– Written by Alex Kountouris, Australia
Lumbar bone stress injury (LBSI) presents in physically active adolescents and young adults. It occurs at the postero-lateral aspect of vertebral arch, typically in the region of the pars interarticularis, including the pedicle, lamina and articular facets1. It is also referred to as part of a spectrum of spinal pathologies known as spondylolysis. The term LBSI is preferred to spondylolysis, because the latter typically describes a larger spectrum of injuries that includes defects (symptomatic and asymptomatic), that are mostly the result of non-united stress fractures and therefore require a completely different management approach2. The injury is often missed in the early stages because the initial symptoms are similar to other non-specific causes of low back pain. It requires a high degree of clinician intuition to make the diagnosis early and attain better outcomes. This paper will highlight that LBSI is as relatively common sporting injury, results in long (6-12 months) recovery times, and has a high risk of complications such as recurrence and non-union. The aim of this paper will be to improve early detection of the injury and describe the management based on the stage of injury, so that athlete-patient can return to their pre-injury level of activity (including elite sport) and attain bone healing.
INCIDENCE
LBSI has been reported in almost every athletic activity that involves repetitive spinal loading, particularly trunk extension, rotation and side flexion3. Some sporting activities, such as cricket fast bowling, gymnastics4,5 (tumbling, landing disciplines), tennis (serving)6,7 and javelin8 have an inherently higher biomechanical risk of LBSI because they involve, repetitive, often asymmetrical, high spinal load. Other sports including soccer9, volleyball7, athletics10, diving7 that don’t have the same asymmetrical or high impact forces (but repetitive lower impact forces instead such running, kicking, jumping and/or twisting activities) have a lower but meaningful incidence of LBSI7 that is sometimes missed in the early stages of pathology, often resulting in a more complicated recovery. Kelly et al.10 reported 9-year injury surveillance data of elite British athletics and found that LBSI (17% incidence) was the third most common bone stress injury (BSI) behind the foot (22%) and pelvis (19%); and the second highest for return to sport (RTS) time behind the tarsal navicular bone, highlighting the relevant incidence and time cost of LBSI in activities that would be considered lower risk based on the activity biomechanics.
MECHANICS AND PATHOGENESIS
Mechanically, the injury occurs because the pars region is located between the inferior and superior articular processes (Figure 1) of the vertebra, so that forces transmitted through the facet joints are also expected to be transmitted to the postero-vertebral arch. Like other BSI, lumbar bone stress is a result of an accumulation of repetitive localised bone loading that exceeds the bone strain threshold11. When mechanical strains exceed the upper boundary of the physiological window, this leads to a breakdown of some bone cells and sets off an osteogenic response to repair and remodel the damage in preparation for future12. When there is insufficient time to remodel and repair before the next loading cycle(s), the repair process is disrupted and micro-fractures can accumulate, eventually developing into radiological and clinical BSI13. The number of loading cycles required to develop a bone stress injury is related to the bone’s strength and geometry, as well as the magnitude and frequency of loading applied14 (Figure 1).
The bone geometry of the pars region of the vertebral arch is an intrinsic factor that explains the reported incidence described with many sporting activities. In particular, the width of the load bearing portion of the vertebral arch is small and therefore not designed to absorb repetitive and/or high impact forces. For example, the transverse width at the pedicle (which is wider than the pars interarticularis) at the L5 vertebra is less than 20mm in most adults and the sagittal width less than 15mm15. Additionally, the pedicle width for 15–17, and 12–14-year-olds is approximately 20% and 45% smaller respectively compared to adults15. This partly explains why adolescent athletes are most vulnerable to LBSI. In addition, there is a lag between peak bone mass (bone mineral content and bone mineral density) that occurs in the mid-twenties in the lumbar spine16, compared to the increase forces that can be generated post-puberty due to increases in muscular strength17 and the longer leavers (and greater forces)18.
BONE STRESS CONTINUUM
Like other BSI, the injury can be graded according to how it is presented, clinically and radiologically, along a continuum. At one end of the continuum is a subclinical but abnormal level of Bone Marrow Oedema (BMO), typically detected through targeted screening for LBSI19 or observed incidentally. This stage can be referred to as pre-symptomatic bone stress2 and should be considered carefully once presented as a blinded prospective study involving 65 adolescent cricket fast bowlers showed that when the BMO intensity exceeded normative values (compared to other spinal levels), the risk of developing into symptomatic LBSI (stress reaction or stress fracture) was very high19. In addition, the study showed every participant who developed a symptomatic LBSI also had a high BMO score in the month before the symptoms developed, with the group mean of 99 days between first presentation of abnormally high BMO and development of symptoms. This highlights the intersection between physiological bone stress and clinical BSI. Progressions along the bone stress continuum based clinical and radiological markers are outlined in Table 1. The findings for chronic or non-united defects at the pars region is also included, to help clinicians with the differential diagnosis (Table 1).
COMPLEX BSI
The unique bone geometry and mechanics that lead to LBSI, are also likely to be related to the high recurrence and non-union rates, and the long RTS times that makes LBSI one of the more complex BSI to manage. Hoenig et al.20 described BSI as either high or low risk, based on the risk of complications (delayed union, non-union, refracture, completed fracture, avascular necrosis, and failure to RTS) and the time taken to RTS. In their meta-analysis of lower limb and pelvic BSI, they reported that the fifth metatarsal, femoral neck, anterior tibial shaft, and tarsal navicular were all anatomical sites that represented high risk BSI based on those criteria (see Table 2). The meta-analysis only considered lower limb and pelvic BSI because they make up over 80% of all BSI in athletes. This paper is somewhat symbolic of the relative lack of attention that LBSI attract in the clinical sports medicine environments, probably because they are undiagnosed or misdiagnosed, and there is a wrongly held assumption that athletes can function unrestricted with non-united LBSI so that non-union is an inevitable (and often acceptable) outcome of LBSI. Table 3 highlights that LBSI has characteristics that could classify them as high-risk based on the criteria used by Hoenig et al.20. Saw et al.21 (Table 3) reported RTS times for LBSI are typically longer than the high-risk BSI reported by Hoenig et al, and with similar high complication rates, particularly with 33% recurrence rate and, with 18% of incomplete stress fractures and 47% of complete stress fractures that result in non-union21. Others have reported similarly high non-union rates, with Watura et al.22 reporting 43% of LBSI in elite athletes achieving partial healing and 19% achieving complete healing.
The high non-union rates result in an unknown outcome when it comes to return to pre-injury activity, RTS and ongoing complications. A study of elite cricket players reported that 100% on non-united defects resulted in ongoing related medical issues including 79% of athletes with ongoing symptoms and 25% of unilateral non-united defects resulting in a LBSI injury on the contralateral side at the same level21.
Added to this, the greater than 200 days (median) time required to achieve bone healing1 makes LBSI worthy of high-risk status and making early diagnosis imperative as it is associated with improved rates of bone healing and faster RTS times (Table 3).
CLINICAL FEATURES
The clinical presentation of LBSI is similar to other causes of low back pain and is one of challenges to early detection. The features include a gradual onset of localised pain and/or stiffness that is typically first noticed post-physical activity (repetitive impact loading activities) but worsens over time to limit physical activity and start to impact on daily activities. Without a high degree of clinician intuition, the diagnosis is only often confirmed once symptoms (and therefore pathology) progress enough to be significantly limiting physical activity. Some of the key clinical features, when ongoing and in combination, which should flag clinicians to the possibility of LBSI are included in Table 4.
If the individual presenting at the initial assessment has some of the clinical features outlined in Table 4 the diagnosis of LBSI must be high on the index of suspicion, and imaging is warranted to confirm the diagnosis.
IMAGING
Whilst the role of imaging in non-specific LBP has been disputed23,24, imaging is reliable and essential in establishing the diagnosis of LBSI2. In addition, targeted imaging can be used as a screening tool for athletes involved in higher risk sports19,25, to determine the estimated healing and RTS times1,21,22,26, and the progress of bone healing during recovery period1,22,27.
There are numerous imaging modalities that have been traditionally used to diagnose and manage LBSI (Table 5). The imaging modality must be capable of detecting active bone stress, including the intensity and extent (spread) , establish the presence of a fracture / bone lesion2,19,25,28, measure size (length/width) of any fracture / lesion1 and provide clarity of fracture / lesion margins to determine the chronicity of any fracture, therefore establish if bone healing is likely. Table 5 highlights the diagnostic capabilities of each imaging modality and highlights why MRI is most utilised, especially as it does not involve ionising radiation2. It can reliably establish the presence of BMO (bone stress), and quantify the intensity and extent BMO using fat suppressed imaging sequences19,22,25 and accurately visualise the presence and extent of any fracture / lesion using fast 3D T1-weighted gradient-echo sequence that provide the spatial resolution and the image contrast provide near-Computed Tomography (CT) bone anatomy quality in three dimensions1,26. Limited (targeted to the spina level being assessed) CT can be used when MRI is equivocal regarding the presence or absence of a fracture, or if additional fracture clarity is required27.
MRI should therefore be the first choice of imaging in the diagnosis and management of LBSI, with three key roles outlined in Table 6.
MANAGEMENT
Once the diagnosis is established, the management of LBSI must commence immediately and involve some level of activity modification with the aim of stopping the progression of the injury along the bone stress continuum. Pre-symptomatic bone stress, to stress reaction, to stress fracture. And when there is a fracture present, ensuring that an incomplete fracture does not progress to a complete fracture, and that complete fractures to result in non-union and/or a bilateral injury.
The rehabilitation plan should be individualised to ensure there is a balance between allowing bone protection to optimise healing whilst preventing deconditioning and facilitating reconditioning when safe to do so. The rehabilitation process can be considered in three overlapping phases.
The rehabilitation phases and estimated timelines post-injury are described below and a summary of the aims, likely MRI findings (if used) and expected clinical findings for each phase outlined in Table 7.
Phase I: Fracture Protection Rehabilitation Phase [stress reaction 6-8 weeks: incomplete fracture 8-10 weeks: complete fracture 10-12 weeks]
Once the diagnosis of LBSI has been established, there must be an immediate cessation of activities that:
- May have contributed to the bone overload – typically the repetitive and/or high impact activities that load the posterior elements of the spine (jumping, landing, extending, and twisting), and
- Any other activity that is likely to disrupt the early bone healing – typically involving end range lumbar spine extension / side flexion / rotation, axial loading (e.g. loaded squatting), and/or repeated low-moderate impact activities (jogging, running).
The aim of the initial period is to ensure that the delicate early stage of bone healing is not disrupted so the initial bone scaffold can be laid down. It is important to remember that the impacted area of bone is very small, with the majority of fractures less than 8mm1, so it may not take many loading cycles, or very high load, to disrupt the early healing of bone. This reduction in activity should result in a quick resolution of symptoms during daily activities (2-4 weeks) and provide reassurance that the bone healing is not being interrupted. Any localised pain or latent stiffness should be used as a guide during this early period to determine whether activity is resulting in excessive load and likely to impact the healing bone.
The length of this period will vary depending on grade of the injury, as a guide, stress reaction (6-8 weeks) and stress fractures; incomplete (8-10 weeks) versus complete fracture (10-12 weeks). Acute bilateral injuries may require even longer periods as they have a higher risk of complications21. To help guide the decision making, a repeat MRI can be performed if feasible, at the latter part of this stage to determine if there has been a quantifiable change in BMO intensity and extent, or changes to any fracture present1,26,32. Reduction in BMO intensity and/or extent, and stability in the size fracture should be considered as positive signs that the rehabilitation in the preceding period was appropriate. For unilateral stress fractures (particularly complete fractures), reviewing the BMO of the contralateral side at the same level is also important to determine if the integrity of the posterior vertebral arch is being maintained and therefore the risk of bilateral injury. Table 7 provides a guide on what could be expected clinically, radiologically, and functionally at each rehabilitation stage, as well as the aim of each stage.
The use of adjunct therapies such as lumbo-sacral bracing or low pulse ultrasound should be considered on a case-by-case basis, given there is no empirical evidence to support their efficacy for LBSI. It is worth considering semi-rigid lumbar-sacral bracing in the initial 2-4 weeks in individuals who have ongoing symptoms with daily activities, are required to perform daily activities (e.g. work) that involve provocative lumbar movements / positions (e.g. lumbar extension) or have bilateral LBSI that may require the additional reinforcement of movement restriction. The aim of the bracing is to restrict or provide feedback with end-range lumbar positions that may disrupt bone healing. More rigid thoracolumbar bracing has been shown to result in improve bone healing outcomes in some studies but is required to be worn for long periods, up to 23 hours per day and for as long to 5 months, to be effective13,32-35. It is likely that any benefit of this protocol for bone healing may be offset by the deconditioning that is likely to result, even if there is patient compliance to it. In addition, the high rates of bone healing demonstrated in recent studies with activity modification and a graduated return to load suggests that rigid bracing may be an overreach in all but extreme cases1,21,26. Low pulse ultrasound can also be considered in those with complete or incomplete stress fractures, as it provides a relatively low cost and safe treatment; and with some studies showing improved healing rates or stress fractures36,37.
Low impact (bodyweight or low axial load) rehabilitation activities that do not load into extension, side flexion, and rotation, such pelvic or trunk control exercises, can commence once the individual is symptom free with daily activities. The aim of these activities is to maintain muscle tone and function and start to build a base for more advanced rehabilitation. Additionally, the use of non-weightbearing (e.g. freestyle swimming) and/or flexion-based conditioning (e.g. stationary bike) can also be incorporated at this stage to reduce the impact of detraining.
Phase II: Protected Reloading Phase [stress reaction 9-12 weeks: incomplete fracture 10-16 weeks: complete fracture 13-20 weeks]
In the next stage of the management (Table 7), the gradual introduction of spinal loading activities can commence (as long as the individual remains symptom free and MRI imaging remains satisfactory if this is utilised). The main aim of this stage is to commence the rebuild of strength and conditioning capacity, improve functional deficits (lumbo-pelvic control) and provide some loading stimulus to the healing bone to encourage further bone healing (mechano-transduction)38. The main activities to be avoided during this stage are those that involve axial loading activities (e.g. barbell squats) or moderate/high impact activities (e.g. jumping / landing). Building up walking endurance, and transition to walk-jog activities during this stage can be included, with the eventual transition to low volume jogging/running. It is important to note that there should be no localised pain or stiffness during or after these activities as there is no physiological reason for this, other than disruption of bone healing.
Where feasible, an MRI can be performed at the completion of this stage (Table 7) to provide reassurance that that the rehabilitation and daily activities of the preceding period have not adversely impacted the bone healing process and that a graded increase in loading can be planned for the next stage of rehabilitation.
Phase III: Transition to Pre-Injury & RTS
a. Advanced Load [stress reaction 13-16 weeks: incomplete fracture 17-24 weeks: complete fracture 21-29 weeks]
During the penultimate rehabilitation stage, the focus needs to be on returning to activities that are associated with higher impact loads. It is expected that the individual remains asymptomatic with all activities and with clinical testing during this stage. Building on the physical conditioning from the previous stage to near pre-injury capacity should be the aim, as well as the commencing low intensity, and low volume sports specific activities. It is important that the reload to sport specific or higher risk activities should be planned and gradual so that intensity and volume are not simultaneously increased, and that recovery periods/days are factored into to each daily, weekly and monthly planning cycles as this has been shown to be the most important risk factor in protecting against bone stress39.
It is highly recommended that MRI is utilised at the end of this stage, to ensure that there is the expected advanced bone healing that is required to cope with the load associated with the transition sports specific training and competition.
b. Return to Sport [stress reaction 17+ weeks: incomplete fracture 25+ weeks: complete fracture 30+ weeks]
It is anticipated that by this stage there is complete bone healing (Table 7). The aims of this stage are to build load and capacity for the person can return to unrestricted training and return to competition. Monitoring of load (intensity and volume) continues to be important, and particularly the inclusion of recovery periods (during each session, day, week and monthly loading cycle) to minimise fatigue and continue to provide a graduated stimulus to the healed area of bone to prevent recurrence as there is no consensus when the new bone will be fully matured to provide optimal bone strength relative to radiological healing40.
The graduated return to pre-injury activity should restore fitness and function to prevent other injuries (e.g. soft tissue injuries) and minimise fatigue. Periodic re-imaging (e.g. every 6-8 weeks for the 6-12 months after the RTS can provide reassurance that bone healing has been maintained. Reimaging after RTS should be jointly decided by clinicians, the athlete, and coaching staff to allow for activity modification if needed.
Alex Kountouris PhD
Sports Physiotherapist
La Trobe University
Melbourne, Australia
Contact: alexkountouris@gmail.com
References
1. Singh SP, Rotstein AH, Saw AE, Saw R, Kountouris A, James T. Radiological healing of lumbar spine stress fractures in elite cricket fast bowlers. J Sci Med Sport. 2021;24(2):112-5.
2. Kountouris A, Saw R, Saw A. Management of Lumbar Spondylolysis in Athletes: Role of Imaging. Current Radiology Reports. 2018;6.
3. Sakai T, Sairyo K, Suzue N, Kosaka H, Yasui N. Incidence and etiology of lumbar spondylolysis: review of the literature. J Orthop Sci. 2010;15(3):281-8.
4. Ciullo JV, Jackson DW. Pars interarticularis stress reaction, spondylolysis, and spondylolisthesis in gymnasts. Clin Sports Med. 1985;4(1):95-110.
5. Kruse D, Lemmen B. Spine injuries in the sport of gymnastics. Curr Sports Med Rep. 2009;8(1):20-8.
6. Ruiz-Cotorro A, Balius-Matas R, Estruch-Massana AE, Vilaro Angulo J. Spondylolysis in young tennis players. Br J Sports Med. 2006;40(5):441-6; discussion 6.
7. Ruddick GK, Lovell GA, Drew MK, Fallon KE. Epidemiology of bone stress injuries in Australian high performance athletes: A retrospective cohort study. J Sci Med Sport. 2019;22(10):1114-8.
8. Schmitt H, Brocai DR, Carstens C. Long-term review of the lumbar spine in javelin throwers. J Bone Joint Surg Br. 2001;83(3):324-7.
9. Gregory PL, Batt ME, Kerslake RW. Comparing spondylolysis in cricketers and soccer players. Br J Sports Med. 2004;38(6):737-42.
10. Kelly S, Waring A, Stone B, Pollock N. Epidemiology of bone injuries in elite athletics: A prospective 9-year cohort study. Phys Ther Sport. 2024;66:67-75.
11. Frost HM. Wolff's Law and bone's structural adaptations to mechanical usage: an overview for clinicians. Angle Orthod. 1994;64(3):175-88.
12. Frost HM. On our age-related bone loss: insights from a new paradigm. J Bone Miner Res. 1997;12(10):1539-46.
13. Sys J, Michielsen J, Bracke P, Martens M, Verstreken J. Nonoperative treatment of active spondylolysis in elite athletes with normal X-ray findings: literature review and results of conservative treatment. Eur Spine J. 2001;10(6):498-504.
14. Crossley K, Bennell KL, Wrigley T, Oakes BW. Ground reaction forces, bone characteristics, and tibial stress fracture in male runners. Med Sci Sports Exerc. 1999;31(8):1088-93.
15. Zindrick MR, Knight GW, Sartori MJ, Carnevale TJ, Patwardhan AG, Lorenz MA. Pedicle morphology of the immature thoracolumbar spine. Spine (Phila Pa 1976). 2000;25(21):2726-35.
16. Walsh JS, Henry YM, Fatayerji D, Eastell R. Lumbar spine peak bone mass and bone turnover in men and women: a longitudinal study. Osteoporos Int. 2009;20(3):355-62.
17. Gillen ZM, Housh TJ, Schmidt RJ, Herda TJ, De Ayala RJ, Shoemaker ME, et al. Comparisons of muscle strength, size, and voluntary activation in pre- and post-pubescent males and females. Eur J Appl Physiol. 2021;121(9):2487-97.
18. Mirwald RL, Baxter-Jones AD, Bailey DA, Beunen GP. An assessment of maturity from anthropometric measurements. Med Sci Sports Exerc. 2002;34(4):689-94.
19. Kountouris A, Sims K, Beakley D, Saw AE, Orchard J, Rotstein A, et al. MRI bone marrow oedema precedes lumbar bone stress injury diagnosis in junior elite cricket fast bowlers. Br J Sports Med. 2019;53(19):1236-9.
20. Hoenig T, Eissele J, Strahl A, Popp KL, Sturznickel J, Ackerman KE, et al. Return to sport following low-risk and high-risk bone stress injuries: a systematic review and meta-analysis. Br J Sports Med. 2023;57(7):427-32.
21. Saw A, Eales B, Jones N, Obst A, Smith M, Kountouris A, et al. Lumbar Bone Stress Injuries and Nonunited Defects in Elite Australian Cricket Players. Clin J Sport Med. 2024;34(1):44-51.
22. Watura C, Mitchell AWM, Fahy D, Houghton J, Kang S, Lee JC. T1-VIBE and STIR MRI of lumbar pars interarticularis injuries in elite athletes: fracture characterisation and potential prognostic indicators. Skeletal Radiol. 2024;53(3):489-97.
23. Darlow B, Forster BB, O'Sullivan K, O'Sullivan P. It is time to stop causing harm with inappropriate imaging for low back pain. Br J Sports Med. 2017;51(5):414-5.
24. Hall AM, Aubrey-Bassler K, Thorne B, Maher CG. Do not routinely offer imaging for uncomplicated low back pain. BMJ. 2021;372:n291.
25. Sims K, Kountouris A, Stegeman JR, Rotstein AH, Beakley D, Saw AE, et al. MRI Bone Marrow Edema Signal Intensity: A Reliable and Valid Measure of Lumbar Bone Stress Injury in Elite Junior Fast Bowlers. Spine (Phila Pa 1976). 2020;45(18):E1166-E71.
26. Saw R, Saw A, Kountouris A, Orchard J. Upper Lumbar Bone Stress Injuries in Elite Cricketers. Clin J Sport Med. 2022;32(2):e121-e5.
27. Ang EC, Robertson AF, Malara FA, O'Shea T, Roebert JK, Schneider ME, et al. Diagnostic accuracy of 3-T magnetic resonance imaging with 3D T1 VIBE versus computer tomography in pars stress fracture of the lumbar spine. Skeletal Radiol. 2016;45(11):1533-40.
28. Taylor J, Saw AE, Saw R, Sims K, Kountouris A. Presence of bone marrow oedema in asymptomatic elite fast bowlers: Implications for management. Bone. 2021;143:115626.
29. Congeni J, McCulloch J, Swanson K. Lumbar spondylolysis. A study of natural progression in athletes. Am J Sports Med. 1997;25(2):248-53.
30. Anderson K, Sarwark JF, Conway JJ, Logue ES, Schafer MF. Quantitative assessment with SPECT imaging of stress injuries of the pars interarticularis and response to bracing. J Pediatr Orthop. 2000;20(1):28-33.
31. Zukotynski K, Curtis C, Grant FD, Micheli L, Treves ST. The value of SPECT in the detection of stress injury to the pars interarticularis in patients with low back pain. J Orthop Surg Res. 2010;5:13.
32. Sakai T, Sairyo K, Mima S, Yasui N. Significance of magnetic resonance imaging signal change in the pedicle in the management of pediatric lumbar spondylolysis. Spine (Phila Pa 1976). 2010;35(14):E641-5.
33. d'Hemecourt PA, Zurakowski D, Kriemler S, Micheli LJ. Spondylolysis: returning the athlete to sports participation with brace treatment. Orthopedics. 2002;25(6):653-7.
34. Micheli LJ, Hall JE, Miller ME. Use of modified Boston brace for back injuries in athletes. Am J Sports Med. 1980;8(5):351-6.
35. Steiner ME, Micheli LJ. Treatment of symptomatic spondylolysis and spondylolisthesis with the modified Boston brace. Spine (Phila Pa 1976). 1985;10(10):937-43.
36. McBride WR, Eltman NR, Swanson RL, 2nd. Blood-Based Biomarkers in Traumatic Brain Injury: A Narrative Review With Implications for the Legal System. Cureus. 2023;15(6):e40417.
37. Arima H, Suzuki Y, Togawa D, Mihara Y, Murata H, Matsuyama Y. Low-intensity pulsed ultrasound is effective for progressive-stage lumbar spondylolysis with MRI high-signal change. Eur Spine J. 2017;26(12):3122-8.
38. Khan KM, Scott A. Mechanotherapy: how physical therapists' prescription of exercise promotes tissue repair. Br J Sports Med. 2009;43(4):247-52.
39. Sims K, Saw R, Saw A, Kountouris A, Orchard J. Multiple risk factors associated with lumbar bone stress injury in youth cricket fast bowlers. The Journal of Sport and Exercise Science. 2001;5(2):92-100.
40. Fisher JS, Kazam JJ, Fufa D, Bartolotta RJ. Radiologic evaluation of fracture healing. Skeletal Radiol. 2019;48(3):349-61.
Header Image by Huard (Cropped)