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Multiple Sclerosis and Transverse Myelitis in Children
[…] and ADLs, as well as equipment assessment, depending on their residual deficits. Some children with MS may initially need outpatient services since after starting treatment they should return to their baseline function as their disease progresses more intensive therapy may […]
Respiratory Impairment in SCI
[…] atelectasis and abnormalities of gas exchange and lung compliance. Expiratory muscle dysfunction results in impaired cough and secretion clearance, increased airway resistance, and persistence of infection when it occurs.4 Loss of sympathetic autonomic signaling to the bronchopulmonary tree results in […]
Acute Herpes Zoster and Postherpetic Neuralgia
[…] and N-methyl-d-aspartate (NMDA) receptor antagonists are ineffective in relieving PHN.22,26 The anticonvulsants gabapentin and pregabalin act as calcium channel alpha-2 delta ligands to inhibit the release of nociceptive neurotransmitters. Side effects include somnolence, dizziness, and peripheral edema.22,26 Compared to gabapentin, pregabalin has increased bioavailability, fewer dose-related adverse side effects, anxiolytic properties, and twice daily dosing with a similar side effect profile.22 TCAs, including amitriptyline, nortriptyline, and desipramine, act by inhibiting the reuptake of norepinephrine and serotonin, inhibiting spinal nociceptive neurons, and by sodium-channel blockade. They are often not tolerated well, particularly in elderly patients, due to anti-cholinergic side effects, such as orthostasis, dry mouth, and urinary retention. Secondary amines (which more selectively block reuptake of norepinephrine), such as desipramine and nortriptyline, are as equally effective as the tertiary amine amitriptyline (which blocks reuptake of both norepinephrine and serotonin), and are better tolerated with fewer side effects, such as sedation.9,27,28 Of note, combining a TCA with an anticonvulsant may be more effective than monotherapy for neuropathic pain states.27,28 Lidocaine, either in transdermal or gel form, affects ectopic activity of sensory nerves involved in nociception. The role of topical lidocaine on neuropathic pain is supported by some anecdotal clinical evidence, though large-scale studies remain conflicted on its efficacy.22,29 As such, lidocaine can be considered a second-line agent for PHN, with selective first line use when there is mild neuropathic pain limited to a defined area of superficial allodynia/hyperalgesia or when systemic therapy is contraindicated or poorly tolerated, such as in the elderly.22,29 Topical capsaicin is a second-line agent for PHN, based on high cost, required in-clinic administration of high-dose treatment (8%), and efficacy. It acts as an agonist for the vanilloid receptors, depleting substance P and desensitizing nociceptors, and is available as an 8% patch or as over the counter 0.075% cream and 0.05% ointment.9,30 High-concentration capsaicin is more efficacious, providing relief up to 3-5 months, than the low-concentration form, though it is associated with more cutaneous irritation.30 Side effects are mainly local application site reactions. Compounded topical agents that include amitriptyline (a TCA) and ketamine (a general anesthetic), in varying concentrations, have shown effectiveness in neuropathic pain states, including PHN.31,32 Opioids have been shown to be effective in PHN and can be considered if first-line therapies fail to achieve adequate pain relief. As a result of their limitations, such as physical dependence and development of analgesic tolerance, opioids are generally considered third-line therapeutic agents. 2,9,33,34 Referral to a pain specialist should be considered especially when higher doses are required.22,26 Of note, multiple agents are often needed for pain relief and combination treatment has been shown to be more effective than single agents. Interventions such as sympathetic and peripheral nerve blocks and epidural injections of both local anesthetic and steroids have short duration benefits.2,35 Spinal cord stimulation potentially provides pain relief, but also has limited supporting evidence.8 Subcutaneous injection of botulinum toxin has been shown to be superior to topical lidocaine with longer lasting benefits.36 Transcutaneous electrical nerve stimulation has been tried for acute HZ and prevention of PHN without consistent evidence supporting efficacy; it can, however, safely be offered as part of treatment.37 Acupuncture has not been shown to be effective.26 At different disease stages In PHN, there can be absence of a pain-free period after the initial rash, or there may be a quiescent period of up to 12 months1 following the rash, after which pain returns. History of rash may not always be present. In such cases, establishing diagnosis may require serial immunologic assays.2,38 Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills VZV immunoglobulin followed by HZ immunization is recommended in immunocompromised seronegative patients who have been exposed to VZV, as well as in neonates, in patients with severe disease, and in pregnant women. 2,39-42 The Centers for Disease Control recommends HZ vaccination in adults over the age of 50 regardless of previous history of HZ. 2,39-42 There are currently two forms of the HZ vaccine approved by the FDA for this age group, one being a live-attenuated zoster vaccine, and the other, a recombinant zoster vaccine.39,40 Of note, HZ vaccines are 14 times more potent than the VZV vaccine and is more efficacious for the prevention of HZ in patients between the ages of 50 to 69, compared to those over 70 years. 2,39-42 The vaccine conferred similar protection against PHN in all age groups but was superior in preventing the incidence and severity of PHN in the older compared to the younger age group.21,26,43 In addition, HZ vaccination was shown to increase quality-life adjusted years.2,39-42 Contraindications to HZ vaccination include primary or secondary immunodeficiency disease, pregnancy or potential pregnancy, and history of allergic reaction to neomycin, gelatin, or vaccine components. The vaccine can be administered with other vaccines.2,39-42 Cutting Edge/Emerging and Unique Concepts and Practice New therapies are under investigation for the treatment and prevention of HZ and PHN. For example, EMA401, an oral highly selective angiotensin II type 2 receptor antagonist, has been shown to provide significant relief against PHN when compared to placebo and demonstrates analgesic efficacy comparable to gabapentinoids.44 Film-forming systems are novel methods of drug delivery that are alternatives to topical and transdermal delivery systems. Bupivacaine, in a film-forming metered-dose dermal spray preparation, is being evaluated for its potential effectiveness for neuropathic pain conditions, like PHN.45 Non-pharmacologic pain control methods for PHN are also being studied. A pilot study demonstrated that patients could alter pain perception by learning to voluntarily regulate over-activation in the rostral anterior cingulate cortex through real-time functional MRI neurofeedback.5 Repetitive transcranial magnetic stimulation (rTMS) has been found to be effective for pain, sleep, and anxiety in patients with PHN. Pei, et al46 conducted a prospective, randomized, controlled clinical trial that concluded that, compared to sham, patients who underwent either 5 Hertz (Hz) or 10 Hz rTMS of the primary motor cortex had significantly lower visual analogue scale (VAS) pain scores at the 3 months post intervention follow up period. In addition, the patients in the treatment groups, compared to sham, had significantly higher scores for quality of life (QOL) scale, sleep quality (SQ) scale, and patient global impression of change (PGIC) scale. Neuromodulation is a means of altering neuronal activity by direct delivery of an electrical or pharmaceutical agent to the target nervous tissue structure.47 There are various forms of neuromodulation, including intrathecal drug delivery and neurostimulator devices that target the dorsal columns of the spinal cord, the dorsal root ganglion, or peripheral nerves.47 These modalities have proven beneficial in PHN, 48 with evidence that early neurostimulation may even prevent PHN, if provided during the acute/subacute phase of HZ.49 Recent advances in peripheral nerve stimulation and current studies have revealed that peripheral nerve stimulation is an effective treatment trigeminal herpetic neuralgia following acute or subacute HZ.50,51 SCRAMBLER therapy is a non-invasive electro-analgesia therapy used to manage a number of pain conditions, particularly neuropathic pain. One explanation by which this therapy works is that it substitutes pain information with “non-pain” information within nociceptive C–fibers, via “artificial neurons” through cutaneous electrodes.52,53 SCRAMBLER was evaluated as a novel method to treat PHN in a study by Smith, et al.52 In this study, 10 patients with refractory PHN were given 30-minute daily sessions of SCRAMBLER therapy for 10 days. The average pain reduction by numerical rating scale improved by 95% at 1 month, and analgesic benefit continued into month 3.52,53 An emerging treatment is the use of platelet rich plasma. A recent study observed that ultrasound guided injections with platelet rich plasma combined with medications to targeted peripheral nerves resulted in better analgesia and fewer side effects when compared to just medication alone.54 Extracorporeal shockwave therapy (ESWT) has also been recently studied as a potential treatment for PHN. A study has recently observed that ESWT combined with conventional treatment could relieve pain associated with PHN.55 Additionally, the treatment with ESWT was shown to improve the psychological state in without serious adverse effects.55 Gaps in the Evidence-Based Knowledge PHN treatment continues to remain challenging and frustrating for patients and clinicians alike. While several oral and topical therapies exist for PHN, it has been shown that meaningful analgesia defined as greater than or equal to 50% pain relief, is provided to roughly 11 to 50% of patients, often at the cost of treatment-related adverse events.44 In addition, the efficacy of different treatment modalities for prolonged periods of time, as is often needed for PHN, remains poorly understood. Indeed, data from clinical trials does not typically extend beyond treatment periods of a few weeks. Furthermore, randomized controlled trials have failed to compare different drug classes and treatment modalities. Combination treatments, which are frequently employed by patients, require further investigation.26 Future studies have focused on phenotypes and genotyping in PHN drug therapy. There are efforts to individualize pharmacological treatment through pain phenotyping.56 References Thakur, R. and A.G. Philip, Chronic pain perspectives: Treating herpes zoster and postherpetic neuralgia: an evidence-based approach. J Fam Pract, 2012. 61(9 Suppl): p. S9-15. Saguil A, Kane S, Mercado M, Lauters R. Herpes Zoster and Postherpetic Neuralgia: Prevention and Management. Am Fam Physician. 2017 Nov 15;96(10):656-663. Reynolds, M.A., et al., The impact of the varicella vaccination program on herpes zoster epidemiology in the United States: a review. J Infect Dis, 2008. 197 Suppl 2: p. S224-7. Argoff, C.E., N. Katz, and M. Backonja, Treatment of postherpetic neuralgia: a review of therapeutic options. J Pain Symptom Manage, 2004. 28(4): p. 396-411. Guan, M., et al., Self-regulation of brain activity in patients with postherpetic neuralgia: a double-blind randomized study using real-time FMRI neurofeedback. PLoS One, 2015. 10(4): p. e0123675. Forbes, H.J., et al., A systematic review and meta-analysis of risk factors for postherpetic neuralgia. Pain, 2016. 157(1): p. 30-54. Marra F, Parhar K, Huang B, Vadlamudi N. Risk Factors for Herpes Zoster Infection: A Meta-Analysis. Open Forum Infect Dis. 2020 Jan 9;7(1):ofaa005. Tontodonati, M., et al., Post-herpetic neuralgia. Int J Gen Med, 2012. 5: p. 861-71. Mallick-Searle T, Snodgrass B, Brant JM. Postherpetic neuralgia: epidemiology, pathophysiology, and pain management pharmacology. J Multidiscip Healthc. 2016 Sep 21;9:447-454. Shah S, Singaraju S, Einstein A, Sharma A. Herpes zoster: A clinicocytopathological insight. J Oral Maxillofac Pathol. 2016 Sep-Dec;20(3):547. Leinweber B, Kerl H, Cerroni L. Histopathologic features of cutaneous herpes virus infections (herpes simplex, herpes varicella/zoster): a broad spectrum of presentations with common pseudolymphomatous aspects. Am J Surg Pathol. 2006 Jan;30(1):50-8. Oh SI. Horner’s Syndrome and Segmental Sympathetic Denervation Following Herpes Zoster Brachial Plexopathy. J Clin Neurol. 2021 Apr;17(2):328-329. Soares BP, Provenzale JM. Imaging of Herpesvirus Infections of the CNS. AJR Am J Roentgenol. 2016 Jan;206(1):39-48. Johnson, R.W., et al., The impact of herpes zoster and post-herpetic neuralgia on quality-of-life. BMC Med, 2010. 8: p. 37. Sreenivasan, N., et al., The short- and long-term risk of stroke after herpes zoster – a nationwide population-based cohort study. PLoS One, 2013. 8(7): p. e69156. Breuer, J., et al., Herpes zoster as a risk factor for stroke and TIA: a retrospective cohort study in the UK. Neurology, 2014. 83(2): p. e27-33. Vrcek I, Choudhury E, Durairaj V. Herpes Zoster Ophthalmicus: A Review for the Internist. Am J Med. 2017 Jan;130(1):21-26. Johnson, R.W., et al., Herpes zoster epidemiology, management, and disease and economic burden in Europe: a multidisciplinary perspective. Ther Adv Vaccines, 2015. 3(4): p. 109-20. Iglar K, Kopp A, Glazier RH. Herpes zoster as a marker of underlying malignancy. Open Med. 2013 Jun 18;7(2):e68-73 Minor M, Payne E. Herpes Zoster Ophthalmicus. . In: StatPearls . Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557779/ de Boer, P.T., J.C. Wilschut, and M.J. Postma, Cost-effectiveness of vaccination against herpes zoster. Hum Vaccin Immunother, 2014. 10(7): p. 2048-61. Gan, E.Y., E.A. Tian, and H.L. Tey, Management of herpes zoster and post-herpetic neuralgia. Am J Clin Dermatol, 2013. 14(2): p. 77-85. Katz J, McDermott MP, Cooper EM, Walther RR, Sweeney EW, Dworkin RH. Psychosocial risk factors for postherpetic neuralgia: a prospective study of patients with herpes zoster. J Pain. 2005 Dec;6(12):782-90. Chen, N., et al., Antiviral treatment for preventing postherpetic neuralgia. Cochrane Database Syst Rev, 2014(2): p. CD006866. Han, Y., et al., Corticosteroids for preventing postherpetic neuralgia. Cochrane Database Syst Rev, 2013(3): p. CD005582. Johnson, R.W. and A.S. Rice, Clinical practice. Postherpetic neuralgia. N Engl J Med, 2014. 371(16): p. 1526-33. Oxman, M.N., Vaccination to prevent herpes zoster and postherpetic neuralgia. Hum Vaccin, 2007. 3(2): p. 64-8. Finnerup, N.B., et al., Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis. Lancet Neurol, 2015. 14(2): p. 162-73. Derry, S., et al., Topical lidocaine for neuropathic pain in adults. Cochrane Database Syst Rev, 2014(7): p. CD010958. Webster, L.R., et al., Tolerability of NGX-4010, a capsaicin 8% dermal patch, following pretreatment with lidocaine 2.5%/prilocaine 2.5% cream in patients with post-herpetic neuralgia. BMC Anesthesiol, 2011. 11: p. 25. Sawynok, J. and C. Zinger, Topical amitriptyline and ketamine for post-herpetic neuralgia and other forms of neuropathic pain. Expert Opin Pharmacother, 2016. 17(4): p. 601-9. Mercadante, S., Topical amitriptyline and ketamine for the treatment of neuropathic pain. Expert Rev Neurother, 2015. 15(11): p. 1249-53. Zin CS, Nissen LM, Smith MT, O’Callaghan JP, Moore BJ. An update on the pharmacological management of post-herpetic neuralgia and painful diabetic neuropathy. CNS Drugs. 2008;22(5):417-42. Khadem T, Stevens V. Therapeutic options for the treatment of postherpetic neuralgia: a systematic review. J Pain Palliat Care Pharmacother. 2013 Aug;27(3):268-83. Shannon HJ, Anderson J, Damle JS. Evidence for interventional procedures as an adjunct therapy in the treatment of shingles pain. Adv Skin Wound Care. 2012 Jun;25(6):276-84 Xiao, L., et al., Subcutaneous injection of botulinum toxin a is beneficial in postherpetic neuralgia. Pain Med, 2010. 11(12): p. 1827-33. Kolsek, M., TENS – an alternative to antiviral drugs for acute herpes zoster treatment and postherpetic neuralgia prevention. Swiss Med Wkly, 2012. 141: p. w13229. Cohen JI. Clinical practice: Herpes zoster. N Engl J Med. 2013;369(3):255-263. Lu, P.J., et al., Shingles Vaccination of U.S. Adults Aged 50-59 Years and >/=60 Years Before Recommendations for Use of Recombinant Zoster Vaccine. Am J Prev Med, 2020. 59(1): p. 21-31. Hurley, L.P., […]
Lower Limb Orthotics/Therapeutic Footwear
[…] maximize function. These interventions apply to all phases of a rehabilitation plan and depend on the patient’s level of imp airment. Medical conditions which warrant the use of limb orthoses or therapeutic footwear may include trauma, stroke, brain injury, spinal […]
Post-Laminectomy Pain
[…] (FBSS). This term can be seen as pejorative, ethically ambiguous, and placing the onus of the “failure” on the patient. 1 With the recommendation of the International Association for the Study of Pain (IASP) and the implementation of International Classification of Disease (ICD-11) on January 1st, 2022, this diagnosis was changed to “chronic pain after spinal surgery (CPSS)”. However, the ICD-11 has yet to be widely adopted. The terms “post-laminectomy pain” and “FBSS” will be used throughout this document for continuity and to improve search engine optimization for this topic, but readers should be aware of the new terminology for future reference. The term “persistent spinal pain syndrome (PSPS)” with two subtypes (T1 – no spine surgery performed and T2 – post-spine surgery) has also been proposed to address some ambiguity with CPSS but has not yet been added to the ICD-11.1,2 Post-laminectomy pain is defined by the IASP as “lumbar spinal pain of unknown origin either persisting despite surgical intervention or appearing after surgical intervention for spinal pain originally in the same topographical location”.3 There may be many causes for this chronic pain creating a complex pathophysiology. Predictive risk factors include preoperative (patient) factors, intraoperative factors, and postoperative factors.4,5,6,7,8 Preoperative: this can be divided into patient-specific and surgery-specific factors. Depression, anxiety, hypochondriasis, obesity, smoking, worker’s compensation or ongoing litigation, and radiographic findings such as disc herniation, stenosis, and fibrosis increase the risk of FBSS.9,10 Psychosocial factors are strongly linked to developing disability from low back pain (LBP).11 However, this does not exclude an organic problem, and these factors should be optimized before the surgery.12 Earlier surgery in patients with poor psychometrics and lumbar disc disease may actually improve pain outcome, as prolonged pain and distress can reduce the efficacy of the surgery.13 Selecting an inappropriate patient for surgical treatment (e.g., isolated axial back pain for microdiscectomy or multiple revision surgeries) or an inappropriate surgical approach (e.g., inadequate decompression) can increase the risk of developing FBSS.6 Patients with previous back surgeries have a lower chance of pain relief following surgery and a higher chance of developing FBSS.8 Surgical: operating at the wrong vertebral level or operating at a single vertebral level when the pain generators are multiple levels can lead to poor pain relief.6,8 Lumbarization of the sacral vertebra or sacralization of the lumbar vertebra can lead to operating at the incorrect level. Poor surgical technique is also significant factor in the development of FBSS, especially if there is inadequate decompression at the lateral recess or neural foramina.14,15 Conversely, spine instability may occur if > 33% of the bilateral articular or 100% unilateral articular surfaces are removed.14 Minimally invasive techniques with limited exposure can increase […]
AIDP/CIDP Part 2: Treatment
[…] positioning, weight shifts, and skin monitoring to prevent skin breakdown and decubitus ulcer formation in immobile patients Initiation of therapy services with a focus on early mobility. Psychosocial support Pain management using neuropathic pain medications, nonsteroidal anti-inflammatories (NSAIDs), and/or opiates. […]
de Quervain Tenosynovitis
[…] ***Tends to develop four to six weeks after delivery. Common mechanisms include lifting a baby or young child into the air by placing the phalanges under their axillae with the thumbs abducted ****Increasing prevalence of de Quervain tenosynovitis in younger […]
Upper Limb Orthotics
[…] between fine motor control in upper extremity and gross motor control and weight-bearing in the lower extremity.3 Along the same lines, the upper extremity has less soft tissue, decreased force requirements, increased sensory requirements, and more precision of movement compared […]
Slipped Capital Femoral Epiphysis
[…] immature physeal growth plate. It is characterized by insidious onset dull hip or referred knee pain, usually without preceding trauma. 1 Etiology Etiology is multifactorial with most cases being idiopathic. Obesity is the most common risk factor with 63% of cases above the 90th weight percentile. Mechanical risk factors for SCFE include rapid growth spurts, femoral retroversion, and femoral neck shaft angle. Renal and endocrine abnormalities such as hypothyroidism, panhypopituitarism and renal osteodystrophy are also linked to the development of SCFE.1 Proper development of the physis requires thyroid hormone, vitamin D, and calcium.3 Epidemiology including risk factors and primary prevention SCFE is the most common hip disorder in pre-adolescents, adolescents, and young adults with an overall prevalence of 10.8 cases per 100,000 children. Prevalence varies widely among race, seasonal and geographic location with higher presentations in the northern and western United States.4 African-Americans, Pacific Islanders and the Hispanic population have greater predisposition for the development of SCFE than Caucasians.5 SCFE usually occurs during adolescence, typically during the ages of 8 through 15 and is more common in males than females (male to female ratio of 1.6:1) with an average age of 13.5 years in males and 12 years in females.1,4 Presentation outside of these age ranges should raise clinical concern for potential endocrinopathies or chronic conditions that lead to high bone turnover.6 Patho-anatomy/physiology Pathogenesis of SCFE has many theories, however, the exact mechanism is still to be determined. It is believed to arise due to a mechanical displacement of the proximal femoral head from the femoral neck due to abnormal physiological loads through a skeletally weak and immature physeal growth plate. Insufficiency of the femoral physis can be attributed to mechanical factors, such as obesity, morphologic abnormalities of the femoroacetabular joint and other external variables that increase the axial load and shear forces applied to the growth plate which ultimately predispose it to slippage.7 Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time) Classification SCFE can be classified according to stability, severity, symptom duration by using the following classification systems8 Stability Loder Classification: classifies cases as stable or unstable based on ability to bear weight. This type of classification is predictive of prognosis and accounts for nearly 90% of all SCFE cases.9 Stable: able to bear weight on the affected side with or without crutches. Unstable: unable to bear weight even with the use of crutches as symptoms are more severe. May have up to a 50% incidence of hip osteonecrosis compared with nearly 50° Figure 1: Southwick head-shaft angle on a frog leg lateral view.10 In cases of bilateral SCFE, 145° for AP radiographs and 10° frog lateral radiographs is used as “unaffected” hip reference. Severity is known to be linked with femoroacetabular impingement. Grading System: radiographic classification based on the percentage of epiphyseal displacement.8 Grade I (mild): 0-33° displacement Grade II (moderate): 33-50° displacement Grade III (severe): >50° displacement Figure 2: Grading of SCFE determined by the percentage of displacement based on radiographic findings.10 Duration Temporal Classification: traditional classification based on the duration of symptoms. Rarely used as it does not yield prognostic information.5 Acute: symptoms present for ≤ 3 weeks Chronic: symptoms present for ≥ 3 weeks; most common Acute on Chronic: acute exacerbation with prior chronic SCFE Specific secondary or associated conditions and complications Secondary conditions and complications11 1. Femoral head osteonecrosis or loss of vascular flow occurs at a higher rate in severe, unstable SCFE and is associated with worse prognosis. Generally, the epiphysis is left in its position since the risk of avascular necrosis is high if manipulation is attempted. It is a detrimental complication resulting in decreased hip motion, increased pain, and lower functional outcomes and activity scores. 2. Chondrolysisis a rapidly progressive loss of articular cartilage that is most commonly seen after pin penetration into the hip joint. Symptoms include decreased range of motion, hip pain, stiffness, and joint space reduction of >50% in the affected hip. 3. Femoroacetabular impingement, a condition that appears mostly in adolescence and in young adults, is […]
Pulmonary Issues in the Athlete/Exercise Induced Bronchoconstriction
Disease/ Disorder: Definition Exercise-induced bronchoconstriction (EIB) is defined as the transient airway narrowing that occurs following exercise without regards to the presence or absence of asthma.1,2 While the term “exercise-induced asthma” (EIA) has been used, the term is misleading as exercise is not an independent risk factor for asthma, but, instead, a trigger for bronchoconstriction in some asthmatics.1 EIB may be present in patients with or without underlying asthma and can affect athletes of all levels.3, 11 Etiology EIB occurs following high-intensity exercise when high minute ventilation dehydrates the airways and ultimately results in the release of inflammatory mediators.4 This occurs more frequently in cold/dry environmental conditions.4,5 The sustained high-level ventilation reached during exercise and the water content of inspired air are the two most important factors of EIB.5 Epidemiology including risk factors and primary prevention The prevalence of EIB is 5%-20% of the general population and is likely underestimated due to lack of gold standard for diagnosis, while the prevalence in asthmatics is 40-90%3. EIB affects athletes of any level with studies showing higher rates (30%-70%) in Olympic/elite athletes.5 Those participating in indoor (i.e. ice hockey, swimming), endurance, and winter sports are more susceptible, and high-intensity training may contribute to the development of EIB.5 Environmental exposures such as cold air, dry air, ambient ozone, airborne particulate matter, gases associated with ice rink resurfacing equipment, and elevated levels of trichloramines in indoor pools are also thought to contribute to EIB.5 Poorly controlled chronic asthma, oral breathing, personal/family history of cardiovascular disease, allergic rhinitis, sinusitis, atopy and urbanization are additional risk factors.1,5 Patho-anatomy/physiology The mechanism of EIB is likely multifactorial and not entirely understood, with several theories existing to explain the pathophysiology12. The osmotic theory is the most universally accepted. It infers that large volumes of cool, dry air inhaled during exercise lead to changes in the osmolarity of the airway surfaces.2,3 A hyperosmolar environment results, triggering a mast cell-mediated release of mediators (i.e. histamine, leukotrienes, prostaglandins) from inflammatory cells, which cause bronchial smooth muscle constriction and edema.1 Uncontrolled underlying airway inflammation may exacerbate this response.1,2 These osmotic and mechanical stresses due to repeated heavy ventilation may also contribute to airway remodeling in the long-term through effects on epithelial cells. Over time this process alters smooth muscle contractile properties, leading to increased bronchial hyper-responsiveness .1,2,12 The re-warming hypothesis has some supporting evidence, but is mostly overlooked for the above hypertonicity mechanism.1 Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time) Symptoms of EIB usually occur during or after exercise, but may only occur in specific environments (i.e. ice rinks or swimming pools), or at a certain intensity or duration.5 In the acute phase, athletes may experience coughing, shortness of breath (SOB), chest tightness, and wheezing, or subtle symptoms such as fatigue, headache, dizziness, or impaired performance.2 Peak onset occurs within a 10-15 of exercise and lasts 30-90 minutes.3 Recovery is spontaneous with FEV1 returning to 95% baseline in 30-90 minutes.5 Patients can be refractory to another exercise stimulus for up to four hours and some can develop symptoms 4-8 hours after exercise, known as a late-phase response.5,13 Airway hyperresponsiveness may improve or normalize (weeks to years) if athletes refrain from competitive participation.2,6 Specific secondary or associated conditions and complications Co-existing conditions, or conditions that may mimic EIB, include asthma, upper-airway cough syndrome, chronic eosinophilic bronchitis, allergies, rhinitis, gastroesophageal reflux (GERD), exercise induced laryngeal obstruction (EILO), central airway obstruction, exercise-induced anaphylaxis, restrictive lung disease, swimming-induced pulmonary edema, and environmental exposures. EILO, is a frequent imitator of EIB, but does not respond to bronchodilators, symptoms resolve upon exercise cessation, and leads to persistent dyspnea.7 Additionally, SOB may be caused conditions other than airway dysfunction including anemia, infectious diseases, cardiovascular disease, and musculoskeletal conditions.7 Potential complications of misdiagnosis include persistent or worsening symptoms, impaired performance, discontinuation of a sport, hypoxemia, and, in extreme cases, death.7 Essentials of Assessment History The history should include when symptoms occur, initial onset, duration, frequency, and severity. Inquire if the patient has difficulty breathing, coughing, excessive mucous production, or chest tightness associated with exercise, that gradually improves upon stopping. Distinguishing inspiratory stridor with or without expiratory wheezing from inspiratory stridor alone is important, especially to help discern EIB from EILO14. Atypical symptoms may include fatigue, feeling out of shape or unable to keep up with peers, and abdominal discomfort. History of prior injury to the head/neck/chest, family/personal history of cardiopulmonary conditions, prior hospitalizations and current/past treatment are relevant. Physical examination A comprehensive physical should include examinations of the head, ear, nose, and throat (HEENT), chest, cardiopulmonary, extremity, and skin systems. HEENT exam should look for any signs of allergic rhinitis, sinusitis, or otitis. Examination of the chest (and back) should look for any structural deformities (such as pectus excavatum) or spinal scoliosis. On cardiopulmonary exam, auscultate for cardiac murmurs, wheezing, rales, or rhonchi and palpate pulse to detect arrhythmias. Examine skin and extremities for signs of eczema, cyanosis, digital clubbing, or edema. Functional assessment The impact of EIB on athletic performance has not been well established.8EIB may hypothetically impair performance due to exercise airflow limitations, increased work/oxygen cost of respiratory muscles, dyspnea/perception of effort, and ventilation/perfusion mismatch.8 Follow-up with patients once a treatment plan has been implemented to ensure compliance with treatment, assess that co-morbidities are adequately addressed, and to monitor for ongoing dyspnea, fatigue, or underperformance.7 From a psychological perspective, recent studies have described the negative emotional burden associated with EIB and EIA. This has been particularly seen in the adolescent population with reports of lower quality of life (QoL) and more mood symptoms including anxiety, depression, and frustration.11,15-17 Laboratory studies Symptoms of EIB are non-specific and have a poor predictive value.5 Serial lung function measurements, using forced expiratory volume in one second (FEV1), objectively determine the presence and severity of EIB.5 Indirect challenges (exercise challenge or surrogate testing) are more sensitive than direct challenge (i.e., methacholine). During an exercise challenge test, spirometry measures FEV1 pre-exercise and at 5, 10, 15, and 30-minute intervals post-exercise.5 An athlete should reach >90% of maximum heart rate at 2 minutes and maintain this level for another 6 minutes during the exercise. Airway response is the percent fall in FEV1 from baseline, […]