Working in cricket the past 2 years, I have seen many athletes who experience pain after bowling. Tim is a very typical case, with multiple areas to address. Meet Tim...
30 year old male, amateur spin bowler
- Sitting 2 hours onset of Pb3/10, walking/stretching into Lx extension for 3 mins eases pain to zero
- Driving 60 mins Pb3/10, Ph1/10, eases with lumbar extension stretching for 3 mins
- Deadlifts 50kg max, Pb5/10 >55kg, nil Ph, awareness for 2 days
- Bowling - 1 hour post-bowling brings on Pb4/10, Ph 1/10 awareness, eases with 24 hours of rest/”cobra” (lumbar extension) stretching
Tim avoids impact or weighted bending (lifting weights, lifting boxes) to prevent flare-ups
24 Hour Behaviour
AM – stiff Pb2/10, 30 mins to ease PM – when Pb >3/10, wakes in night when changing position
- Pb increased one month ago, previously Pb 2/10 max, now 5/10 max, coincided with increase in cricket load
- Tues/Thurs 15-20 overs (90-120 balls), Sat 10-20 overs (60-120 balls), total ~50 overs/week (300 balls/week)
- 7 weeks ago – 3 hour flight, Pb3/10 by end of flight, next day Pb6/10 on bending/sitting, eased after 5 days with rest & avoiding aggs
- 4 yrs ago post-cricket onset of Pb, sharp 8/10, had started working in pub at same time, lifting 65kg kegs of beer 5-10x a day, saw physio, diagnosed “bulging disc”, resolved with lumbar extension, stretching & off-season of cricket so not aggravating back
- Works in sales, sit/stand/walking during day, minimal gym/strength work, often driving between clients,
Following subjective questioning, I already have a list of possible diagnoses in my head. Based on the patient's aggravating and easing factors, location of pain, age, occupation and previous injury history, this was the prioritised list of diagnoses I had to confirm or refute, during my physical examination.
My goals for the initial physical examination were:
- Determine source of Pb, confirm primary hypothesis of discal pathology with neural irritation, isolate lumbar pain to specific level/s.
- Determine contribution of neurodynamic dysfunction to Ph.
- Determine contribution of secondary hypotheses to primary presentation (e.g. QL muscle spasm, facet joint stiffness) or clear secondary hypotheses.
- Determine contribution of bowling technique and biomechanical factors (gluteal, calf strength, lumbosacral control) to pain.
If I achieved all of these goals in my day 1 assessment, I would have a solid understanding of the patient's presentation and a clear plan for the following few sessions.
- PA R L5/S1 hypo Pb4/10, Ph1/10
- Central PA L5 hypo + Pb3/10, nil Ph
- R SLR 80° Ph1/10, with ankle DF Ph2/10, slight Pb awareness
- Muscle spasm R QL (reproduce Pb1/10), gluteus medius
- Lx flexion = fingers to ankles, Pb1/10 EROM (end-range)
- Flexion/L sideflexion/rotation (opening Quadrant) = symmetrical range, Pb3/10, Ph awareness
- Lx/hip Quadrant clear
- Glut med endurance (sidelying hip abduction) L 12 repetitions fatigue, RPE 6/10, R 15 reps, RPE 3/10
- Glut max strength L 160mmHg, RPE 8/10, 190mmHg, RPE 7/10
- SLCR L = supinates midfoot, left trunk lean, ¾ plantarflexion range, when corrected L fatigues 5 reps, R 8 reps
- SLSquat BL = Moderate dynamic knee valgus, Trendelenberg with anterior pelvic tilt, trunk lean forward (Crossley et al., 2011)
- Reduced muscle tone/bulk bilateral lower glute max, medial gastrocnemius
- Hop – bilateral excessive arm/trunk/hip strategy to initiate movement, dynamic knee valgus & Trendelenberg on land, reduced hop height
Sporting / Functional Limitations
- No cricket limitation
- Deadlifts 50kg max, Pb5/10 >55kg
- Sitting >2hours, Pb3/10
Contributing / Predisposing Factors
- Currently 240 – 360 balls/week, Tuesday/Thursday/Saturday
- Bowling >188 balls/week correlated with increased injury risk (Dennis, Farhart, Goumas, Orchard, & Farhart, 2003)
- <2 days rest between sessions gives 2.4x injury risk, with 1.4x with 2-3 days rest (Dennis et al., 2003)
- Bowling 200% of monthly average (chronic load) gives 3.3x greater risk of injury (Hulin et al., 2014)
- Patient bowling >188 balls/week, having <2 days rest between sessions, and had large acute load spike, giving high injury risk
Psychosocial Impairments, Attitudes, Beliefs
Displays poor pacing, avoidance behaviour with ADL’s, maladaptive coping (Fersum, O'Sullivan, Skouen, Smith, & Kvale, 2013)
1. R PA L5/S1 III 3x30sec
- Reproduced both Pb and Ph symptoms, no worsening of symptoms following PAIVM’s assessment
- Provocative segment consistent with body chart, AROM restrictions and functional deficits
- Movement diagram shows muscle spasm, pain is limiting factor not resistance, consistent with chemically sensitised disc and somatic referral to hamstring
- Technique addressing pain, rather than resistance, so mobilisation applied at mid-range (G3 not ++)
- Larger amplitude technique chosen to reduce risk of latency to sensitised structures
- Dosage conservative, care taken with sensitised disc/neural structures
// Lx flex = full, no pain // Opening Quadrant = full, no pain // QL – nil spasm, nil Pb // R SLR 90° stretch, nil Ph, with ankle DF Ph1/10, nil Pb
2. Modified Bridge
- Push through heel closest to hips, ensure hips level (addressing rotational deficit in single leg squat), encourage posterior pelvic tilt (biasing inferior glut max), neutral thoracolumbar junction
- Fatigued 15 reps L, 19 reps R, complete 3x sets to fatigue daily, targeting activation and endurance with high repetitions and repeated daily (no rest days between)
- Co-contraction of gluteus medius, biasing glute max but addressing activation/endurance deficits in both glute max and med (Selkowitz, Beneck, & Powers, 2013)
// Opening Quadrant = full, no pain // R SLR 90° stretch, nil Ph, with ankle DF nil Ph/Pb // Prone hip extension L RPE 5/10 (previously 8/10), R 4/10 (previously 7/10) // Sidelying hip abduction L RPE 3/10 (previously 6/10), R 2/10 (previously 3/10) // L SLSquat = mildly improved dynamic knee valgus, reduced trunk lean to left
3. Single Leg Calf Raise
- Weight on big toe to encourage neutral midfoot and medial gastrocnemius/evertor co-contraction
- Perform in front of mirror to increase external feedback on technique
- Fatigued 5 reps L, 8 reps R, 3 sets to fatigue completed in treatment, home exercise – complete 6x sets to fatigue daily, targeting activation and endurance with high repetitions and multiple sets (achieve neural adaptation) (Joyce, 2014)
- Improved foot biomechanics to allow improved “push-off” (Oatis, 2009; Silbernagel et al., 2001)
// Flexion/L sideflexion/rotation = full, no pain // SLCR L = 10 rep fatigue, R 13 rep fatigue // SLSq L R = improved trunk control, dynamic knee valgus ISQ // Hop L R = ~30% reduced arm/trunk/hip strategy, slightly increased hop height
The exercises from Day 1 would be progressed over the next 6 weeks, as described in the tables below.
Return To Sport Plan
The patient presents with three common bowling technical faults, planting his foot too front-on, poor pelvic drive and increased lumbar counter-rotation. Assessing and modifying technique errors, consistent with back pain (such as poor foot position and excessive counter-rotation), decreases incidence and progression of lumbar disc degeneration (Elliott & Khangure, 2002).
Poor bowling load management is a consistent factor in cricketer’s low back pain (Hulin et al., 2014; Orchard et al., 2015; Orchard, James, Portus, Kountouris, & Dennis, 2009). By effectively managing bowling load, while addressing strength, motor control and technique, Tim's pain should resolve.
Both Pb and Ph were resolved during the initial treatment session, indicating a mechanical loading dysfunction, rather than loss of structural integrity and tissue damage. There is gross lower limb kinetic chain weakness and poor control, with great potential for improvement. Addressing the causes of dysfunction, by providing greater lower limb strength/endurance and lumbopelvic control, should protect sensitised structures and prevent recurrence. Currently, there is poor bowling load management; monitoring and managing this more closely can greatly reduce risk of recurrence. (Dennis, Farhart, Clements, & Ledwidge, 2004; Hulin et al., 2014; Orchard et al., 2009)
Most acute lumbar incidents resolve within a month, however recurrence rates within 12 months are up to 78% (Van Dillen et al., 2016), with poor recovery. This is attributed to cognitive factors (Vlaeyen & Linton, 2012), physical factors (Peter O'Sullivan et al., 2006) and lifestyle conditions (Fersum et al., 2013). There is also poor diagnosis, with 90% of low back pain considered non-specific, due to absence of strong radiological findings (P. O'Sullivan, 2005). The patient shows signs of maladaptive coping strategies and poor pacing, global deconditioning, altered body schema, muscle guarding and altered movement patterns, increasing the likelihood of recurrence.
Tim has now returned to full bowling load, and is currently bowling pain-free at amateur level cricket, bowling ~250 balls/week. The combination of manual therapy, strength/rehabilitation and monitoring and controlling bowling load successfully achieved full return to pain-free sport. I believe previous treatment had only addressed one or two aspects, without addressing all pathology and contributing factors. Hopefully, this case study can be applied to any musculoskeletal condition, so the next time you treat a cyclist, carpenter, office worker or lecturer, you address their physical impairments, contributing factors and ensure a graded return to loading plan.
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