in three patients. Continuation of the study with more patients may indicate whether BoNT-A injections could be a treatment of FPAES, which has no appropriate treatment as of today.

Changes in Muscle Oxygen Saturation Have Low Sensitivity in Diagnosing Chronic Anterior Compartment Syndrome of the Leg.

Near-infrared spectroscopy measures muscle oxygen saturation (StO2) in the skeletal muscle and has been proposed as a noninvasive tool for diagnosing chronic anterior compartment syndrome (CACS). The purpose of this study was to investigate the diagnostic value of changes in StO2 during and after exercise in patients with CACS. The study comprised 159 consecutive patients with exercise-induced leg pain. Near-infrared spectroscopy was used to measure StO2 continuously before, during, and after an exercise test. One minute post-exercise, intramuscular pressure was recorded in the same muscle. The cohort was divided into patients with CACS (n = 87) and patients without CACS (n = 72) according to the CACS diagnostic criteria. Reoxygenation at rest after exercise was calculated as the time period required for the level of muscular StO2 to reach 50% (T50), 90% (T90), and 100% (T100) of the baseline value. The lowest level of StO2 during exercise was 1% (range, 1% to 36%) in the patients with CACS and 3% (range, 1% to 54%) in the patients without CACS. The sensitivity was 34% and the specificity was 43% when an StO2 level of ≤8% at peak exercise was used to indicate CACS. The sensitivity and the specificity were only 1% when an StO2 level of ≤50% at peak exercise was used to indicate CACS. The time period for reoxygenation was seven seconds (range, one to forty-three seconds) at T50, twenty-eight seconds (range, seven to seventy-seven seconds) at T90, and forty-two seconds (range, seven to 200 seconds) at T100 in the patients with CACS and ten seconds (range, one to forty-nine seconds) at T50, thirty-two seconds (range, four to 138 seconds) at T90, and forty-eight seconds (range, four to 180 seconds) at T100 in the patients without CACS. When thirty seconds or more at T90 was set as the cutoff value for a prolonged time for reoxygenation, indicating a diagnosis of CACS, the sensitivity was 38% and the specificity was 50%. Changes in muscle oxygen saturation during and after an exercise test that elicits leg pain cannot be used to distinguish between patients with CACS and patients with other causes of exercise-induced leg pain.

Medial Tibial Stress Syndrome (MTSS): ‘New thoughts’ and proposed pathomechanical model

MTSS is the most common cause of exercise-induced leg pain and is prevalent in athletes and military personnel. Though there is much written about this entity there is much controversy concerning many aspects of this problem including it's pathology, pathomechanics, pathoanatomy, clinical presentation, diagnostic imaging, treatment and prevention. Two popular theories have been proposed to account for this condition: tibial bending and fascial traction. This presentation begins with a brief review and summarizes current thinking and concerns about the present state of MTSS. Based on a critical review of the literature and personal clinical experience, a proposed pathomechanical model involving fascial traction is suggested. A study was performed to evaluate the role of fascial traction as a possible mechanism responsible for MTSS.

Patient pain drawing in diagnosing the cause of exercise-induced leg pain

IntroductionClassifying symptoms by patient pain drawing (PPD) may be helpful in diagnosing chronic anterior compartment syndrome (CACS). We have investigated the sensitivity and interobserver reliability of the PPD to diagnose...

Popliteal artery entrapment syndrome.

Popliteal artery entrapment syndrome (PAES) is a rare cause of exercise-induced leg pain. Entrapment occurs because of an abnormal relationship between the popliteal artery and the surrounding myofascial structures in the popliteal fossa. Arterial insufficiency in the affected limb arises with entrapment of the artery, commonly giving leg symptoms with exertion. The true incidence of PAES in the general population is not known. The aetiology of PAES has an embryological basis related to the development of the popliteal artery and the surrounding musculature. Many different classification schemes have been developed to differentiate the various types of abnormal anatomy that are associated with the syndrome. Repeated popliteal artery compression causes trauma to the arterial wall, leading to premature localised atherosclerosis. The pathology of PAES is believed to be progressive, with arterial thrombosis occurring in some individuals as a natural progression of the disease process. Acute ischaemia can occur if there is an occlusion of the artery or thrombosis within an aneurysm. Clinically, up to 85% of individuals diagnosed with the syndrome are males. The mean age of individuals in a large series was 28 years. The condition can be found bilaterally in 25% of cases. Most individuals present with exercise-induced leg pain, the remainder presenting with acute or chronic ischaemia. The condition can result in significant functional loss for active individuals. Surgery has been advocated to prevent the progression of the disease that is believed to be the natural history of untreated PAES. However, the little research that has been done to determine the prognosis for individuals who have undergone surgery has focused on the patency rate of the arteries after surgery and the presence or absence of complications. Research needs to be done to look at the natural history of untreated PAES and the functional status of athletes after undergoing PAES surgery.

EXERCISE-INDUCED LEG PAIN

1494 Leg pain which occurs only with exercise and disappears on cessation of exercise is a common presenting complaint. The primary source of this pain could be bone, muscle compartment, vascular or neural tissue. These different sources can usually be differentiated on the basis of history and physical examination. Bone stress occurs as a continuum from normal bone at one end of the continuum to the development of a stress fracture at the other end. The main characteristic of bone injury is the presence of focal tenderness over the bone. The two main sites of compartment syndrome are the anterior compartment and the deep posterior compartment. Patients with compartment syndrome complain of a characteristic feeling of tightness in the relevant area. This pain is alleviated as soon as exercise ceases. Vascular and neural causes of exercise-induced leg pain are relatively uncommon but should be considered in cases with atypical presentations. Vascular entrapments present with claudication-type pain and a vascular bruit can often be heard over the site of the narrowing if the patient is examined immediately following exercise. Neural entrapments may present as exercise-induced pain rather than the classic presentation with neurological symptoms.

Peroneal nerve entrapment in athletes.

Peroneal nerve entrapment is one of the less common causes of exercise-induced leg pain in competitive athletes. This type of lower extremity peripheral nerve dysfunction is usually associated with activities that subject the nerve to constant compression or repetitive trauma. Herein, we present our experience with 12 competitive athletes treated for peroneal nerve entrapment. Diagnostic electromyography results, intraoperative findings, and the results of cadaveric dissections are discussed.

The evaluation and treatment ofexertional compartment syndrome

Exertional compartment syndrome (ECS) is becoming increasingly recognized as a cause of exercise-induced legpain in the athletic population. Unfortunately, the pathophysiology is not clearly understood. The use of 31P-NMR has shown that ischemia is not a significant component of ECS because it is in the acute syndrome. A primary diagnosis can be made after a thorough history and physical examination. In a young patient with leg pain that is only exercise induced, reproducible and associated with a normal physical examination, a diagnosis of ECS is likely and does not need to be a diagnosis of exclusion. Confirmation with intracompartmental pressure measurement still remains the gold standard before further management. Nonoperative management is usually ineffective and fasciotomies of the affected leg(s) and compartment is the recommended treatment in the symptomatic patient. At our center, the use of a two-incision anterior and lateral compartment release, and a one-incision posterior compartment release has been very successful in returning athletes symptom free to their sporting level.

Chronic compartment syndrome of the leg

Chronic compartment syndrome is an uncommon but important cause of exercise-induced leg pain. The author provides a comprehensive review of chronic compartment syndrome of the leg. Case reports are presented to stress the clinical importance of chronic compartment syndrome to the podiatric physician.

The use of transcutaneous oxygen tension measurements in the diagnosis of peripheral vascular insufficiency.

Transcutaneous tissue oxygen tension (PtcO2) was evaluated as a noninvasive diagnostic test for peripheral arterial insufficiency; PtcO2 was measured at rest, during exercise, and following exercise at three leg sites in 36 controls and 138 patients with exercise-induced leg pain. Resting foot PtcO2 differed significantly in controls and in patients with rest pain (32/138) and was 60.1 +/- 6.82 mmHg and 3.66 +/- 3.68 mmHg, respectively (p less than 0.001). Abnormal resting PtcO2 values occurred in 80% of claudicants (85/138) and 20% had normal values. However, all vascular claudicants exhibited a decline in PtcO2 following exercise, a finding that distinguished them from controls (p less than 0.001). The PtcO2 values in 21 patients who were subsequently shown not to have vascular disease did not differ significantly from controls (p greater than 0.5). Comparison with angiograms (48) showed that PtcO2 following exercise had a 100% sensitivity and specificity in detecting the presence of arterial disease. If resting values alone are considered, sensitivity falls to 77%. This study demonstrates that measurement of PtcO2 at rest and particularly after exercise is a simple and sensitive noninvasive diagnostic test for peripheral arterial insufficiency. This test will serve to distinguish between vascular and other causes of exercise-induced leg pain.