Spinal pain CPD: osteoporosis fill-in, when MRI beats X-ray, and a component approach to degeneration

Dr Gus Ovalton — osteoporosis & bone health (fill-in)

Irish endocrinologist / general medicine. Narelle introduces him clearly as Gus Ovalton (Otter also hears “Obolt,” “Obolcian”). Do not invent an alternate surname. He stepped in after Dr Yang apologised — emergency spine surgery overnight.

Dr Wayne Ng — choosing spine investigations

Neurosurgeon. Host notes he has taken over many of Dr Leon Tan’s patients and practice. Speaks on imaging choice, CT-guided diagnostic blocks, and case-based pitfalls.

Dr Charles Chow — chronic spinal pain / component approach

Pain and rehabilitation specialist. Kirkaldy-Willis cascade, disc / facet / Modic / stenosis / listhesis / Baastrup / SI joint / DISH, then rehab and hydrotherapy.

Host

Narelle. Self-record CPD event (no activity number — write “self-record”).

Setup — Dr Yang’s apology and Gus fills in

Narelle opens: this is a self-record event — no approved activity number; write “self-record” on your form and complete the evaluations. Dr Yang (neurosurgery) sends apologies — he is in emergency spine surgery that came through overnight (about six hours). In his place, a new endocrinologist / general medicine doctor — Irish — Dr Gus Ovalton — fills in with osteoporosis and bone health, which Narelle notes is still relevant to the day’s orthopaedic / spinal theme (she had also circulated his fact sheet).

Part 1 — Osteoporosis & bone health (Dr Gus Ovalton)

Learning aims he races through in ~20 minutes: identify high fracture-risk patients; relative efficacy of therapies; PBS framing for anabolics; prevent denosumab (Prolia) withdrawal fractures; counsel on osteonecrosis of the jaw (ONJ) and atypical femoral fractures; and a few clinic tricks.

Why fracture risk beats BMD alone

• Rough Australian burden he quotes: ~66% of people over 50 have osteoporosis or related disease context; ~200,000 fragility fractures/year; lifetime osteoporotic fracture risk ~50% women / ~30% men.
• Fracture risk matters more than bone mineral density alone — BMD explains only ~50–70% of risk.
• FRAX (2008): age, sex, prior fracture, steroids, smoking, alcohol, BMD → 10-year fracture probability. Limits: not dose-dependent for steroids; misses frequent fallers / Parkinson’s with “good” BMD; underestimates type 2 diabetes and multiple prior fractures.
• Garvan fracture risk calculator can help when falls dominate the picture.

LiftMore / Onero — heavy resistance

The LiftMore trial (~2018, Griffith University; Belinda Beck / Linda Beck as heard) put postmenopausal women through powerlifting (deadlifts, back squats, overhead press, bench press) at ~80–85% of one-rep max, five sets of five. ~2.9–3% spine BMD gain at six months — comparable to weak pharmacotherapy at the spine (bisphosphonates ~5–8%; raloxifene ~2–3%). Onero / supervised bone-loading programs (licensed; Brisbane “bone living” network referenced) are the practical referral path when you will not personally coach an 80-year-old into back squats.

Bisphosphonates — oral and zoledronate

• Oral cornerstones: alendronate and risedronate (Actonel) — decades of use.
• Zoledronate (zoledronic acid): 5 mg IV roughly every 18 months × three doses for many patients, then reassess / drug holiday. Much more convenient than weekly oral therapy.
• Infusion (flu-like) reaction ~30%. Professor Ian Reid (NZ) dexamethasone day 1–2–3 protocol — Gus says Reid reports essentially no reactions when used.
• Ian Reid NEJM osteopenia trial: women >65 with osteopenia, zoledronate 5 mg q18 months ×3 → ~37% fracture risk reduction; NNT ~15. Majority of fractures occur in osteopenic (not osteoporotic) patients simply because there are more of them.
• Residual effect allows genuine drug holidays with bisphosphonates — unlike denosumab.

Denosumab / Prolia — cannot stop cold

Marketed from ~2013: six-monthly injection, very effective. From ~2016, case reports of rebound vertebral fractures after stopping or missing a dose — patients can lose all (or more) of their gains. First year after a missed dose is the danger window. You need an exit strategy before starting, especially in younger patients who may face decades on therapy. Approaches discussed: run teriparatide alongside then switch to zoledronate at the next due dose; if <~6 Prolia doses, zoledronate alone may suffice; after more doses you may still lose some gains. Bisphosphonates contraindicated in significant CKD may force denosumab — deal with exit when you must.

Anabolics — sequence matters

• Romosozumab: best BMD gains in his comparisons (~11–12% lumbar spine, ~4% hip/femoral neck in ARCH/FRAME-era framing; meta-analysis blue bars “far superior”). Monthly for a year, then must consolidate with antiresorptive (zoledronate or alendronate). PBS: specialist-initiated; high fracture risk / T-score criteria (treatment-naive first-line romo can use T < −2.5 with recent hip or symptomatic vertebral fracture in 24 months; rescue after antiresorptive failure also discussed). Private Amgen co-pay: roughly every third month covered → ~$400 patient / month framing (~$3200–4000/year investment for one year).
• Teriparatide: intermittent PTH analogue; PBS 18 months then often +6 months private (~$170/month as quoted); daily injections; also needs lock-in.
• Abaloparatide: PTHrP analogue — superior to teriparatide in overseas data; coming to Australia, not yet available at the talk.
• Sequence: anabolic then antiresorptive gets far better BMD response than anabolic after years of antiresorptive (example numbers he showed: ~6.2% vs ~2.9% when order flipped). Prefer anabolic first in treatment-naive high-risk patients when you can.
• Clinic tip: lateral thoracolumbar X-ray can uncover old symptomatic vertebral fractures that unlock PBS criteria; ask for distal radius on DEXA to improve chance of capturing a worse T-score (three sites).

Tibolone plug

Brief MHT aside: tibolone as effective for bone as estrogen in his framing, one tablet, estrogenic + androgenic (libido) “triple whammy.” Lower breast-cancer signal discussed with caveats (prior breast cancer — recurrence concern). Audience note: not on PBS; patches often preferred currently. Start peri-/early post-menopause to mitigate the precipitous BMD drop — it is not anabolic if you wait years.

Part 2 — Choosing spine investigations (Dr Wayne Ng)

Impetus: step back from “operate or not” to the investigations that lead there. Structural options: X-ray, CT, MRI. Functional: SPECT-CT. Mimics: ultrasound. Diagnostic lock-in: CT- or US-guided blocks. Adjunct: nerve conduction studies (limitations for pain fibres).

Ng cases — false reassurance, soft vs hard disc, double crush

1. 34-year-old, L3/4 radicular pattern. X-ray reassuring → CT hints at L3/4 → MRI shows large disc and tight canal. Classic false reassurance from plain films.
2. 46-year-old, C6 radiculopathy 12 months. MRI disc bulge alone might suggest spontaneous resolution; CT shows osteophyte — chronic hard disc/osteophyte unlikely to vanish. After C5/6 ACDF she develops new shoulder pain within six months: adjacent soft disc at C4/5 (inflammatory, more painful, more chance of self-resolution — worth waiting if the patient can, to avoid a second fusion).
3. 45-year-old, whiplash, huge asymptomatic cord-compressing disc that settles — then six months later myelopathy from the adjacent level blowing out → two-level disc replacement. Motion X-rays still useful to show preserved motion / instability.
4. Post-hemilaminectomy spondylolisthesis in RA (rare <1% instability after hemilaminectomy): mechanical back pain years later; progressive slip; patent canal on MRI → needs fusion/stabilisation, not further decompression. SPECT facets light up as they try to stabilise.
5. Type 1 diabetic double-crush: prior C6/7 foraminotomy for C7 radiculopathy; later medial forearm pain with good nerve-root block; then recurrent C7 pattern with triceps wasting — NCS/EMG plus brachial plexitis (plexus MRI abnormal) plus recurrent foraminal compression. Diabetes likely drives the neuritis. Surgical options limited; guarded prognosis; counsel honestly.

Closing imaging point: tumour cases sometimes need both CT and MRI — subtle foraminal widening on CT only makes sense once MRI shows the lesion. “Sky is blue — which blue?” applies to radiology opinions too: correlate to the clinical question.

Epidurals vs focal blocks

Part 3 — Component approach to degeneration (Dr Charles Chow)

Chronic spinal pain framed via Kirkaldy-Willis degenerative cascade: dysfunction (disc water loss, annular fissures, endplate and cartilage wear) → instability / laxity → restabilisation — often at different stages at different levels. Tell patients degeneration is like white hair and wrinkles: common, not automatically the pain source. >50% of people over 50 scanned have some degeneration — imaging ≠ pain.

Disc

• “Black disc” on T2, vacuum phenomenon (nitrogen with motion/traction) — often flexion-sensitive somatic referred pain to buttock; not always.
• Herniation spectrum: bulge → protrusion → extrusion → sequestration. Chemical radiculitis / extrusion often helped by nerve root injection; if extrusion settles but root stays sensitised → consider pulsed radiofrequency to the root. Most herniations, especially in younger patients, resolve.

Facets

• Common with age; can crowd lateral recess. Textbook: worse in extension / quadrant testing (vs disc in flexion) — not highly specific.
• Diagnostic path: medial branch block + pain diary (formal dual LA protocol rarely done in practice).
• Key teaching: the most arthritic-looking joint is often not the most painful — adjacent or contralateral joints may be the generators (even without SPECT).

Modic type 1

Endplate edema/inflammation: low T1 / high T2. Type 1 is the best-recognised pain phenotype (types 2 and 3 can hurt too). Overseas: basivertebral nerve ablation for axial pain not clearly discogenic or facetogenic. Australia: makeshift kits historically; formal kits going through TGA at the time of the talk.

Stenosis & the tripod

Multifactorial: ligamentum flavum, facet osteophytes, disc. Claudication → prefer neurosurgical assessment first if progressive, to judge urgency. Therapeutic (not diagnostic) epidurals for surgery-averse patients — results variable; be honest. Tripod metaphor: when the spine “drops,” central canal, lateral recess (traversing root), and foramen (exiting root) all crowd.

Spondylolisthesis, Baastrup, SI joint, DISH

• Mild listhesis: strengthen, treat associated facet/disc pain. Moderate–severe with giving-way: refer neurosurgery. Flexion–extension X-rays helpful; dynamic MRI appearing in some pathways.
• Baastrup (kissing spines / interspinous bursitis): guided steroid often helps.
• SI joint: provocative exam; somatic referral can go past the knee even to the ankle — do not assume “below knee = radicular only.”
• DISH (diffuse idiopathic skeletal hyperostosis): anterior bridging ± PLL; caution aggressive chiropractic / osteopathy — cervical myelopathy risk; therapists should see the films; consider neurosurgical review.
• Degenerative scoliosis in older patients: often intermittent RF denervation + diligent rehab / hydrotherapy rather than big reconstructive surgery.

Take-home messages for clinic

• Bone: treat fracture risk, not T-score alone; vit D >75, calcium ~1000 mg, lift heavy via supervised programs; zoledronate 5 mg q18 months ×3 is a powerful, holiday-friendly option (incl. osteopenia data, NNT~15); never start denosumab without an exit plan; anabolic then antiresorptive when you can; ask for distal radius on DEXA and lateral TL X-ray when hunting PBS criteria.
• Imaging: clinical question first; MRI for soft tissue; CT for bone; X-ray for dynamics/alignment (and false reassurance risk); SPECT hot ≠ pain; counsel the 24-hour LA window after diagnostic blocks.
• Injections: prefer focal over epidural; ~3–4/year then refer.
• Degeneration: component approach; imaging ≠ pain; neurosurg first for progressive claudication / giving-way listhesis; caution aggressive manipulation in DISH; rehab is the long game.

spinal-pain.drkotha.com · cerulean theme · CPD education for Australian general practice